The Shapes of Epidemics and Global Disease [1 ed.] 9781527558960, 9781527556935

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The Shapes of Epidemics and Global Disease Edited by

Andrea Patterson and Ian Read

The Shapes of Epidemics and Global Disease Edited by

Andrea Patterson and Ian Read

The Shapes of Epidemics and Global Disease Edited by Andrea Patterson and Ian Read This book first published 2020 Cambridge Scholars Publishing Lady Stephenson Library, Newcastle upon Tyne, NE6 2PA, UK British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Copyright © 2020 by Andrea Patterson, Ian Read and contributors All rights for this book reserved. No part of this book may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior permission of the copyright owner. ISBN (10): 1-5275-5693-X ISBN (13): 978-1-5275-5693-5 Cover, SHAPES Logo images (left to right): S:

Blood Vessel, Blood, Vein, Cardiovascular System, Human Vein © iStock.com/Giang Nguyen.

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The Temptation of Saint Anthony (detail). Matthias Grünewald, ca. 1515. Web Gallery of Art. CC-PD 1.0. Epidemic ergot poisoning (St. Anthony’s fire) was a devastating medieval scourge caused by a rye fungus. The monastic order of St. Anthony began treating its victims in the 11th century, initiating one of the first “specialized” medical and surgical therapies.

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Anna’s Suicide Attempt, 1815 (detail). Jesse Torrey, A Portraiture of Domestic Slavery in the United States, 1817. RB 187796, The Huntington Library, San Marino, California.

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Structure of DNA. Виталий Смолыгин. PublicDomainPictures.net. CC-PD 1.0.

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Lübecker Totentanz (detail). Carl Julius Milde, 1852. Wikimedia Commons. CC-PD 1.0. This medieval allegorical concept (Dance of Death) provided a visual representation on the universality of death. Milde’s painting refers to a bubonic plaque episode in the German city of Lübeck during the 15th century.

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Covid-19 (detail). Gerd Altmann. PublicDomainPictures.net. CC-PD 1.0.

TABLE OF CONTENTS

List of Figures.......................................................................................... viii About the Authors ...................................................................................... x Acknowledgments ................................................................................... xiii Foreword ................................................................................................. xv Jonathan D. Katz Introduction ................................................................................................ 1 SHAPES of Epidemics: Socio-Historic, Artistic, Political, and Ecological Significance Andrea Patterson and Ian Read Part I: The Shape and Shaping of Epidemics in Webs of Meaning Chapter One .............................................................................................. 42 Suicide, Slavery, and Epidemics: A Perspective from Early Modern British America Terri L. Snyder Chapter Two ............................................................................................. 64 Suicide Epidemics, Post-colonial Governance, and the Image of the Recalcitrant Native in Oceania Edward Lowe Chapter Three ........................................................................................... 87 Leprosy Control in Imperial Japan Michael Weiner Chapter Four ........................................................................................... 110 Epidemics of Inequity: Challenging the Racial Predisposition Hypothesis Andrea Patterson

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Table of Contents

Chapter Five ........................................................................................... 132 Epidemics as Complex Systems: Sexual Meanings and HIV among Latino Gay and Bisexual Men Jorge Fontdevila Chapter Six ............................................................................................. 168 A Picture is Worth a 1000 Lived Experiences of Illness: Photovoice as an Emancipatory Approach to Public Health and HIV Research Michelle Teti and Amy Slaton Part II: The Shape and Shaping of Epidemics in Webs of Matter Chapter Seven......................................................................................... 196 Four Turning Points in the Treatment of HIV/AIDS John E. Lesch Chapter Eight .......................................................................................... 222 “Damage Control” and the HIV/AIDS Epidemic in Henan China Xiaoxing Liu Chapter Nine........................................................................................... 242 Non-communicable Disease Epidemic: Ideologies and Institutions of Modernity Joshua S. Yang Chapter Ten ............................................................................................ 263 Industry’s Role in the Metabolic Disease Pandemic Lisa Crummett Chapter Eleven ....................................................................................... 293 Evolution of Infection Resistance in Large Populations Parvin Shahrestani Chapter Twelve ...................................................................................... 307 Tragedy at the Tropic of Capricorn: Nineteenth Century Globalization and Epidemiological Change on Two Sides of South America Ian Read

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Part III: Co-emergence and Co-resolution of Epidemics Chapter Thirteen ..................................................................................... 328 What Places Ebola in the Realm of the “Global”? A View from History Monica H. Green Chapter Fourteen .................................................................................... 363 Immemorial: The Poetics of AIDS—A Conversation with Rudy Lemcke Tina Takemoto and Rudy Lemcke Epilogue.................................................................................................. 377 Index ....................................................................................................... 383

LIST OF FIGURES

Ideological and Physical Worlds of Epidemics ........................................ 10 Thomas Day, The Dying Negro, 1775 ...................................................... 43 Anna’s Suicide Attempt, A Portraiture of Domestic Slavery, 1817 ......... 45 Speculum Oris, 1786 ................................................................................ 57 Germs Know No Color Line, Atlanta Constitution, 1914 ...................... 118 Tianna’s Photo of a Flower .................................................................... 185 Anna’s Photo of the Community Garden ............................................... 186 Anna’s Photo of a Cleared Lot ............................................................... 187 Top Ten Global Causes of Death, 2016.................................................. 264 Top Ten Global Causes of Death, 2000.................................................. 264 Fructose Metabolism in the Liver ........................................................... 272 Infant Mortality in Chile and Argentina ................................................. 316 Pandemics and Epidemics, 1780 – 1910 ................................................ 320 Molecular Dating of the 2014 Ebola Outbreak ....................................... 335 The Killers: Deaths Per Day, Ebola Affected Countries, 2014 .............. 349 Immemorial—The Poetics of AIDS ................................................. center Where the Buffalo Roam, 2007 Are You Sleeping, 1987 Untitled Installation for Breathing, 1979 Iscador, 1989 Foscarnet, 1989

The Shapes of Epidemics and Global Disease

AIDS Timeline, 1990 Glinda, 1988 Untitled photograph of pedestrians outside Star Pharmacy, 1982 Cinders, 1996 Detail of Cinders, 1996 Immemorial, 1992 Immemorial, 1996 Immemorial, 2005 Shadow puppet for The Uninvited, 2003 The Uninvited, 2003 The Poetics of Finitude, 2014 New World, 2017

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ABOUT THE AUTHORS

Lisa Crummett is Associate Professor of Biology at Soka University of America. She is an evolutionary ecologist and has taught a variety of courses on the role of diet in the development of metabolic disease. Some of her current research focuses on the causes, risk factors, and prevention of type 2 diabetes associated with diet. Jorge Fontdevila is Professor of Sociology at California State University, Fullerton. He has conducted extensive socio-behavioral research among US populations disproportionately affected by HIV/AIDS. He has published widely in leading academic journals, including Social Theory & Health, Journal of Urban Health, AIDS and Behavior, Sexualities, and Archives of Sexual Behavior. Monica H. Green is a historian of medicine, specializing in the intellectual and social history of medicine in pre-modern Europe, and in the history of humankind's leading infectious diseases. Recent works have addressed plague, leprosy, tuberculosis, and smallpox. She is currently writing The Black Death: A Global History. Jonathan D. Katz is an art historian, curator and queer activist. Now Associate Professor of Practice in Art History and Gender, Sexuality and Women’s Studies at the University of Pennsylvania, Katz is a pioneering figure in the development of queer art history, and author of a number of books and articles. He has curated many exhibitions, nationally and internationally. Rudy Lemcke is a new media artist who lives and works in San Francisco. His artworks concerning HIV/AIDS have been presented in the exhibitions: From Media to Metaphor (1987—1992), Group Material’s AIDS Timeline (1989—1991), Inside/Out: Voices from Home (1990) and Art AIDS America (2015—2017). John E. Lesch is Professor Emeritus of History at the University of California, Berkeley. His publications include The First Miracle Drugs: How the Sulfa Drugs Transformed Medicine.

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Xiaoxing Liu is Professor of Chinese Language and Culture at Soka University of America. She received her Ph.D. in cultural anthropology with a focus on medical anthropology from University of Illinois at UrbanaChampaign. She has written about health care system and practices of the Yi, an ethnic minority group in China. Edward D. Lowe is Professor of Anthropology at Soka University of America. A recent chapter on comparative suicidology is “A Critical Comparative Analysis of Late 20th Century Suicide Epidemics in Chuuk and Samoa,” in M. Schnegg and E.D. Lowe (eds), Comparing Cultures: Innovations in Comparative Ethnography (Cambridge University Press, 2020). Andrea Patterson is Associate Professor of Liberal Studies at California State University Fullerton. She is a historian of medicine and public health with a focus on the intersections of gender, race and science. Her publications include journal articles and book chapters on African American health and healthcare under Jim Crow. Ian Read is Associate Professor of Latin American Studies and Director of International Studies at Soka University of America, USA. His publications include journal articles and book chapters on Brazil, Mexico, and Central America, and the book Hierarchies of Slavery in Santos Brazil, 1822—1888 (Stanford University Press, 2012). Parvin Shahrestani is Assistant Professor in the Department of Biological Science at California State University, Fullerton. Her research team focuses on the population genetics of health-relevant traits, including immune defense, using the model organism Drosophila melanogaster. Amy E. Slaton is Professor of History at Drexel University in Philadelphia, Pennsylvania. Her research focuses on the social character of technical expertise and aptitude, with particular emphasis on the role of race, disability and other classificatory systems. Her most recent book is Race, Rigor, and Selectivity in U.S. Engineering: The History of an Occupational Color Line (Harvard University Press, 2010); she is currently writing a critical history of STEM Diversity in the United States. Terri L. Snyder is Professor of American Studies at California State University, Fullerton, and her research focuses on the history of gender, race, and the law in British North America. She is the author of The Power to

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About the Authors

Die: Slavery and Suicide in British North America (University of Chicago Press, 2015). Tina Takemoto Tina Takemoto is the Dean of Humanities & Sciences at California College of the Arts. They are a visual studies scholar and artist whose work explores issues of race, illness, queer identity, memory, and grief. Their work has been exhibited and performed widely, and Takemoto was awarded Grand Jury Prize for Best Experimental Film at Slamdance and Best Experimental Film Jury Award at the Austin Gay & Lesbian International Film Festival. Michelle Teti is Associate Professor and Associate Chair of the Department of Public Health, and a program affiliate in the Black Studies Program, at the University of Missouri. The goal of her research is to improve the lives of people at risk for and living with HIV. Michael Weiner is Professor of East Asian History and International Studies, and Associate Dean of Faculty, Soka University of America. He is a former Managing Editor of the Japan Forum. Major publications include Race, Migration and Ethnicity in Modern Japan (2004), Japan’s Minorities, the Illusion of Homogeneity (2009), The Pacific Basin: An Introduction (2017), Race and Ethnicity in Asia (forthcoming 2021). Joshua S. Yang is Associate Professor of Public Health at California State University, Fullerton. His research examines how the intellectual history of economic and political discourse affect public health, with an emphasis on noncommunicable diseases and tobacco control.

ACKNOWLEDGMENTS

We wish to convey our appreciation to the many people who have supported us throughout the preparation of this volume and who helped to shape its final form. We are grateful for the assistance of our authors, editors, readers, and students for sharing their thoughts and brilliance to make this book possible. The idea for this project resulted from the collaborative work with our dear colleague Margaret Garber at California State University, Fullerton (CSUF), who we cannot thank enough for setting us on this path. Michael Weiner at Soka University of America (SUA) encouraged this project at its inception and cheered it on to its publication. We are indebted to Navid Madani, Harvard Medical School and Dana Farber Cancer Institute, for her excellent insights and to Terri Snyder, CSUF, who provided guidance at every stage of the process. Above all, we want to credit the contributing authors to this volume for their scholarship, cooperation, and patience in seeing this book through its completion. Angeles Sancho-Velazquez, Philip Minehan, Kay Read, and Edward Read reviewed early drafts and offered invaluable commentary in matters both of style and substance, and their thoughtful recommendations resulted in many improvements to the text. We thank the anonymous readers during the scholarly review process who suggested useful criticisms that helped revise the manuscript. We also would like to recognize the enriching conversations and enthusiasm of our students, and the hard work of the Liberal Studies Student Association at CSUF, and Karen Rogers-Bronstein and Clare Lorenzo at SUA in facilitating the conference proceedings. We acknowledge generous institutional support provided by the College of Humanities and Social Sciences and the Liberal Studies Department at CSUF, and from Academic Affairs at SUA. Funds made available by these universities permitted consecutive conferences at each institute, and a platform for discussion among scholars from fifteen disciplines across the natural sciences, social sciences, and arts and humanities that contributors concerted into this book. At CSUF, we especially thank the Chair of Liberal Studies, Jim Hofmann, for his administrative support and collegial advice and Ronald Clapper for his most generous donation. At SUA, Ed Feasel, Vice-President of Academic Affairs, and Bryan Feasel, Dean of Faculty, provided institutional support and kind praise.

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Acknowledgments

We want to express our gratitude to our publishing and production team, who aided us in the physical preparation of the manuscript. Carolyn Millar expertly copyedited and prepared the manuscript, Brad Colin and Daria Early delivered invaluable services with the index and reference sections, and Mari Migliore lent her treasured skills in designing the cover page. We thank our Cambridge Scholars Publishing Editor, Rebecca Gladders, for her continued assistance and encouragement. Last but foremost, our families deserve to be recognized for their love, support and endless patience, without none of this would be possible.

FOREWORD JONATHAN D. KATZ

The logical outcome of testing is a quarantine of those infected. We used to quarantine for typhoid fever and scarlet fever, and it did not ruin the civil liberties of anybody to do that. —Senator Jesse Helms1

The most consistent casualty of any epidemic is social and political progress. As an epidemic cleaves, splinters, and ultimately shatters any imagined human collectivity, people turn on one another, othering the afflicted, and in the process generally reinforcing with a new virulence the established social hierarchy that existed before the epidemic hit. The rationale, of course, is self-protection, but beneath that lies an all too human desire to locate, name, enumerate and then excise the unknowable threats that haunt all existence. Epidemics thus favor conservative political ideologies, the very ideologies that are propagated against the prospect of social and political change, and by extension, against the agents of that change. They are a centrifugal force in culture, routinely deployed then and sadly still now, to call a people backwards, towards credence in old gods, old values, old social and political beliefs. Epidemics have pushed humanity relentlessly backwards, instrumentalized by conservative social forces to further their agenda of stasis and the replication of outmoded social norms and hierarchies. Epidemics are political crises every bit as much as they are health crises, so much so that the two are inseparable. In fact, I often hear that we have AIDS to thank for the resurgent attention to, and victories in the queer rights struggle today. AIDS, the thinking goes, moved queerness into general discourse, and thus forced political attention, a harbinger of recent victories such as marriage equality. But nothing could be further from the truth, and AIDS actually set back the queer rights 1 Cited in Douglas Crimp, ed, AIDS: Cultural Analysis, Cultural Activism (Cambridge, MA: MIT Press, 1988), p.8. and 262.

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movement by decades. It did so, as Helm’s quotes above underscore, by reifying and naturalizing a firm boundary between the population at risk for infection and the rest of the country. No less an authority than President Ronald Reagan’s spokesman, Gary Bauer, remarked on the Face the Nation television program in 1987 that the reason the President hadn’t so much as uttered the words AIDS until 1985, at least 3 years into the epidemic, was due to the fact that, [“i]t hadn’t spread into the general population yet.” Worse, AIDS gave new life to dying old canards long associated with queerness, such as the association of homosexuality with illness or the idea of an invisible contagion that corrupts the vulnerable young, causing a miserable life and early, tragic death. AIDS, in short, breathed new life into rapidly disappearing prejudice, and the cost to individuals and to the social and political movement as a whole is incalculably high.2 Horrifying as it is to admit, epidemics serve not to equalize everyone as potentially vulnerable, but to differentiate. They thus accommodate multiple, highly fraught social intents, not least giving prejudice, selfishness, and even cruelty the gloss of rationality it desperately lacks. Under the pressure of an epidemic, bias and cupidity is magically transformed into ethical scrupulousness. And in facilitating a false binary between the diseased and undiseased, an epidemic allows us to at least temporarily forget all the other threats to our existence, while rallying around a vision of a necessary social hygiene that has been responsible for all the greatest of human cruelties. Epidemics are therefore among the most formative, but invisible, of social forces in human history. As such, they by definition call for interdisciplinary approaches combining scientific, medical, political and social historical scholarship—precisely the kind of scholarship to be found in this book. Indeed, as the various essays in this book illuminate, epidemics have been as primary a force in human evolution, migration, and settlement as they have been in social stratification, murder and barbarity. Epidemics have thus not only fundamentally shaped what it is to be human, they have consistently reified hierarchies that benefit the few at the expense of the many, the strong in the face of the weak, the wealthy before the poor, and the healthy over the sick. Above all then, epidemics have served to naturalize what were previously merely social distinctions, and thus as artifacts of the social, subject to change. But epidemiology of all stripes can 2

See my “‘The Senators Were Revolted:’ Homophobia and the Culture Wars,” a chapter in A Companion to Contemporary Art Since 1945, ed. Amelia Jones (Oxford: Blackwell Publishing, 2006), pp. 231-248.

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recast human values as natural ones, allying human prejudice to deities, nature, and other uncontrollable forces. Under an epidemic, the nakedly selfish and self-interested is easily transubstantiated into the selfless protection and nurturance of the social collective. If AIDS is a central organizing principle of this book, it’s in part because AIDS has cast these often camouflaged socio-political machinations into high relief. But AIDS isn’t a particularly unusual epidemic and the catalog of social horrors that have followed in its wake are hardly novel. Rather, AIDS allows us to diagnose with social historical specificity some of the defining social patterns that follow in the wake of an epidemic. For example, in the United States, it was largely the Republican Party that instrumentalized AIDS, wielding it as a wedge issue, a scare tactic with profound, in-thestreets social traction. Demonizing people at risk of AIDS in fact revived the party, reanimating its conservative wing and helping to birth such now broad-based US political lobbying heavyweights as Christian Conservatives and the Tea Party. These forces in turn led to the election of Donald Trump, a man who has continually mobilized a bifurcated us/them dichotomy as his core, arguably sole, political stratagem. We are thus now inheritors of a political landscape, that, if not fundamentally restructured by an epidemic, found its most base instincts reinforced by one, the ramifications of which can be felt across a range of social issues that have no obvious connection to disease. In this book, the invisible hand of the epidemic is finally given the complex, multi-disciplinary attention it deserves. —Jonathan D. Katz, October 2019. Jonathan D. Katz is Associate Professor of Practice, Art History and Gender, Sexuality and Women's Studies, University of Pennsylvania. He is a pioneering American academic and activist. Katz founded Harvey Milk Institute, the world’s largest queer studies institute, and curated the first major museum queer exhibition at the Smithsonian National Portrait Gallery.

INTRODUCTION SHAPES OF EPIDEMICS: SOCIO-HISTORIC, ARTISTIC, POLITICAL, AND ECOLOGICAL SIGNIFICANCE ANDREA PATTERSON AND IAN READ

Epidemics shape us as much as we shape them. This book examines how the physical threat of epidemic disease is irrevocably linked to culture, economic resources, social class, and power. In particular, our core example of HIV/AIDS illustrates how disease not only affects patients and health providers but may alter social and political landscapes. Like other epidemics, HIV/AIDS cannot be confined to its frightening devastation but needs to be recognized for its important role in promoting scientific discovery, changing policy, and influencing the arts. Yet, as much as epidemics affect us, humans often provide the conditions for them to emerge, transform, or disappear. For example, biological and physical processes can modify disease environments among animals, while our particular interactions with these animals may cause the disease to “spillover” to humans. At the same time, causes of disease must be made legible and potentially resolvable within the cultural, economic, and political contexts of communities. Therefore, epidemics are situated at the intersections of nature, society, human rights, and global public health efforts. We believe their study requires far-reaching collaboration of experts from across academia to grasp their complexity more fully and ethically. What is an epidemic? In the popular imagination, epidemics evoke fear, contagion, pain, or death. Film, literature, and the arts use epidemics as a vehicle to explore a collective tragedy, especially when elements of intimacy, scientific experimentation, or state security can themselves cause apocalyptic

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Introduction

destruction through “contagion.”1 The term “epidemic” was first used in a medical context by Hippocrates over 2,500 years ago,2 describing either “groups of different diseases occurring at the same place” (or time), or a symptom such as “epidemic cough” associated with multiple maladies.3 However, it was not until the Middle Ages when physicians began to identify an epidemic with a single disease, then with a microbe in the nineteenth century, and finally a specific “epidemic strain” in the twentieth century. In contrast, over the past decades, we have witnessed a semantic expansion of the term to include noninfectious and sometimes even nonmedical phenomena such as obesity and computer “viruses.” In mass media, “anything that affects a large number of persons or objects and propagates like a disease” may be referred to as an “epidemic.”4 The academic disciplines contribute their distinct version of what constitutes an epidemic. At its most basic, dictionaries of epidemiology define “epidemic” as a sudden increase of cases in a geographic area, as compared to “endemic” (constant presence or prevalence) and “pandemic” (involving large numbers of people in several countries or continents).5 Yet, an epidemic is never by itself some measurable overstep of a numerical threshold of mortality or morbidity, the emergence of a belief category, or the vividly painted reaping hook sweeping down a cowering crowd. An epidemic is usually part of all of these. The ways they come together to give diseases their intriguing “personalities” are determined by a process that begins well before and continues long after the first death.

1

Kristen Ostherr, Cinematic Prophylaxis: Globalization and Contagion in the Discourse of World Health (Durham: Duke University Press, 2005); Elaine Showalter, Hystories Hysterical Epidemics and Modern Media (Charlesbourg, Québec: Braille Jymico Inc, 2003); Priscilla Wald, Contagious: Cultures, Carries, and the Ourbreak Narrative (Durham: Duke University Press, 2008). 2 The Greek word epidemios can be traced back to the Greek poet Homer and, prior to Hippocrates, described “almost anything (persons, rain, rumors, war), except diseases;” Paul M.V. Martin and Estelle Martin-Granel, “2,500-year Evolution of the Term Epidemic,” Emerging Infectious Diseases 12, no. 6 (June 2006): 976-980, https://doi:10.3201/eid1206.051263. 3 Cough of Perinthus described by Hippocrates has been associated by historians of medicine with diphtheria, influenza, whooping cough, dengue fever, among many others ailments; Georgios Pappas, Ismene J Kiriaze and Matthew E. Falagas, “Insights into Infectious Disease in the Era of Hippocrates,” International Journal of Infectious Diseases 12, no. 4 (July 2008): 347-350. 4 Martin, Kiriaze, and Falagas, Evolution of the Term Epidemic, 979. 5 Miquel Porta, ed., A Dictionary of Epidemiology (New York: Oxford University Press, 2008), https://doi:10.1093/acref/9780195314496.001.0001.

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We intend to contribute to this topic at a time when infectious diseases pose a rising global threat due to factors such as antibiotic resistance, a worldwide opioid crisis,6 and profound environmental and demographic changes, all of which contribute to the evolution and spread of new pathogens.7 As we were completing this book, COVID-19 “spilled over” from a wild animal population and has spread uncontrollably, killing hundreds of thousands. Authors analyze the human body’s defense to infectious disease (see Shahrestani) and investigate epidemics in the context of past plagues to offer insights into how we might prepare ourselves for emerging diseases such as Ebola (see Green) and COVID-19 (epilogue). Furthermore, we go beyond infectious and microbial diseases to define epidemics in the context of contagions of suicide (see Snyder, Lowe) and non-communicable or degenerative diseases (see Yang, Crummett). How we define epidemics matters. We expand the discourse on epidemics by drawing attention to phenomena that cause widespread mortality and morbidity but are not (adequately) addressed because we do not consider (or respond to) them as epidemics. To identify, measure, and contain epidemics, the processes that drive them must be better understood. We challenge conventional views of infection and transmission by associating diseases with ideologies and their accompanying institutions, such as colonialism (see Snyder, Lowe, Lesch, Read, Green), imperialism (see Weiner), neoliberal capitalism (see Yang, Crummett), communism (see Liu) and racial segregation (see Patterson, Fontdevila, Teti/Slaton). Approaches to ideology include discussion of diverse religious beliefs (see 6

Growing evidence in support of opioid dependency and its immunosuppressive effects suggest that the opioid epidemic could be responsible for the next major infectious disease outbreak; Sabita Roy, Jana Ninkovic, Santanu Banerjee et al., “Opioid Drug Abuse and Modulation of Immune Function: Consequences in the Susceptibility to Opportunistic Infections,” Journal of Neuroimmune Pharmacology 6, no. 4 (December 2011): 442-65, https://doi.org/10.1007/s11481-011-9292-5. 7 David Bloom, Steven Black, and Rino Rappuoli, “Emerging Infectious Diseases: A Proactive Approach,” Proceedings of the National Academy of Sciences of the United States of America 114, no. 16 (April 2017): 4055–4059. https://doi:10.1073/pnas.1701410114. Of growing concern are infectious diseases as they relate to environmental change, such as the drug-resistant fungus candida auris that suddenly became a human pathogen on three separate continents (diff. genetic strains). Research suggests that as fungal lineages become more thermally tolerant due to climate change, they will more likely breach human thermal barriers. This pathogen causes high mortality among hospital patients with immunodepressed systems; Arturo Casadevall, Dimitrios P. Kontoyiannis, and Vincent Robert, “On the Emergence of Candida Auris: Climate Change, Azoles, Swamps, and Birds,” mBio 10, no. 4 (July 2019), https://doi:10.1128/mBio.01397-19.

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Introduction

Snyder, Weiner, and Lowe) and studies of media representation (see Yang and Takemoto/Lemcke). We argue that epidemics are always more than physical processes, and it is especially their catastrophic and degenerative qualities that demand explanations from pre-existing cultural tropes. Therefore, what appears at first glance the most basic question, “what is an epidemic?” can hardly be answered in a few sentences, or by a single discipline. What is the best method for understanding how epidemics shape and are shaped? In this book, seventeen scholars from fifteen disciplines across the natural sciences, social sciences, and arts and humanities came together in a collaborative effort to offer insightful suggestions on the kind of radical interdisciplinarity we believe is needed to recognize, moderate, and coexist in the face of epidemic disease. We argue for this approach not because “interdisciplinarity is fashionable in academia right now,” but from a conviction that to do justice to the complexity of this topic, to create innovative ways to address human suffering, and to find real solutions that may determine whether people live or die, we need broad and inclusive participation. Solving specific problems requires more than the collection of diverse (autonomous) disciplinary insights—what may be better described as a multidisciplinary or pluralist approach.8 Instead, we aim to create conceptual connections and integrate knowledge from across closely related as well as vastly distant fields of study.9 Such an approach is needed within an increasingly interconnected world where both pathological diseases and health behaviors are infectious. Epidemics involve the infected and non-infected; they are influenced by control and neglect and affect the local and global. Therefore, we need a willingness to abandon the most basic assumptions that can accompany particular academic tracks, such as the belief that science may observe and measure with objectivity, or that our 8

Troy Camplin, “The Fading Hope of Interdisciplinary Study,” James G. Martin Center for Academic Renewal. Last modified January 30, 2011, https://www.jamesgmartin.center/2011/01/the-fading-hope-of-interdisciplinarystudies/. Camplin notes that some attempts at interdisciplinarity fail to go beyond closely related disciplines, or don’t go deep enough in understanding each of the disciplines to truly interrelate and integrate the knowledge, ending up with a “multidisciplinary cobbling-together.” 9 Ruth Wodak and Paul Chilton, eds., New Agenda in (Critical) Discourse Analysis: Theory, Methodology and Interdisciplinarity (Philadelphia: John Benjamin Publishing Company, 2007), 7-11.

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cultural beliefs are separate from ecological processes. Scholars in this volume came together in an effort to find “common ground” and establish how distinct disciplines can interact and correlate.10 They investigated shared problems within a theoretical framework that emphasizes the meaning we attach to epidemics as well as their material reality; both of which we contend are essential for a more complete understanding of how epidemics shape and are shaped. The central purpose that connects this diverse set of chapters is to illustrate that both the ideological and physical world mediate how we make sense of epidemics. Malaria’s old theorized relationship with race is a good example. In one way, malaria has everything to do with race because, between the sixteenth and nineteenth centuries, imperial regimes, merchants and planters across the Atlantic world believed that lower rates of malaria, incorrectly attributed just to black people and their descendants, helped justify their enslavement and labor in tropical environments.11 In other words, the legacy of slavery is deeply associated with theories of racialized disease predisposition (see Patterson). But in another way, malaria also has nothing to do with race because it is a geographic trait with no alignment with phenotypical and physiological characteristics that are unevenly, inconsistently, and always impermanently applied to “race.”12 Since the discovery of sickle cell disease in 1910, scientists began to document how sickle trait and disease are more common among communities in geographic 10

Allen F Repko, Interdisciplinary Research: Process and Theory (Thousand Oaks, Calif.: SAGE Publications, 2012). Repko provides a very useful discussion of possible theoretical frameworks and practical approaches to interdisciplinary research and scholarship. He emphasizes “common ground” and “shared problems” and notes that the diverse and often “incongruent” methods of distinct fields can complement each other and create a better and deeper understanding of complex problems; Rick Szostak, “How and Why to Teach Interdisciplinary Research Practice.” Journal of Research Practice 3, no. 2 (2007), retrieved August 25, 2019 from http://jrp.icaap.org/index.php/jrp/article/view/92/89. 11 Kenneth Kiple and Virginia Kiple, “The African Connection: Slavery, Disease and Racism,” Phylon 41, no. 3 (1980): 211-22, https://doi.org/10.2307/274784. For further evidence on inherited differences in black people that were used to justify slavery in the 19th century see Stephen J. Gould, Mismeasure of Man (New York: W. W. Norton, 1996), 101–103. 12 Andrea Manica, Franck Prugnolle and Francois Balloux, “Geography is a Better Determinant of Human Genetic Differentiation than Ethnicity,” Human Genetics 118, no. 3 (December 2005): 366-371, https://doi.org/10.1007/s00439-005-0039-3; James H Jones, Bad Blood: The Tuskegee Syphilis Experiment (New York: Free Press, 1993), 29. Jones’ book provides an excellent discussion on racialized medicine and pathology due to the continued confusion over what role biology, culture, and environment played in the contraction of disease.

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Introduction

regions with a high incidence of malaria, and that individuals with this “faulty gene” are less likely to be sickened by malaria. More recently, a group of scientists was celebrated for discovering the “elusive mechanism” that affords this “protection.” They genetically modified mice (see Shahrestani’s discussion of model organisms) to carry the sickle trait and discovered that the crucial process involved a component of hemoglobin, or a slightly different chemical composition of the blood in the mice with the sickle gene.13 Yet for much of the twentieth century, physicians presumed an association between sickle cell and “race” (erroneously defined by skin color and other phenotypical traits) and even used it to determine racial identity: physicians either called into question their own diagnosis when “no evidence of Negro blood could be found,” or doubted the “racial purity” of white people burdened with it.14 To confront the unjust legacies of discrimination and continued use of rigid racial categories by scientists and doctors, we must see epidemic diseases as enduring social and biological processes and investigate both their meaning and their material realities. Like the history of malaria, the essays in this volume illustrate that culture matters and provides an essential framework for understanding disease. On the one hand, the concept of “epidemic” is culturally mediated and ideologically defined. We understand shared disease within our cultural vocabulary and concomitant power structures that help us explain and control epidemics. History and contemporary health demographics reveal that the meaning attached to epidemics result in approaches that can oppress (see Lowe’s discussion of adolescent suicide) as much as emancipate or cure (see Snyder and Teti/Slaton). For example, smallpox was not one scourge, but many afflictions understood distinctly and in contradictory webs of meaning in different times and places. When smallpox was carried to the New World in the early sixteenth century, Europeans and Native Americans made sense of the resulting plagues in nearly opposite ways. In this particular and tragic “Colombian exchange,” Europeans took advantage by claiming and colonizing the Americas in the wake of epidemic

13 Marek Cyrklaff, Cecilia Sanchez, Nicole Kilian et al., “Hemoglobins S and C Interfere with Actin Remodeling in Plasmodium falciparum–Infected Erythrocytes,” Science 334, no.6060 (December 2011):1283-1286. https://doi.org/10.1126/science.1213775. 14 Melbourne Tapper, In the Blood: Sickle Cell Anemia and the Politics of Race (Philadelphia: University of Pennsylvania Press, 2011), 17-18, 35, 39; similar questions regarding racial identity and presumed prevalence of certain diseases could be observed with many others, such as syphilis and polio; the practice of “racial profiling” continues in contemporary medicine (see Patterson, this volume).

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devastation, including that by smallpox.15 No single category of “smallpox” does justice for who this disease killed and how its epidemics allowed the detriment and death of many to become the benefit and wealth of others. On the other hand, the essays in this volume emphasize that matter cultures epidemics and scholars also approach them through their materiality. The authors investigate biological and chemical processes that can cause or contain epidemics. They study migratory movements of organisms and relate disease to the transfer of resources or transformation of physical environments. Scholars further study reconfigurations to the human body’s ecosystem, in the contexts of exposure to harmful matter as well as evolutionary advantages and disadvantages. In these ways, biological, environmental, and ecological analyses of matter can create an important framework for understanding disease pathology. Today, we may realize that illnesses of the past, often called by different names, constitute a single disease. For example, Ebola or H1N1 influenza demonstrate zoonosis (when diseases evolve in animals before spreading to humans), while smallpox evolved from common microbial ancestors thousands of years ago and traveled across large parts of the world as a uniquely human disease.16 Scientifically, we would have difficulty refuting the “diagnosis” that the child who died in the seventeenth century, and whose body provided genetic material for analysis of a specific virulent strain, is more than the variant of a single disease category.17 Human control over smallpox is similarly physical and material. Less than fifty years ago, smallpox became the only major disease that humans successfully eradicated. A vaccine, manufactured in mass quantities, prompted the immune system to “accidentally” defend the body by developing antibodies to a close cousin, and much more benign disease, cowpox.18 Smallpox rarely evokes our fears even as it physically exists in two places 15 Noble David Cook, Born to Die: Disease and New World Conquest, 1492-1650 (Cambridge: Cambridge University Press, 2004); and Alfred W. Crosby, The Columbian Exchange: Biological and Cultural Consequences of 1492 (Westport, Conn.: Greenwood Press, 1972). 16 Yu Li, Darin S. Carroll, Shea N. Gardner et al., “On the origin of smallpox: Correlating variola phylogenics with historical smallpox records,” PNAS 104, no. 40: 15787-15792, https://doi.org/10.1073/pnas.0609268104. 17 Recent genetic sequencing of this virus taken from mummified victims has suggested that more or less virulent strains also diverged fairly recently. J. O. Wertheim, “Viral Evolution: Mummy Virus Challenges Presumed History of Smallpox,” Current Biology 27, no. 3 (February 2017): R119-R120, https://doi: 10.1016/j.cub.2016.12.008. 18 Donald R. Hopkins, The Greatest Killer: Smallpox in History (Chicago: University of Chicago Press, 2002).

8

Introduction

(that scientists know of): heavily guarded military laboratories of Russia and the United States.19 This book’s interdisciplinarity and purpose are driven not only by the idea that “culture matters” and “matter cultures,” but by the recognition of their interdependence. In essence, we want to make evident that meaning and matter are irrevocably entangled when it comes to epidemic disease. Accordingly, we challenge the common assumption that diseases and their epidemic manifestation are primarily “physical,” that scientific medicine is primarily “heroic,” and that we can easily distinguish between the ideological and natural worlds. In approaching this topic, SHAPES is inspired by the growing field of the medical humanities, but contrary to much of its recent scholarship, we do not assume that the humanities must serve as a “corrective” to medical-based or science-based approaches to epidemics. We intend to show that discoveries and paradigms about disease derive much less from the amelioration of disciplinary deficiencies than from learning of each other’s work and perspectives. This project began with meetings at two consecutive university conferences in Southern California in February and September of 2017. We asked experts to address a series of interrelated questions on epidemics and explore significant intersections to facilitate an exchange of ideas among researchers who employ vastly different methodologies and seldom communicate across the divide of academic disciplines. Researchers may be unaware of what each field could contribute to alternative therapeutic approaches and innovative ways of thinking about epidemics. This volume is the outcome of subsequent cooperative development of these themes. The first part (chapters 1-6) emphasizes epidemics in webs of meaning, while the second part (chapters 7-12) emphasizes their materiality. This structure is intended to show that both explanatory frames are equally important and, indeed, complement and depend on each other. We are careful to illustrate their interdependence without collapsing these concepts in our discussion. The first two sections of the book are organized around a series of important guiding questions that highlights the intersections and inter-relatedness of phenomena manifested in epidemic diseases, even though they may otherwise be separated by time, geography and culture (Part I); or divided by living or abiotic matter across extremely diverse ecosystems (Part II). However, throughout the book, and above all 19 Bob H. Reinhardt, The End of a Global Pox: America and the Eradication of Smallpox in the Cold War Era (Chapel Hill: The University of North Carolina Press, 2018), 174-76. Some virologists fear that new technology permits smallpox to be “synthesized” in a laboratory; and Kai Kupferschmidt, “Labmade smallpox is possible, study shows.” Science 357, no. 6347 (July 2017): 115-116.

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demonstrated by Part III (chapters 13-14), our interdisciplinary and integrative approach makes apparent that neither meaning nor matter is ultimately sufficient to grasp how epidemics shape and are shaped; nor can they be easily separated as the many ways of their entanglement illustrate in all chapters.20 This is our point: the strict boundaries around the disciplines of academia are untenable when it comes to epidemics. In fact, we gain a much deeper understanding of the SHAPES of epidemic and global disease—their socio-historic, artistic, political and ecological significance when—for instance, Monica Green “treats the disease organism itself as a historical ‘actor’.” Her analysis of the 2014 Ebola outbreak in West-Africa, chapter 13, demonstrates the consilience we need to bridge the gap between the biophysical and cultural environments.21 Similarly, Rudy Lemcke’s observation on AIDS artwork, chapter 14, shows that material objects—for instance photographs of people dying of AIDS—not only document the physical manifestations of the disease but give “voice to how we see and speak about ourselves and that this process can change culture.” The book’s structure is illustrated by Figure 1, along with its core case study, HIV/AIDS (chapters 5-8, 14). The prominent place we give to HIV/AIDS serves several purposes. First, this pandemic exposed new dangers when the relationship between microbes (a virus) and humans altered zoonotic boundaries. Second, while most pandemics were exaggerated by prejudice, racism, and xenophobia, HIV/AIDS provides a vivid example of how this can endure in a world defined by our interconnectivity and reliance on technology and science. Third, even as it transformed into a chronic “controlled” disease, HIV/AIDS continues to plague global communities, and survival rates still depend on nationality, race, gender, class, and sexuality. Finally, we employ a broader view and examine the effects of this disease in the framework of historical and alternate epidemics.

20

Theo van Leeuwen, “Three Models of Interdisciplinarity,” in New Agenda in (Critical) Discourse Analysis: Theory, Methodology and Interdisciplinarity, eds. Ruth Wodak and Paul Chilton (Philadelphia: John Benjamin Publishing Company, 2007), 7-11; Leeuwen discusses various models of interdisciplinarity. In contrast to the centralist or pluralist model that treat disciplines as autonomous disciplines, which may not be equally valued (centralist model), the aim in this book, as discussed above, is to establish the interdependency of the disciplines and to highlight their equal value in contributing understanding to epidemic disease. 21 Edward O. Wilson, Consilience: The Unity of Knowledge (New York: Vintage Books, 1998).

10

Introduction

Figure 1. This multidisciplinary set of chapters–written by scientists, social scientists, humanists, and artists–illustrates that our understanding of epidemics is mediated by both a physical and ideological world. Moreover, the result of this collaborative development shows that culture and matter are invariably linked, and neither framework alone can fully show how epidemics affect and reflect the varied human experience.

Part I: The Shape and Shaping of an Epidemic in Webs of Meaning What can the emphasis on meaning tell us about epidemics? The essays in this section show that epidemics are part of a complex system of phenomena that interact nonlinearly in deeply symbolic webs of ethnicity, class, gender, sexuality, and power. The burden of disease is not solely the result of pathogens, and in some instances may even be independent of, or only marginally dependent on biological agents. Social determinants, such as discrimination, racism, poverty, stigma, violence, and incarceration contribute to and amplify epidemic diseases.22 Despite the vast cultural, 22 Colonial British America provides an infamous example of epidemic amplification. In 1691, three young girls in Salem Village, Massachusetts, displayed “distempers” and complained of pains. A local minister wrote, “These Children were bitten and pinched by invisible agents; their arms, necks, and backs turned this way and that way, and returned back again, so as it was impossible for them to do of themselves, and beyond the power of any Epileptick Fits, or natural Disease to effect.” Soon

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temporal and geographic differences that set apart the epidemics discussed here, scholars raise many related concerns: the power relations negotiated between western and indigenous societies and their respective cultural reference frames; the transforming power of ideologies or scientific discovery that helps frame public health policies as social or individual responsibilities; and social and cultural differences that inform mainstream and marginalized spaces. How are epidemics perceived and explained? Determining what, in fact, constitutes an epidemic depends not merely on formal recognition by the medical community or institutions of governance, but is subject to how a disease is measured, perceived, and consequently understood by both the “infected” and “non-infected.” Epidemics are not always captured by mortality and morbidity statistics, and as such, may evade conventional depiction or result in competing and contested narratives. In the first two chapters, Terri Snyder and Edward Lowe expose the intricate processes involved in the realization and interpretation of epidemics. Their discussions of very distinct suicide “epidemics,” involving African slaves in British North America/early United States and indigenous youth in Oceania, reflect on who has the authority to “define, describe, explain and intervene” in epidemics and what impact that may have on the afflicted. The authors explore the shape epidemics may take when western and indigenous cultural and political reference frames interact, revealing a wide range of meanings attached to suicide, as well as their complex networks of power and resistance. Snyder, in chapter 1, poses the question of whether, even without reliable statistical data, slave suicide may still be described as an “epidemic.” She notes that in early British America, epidemics were defined as “common to or prevalent among a people or a community at a special time.” Certainly, many of the risk factors, widely acknowledged in modern after, three women were accused of witchcraft. By the end of the Salem trials in 1693, more than 200 people had been accused, mostly women, and at least 24 were executed or died in jail. George Lincoln Burr, “From ‘A Modest Inquiry into the Nature of Witchcraft,’ by John Hale, 1702.” Narratives of the Witchcraft Cases, 1648-1706 (New York: C. Scribner’s Sons, 1914), 413; and Frances Hill, The Salem Witch Trials Reader (Cambridge, Mass: Da Capo Press, 2009). For a contemporary example, see Ingrid T. Katz, Annemarie E. Ryu, Afiachukwu G. Onuegbu et al., “Impact of HIV-related Stigma on Treatment Adherence: Systematic Review and Meta-synthesis,” Journal of the International Aids Society 16, no. 3, suppl. 2 (November 2013): 1-25.

12

Introduction

epidemiological studies of suicide, were present. Stress and depression were constant features in a slave system that was characterized by permanence, extended transporting, excessive disease and death, and frequent kin separation. Moreover, the author argues that “the perception that there was an epidemic of suicide among enslaved people” can be well established, although explanations varied greatly depending on the historical and cultural frameworks. Abolitionists exposed and politicized suicides in an effort to end slavery, while slave owners categorically denied any relationship between the system of slavery and suicide and resorted to “blaming the victims” for their “inferior” biological and cultural dispositions (see Lowe, Patterson, Weiner, Takemoto/Lemcke). Nevertheless, and indicative of an epidemic, slavers also expressed fear and apprehension as they associated suicide episodes with possible onset of insurrection. Finally, slaves themselves may have understood suicides as emancipatory acts of rebellion, as liberation from suffering, or means of spiritual homecoming. As such, slave suicides and their complex webs of meaning resemble other epidemics in which people seek to control the narrative regarding their existence, their possible causes, and ways of interventions. The critical role of perception and explanation in determining what establishes an epidemic is further illustrated in chapter 2, where Lowe investigates how the image of “the recalcitrant native” served as means to reinstate “a relationship of dependency and subordination.” In the 1970s and 1980s, in the wake of gaining political independence from New Zealand and the United States, Pacific Islanders experienced an apparent rise in suicides among indigenous youths. A network of western experts studied, explained and intervened in two epidemics in Samoa and the Micronesian Pacific Islands, using this health crisis to create “governance at a distance.” Conditions that rendered local populations vulnerable to the epidemic were transformed into a reductionist narrative that served “larger, distant bureaucratic interests.” Efforts to promote social and political reforms failed to convey the complex and conflicting interpretations of the epidemic. Instead, academic specialists disassociated the US policy of rapid modernization from its connection to suicide and “blamed the victim,” finding fault with local peoples for their adherence to indigenous cultural values and power structures. Explanatory frameworks often persist within enduring belief systems, in this case, the western idea of “the inevitability of civilizational progress” and the need to reform those suffering from “the conservative forces of superstition and tradition.” Lowe’s analysis reveals the importance of a counter-narrative for any meaningful post-colonial epidemiology. He calls for “a greater reflexive awareness” among experts,

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so that “we may be more careful about our complicity in ongoing forms of colonial domination and more open-minded,” especially as it concerns the inclusion of indigenous perspectives (see Green). What is the relationship between epidemics and ideology? Epidemics then are not only a matter of life and death, but also serve as ideological battlegrounds. Discussions of political, social and economic ideologies indicate that (predominantly) western commentary can prompt policies of inaction as well as extreme intervention, such as: x Prohibiting medical care and shaping public health policies in a racially segregated Jim Crow America (see Patterson) x Fostering an economic climate that advances corporate profits over community health (see Yang, Crummett) x Placing impoverished peasants at the mercy of a “culture of bureaucratic obedience” in communist China (see Liu) x Preventing or impeding research that challenges prevailing belief systems (see Lesch, Shahrestani, Green, Takemoto/Lemcke) In a case study for extreme intervention, Michael Weiner, in chapter 3, unravels how Japan’s desire to become an imperial power shaped public policies in the early 1900s. Disease control addressed not merely “medical or epidemiological knowledge but also questions of national identity and preexisting understandings of leprosy.” The Japanese government accused those afflicted with infectious diseases of giving the country an image of “backwardness and lack of civilization” (see Lowe). Officials embarked on a mission to sanitize public spaces from those “creating an unfavorable impression among westerners.” One disease, in particular, gave great offense: leprosy (Hansen’s disease). Historically, this disease has been fraught with immorality and inundated with symbolic images of fear, shame, and ostracism. The rise of social Darwinism and eugenics reinforced preexisting meaning systems, while gradually incorporating new “scientific” theories that increasingly defined leprosy as a hereditary disease. Control extended beyond the ill. Conceptualization of leprosy as hidden “poison” in family lines of the non-infected warranted more drastic measures of isolation and reproductive control. Weiner argues that scientific discourse had “infected” the public, consequently shaping epidemic diseases as social and political problems that required an unflinching commitment to progressivism, especially from a modernizing nation like Japan. Patients

14

Introduction

throughout the empire were subjected to physical abuse and forced labor until laws mandating incarceration were repealed in 1996. Andrea Patterson, in chapter 4, also explores the influence of ideology in interpreting disease. In the early twentieth century, Jim Crow public health policies developed in response to popular theories from newly emerging disciplines such as physical anthropology, evolutionary biology, and genetics. She argues that academia lent a distinctly scientific aura to pre-existing racial biases. White supremacist ideology informed scientists, doctors and public officials who agreed that innate physiological and biological differences separated the races. Excessive morbidity and mortality among black people were blamed on racial “inferiority.” Hence, denial of medical care was justified and rooted in the medical opinion that “the rapid dying out of the Negro is natural.” Disavowing the social and economic inequities of a highly structured racial caste society as diseasecausing factors, politicians and healthcare providers placed unshaken confidence in the accuracy of scientific theories which promoted the medicalization of racism. The essays of Weiner and Patterson raise an additional important question: to what degree is our contemporary epidemiological discourse reflective of past stigma and notions about racial inferiority? In other words, does it affect our perception, or even acceptance of pathology among some patients, but not others? While we may view the ideologies discussed by these authors as “pseudoscience” today, preoccupation with racial, social, and cultural differences in research and therapeutic control persists, as does the “epidemic of inequity.”23 Unless public health systems acknowledge and address the crucial role discrimination plays in generating and sustaining disease, vulnerable communities will continue to carry a disproportionate disease burden, including shorter lifespans and higher rates of death (see Fontdevila, Teti and Slaton).24 Joshua Yang, in chapter 9, directs us to the role ideology plays in noncommunicable diseases (NCDs) that claim millions of lives annually and are projected to increase rapidly. As such, they constitute an epidemic and 23 Leonard E. Egede, “Race, Ethnicity, Culture, and Disparities in Health Care,” Journal of General Internal Medicine 21, no. 6 (2006): 667–669. https://doi:10.1111/j.1525-1497.2006.0512.x. 24 African American men continue to have the highest mortality rate among all ethnic and gender groups in the United States. Infant mortality for African Americans is more than twice that of whites (11.11and 5.06 respectively per 1000 births); see T.J. Matthews, Marian F. MacDorman and Marie E. Thoma, “Infant Mortality Statistics from the 2013 Period Linked Birth/Infant Death Data Set,” National Vital Statistics Reports 64, no. 9 (August 2015): 1-30.

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require global intervention as articulated by both the World Health Organization and the United Nations. NCDs are not caused by pathogenic organisms but result from the consumption of unhealthy goods massproduced by large industries (see Crummett). Neoliberal capitalism, as Yang claims, enables transnational corporations to “produce disease through active and intentional efforts to maximize consumption.” The author links the emergence of the epidemic to the rise of corporate power and the simultaneous decline in public health services. He argues that lower taxes for corporations, fewer resources for public health services, deregulation, and extensive campaigns that shape public opinion and create misleading scientific information all work in concert to amplify potential harm to consumers and undermine efforts to control and prevent NCDs. A final case illustrates the powerful role ideology can play in producing and even prolonging epidemics. In a remote region in China, a devastating AIDS crisis developed through a tainted blood supply, despite full cognizance of the authorities. Xiaoxing Liu, in chapter 8, reports that poor villages found themselves and their health at the mercy of unsympathetic government doctrine. Local government valued obedience and “saving face” over patient protection and turned a blind eye to the epidemic. Liu observes that in communist China, ordinary people will suffer because “officials ultimately remain responsible not to the public but to the higher authorities.” These examples across such different regions, political and cultural theaters, and temporal spaces illustrate the importance of ideology in disease. Researchers and health professionals must develop a greater awareness of these important connections, as it may offer an opportunity for new approaches to prevent and control disease. Additionally, it will shift some of the individual responsibility and burden away from the patient, especially in marginalized spaces. For this, some reckoning must occur. Society and public health systems would have to acknowledge and address the crucial role ideology can play in causing and sustaining disease and in controlling research, methodology and policy. How are epidemics transformed by scientific discovery? Research and methodology within the scientific process have the potential to lead to discoveries that transform public health policy. Patterson suggests that an increased understanding of disease-causing microorganisms challenged the racial predisposition hypothesis and provided a persuasive counter-narrative. “Amidst fear of contagion and concern for white health,” the idea that germs as “the original democrats” affected all Americans proved a powerful force in transforming health care to include black

16

Introduction

people.25 As a result, black mortality rates declined dramatically. Likewise, Yang points out that the initial response to the discoveries in microbiology was characterized by large-scale investment in infrastructure, engineering, and social reform. This was followed by a biomedical and technological revolution leading to antibiotics, antiviral drugs, and vaccines. Together they had a significant impact in reducing infectious disease. Yet, at the same time, responsibility gradually shifted away from the environment to “the individual bodies in which they [germs] were housed,” transforming public health services by redirecting attention to individual lifestyle and behaviors regarding the “sanitation” of the body (see Read). The subsequent political disengagement and lack of social reforms impede biomedical control of both infectious diseases and NCDs. In the context of scientific discovery and public health policy, Weiner’s discussion of Hansen’s disease is especially noteworthy. Because the image of the “leper” was so imbued with meanings of personal failings and even “bad blood,” biomedical control had initially little effect on reversing the policy of segregation. The apparent peril posed by leprosy patients was so ingrained in the thinking about this disease that many officials, researchers, and medical health professionals continued to perceive Hansen’s disease as a risk to public health. Indeed, many argued for a continued policy of isolation and sterilization. Nearly 3,000 patients were still in leprosaria by the first decade of the twenty-first century, even though biomedical control had become available in the form of the highly effective Sulfone drug Promin in 1946. Evidently, scientific discovery alone holds no power over making an epidemic, real or imagined, disappear. Several other authors raise the complicated relationship between scientific discovery and epidemics. Parvin Shahrestani, in chapter 11, reports that continued ideological resistance to evolution prevents adequate funding for experiments in evolutionary biology, despite promising results with important therapeutic implications for the human immune response to infectious diseases. Likewise, Lisa Crummett, in chapter 10, indicates that extensive biological studies establish the addictive and harmful nature of excess sugar and its potential impact on metabolic and neurological 25

Stuart Galishoff, “Germs Know No Color Line: Black Health and Public Policy in Atlanta, 1900–1918,” Journal of the History of Medicine and Allied Sciences 40 (January 1985): 22–41; Galishoff discusses the construction of a sewage system in Atlanta that extended into (some) of the black neighborhoods to stem infectious diseases affecting white neighborhoods. Atlanta officials, like in other cities in the American South, realized that daily contact with predominantly black domestic servants allowed pathogens to cross the otherwise firmly established lines of segregation.

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pathways. Yet overwhelming scientific data does not result in the appropriate health policies or regulations that would effectively combat the global metabolic disease epidemic. These examples reveal that scientific progress and effective therapies often require drastic changes in cultural, economic and political structures. A daunting challenge, even more so in the latter case, because of the gradual demise associated with metabolic disease. Even a sudden and fatal epidemic depends greatly on the intricate relationships among scientists, doctors, patients, politicians and activists to negotiate and design new therapy. In chapter 7, John Lesch unravels this complex process and argues that effective therapy for HIV/AIDS derived from nearly a century of scientific research. His essay traces scientific and cultural forces crucial for this development as far back as 1916. The final “drug cocktail” that transformed the epidemic was not solely a teleological march of scientific progress, but the result of multiple cooperative forces responding to each other over decades. Moreover, it presents a successful example of how to confront powerful economic and political institutions and thereby sets an important precedent. ACT-UP (AIDS Coalition to Unleash Power) confronted discrimination and stigma as much as government inaction and corporate greed, and ultimately succeeded in fundamentally changing public funding, policy and opinion (see Teti, Slaton, Lesch, Takemoto/Lemcke).26 How are epidemics linked to emancipation and control? The final two chapters in Part I illuminate how ideas about perception, identity and power can influence therapeutic control. In chapters 5 and 6, Jorge Fontdevila and co-authors Michelle Teti and Amy Slaton take us into the field for qualitative ethnographic studies of two vulnerable populations in the United States who, despite the (relative) accessibility of medical care, still evade detection, prevention, and consistent treatment for HIV/AIDS. The epidemic persists as a public health problem and the statistics remain alarming. Rates of infection are increasing among the most disadvantaged: 26

The protests pitched activists against powerful politicians, pharmaceutical companies, researchers and health care professionals. The movement used a combination of civil disobedience and distinct cultural expressions—slogans, images, art, media—to appeal to a mass audience; see T. V. Reed, The Art of Protest: Culture and Activism from the Civil Rights Movement to the Streets of Seattle (Minneapolis: University of Minnesota, 2005). Benjamin Shepard and Ronald Hayduk, eds., From ACT UP to the WTO: Urban Protest and Community Building in the Era of Globalization (London and New York: Verso, 2002).

18

Introduction

the poor, ethnic and racial minorities, and men having sex with men (MSM).27 The authors discuss some of the reasons why far too many are not captured by conventional public health approaches. Viral transmission is linked to behaviors that continue to be subjected to moral judgment and discrimination.28 The authors point out that this epidemic continues to be driven by a lack of understanding of the complex web of social conditions and power relations that shape the decisions of those most at risk. Fontdevila’s research among Latino gay and bisexual men in Southern California introduces cultural spaces with complex psychosocial meaning systems that resist monolithic categories used in epidemiology, such as “MSM,” “Latino,” or “gay.” For example, cultural interpretations and behaviors during sex may be prompted or altered by stigma and discrimination. Depending on the context, gaps in interpretation may directly impact the transmission of HIV and other sexually transmitted diseases. In a cultural framework in which silence means actively resisting the stigma of HIV, not revealing the condition may feel empowering. This practice, however, can elevate the spread of infection significantly for recent Latino immigrants who attach a different cultural meaning to non-disclosure of one’s HIV status. In other words, multiple sexual meanings for individuals of a diverse group defy a one-method-fits-all behavioral protocol. Additionally, biomedical intervention can carry meanings that have unexpected consequences and may ultimately prove “insufficient to counter the sociocultural complexities.” Young Latino gay men often associate the meaning of sexual promiscuity with the pre-exposure prophylaxis (PrEP). As result, intervention may be rejected despite its significant ability to prevent infection. From a perspective of healthcare professionals, it defies a “logical” explanation that so many actively resist the existing biomedical and behavioral protocols that would protect their health and prevent transmission. Fontdevila’s study points to the importance of “meaning in context” in designing healthcare approaches. His analysis shows that continued social shaming and medical protocols that mask the diversity of 27

The Center for Disease Control and Prevention (CDC) estimates that new HIV infections in the US have increased among certain sub-populations, while they remained relatively stable overall at about 50,000 new infections per year. African Americans, Latinos, and Gay Men continue to be disproportionately affected, and MSM show a 22% increase in infection rates; see Centers for Disease Control and Prevention, “CDC Fact Sheet 2016: New HIV Infections in the United States,” Last modified February, 2016, https://www.cdc.gov/nchhstp/newsroom/docs/factsheets/new-hiv-infections508.pdf. 28 Katz et al., “Impact of HIV-related Stigma.”

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sociocultural experiences prevent therapeutic success and “relentlessly drive the epidemic.” Instead, we need alternative methods that focus on empowering and emancipating patients. Authors Teti and Slaton discuss one promising alternative. They argue that traditional epidemiological models “discourage researchers’ reflection about power and privilege.” When researchers conform to their own secure social and economic status, they risk creating public health solutions that ignore significant sociocultural patterns of disease. Teti and Slaton suggest that existing approaches “can inadvertently sustain the marginality of people with HIV and reinforce the social structures (racism, sexism, and poverty) that allow HIV to thrive.” Conventional public health interventions increasingly emphasize individual responsibility in controlling the spread of disease (see Yang, Crummett). In its place, Teti and Slaton focus on building community strengths, identity and participation, rather than risky behaviors of individuals. Research has firmly established that epidemiological models “that link the concept of risk to sexuality and cultural practice” will compromise or render ineffective most methods of intervention and therapy.29 To facilitate an “emancipatory power of public health,” Teti and Slaton engage in Community Based Participatory Research (CBPR). Specifically, they discuss the potential of photovoice, a method of documentary photography that enables marginalized groups to visualize their concerns, and empowers participants by creating a counter-narrative to the often demeaning assumptions about HIV and experts’ definitions of “risk.” Assessment of “risk” is often dramatically different among low-income women who face more immediate challenges such as violence, addiction, homelessness, and hunger. Traditional interventions with prohibitive messages regarding sexual behaviors undermine results. Yet, when the women in this study became active participants in their healthcare, they not only came to terms with HIV but often took control of other aspects of their lives. Teti and Slaton’s work provides a much needed emancipatory perspective that challenges biological interpretations and mainstream assumptions (see Lowe, Fontdevila, Takemoto/Lemcke). Finally, this brings us to the question Snyder poses at the beginning of this section on epidemics in webs of meaning. She contemplates whether we “can understand self-killing by enslaved people as an epidemic of choice,” given the “egregiously narrow range of possibilities” that presented suicide as an increasingly acceptable path to freedom, power, and control. This kind of emancipation is very different from the liberating, life29

Ann D. Herring and Alan C. Swedlund, eds., Plagues and Epidemics: Infected Spaces Past and Present (New York: Berg Publishers, 2010), 16.

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Introduction

affirming choice by the women in Teti and Slaton’s ethnography. Nonetheless, we may consider the intervention of suicide “therapy,” especially (but not exclusively) in the context of contemporary discussion of the right to end one’s life in cases of a terminal illness.30 Though this raises important issues concerning social responsibility and the suffering of others, it also provides an emancipatory path to freedom and control.

Part II: The Shape and Shaping of Epidemics in Webs of Matter What can the emphasis on “matter” tell us about epidemics? We live in a world of continually transforming macro- and microcosms in which we compete and cooperate with other living organisms. Studies of the biological, chemical, and ecological exchanges of matter within these animated and physical environments provide an integrative understanding of processes that enable or disable epidemics.31 Scholars in this section discuss issues from tropical medicine to immunology and pathology to explain disease emergence and health impacts. Their essays raise many related concerns as they focus on the physicality of disease: they study biological and chemical processes and medical manipulations of molecules that can either contain or cause epidemics; they discuss ecosystemic reconfigurations that provide evolutionary advantages or disadvantages; they place epidemics within their ecological relationships by analyzing migratory movements of organisms, vectors and human bodies; and they relate the materiality of disease to the governance and transfer of physical resources. In short, scholars argue that in epidemic disease, matter matters. 30

John R. Cutcliffe and Paul S. Links, “Whose Life is it Anyway? An Exploration of Five Contemporary Ethical Issues that Pertain to the Psychiatric Nursing Care of the Person who is Suicidal: Part One,” International Journal of Mental Health Nursing 17, no. 4 (August 2008): 236-245. https://doi:10.1111/j.1447-0349. 2008.00539.x; Stewart Cameron, "Learning from Amy: A Remarkable Patient Provokes Anguished Debate about Rationality, Autonomy and the Right to Die," Journal of Canadian Medical Association 156, no. 2 (April 1997): 229-31; and Hadi Karsoho, Jennifer R. Fishman, David K. Wright, and Mary E. Macdonald, “Suffering and Medicalization at the End of Life: The Case of Physician-assisted Dying.” Social Science & Medicine 170 (December 2016): 188-96. https://doi.org/10.1016/j.socscimed.2016.10.010.; Jukka Varelius, “Voluntary Euthanasia, Physician-Assisted Suicide, and the Right to Do Wrong,” Healthcare Ethics Committee Forum 25, no. 3 (September 2013): 229-43. 31 Warwick Anderson, "Natural Histories of Infectious Disease: Ecological Vision in Twentieth-Century Biomedical Science," Osiris 19 (2004): 39-61.

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How do epidemics become a physical reality? At what point does a disease begin to exist? Does it depend on how we define its materiality? Or when we understand its pathogenesis?32 Many epidemics (e.g., bubonic plague, malaria, smallpox) have old pedigrees we can decipher from skeletal remains, descriptions of ancient outbreaks, and archaeogenetics. For instance, cholera likely never moved beyond a river delta region in South Asia until imperial expansion, migration, and trade created the global networks for it to be felt and “known” across the world in the early 1800s.33 Araetus of Cappodocia (81-133 AD) first used the term “diabetes,” but it did not gain its second name “mellitus” (sweet) until doctors tasted the urine of people with diabetes and noticed a slight taste of honey.34 And even though Muhammad ibn Zakariya al-Razi (Rhazes) distinguished smallpox from measles around 910 AD,35 confusion over symptoms in their early phases continued to have vital public health implications.36 Retro-diagnosis based on mostly scientific understanding of pathological properties can assume ontological superiority. Retro-diagnosis may also remain ignorant of the historical “constructiveness” of knowledge (see Green). Nevertheless, communities suffering from an epidemic are rarely aided when we tell them their disease is not entirely “real” or no more than a society’s collective imagination (see Snyder, Lowe, Weiner). Certainly, AIDS was real even though its original identity was believed to be carcinogenic (derived from Kaposi’s sarcoma lesions). And victims suffered, maybe even to a greater extent, because it was inappropriately named gay-related immune deficiency (GRID) or “gay cancer” for the biological and physical “spaces” it appeared to have affected most (see Takemoto/Lemcke). Subsequent scientific discovery of its biological 32

A commonly used quote by Charles E. Rosenberg, historian of medicine: “In some ways disease does not exist until we have agreed that it does, by perceiving, naming and responding to it.” Charles E Rosenberg, “Disease in History: Frames and Framers,” The Milbank Quarterly 67, suppl. 1 (1989): 1-15. 33 Dhiman Barua, Cholera (New York: Plenum Medical Book, 1992), 1-35. For a discussion that casts doubt on cholera’s bio-historical evolution and geographic origins; see Christopher Hamlin, Cholera: The Biography (Oxford: Oxford University Press, 2009). 34 Doctors also noticed the urine became thicker and syrupy. Robert Tattersall, Diabetes. (Oxford: Oxford University Press, 2009). 35 Abbas M. Behbehani, “The smallpox story: life and death of an old disease,” Microbiological Review 47, no. 4 (December 1983):455–509. 36 B. A. Cunha, “Smallpox and Measles: Historical Aspects and Clinical Differentiation,” Infectious Disease Clinic North America 18, no. 1 (March 2004): 79-100.

22

Introduction

pathways provided a different “name,” establishing a viral identity for HIV/AIDS and thus offered an explanatory frame rooted in its materiality. How are epidemic diseases contained with matter? Furthermore, John Lesch, in chapter 7, explains how this fatal disease could be contained with matter that alters or blocks the operation of the HIV virus. Lesch marks four distinct “turning points” in pharmaceutical history that advanced the therapy. In the first phase, before the virus was identified, scientists focused on drugs already known from cancer research (e.g., Interferon). In the second and third phases, medical laboratories created the first classes of effective drugs such as AZT. The final stage has been the most “recognizable,” leading to the development of combination “drug cocktails” that can suppress and control the disease as long as patients have access to prolonged treatment.37 While the period from onset of the epidemic to the beginning of effective treatment (1981-1996) seemed painstakingly slow progress for communities devastated by the disease, Lesch points out that this (comparative) short time frame was made possible by knowledge production that benefited from “longstanding treatment regimens” of other illnesses: tuberculosis, pneumonia, cancer, herpes, and several tropical diseases. Research “repurposed” chemical agents that previously showed anti-metabolite or antiviral activity, thereby accelerating drug development. Apparently, the reframing of the disease from “cancer” to “virus” had significant implications in selecting chemical compounds for research. Lesch notes that the idea that cancer was caused by retroviruses, so dominant in the 1970s, “smoothed the way from antiviral therapy as cancer therapy to antiviral therapy as AIDS therapy.” HIV/AIDS therapy does not eliminate the virus from the HIV-positive body, but it can prevent it from replicating and overwhelming the immune system. The resulting stasis is therapeutic but not fully curative, controlling by containing rather than destroying. Since 2012, HIV/AIDS therapy includes antiviral drugs that protect the HIV-negative body and reduce

37 Fontdevila, in chapter 5, reports that biomedical therapy is far from being a “magical bullet.” Studies show that national average for viral suppression is about 60% in the United States. Health Resources and Services Administration (HRSA), “HRSA Announces Highest HIV Viral Suppression Rate in New Ryan White HIV/AIDS Program Client-Level Data Report,” (Dec 2018). Last modified December 2018, https://www.hrsa.gov/about/news/press-releases/hrsa-announceshighest-hiv-viral-suppression-rate.

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infection risk by 92 percent.38 It is worth mentioning, however, that preexposure prophylaxis (PrEP) has an unintended relationship with another material object of prophylaxis, the condom. PrEP can lead to lower rates of condom use that in turn increases the spread of other sexually transmitted diseases (see Fontdevila). The therapeutic approach of photovoice in the fight against HIV/AIDS involves a very different physical “matter.” This method utilizes images captured with a camera.39 The photos are engineered in a photography rather than pharmaceutical laboratory, or produced digitally, and prove an effective material component in containing HIV/AIDS. Patients articulate their debilities and progress through physical documents, thereby facilitating intervention. Researchers Teti and Slaton illustrate how a focus on these particular objects alters a different kind of structural boundary by “effectively decentering the researcher’s experiences and any pre-existing research questions to allow consideration of participant perspectives.” As such, it has the potential to reduce the physical pressure of living with HIV/AIDS, while increasing patient compliance with biomedical protocols. How does matter fuel epidemic diseases? In epidemics, matter can transform and contain disease, and reduce or prevent infection. In another pharmaceutical enterprise, however, “matter” granted a virus unimpeded access to thousands of unsuspecting victims. In Henan, China, a cottage industry emerged to extract human blood and sell its plasma. As Xiaoxing Liu reports, in chapter 8, impoverished villagers became infected when they sold their blood at clandestine stations in the mid-1990s. Typically, when plasma is extracted by centrifuge, the remaining red blood cells and other cellular components are mixed with a saline solution and returned to the body. In this case, blood of the same type from multiple donors was combined for efficiency and profit. Station operators did not screen for HIV, and the reinjected blood provided a quick pathway for infection. Some individuals donated repeatedly to provide a steady source of income that may have alleviated poverty but ensured the 38

David Sidebottom, Anna Mia Estrom and Susanne Stromdahl, “A Systematic Review of Adherence to Oral Pre-exposure Prophylaxis for HIV – How Can We Improve Uptake and Adherence?” BMC Infectious Diseases 18 (November 2018): 581. https://doi:10.1186/s12879-018-3463-4. 39 Nicole Mareno, “Exploring Parental Perceptions of Healthy Eating and Physical Activity Using the Photovoice Method” in Nursing Research Using Participatory Action Research: Qualitative Designs and Methods in Nursing, ed. Mary de Chesnay (New York: Springer Publishing Company, 2016), 178.

24

Introduction

spread of the virus. Evidently, a growing marketplace for plasma, falling prices in centrifuges, corrupt officials, and poor rural villagers created a dystopian combination of bodies, blood, and machines for highly efficient viral delivery and epidemic manufacturing. In Liu’s case study, pathology was the result of a mechanism that massproduced living microbes. Epidemics can also arise from the mass production of non-living and non-infectious matter. Yang, in chapter 9, identifies “Big Tobacco,” “Big Food,” and “Big Pharma”40 as large-scale producers and distributors of harmful goods that significantly contribute to non-communicable disease epidemics. Indeed, scholars have argued that the cigarette is one of the world’s deadliest artifacts.41 By the 1950s, scientific studies had already established an indisputable link between smoking and lung cancer, yet global sales of cigarettes increased more than three-fold until its (temporary?) peak in 2017.42 That year, tobacco use was responsible for approximately seven million deaths globally,43 and it is estimated that as many as one billion people will die from this product in the twenty-first century.44 Firearms provide an analogous example of non-living matter “infecting” spaces and producing epidemics. As a result, public health models are increasingly used to address gun violence in the United States.45 In 2013, the Center for Disease Control and Prevention (CDC) reported 84,000 gunrelated injuries and 33,000 deaths. Gun-related homicide rates are 25 times higher in America than in other countries with comparable economies;

40

The pharmaceutical industry is implicated in playing a crucial role in the current opioid epidemic; see Scott E Hadland, Ariadne Rivera-Aguirre, Brandon D. L. Marshall et al., “Association of Pharmaceutical Industry Marketing of Opioid Products with Mortality from Opioid-Related Overdoses,” JAMA 2, no. 1 (2019): e186007, https://doi:10.1001/jamanetworkopen.2018.6007. 41 Robert N. Proctor, Golden Holocaust: Origins of the Cigarette Catastrophe and the Case for Abolition (Berkeley: University of California Press, 2012). 42 Ibid., “The History of the Discovery of the Cigarette-Lung Cancer Link: Evidentiary Traditions, Corporate Denial, Global Toll,” Tobacco Control 21, no. 2 (January 2013): 87-91. 43 Hillary Wasserman and Becky Bunn, “Lung Cancer Facts and Statistics” International Association for the Study of Lung Cancer, accessed August 21, 2019 from http://wclc2017.iaslc.org/wp-content/uploads/2017/09/2017-WCLC-FactSheet-Lung-Cancer-Final.pdf. 44 Proctor, Golden Holocaust. 45 Caterina Gouvis Roman, Jeffrey A. Butts, Jeremy R. Porter, and Lindsay Bostwick, “Cure Violence: A Public Health Model to Reduce Gun Violence,” Annual Review of Public Health, 36 (March 2015): 39-53.

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among 15 to 24-year-olds the rate is 49 times higher.46 The United States Congress inhibited funding of federal research on gun violence in 1996,47 and it took more than twenty years for congressional language to finally “allow” research in 2018. Still, the CDC cannot advocate for gun control.48 In some ways, this is akin to allowing research for breast cancer, but withholding permission to deploy a potential cure. Protecting patients may be more challenging when the matter that causes disease is inanimate, develops debilitating features only gradually, or cannot be directly (or immediately) linked to illness and death. Cigarettes harm not instantly, and even as they lead to illness and death, they do so discriminately. Lisa Crummett, in chapter 8, addresses some of these challenges, focusing on a third example of an industrially mass-produced substance that fuels epidemic disease. Crummett discusses sugar in its many forms, such as caramel, agave nectar, evaporated cane juice, and many others. She argues that extrinsic (added) sugar is a major factor in the global epidemic of metabolic syndrome (MetS), a “cluster of metabolic disorders” with longterm health implications such as Type 2 diabetes and cardiovascular disease.49 Her essay, together with others in this volume, shows that to 46

Debra Malina, Stephen Morrissey, and Edward W. Campion et al., “Rooting Out Gun Violence,” New England Journal of Medicine 374, no. 2, (January 2016): 175176. 47 Christine Jamieson, “Gun violence research: History of the federal funding freeze,” American Psychological Association, last modified February 2013, https://www.apa.org/science/about/psa/2013/02/gun-violence. 48 Alana Wise, “U.S. House Votes to Fund Gun Violence Research for The First Time in Decades,” KUNC, accessed August 21, 2019 from https://www.kunc.org/post/us-house-votes-fund-gun-violence-research-first-timedecades#stream/0. 49 Extrinsic (added) sugar is metabolically not equivalent to intrinsic sugar (contained within whole fruits and vegetables). Lisa Crummett reports that NCDs are responsible for 71% of deaths globally; and 88% in high-income countries. Furthermore, diabetes is the third leading cause of death in the US; the Global Burden of Disease Study (GBD) reaffirms Abdel Omran’s prediction, made in 1971, that the world was undergoing a remarkable transition from infectious to noncommunicable diseases. The GDB found that total deaths and age-standardized death rates due to communicable, maternal, neonatal, and nutritional conditions significantly declined from 2005 to 2015. In contrast, NCDs worsened across the world, including several types of cancer, ischemic heart disease, cirrhosis, and Alzheimer’s disease and other dementias.” Global Burden of Disease (GBD) 2015, “Mortality and Causes of Death Collaborators, "Global, Regional, and National Life Expectancy, All-Cause Mortality, and Cause-Specific Mortality for 249 Causes of Death, 1980-2015: A Systematic Analysis for the Global Burden of Disease Study 2015,” Lancet 388, no. 10053: 1459-1544. Abdel R. Omran, “The Epidemiological

26

Introduction

effectively change disease trajectory we must accept and respond to shared diseases as true epidemics (see Yang, Snyder, Lowe, Patterson, Weiner). After all, epidemics are experienced collectively not individually. A medical discourse that emphasizes “personal choices” and “individual lifestyle” is insufficient, or even prohibitive, in successfully confronting an epidemic (see Teti and Slaton). Instead, it is essential to recognize and communicate how they are promoted by biological and chemical processes. How does matter exert pressure on the human body in epidemics? Crummett’s research provides a clear link between a non-communicable disease matter and its associated pathologies by establishing the intricate relationships between excess sugar and its biological effects on the human body. Metabolic dysfunction begins with the liver but ultimately leads to systemic insulin resistance. She explains insulin resistance as “the core abnormality that ties together” all disorders associated with MetS, such as hypertension, obesity, and hyperlipidemia. It is particularly noteworthy that Crummett identifies the “matter” as the primary cause for subsequent debility. She documents that high intake of added sugars triggers biochemical processes that stimulate “excessive hunger,” “fat storage,” and “sluggishness.” In essence, being sedentary or obese are “downstream consequences” resulting from “high sugar consumption interfering with hormonal signaling.” Contrary to prevailing opinion, Crummett’s research implies that the toxic and addictive nature of the substance (rather than behavior alone) is the root cause of this epidemic. The shared symptoms and similar patterns of tissue damage across many bodies of a community can help identify a “gap” in the understanding in what creates widespread abnormal health effects. A better understanding could shift (sole) responsibility in this epidemic disease away from the individual. In Crummett’s example, one of the most universal sweeteners, corn syrup, is chemically altered to contain fructose, the sweeter and more harmful component in sugar. This increases the toxicity of the sweetener.50 Transition: A Theory of the Epidemiology of Population Change,” Millbank Memorial Fund Quarterly, no. 49 (October 1971): 509-538. See also chapter 9 in this volume by Joshua Yang. 50 Fructose is mostly metabolized by the liver alone (> 95%). In contrast, glucose is metabolized by every cell in the body. Corn syrup naturally consists of glucose and does not contain fructose. Jung Sub Lim, Michele Mietus-Snyder, Annie Valente et al., “The Role of Fructose in the Pathogenesis of NAFLD and the Metabolic Syndrome,” Nature Reviews Gastroenterology and Hepatology 7 (November 2010): 251-264.

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Scientific studies have identified fructose as the major contributor to insulin resistance. Crummett joins other authors in this volume by suggesting that increased awareness of the harmful nature of mass-produced matter should create or change regulatory structures (see Lowe, Yang, Liu). Edward Lowe points to a specific kind of herbicide called paraquat, which became a common method of self-poisoning in places as diverse as Trinidad and Tobago, Sri Lanka, and South Korea.51 In a case study of Samoa, Lowe provides evidence that the availability and level of regulation of this product is related to rates of suicide. Correlation is better confirmed as causation when we see suicide rates fall after paraquat is more carefully regulated or its formula altered to be less toxic.52 In sum, while we cannot compare the toxicity of excess sugar to that of paraquat, these and other examples discussed in this book help reveal how matter can impact and exert pressure on the human body’s ecosystem in different ways. Such revelation is needed for protecting consumers and containing disease epidemics. How are epidemics linked to changing physical and living environments? The relationship between changing ecosystems and epidemic disease is at the center of the final two essays in Part II. While metabolic diseases are defined and studied in niche-like spaces within the human body (e.g., liver, pancreas, brain), they often provide pathophysiological links to infections. In fact, all NCDs have the potential to compromise the immune system and the ultimate cause of death is usually prompted by an infectious microbe. Parvin Shahrestani, in chapter 11, takes an evolutionary biology approach to understanding infectious diseases by investigating ecological relationships between humans and microbes. She argues that to understand the human body’s defense to infectious disease, we need far-reaching studies of host-pathogen interactions in a “context of their evolutionary histories.” In her research on fungal infections,53 she uses fruit flies 51

IB Gawarammana and NA Buckley, “Medical Management of Paraquat Ingestion,” British Journal of Clinical Pharmacology 72, no. 5 (November 2011): 745-57; and H. Daisley and V. Simmons, “Forensic analysis of acute fatal poisonings in the southern districts of Trinidad,” Veterinary and Human Toxicology 41, no. 1 (February 1999): 23-5. 52 Martin F. Wilks, John A. Tomenson, Ravindra Fernando et al., “Formulation changes and time trends in outcome following paraquat ingestion in Sri Lanka,” Clinical Toxicology 49, no. 1 (2011): 21-28; and Eun Shil Cha, Shu-Sen Chang, David Gunnell, et al., “Impact of paraquat regulation on suicide in South Korea,” International Journal of Epidemiology 45, no. 2 (November 2015): 470-479. 53 Understanding defense mechanisms for fungal infections may provide important insights for global human health and food security. Shahrestani’s research has wider

28

Introduction

(Drosophila melanogaster) that share 70 percent of disease genes with humans and present similar innate immune defenses. When Shahrestani exposed multiple generations of this model organism to a fungus, she noticed that some populations evolved a more effective immune response and increased survival rates. Her research further shows that adaptation to survive in the presence of the fungus compromised life expectancy in the absence of infection. In other words, “immune defense is costly and trades off with other traits.” Shahrestani’s contribution has important implications for prevention and therapy of infectious diseases. Humans are clearly at a disadvantage in the “co-evolutionary arms race with pathogens.” Our longer lifespans and (relative) small population size allow pathogens to evolve faster. Hence we remain susceptible. Yet genetic material from flies with better survival rates helps Shahrestani identify “potential candidate genes” that already exist in natural populations. She argues that “we need to consider evolutionary forces acting on those genes” to reveal the genetic and environmental factors relevant to human immune defense variations. Her method reflects the willingness of other SHAPES authors to think broadly and creatively. She observes that “traditional molecular genetic approaches are insufficient.” Instead, she provides crucial additional insights by 1) using model organisms in “experimental evolution,” 2) conducting genome-wide analysis, and 3) considering immune response regulation at the level of the whole organism.54 These insights show the kinds of evidence needed for more informed disease ecology in epidemiology. Disease ecology focuses on how diseases are shaped by the interactions of biological agents and their abiotic environment.55 Microbes demonstrate their physicality by occupying and colonizing niches within boundaries and bodies. Their “home environments” vary widely. For example, a single bacterium of tetanus (causing “lockjaw”) can live enveloped in an endosporic state for a millennium. These organisms inhabit soil, water, and even house dust, but will not cause harm unless entering the human body through a dirty wound. In contrast, the HIV virus is an “obligate” implications and may offer potential for “biological control of insect crop pests and insect vectors of human disease.” 54 For a detailed description on how model organisms are recently used for “wholeorganism physiology,” see Nicolas Buchon, Neal Silverman, and Sara Cherry, “Immunity in Drosophila melanogaster—from microbial recognition to wholeorganism physiology,” Nature Reviews Immunology 14, no. 12 (December 2014): 796-810. https://doi:10.1038/nri3763. 55 Linda Nash, Inescapable Ecologies: A History of Environment, Disease, and Knowledge, (Berkeley: University of California Press, 2016).

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intercellular parasite and cannot survive outside the body (or artificial and regulated conditions). Other epidemics require synchronized interaction, such as Yersinia pestis (bacterium of bubonic plague) that involves accidental cooperation between humans, rodents, and fleas.56 Ian Read, in chapter 12, explores a pronounced shift in the interaction of hosts and pathogens in South America. He argues that during the second half of the nineteenth century, three countries in particular (Brazil, Chile, and Argentina) experienced the most “fertile” epidemic environment since the first arrival of Europeans and their pathogens in the Americas. Several new epidemic diseases appeared while others worsened. Cholera and yellow fever, well-known in the North Atlantic, killed hundreds of thousands of people in the first recorded outbreaks.57 The bubonic plague arrived and smallpox outbreaks intensified. All of these involved distinct relationships between microbes, vectors, and humans. Yellow fever depends on a virus spread by particular species of mosquito and one type, the Aedes aegypti, was especially well suited for urban outbreaks because of its propensity to breed on ships and within small amounts of water that accidentally collected in human receptacles. In contrast, cholera requires no intermediary vector, causing illness when people drink polluted water. Finally, smallpox requires close human interaction as the virus spreads by contact with contaminated objects or bodily fluids. Taken together, these “new” epidemics were manifestations of rapidly transforming physical environments resulting from urbanization and global transport of physical resources (see Patterson, Green, Liu, Lowe, and Yang). Read comments aptly, “with people and goods travel germs.” In this case study, the transforming physical environment also changed the relationship between “matter” and disease. Prevalent medical opinion in South America, according to Read, had reflected Hippocratic views that its 56 The life cycle of the bacteria that causes bubonic plague depends on a cycle of transmission that mostly involves rodents and their fleas. Among some rodents, the bacteria may be able to maintain itself in low-levels. Among other species, such as rats, the disease can spread rapidly and cause a large population to die. When these epizootic (animal outbreak) occurs near humans, infected fleas which had previously been hosted by the rats will seek its blood meals from other animals. In urban areas with dense populations and high rat infestation, a human epidemic of plague may occur when preceded by a die-off of rats. This type of epizootic was noticed before the outbreak of plague in San Francisco in 1900, for example; see Marilyn Chase, The Barbary Plague (New York: Random House, 2004), 189. 57 Donald B. Cooper, “Oswaldo Cruz and the Impact of Yellow Fever on Brazilian History,” The Bulletin of the Tulane University Medical Faculty 26 (February 1967), 49-52; Ibid., "The New “Black Death”: Cholera in Brazil, 1855-1856," Social Science History 10, no. 44 (1986): 467-488.

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Introduction

good health was “pieced together by earth, wind, rain, and heat.” For nearly three centuries, this seemed particularly true for the region and these chemical “elements” were considered purifying and conducive to longevity. Numerous records attest to “fertile soil,” “healthy air,” “rising mists,” and “temperate heat.” By the end of the nineteenth century, the very same matter was described as polluted, pestilential, torrid, and deadly. Instead of cleansing the body, matter had become the source of epidemic disease. Doctors, visitors, and officials very quickly accepted long-held negative stereotypes about the unwholesome tropics (including their human population), thereby suppressing or eliminating centuries of positive views about the region. Transformation of matter and physical environment was evidently accompanied and conditioned by attitudinal shifts, as we have similarly observed in other epidemics (see Snyder, Weiner, Patterson). Read concludes, “Interdependent relations of living things, micro- or macroscopic, matter as much as the way that these things are culturally understood, but neither comes first.”

Part III: The Co-emergence and Co-resolution of Epidemics Indeed, all chapters in this volume show this interdependence between meaning and matter. Our discussion in Part I and II views epidemics through each explanatory frame to delineate their equal importance and to illustrate the specific ways they contribute to creating, sustaining, transforming, or containing outbreaks. We intend to carefully establish important intersections without confounding or collapsing the roles that meaning and matter play in the process. While our discussion describes some of the distinct processes through which they operate, the chapters clearly show that meaning and matter are invariably linked and co-emerge and react to one another. Understanding the biochemical and physical processes leading to disease (e.g., suicide, insulin resistance, leprosy, HIV/AIDS) will not necessarily affect containment or a cure in an adverse cultural, economic or political climate. And social, economic, and political forces can equally facilitate or curb pathogenic development. To better understand and address the complex challenges posed by epidemics, we need to focus on their coemergence and find co-resolution to the problems posed by both the material and ideological worlds. Monica Green’s synthesis of historical and genetic sources related to the Ebola epidemic serves as a vivid example to illustrate this process of coemergence and co-resolution. The author’s investigation provides an important counter-narrative to the “perfect storm” accounts of “unprecedented (and

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unpredictable) coincidence of circumstance and bad luck” that explained the outbreak in West Africa in 2014. Most interpretations blamed civil war, poverty, inadequate infrastructure, and the “sudden” presentation of this virus in an urban environment. Green contradicts the notion “that Ebola had never been present in West Africa before,” having arrived at her conclusion nearly eight months before other public health researchers reported, “We Were Warned About Ebola.” In her survey of published Ebola Viral Disease (EVD) research, Green applied approaches she has used in studying the evolutionary histories of several other global pathogens, looking for indications of “how those histories intersect and intertwine with human history.” Taking the “deep and long view” by extending geographic, political, and temporal boundaries, she was able to appreciate the severity of EVD. Green predicted it might become a global epidemic long before the 2019 Congo Outbreak was declared a global health emergency. She delivered a warning (five years before the recent announcement by the WHO) and predicted that EVD would remain a “permanent threat to humankind, demanding vigilant monitoring,” as well as vaccination programs comparable to smallpox. What had gone wrong to bring EVD so “unexpectedly” and violently into the social and physical realm in 2014? Green finds that researchers had published warning signs years before the first presumed outbreak, but these publications remained obscured, because of the “colonial practice of scientific research done by, and published for, non-Africans.” As a result, local health workers and populations had insufficient warning and remained vulnerable and exposed. Green points out that “global” disease can be affected by more than just geography. While “germs” may not observe geographic or cultural borders (see Patterson, Read), knowledge production often does (see Lowe). In this instance, the serological studies that revealed Ebola’s long history were conducted by German and Dutch researchers and published in French and Dutch journals (in English). Thus the story successfully evaded local cognizance. While history is certainly in no position to offer immediate relief to suffering during the “event” of an epidemic, Green contends that it can provide pertinent information about its severity and possibly expedite intervention. She suggests that by not treating “a situation [as] so unique that it sits outside our ability to interpret it,” we can see patterns and trajectories and learn from them. Setting an emerging epidemic in the context of other pandemics such as the plague, smallpox, or HIV/AIDS offers relevant information on how “diseases exploit” distinctly human behaviors that drive epidemics. As a result of a broad approach that historicizes the disease organism, including in the context of genetics, the

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2014 Ebola outbreak was not an unpredictable event. Rather, it appeared “as a process, and as an emerging zoonotic disease that was beginning to establish it[self] in the realm of the knowable.” Combined methodologies from different disciplines can help establish the “silent” phases of epidemics (e.g., the decades between the emergence of HIV around 1920, and its first clinically documented cases in the 1980s). Green reminds us of the inept response to HIV/AIDS, mainly in its early stages, when “firewalls between disciplines” prevented a much needed deeper understanding. She joins the other authors in SHAPES in a move toward consilience, so we may recognize “the critical ways in which human uses of biophysical and cultural environments have exacerbated, limited, or ameliorated the effects of pathogens on human communities.” The conversation between Tina Takemoto and the artist Rudy Lemcke, in chapter 14, illustrates another move towards consilience. Lemcke’s artistic expressions “make visible” the otherwise invisible: a minuscule, but highly deadly pathogen and the countless lives it claimed. In 1992, the artist performed Immemorial at the de Young Museum in San Francisco for Day Without Art, enacting a die-in that simultaneously represented loss and memory while constituting a political act of protest. AIDS Art not only was shaped by the epidemic but also fundamentally shaped perceptions of the disease, medical and pharmaceutical professions, AIDS activism, and LGBT identity.58 In another example, Lemcke transforms the name for a material object, Foscarnet, a drug used to treat blindness affecting people with HIV, into a mesostic poem. He shows “the range of emotions attached to these drugs: the evasiveness, uncertainty, and precarity of hope for possible ‘cures.’” Additionally, the matter intended to cure blindness was imbued with meaning and served “as a metaphor for the ability or willingness to see or not see the HIV/AIDS pandemic.” Lemcke’s art illuminates the multivalent ways physical disease manifests itself within the context of socio-political systems of power and control that—in the case of HIV/AIDS and many of the epidemics discussed here—were “literally killing people.” In essence, meaning and matter do not interact in a fixed, one-directional way, neither in their co-emergence nor in their coresolution.

58 Jonathan D. Katz, Art AIDS America (Seattle: University of Washington Press, 2015).

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Conclusion In exploring any complex process, the interdisciplinary approach requires a patient, scholarly intimacy in which the learning objective of making creative connections and arriving at innovative solutions is as important as retaining foundational knowledge. This approach or attitude usually comes naturally to our students (and most people outside of academia, in fact) who may be more guided by a curious search for answers or resolutions than the thick stitches that hem in disciplinary training. Nevertheless, it is not uncommon to hear concerns regarding “the current focus on interdisciplinarity.”59 For instance, a recent article in Nursing Outlook sounded an alarm over the state of disciplinary integrity in the nursing profession. The authors stated, “that many nurses who conduct research that is not explicitly based on nursing perspectives … may well be serving the human good, but it is questionable whether such research will contribute to the development of unique nursing knowledge.” The scholars noted that “interdisciplinary endeavors can be useful, even critical,” but pointed out that “we are at risk of losing our identity.”60 We advocate for a different vision. Scholars must take the leap beyond the typical constraints of disciplinary boundaries, challenge established power relationships, and redefine the often one-directional, hierarchical flow of knowledge production so often embedded in biomedical and behavioral protocols (see Lowe, Fontdevila, Teti/Slaton, Liu, Weiner, Patterson, Crummett). Who says that pathologists should not use historical and cultural evidence to unravel transmission patterns and predict emergence of future “hot spots” (see Yang, Crummett, Shahrestani); that historians cannot depend on biochemistry or genetics for their claims (see Lesch, Green); that public health experts cannot use photographs as objects of empathetic ethnography to enhance therapeutic success (see Teti/Slaton); or that artists cannot use music, philosophy, literature and technology to inspire their work and galvanize political revolution and scientific discovery (see Takemoto/Lemcke)? Not long ago, a group of scholars described their collective mission as “the ideal of learning as an act of community, in which students and faculty come together to explore and extend the foundations of knowledge.”61 This mission is particularly important for the study of 59 Pamela J. Grace, Danny Willis, Callista Roy and Dorothy A. Jones, “Profession at the Crossroads: A Dialog Concerning the Preparation of Nursing Scholars and Leaders.” Nursing Outlook 64, no. 1 (October 2015): 62. 60 Ibid. 61 Scott Beardsley. Higher Calling: The Rise of Nontraditional Leaders in Academia (Charlottesville: University of Virginia Press, 2017), 63.

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epidemics as they are situated at crucial intersections of our human experience, requiring the far-reaching collaboration of experts from across academia. In fact, as shown by Rudy Lemcke’s beautiful art, which one day may outlive the plague it helped transform: this is no pedantic debate but a strategy for survival, truth, and justice.

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https://www.cdc.gov/nchhstp/newsroom/docs/factsheets/new-hivinfections-508.pdf. Cha, Eun Shil, Shu-Sen Chang, David Gunnell et al. “Impact of paraquat regulation on suicide in South Korea.” International Journal of Epidemiology 45, no. 2 (November 2015): 470-479. Chase, Marilyn. The Barbary Plague. New York: Random House, 2004. Cook, Noble David. Born to Die: Disease and New World Conquest, 14921650. Cambridge: Cambridge University Press, 2004. Cooper, Donald B. “Oswaldo Cruz and the Impact of Yellow Fever on Brazilian History.” The Bulletin of the Tulane University Medical Faculty 26 (February 1967), 49-52. Cooper, Donald B. “The New “Black Death”: Cholera in Brazil, 18551856.” Social Science History 10, no. 44 (1986): 467-488. Crosby, Alfred W. The Columbian Exchange: Biological and Cultural Consequences of 1492. Westport, Conn.: Greenwood Press, 1972. Cunha, B. A. “Smallpox and Measles: Historical Aspects and Clinical Differentiation.” Infectious Disease Clinic North America 18, No. 1 (March 2004): 79-100. Cutcliffe, John R., and Paul S. Links. “Whose Life is it Anyway? An Exploration of Five Contemporary Ethical Issues that Pertain to the Psychiatric Nursing Care of the Person who is Suicidal: Part One.” International Journal of Mental Health Nursing 17, no. 4 (August 2008): 236-245. https://doi:10.1111/j.1447-0349.2008.00539.x. Cyrklaff, Marek, Sanchez, Cecilia, Kilian Nicole, et al. “Hemoglobins S and C Interfere with Actin Remodeling in Plasmodium falciparum–Infected Erythrocytes.” Science 334, no. 6060 (December 2011): 1283-1286. https://doi.org/10.1126/science.1213775. Daisley, H. and V. Simmons. “Forensic analysis of acute fatal poisonings in the southern districts of Trinidad,” Veterinary and Human Toxicology 41, no. 1 (February 1999): 23-5. Egede, Leonard E. “Race, Ethnicity, Culture, and Disparities in Health Care.” Journal of General Internal Medicine 21, no. 6 (2006):667–669. https://doi:10.1111/j.1525-1497.2006.0512.x. Galishoff, Stuart. “Germs Know No Color Line: Black Health and Public Policy in Atlanta, 1900–1918.” Journal of the History of Medicine and Allied Sciences 40 (January 1985): 22–41. Gawarammana, IB and NA Buckley. “Medical Management of Paraquat Ingestion,” British Journal of Clinical Pharmacology 72, no. 5 (November 2011): 745-57. Global Burden of Disease (GBD) 2015, “Mortality and Causes of Death Collaborators, “Global, Regional, and National Life Expectancy, All-

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Cause Mortality, and Cause-Specific Mortality for 249 Causes of Death, 1980-2015: A Systematic Analysis for the Global Burden of Disease Study 2015,” Lancet 388, no. 10053: 1459-1544. Gould, Stephen J. The Mismeasure of Man. New York: W. W. Norton, 1996. Grace, Pamela J., Willis, Danny, Roy, Callista, and Dorothy A. Jones. “Profession at the Crossroads: A Dialog Concerning the Preparation of Nursing Scholars and Leaders.” Nursing Outlook 64, no. 1 (October 2015): 61-70. Hadland, Scott E., Ariadne Rivera-Aguirre, Brandon D. L. Marshall et al. “Association of Pharmaceutical Industry Marketing of Opioid Products with Mortality from Opioid-Related Overdoses,” JAMA 2, no. 1 (2019): e186007. https://doi:10.1001/jamanetworkopen.2018.6007. Hamlin, Christopher. Cholera: The Biography. Oxford: Oxford University Press, 2009. Health Resources and Services Administration (HRSA). “HRSA Announces Highest HIV Viral Suppression Rate in New Ryan White HIV/AIDS Program Client-Level Data Report.” Last modified December 2018, https://www.hrsa.gov/about/news/press-releases/hrsa-announceshighest-hiv-viral-suppression-rate. Herring, Ann D., and Alan C. Swedlund, eds., Plagues and Epidemics: Infected Spaces Past and Present. New York: Berg Publishers, 2010. Hill, Frances. The Salem Witch Trials Reader. Cambridge, MA: Da Capo Press, 2009. Hopkins, Donald R. The Greatest Killer: Smallpox in History. Chicago: University of Chicago Press, 2002. Jamieson, Christine. “Gun violence research: History of the federal funding freeze.” American Psychological Association, accessed August 21, 2019. https://www.apa.org/science/about/psa/2013/02/gun-violence. Jones, James H. Bad Blood: The Tuskegee Syphilis Experiment (New York: Free Press, 1993). Karsoho, Hadi, Jennifer R. Fishman, David K. Wright, and Mary E. Macdonald. “Suffering and Medicalization at the End of Life: The Case of Physician-assisted Dying.” Social Science & Medicine 170 (December 2016): 188-96. https://doi.org/10.1016/j.socscimed.2016.10.010. Katz, Ingrid T., Annemarie E. Ryu, Afiachukwu G. Onuegbu et al. “Impact of HIV-related Stigma on Treatment Adherence: Systematic Review and Meta-synthesis.” Journal of the International Aids Society 16, no. 3, suppl. 2 (November 2013): 1-25.

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Katz, Jonathan D. Art AIDS America. Seattle: University of Washington Press, 2015. Kiple, Kenneth and Virginia Kiple. “The African Connection: Slavery, Disease and Racism.” Phylon 41, no. 3 (1980): 211-22. https://doi.org/10.2307/274784. Kupferschmidt, Kai. “Labmade smallpox is possible, study shows.” Science 357, no. 6347 (July 2017): 115-116. Leeuwen, Theo van. “Three Models of Interdisciplinarity,” in New Agenda in (Critical) Discourse Analysis: Theory, Methodology and Interdisciplinarity, edited by Ruth Wodak and Paul Chilton. Philadelphia: John Benjamin Publishing Company, 2007. Li, Yu, Darin S. Carroll, Shea N. Gardner et al. “On the origin of smallpox: Correlating variola phylogenics with historical smallpox records.” PNAS. 104, no. 40: 15787-15792. https://doi.org/10.1073/pnas.0609268104. Lim, Jung S., Michele Mietus-Snyder, Annie Valente, et al. “The Role of Fructose in the Pathogenesis of NAFLD and the Metabolic Syndrome.” Nature Reviews Gastroenterology and Hepatology 7, no. 5 (2010): 251264. Malina, Debra, Stephen Morrissey, Edward W. Campion et al. “Rooting Out Gun Violence”. New England Journal of Medicine. 374, no. 2, (January 2016): 175-176. Manica, Andrea, Franck Prugnolle, and Francois Balloux. “Geography is a Better Determinant of Human Genetic Differentiation than Ethnicity.” Human Genetics 118 (December 2005): 366-371. https://doi.org/10.1007/s00439-005-0039-3. Mareno, Nicole. “Exploring Parental Perceptions of Healthy Eating and Physical Activity Using the Photovoice Method” in Nursing Research Using Participatory Action Research: Qualitative Designs and Methods in Nursing, ed. Mary de Chesnay. New York: Springer Publishing Company, 2016. Martin, Paul M.V. and Estelle Martin-Granel. “2,500-year Evolution of the Term Epidemic.” Emerging Infectious Diseases 12, no. 6 (June 2006): 976-980. https://doi:10.3201/eid1206.051263. Matthews, T.J., MacDorman, Marian F., and Marie E. Thoma. “Infant Mortality Statistics from the 2013 Period Linked Birth/Infant Death Data Set.” National Vital Statistics Reports 64, no. 9 (August 2015): 130. Nash, Linda. Inescapable Ecologies: A History of Environment, Disease, and Knowledge. Berkeley: University of California Press, 2016.

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Omran, Abdel R. “The Epidemiological Transition: A Theory of the Epidemiology of Population Change.” Millbank Memorial Fund Quarterly, no. 49 (October 1971): 509-538. Ostherr, Kristen. Cinematic Prophylaxis: Globalization and Contagion in the Discourse of World Health. Durham: Duke University Press, 2005. Pappas, Georgios, Kiriaze, Ismene J., and Matthew E. Falagas. “Insights into Infectious Disease in the Era of Hippocrates.” International Journal of Infectious Diseases 12, no. 4 (July 2008): 347-350. Porta, Miquel, ed. A Dictionary of Epidemiology. New York: Oxford University Press, 2008. https://doi:10.1093/acref/9780195314496.001.0001. Proctor, Robert N. Golden Holocaust: Origins of the Cigarette Catastrophe and the Case for Abolition. Berkeley: University of California Press, 2012. Proctor, Robert N. “The History of the Discovery of the Cigarette-Lung Cancer Link: Evidentiary Traditions, Corporate Denial, Global Toll.” Tobacco Control 21, no. 2 (January 2013): 87-91. Reed, T. V. The Art of Protest: Culture and Activism from the Civil Rights Movement to the Streets of Seattle. Minneapolis: University of Minnesota, 2005. Reinhardt, Bob H. The End of a Global Pox: America and the Eradication of Smallpox in the Cold War Era. Chapel Hill: The University of North Carolina Press, 2018. Repko, Allen F. Interdisciplinary Research: Process and Theory. Thousand Oaks, Calif.: SAGE Publications, 2012. Roman, Caterina Gouvis, Jeffrey A. Butts, Jeremy R. Porter, and Lindsay Bostwick. “Cure Violence: A Public Health Model to Reduce Gun Violence.” Annual Review of Public Health, 36 (March 2015): 39-53. Rosenberg, Charles E. “Disease in History: Frames and Framers.” The Milbank Quarterly 67, suppl. 1. (1989): 1-15. Roy, Sabita, Jana Ninkovic, Santanu Banerjee et al. “Opioid Drug Abuse and Modulation of Immune Function: Consequences in the Susceptibility to Opportunistic Infections.” Journal of Neuroimmune Pharmacology 6, no. 4 (December 2011): 442-65. https://doi.org/10.1007/s11481-011-9292-5. Shepard, Benjamin, and Ronald Hayduk, eds. From ACT UP to the WTO: Urban Protest and Community Building in the Era of Globalization. London and New York: Verso, 2002. Showalter, Elaine. Hystories Hysterical Epidemics and Modern Media. Charlesbourg, Québec: Braille Jymico Inc, 2003.

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Sidebottom, David, Anna Mia Estrom and Susanne Stromdahl, “A Systematic Review of Adherence to Oral Pre-exposure Prophylaxis for HIV – How Can We Improve Uptake and Adherence?” BMC Infectious Diseases 18 (November 2018): 581. https://doi:10.1186/s12879-0183463-4. Szostak, Rick. “How and Why to Teach Interdisciplinary Research Practice.” Journal of Research Practice 3, no. 2 (2007): 2. Retrieved August 25, 2019 from http://jrp.icaap.org/index.php/jrp/article/view/92/89. Tapper, Melbourne. In the Blood: Sickle Cell Anemia and the Politics of Race. Philadelphia: University of Pennsylvania Press, 2011. Tattersall, Robert. Diabetes: The Biography. Oxford: Oxford University Press, 2009. Varelius, Jukka. “Voluntary Euthanasia, Physician-Assisted Suicide, and the Right to Do Wrong.” Healthcare Ethics Committee Forum 25, no. 3 (September2013): 229-43. Wald, Priscilla. Contagious: Cultures, Carriers, and the Outbreak Narrative. Durham: Duke University Press, 2008. Wasserman, Hillary and Becky Bunn, “Lung Cancer Facts and Statistics” International Association for the Study of Lung Cancer, accessed August 21, 2019, http://wclc2017.iaslc.org/wp-content/uploads/2017/09 /2017-WCLC-Fact-Sheet-Lung-Cancer-Final.pdf. Wertheim, J. O. “Viral Evolution: Mummy Virus Challenges Presumed History of Smallpox.” Current Biology 27, no. 3 (February 2017): R119R120. https://doi: 10.1016/j.cub.2016.12.008. Wilks, Martin F. John A. Tomenson, Ravindra Fernando et. al. “Formulation changes and time trends in outcome following paraquat ingestion in Sri Lanka.” Clinical Toxicology 49, no. 1 (2011): 21-28. Wilson, Edward O. Consilience: The Unity of Knowledge. New York: Vintage Books, 1998. Wise, Alana. “U.S. House Votes to Fund Gun Violence Research for The First Time in Decades.” KUNC. Accessed August 21, 2019 from https://www.kunc.org/post/us-house-votes-fund-gun-violenceresearch-first-time-decades#stream/0. Wodak, Ruth, and Paul Chilton, eds. New Agenda in (Critical) Discourse Analysis: Theory, Methodology and Interdisciplinarity. ProQuest Ebook Central, 2005. https://doi.org/10.1075/dapsac.13.

PART I: THE SHAPE AND SHAPING OF EPIDEMICS IN WEBS OF MEANING

CHAPTER ONE SUICIDE, SLAVERY, AND EPIDEMICS: A PERSPECTIVE FROM EARLY MODERN BRITISH AMERICA TERRI L. SNYDER

In May 1773, the following item appeared in several London newspapers: Tuesday a Black Servant to Capt. Ordington, who a few days before ran away from his Master and got himself christened, with the intent to marry his fellow-servant, a White woman, being taken and sent on board the Captain’s ship in the Thames, took an opportunity of shooting himself through the head.1

Over the next few months, the account of this unnamed enslaved man appeared in the North American press as well. Which details of his story most fascinated readers? That he had been brought to London and escaped his enslaver? That he and a similarly unnamed English woman planned to marry? Or that he shot himself rather than face transport back to American slavery as he waited, imprisoned in a ship anchored in the Thames River?2 Whatever the sources of the story’s appeal, it sparked an immediate reaction, and two London lawyers quickly composed a poem based on this incident (Fig. 1). The resulting publication, The Dying Negro, a lengthy melodramatic verse, was something of an overnight sensation. It spawned multiple editions by 1780 and was reprinted well into the nineteenth century; it inspired songs and even a few imitators. As its authors had intended, the dramatic account of the enslaved man’s suicide — illustrated

1

The Morning Chronicle and London Advertiser, May 28, 1773, 25; General Evening Post, May 1773, 25–27; and Lloyd’s Evening Post, May 1773, 26–28. 2 Virginia Gazette (Purdie &Dixon), July 22, 1773.

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Figure 1. Thomas Day and John Bicknell. The Dying Negro, A Poem. 3rd edition, corrected and enlarged. London: W. Flexney; J. Wilkie; and J. Robson, 1775. The Dying Negro sentimentalized the theme of slave suicide and was an overnight sensation, enjoying wide publication in newspapers in England and America beginning in 1773. Source: Thomas Day and John Bicknell The Dying Negro, The Dying Negro, a Poetical Epistle supposed to be written by a Black (Who later shot himself on board a vessel in the river Thames;) to his intended Wife (London, 1773). This image is reproduced by permission of The Huntington Library, San Marino, California.

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on the cover of the printed poem as seen above—ignited antislavery debate across England and British North America. 3 About forty years later, in November 1815, an enslaved woman named Anna was brought to the District of Columbia. Without notice, her owner had sold her and two of her daughters to a “Georgia-man” who forced them away from the Maryland plantation on which her family had labored. The trader temporarily lodged them in a tavern. Imprisonment weighed heavily on Anna, and early one morning she became so “confused and distracted” that she jumped out of the third-story garret window (Fig. 2). She survived the fall. The story of her sale, imprisonment, and self-destructive leap sparked the already smoldering debate over slave trading in the nation’s capital. Along with other accounts of slave trafficking and suicide, Anna’s story spurred a congressional investigation (1816) and a printed exposé on slavery in the District of Columbia (1817). Like The Dying Negro, accounts of Anna were reprinted in antislavery periodicals and newspapers through the eve of the Civil War.4 While these stories and images may appear to be novel to us, the connection between suicide and slavery was a familiar theme in early modern Anglo-American culture. As The Dying Negro and Anna’s stories illustrate, from the last quarter of the eighteenth century forward, antislavery reformers on both sides of the Atlantic drew on accounts of enslaved peoples’ suicides in order to protest slavery, often with great success. In the hands of antislavery reformers, the suicides featured in The Dying Negro and Anna’s leap took aim at specific moral, physical, and political harms of slavery: the international and domestic slave trades, the separation of families, forced confinement, the denial of natural rights, and physical and

3

Thomas Day and John Bicknell, The Dying Negro, a Poetical Epistle (London, 1773). On the poem’s history, see Brycchan Carey, British Abolitionism and the Rhetoric of Sensibility: Writing, Sentiment, and Slavery, 1760–1807 (New York: Palgrave Macmillian, 2005), 75–84; Richard Bell, We Shall Be No More: Suicide and Self-Government in the Newly United States (Cambridge, MA: Harvard University Press, 2012), 205–08; and Terri L. Snyder, The Power to Die: Slavery and Suicide in British North America (Chicago: University of Chicago Press, 2015), 121–26, 131–36. 4 Jesse A. Torrey, A Portraiture of Domestic Slavery in the United States (Philadelphia: John Bioren (printer), 1817), 42–44; E. A. Andrews, Slavery and the Domestic Slave-Trade in the United States (Boston: Light & Stearns, 1836), 130–33; Secondary treatments of Anna’s story include Robert Gudmestad, A Troublesome Commerce: The Transformation of the Interstate Slave Trade (Baton Rouge: Louisiana State University Press, 2003), 35–37, 61; Bell, We Shall Be No More, 216–20; and Snyder, Power to Die, 1–6.

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Figure 2. Engraving of Anna’s suicide attempt, 1817. “—but I did not want to go, and I jump'd out of the window. —” This illustration was used in an anti-slavery tract, focusing on the separation of mother and child that led the former to suicide. The theme of suicide was a common trope used in abolitionist writings to illustrate the wrongs of slavery. Source: Jesse Torrey, A Portraiture of Domestic Slavery in the United States (Philadelphia, 1817). This image is reproduced by permission of The Huntington Library, San Marino, California.

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sexual brutality. Suicide by enslaved people was a shorthand representation for the wrongs of slavery. Suicide and slavery had a long history. From at least the seventeenth century forward, observers of the slave trade and participants in enslaving regimes remarked on captive Africans’ propensities for self-killing. Jean Barbot (1655–1712), for instance, a commercial agent who accompanied French slaving expeditions to the African coast, wrote that Africans were “steadfast and fearless” in their pursuit of death, regardless of their sex. Similarly, ship captains, surgeons, and crews engaged in the eighteenthcentury transatlantic slave trade routinely wrote about self-destruction by their captive cargos. Acts of suicide were frequent on Middle Passage that brought Africans across the Atlantic to the Americas. Rumors of slave selfdestruction circulated beyond the ship, and affected market values onshore as well. One North American factor asked his shipper to obtain “stout healthy fellows” but warned him that selling Calabar slaves was difficult because, as he wrote, significant numbers of enslaved people in every cargo “destroy [ed] themselves.”5 Self-destruction by enslaved women and men did not abate upon arrival in British America. Suicide was widely associated with the period of “seasoning,” the “amount of time an African must take to be so accustomed to the colony, as to be able to endure the common labour of a plantation.” Even after 1807, however, when the Constitution banned international slave imports to the U.S., suicide remained a visible feature of the domestic slave trade. The years between 1820 and 1860 marked the expansion of slavery in the U.S. In what some reformers called the “American Middle Passage,” millions of enslaved people were trafficked from the Mid-Atlantic region to service the expansion of cotton production south and westward. Moreover, almost every single American-born enslaved person who escaped slavery and wrote about their experiences not only admitted to their own selfdestructive thoughts but also wrote about the suicides of other enslaved people. Perhaps this is why the famous, formerly enslaved, black antislavery activist Frederick Douglass cautioned slaves not to “abandon yourselves, as

5

P. E. H. Hair, Adam Jones, and Robin Law, eds., Barbot on Guinea: The Writings of Jean Barbot on West Africa, 1678–1712, vol. 2 (London: Hakluyt Society, 1992), 639–40 (“steadfast and fearless”). “Henry Laurens to Peter Furnell, 6 September 1755,” in The Papers of Henry Laurens, eds. Philip M. Hamer, George C. Rogers, Jr., and Peggy J. Wehage, vol. 1 (Columbia: University of South Carolina Press, 1970), 331 (Callabar slaves). On Suicide and the Middle Passage, see Sowande M. Mustakeem, Slavery at Sea: Terror, Sex, and Sickness in the Middle Passage (Urbana-Champaign: University of Illinois Press, 2016), chap. 5.

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have many thousands of American slaves [have done], to the crime of suicide.”6 Do these reports reflect that an epidemic of suicide accompanied the rise of slavery in eighteenth-century British America and the early U.S.? Perhaps. Today, observers often assume that epidemics are objectively defined and quantitatively measured. We should bear in mind, however, that labeling diseases as “epidemics” casts a value judgment that is often politically fraught and can be a means by which the powerful marginalize other social groups. In contemporaneous accounts of British American slavery, for instance, descriptions of Africans as prone to suicide sustained assumptions about white supremacy and racial difference, and fed the enslavers’ claims about the putative brutish and heathen nature of Africans. Many of the sources for studying slave suicide—surgeon’s logs, coroner’s reports, legislative records, and enslavers’ diaries, for instance— are unreliable for establishing mortality rates. While captains and surgeons on slave ships were required to keep accounts of cargo losses for insurers and investors, these provide some quantitative measures of shipboard suicide, and studies using them exhibit a wide variation. One study of ship surgeons’ logs (1788–1797) finds that nearly one-third of slaving ships witnessed suicide by captive Africans. However, the study’s author describes that percentage as a “serious understatement,” and in any case, that number does not tell us how many slaves resorted to suicide. Another study of surgeons’ logs (1792–1796) finds that 7.2% of slave deaths during embarkation on the African coast and along the Middle Passage were attributed to suicide. It is worth noting that in 2018 the American Association for Suicidology found that 1.7% of deaths in the U.S. were caused by suicide, a comparison that suggests that the eighteenth-century percentages were sharply elevated. In addition, key legal decisions in the late 18th century gave incentives for shippers to underreport suicide, and so 6

Thomas Clarkson, An Essay on the Slavery and Commerce of the Human Species (London: Joseph Crukshank, 1785), 93 (quotation on seasoning). On slavery’s expansion in the early national U.S., see Damian Alan Pargas, Slavery and Forced Migration in the Antebellum South (New York: Cambridge University Press, 2015), 1–3; Adam Rothman, A Slave Country: American Expansion and the Origins of the Deep South (Cambridge MA: Harvard University Press, 2005), x–xi; Robert Gudmestad, A Troublesome Commerce: The Transformation of the Interstate Slave Trade (Baton Rouge: Louisiana State University Press, 2003), and 6–34, 210; Michael Tadman, Speculators and Slaves: Masters, Traders, and Slaves in the Old South (Madison: University of Wisconsin Press, 1989), 5–7, 22–52. Letter from Frederick Douglass [Emphasis mine], September 5, 1850, Frederick Douglass: Selected Speeches and Writings, Philip S. Foner, ed. (Chicago, 1999), 162 (quote), (158–62, inclusive).

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their numbers likely underestimate self-destruction by captive Africans. In British North America and the early United States, coroners' inquests on slaves were erratic and irregular; no law required that inquests be held for the enslaved. Under certain circumstances, owners could ask for compensation for deceased slaves—even for those who died by their own hands—but such requests were limited to slaves who were felons. To put it simply: the data from ship logs, coroners’ reports, and legislative petitions undercount suicides, and give us no way to determine the actual numbers of suicides by enslaved people in early modern British America.7 If we lack reliable numbers on slave suicide, however, the perception that there was an epidemic of suicide among enslaved people was widely shared by traders, shipmasters, sailors, surgeons, planters, enslaved people, and reformers connected to British American slavery. Those perceptions fit many of the early modern scientific markers of epidemics. Then as now, epidemics were typically described as maladies “common to or prevalent among a people or a community at a special time.” Epidemics were understood to be diseases that were produced by “special”—e.g. novel— causes that were not “naturally or generally present” in an affected locality. If an endemic disease is “constantly present,” an epidemic disease “occurs at levels beyond those expected.”8 Slavery and suicide had existed in African nations, of course. However, the rising scale of the Atlantic slave 7

Marcus Rediker, The Slave Ship: A Human History (New York: Viking, 2007), 291 (one-third statistics, quote); David Eltis, The Rise of African Slavery in the Americas (Cambridge: Cambridge University Press, 2000) 157n73 (7.2% statistics); American Association of Suicidology/Resources/Fact Sheets https://suicidology.org/ . Terri L. Snyder, “Suicide, Slavery, and Memory in North America,” Journal of American History 97, no. 1 (June 2010): 39–62; Snyder, Power to Die, 19–21, 167–169; and Geoffrey Clark, Betting on Lives: The Culture of Life Insurance in England, 1695–1775 (Manchester, UK: Manchester University Press, 1999), 16–17. 8 For a parallel study that explores the early modern preoccupation with melancholy—rather than its quantitative frequency—see Angus Gowland, “The Problem of Early Modern Melancholy,” Past and Present, 141 (May 2006), 77–120. On suicide by enslaved people, see Snyder, Power to Die, passim; William Pierson, “White Cannibals, Black Martyrs: Fear, Depression, and Religious Faith as Causes of Suicide among New Slaves,” Journal of Negro History, 62 (1977), 147–59; John Thornton, “Cannibals, Witches, and Slave Traders in the Atlantic World,” William and Mary Quarterly 3rd ser, 60 (2003), 273–94; and Henry Power and Leonard W. Sedgwick, eds., New Sydenham Society’s Lexicon of Medicine and the Allied Sciences, (London: New Sydenham Society, 1882), 563. See Dale H. Hutchinson, Disease and Discrimination: Poverty and Pestilence in Colonial Atlantic America (Gainesville: University Press of Florida, 2016), 16–17 for quoted definitions of epidemics.

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trade and the expanding scope of colonial slave regimes changed the nature of slavery. A distinctive form of slavery became an “embedded feature of the human and social landscape” of colonial British America. The distinguishing characteristics of colonial American slavery, according to the perceptions of participants and onlookers, may have indeed caused an epidemic of suicide among enslaved Africans and their descendants in early modern British America.9 The first among these causes would be the scale of the slave trade. Of the estimated 12.5 million Africans who were forcibly transported from Africa to the Americas, traders bought nearly 2.32 million to the British Caribbean and another 388,000 to mainland North America. Most of these captive Africans arrived in the eighteenth century when the sheer volume of human imports to British colonies grew exponentially. For instance, while an estimated 207,576 captive Africans disembarked in British possessions in the Americas in the last quarter of the seventeenth century, that number more than tripled, reaching 699,646 by the third quarter of the eighteenth century. The rising demand for slaves in the Americas had profound effects on captive Africans. Accelerated warfare necessary to procure captives extended forced marches from the African interior to the coast, warehousing of captives for months in coastal forts, and for those who had survived all of the above, transport across the Atlantic. In addition, for some Africans, the meaning of slavery changed dramatically in the Americas. Many forms of slavery existed in Africa—debt slaves, pawns, concubines, and chattel slaves—and in some regions, slaves enjoyed a modicum of rights and mobility from slavery was possible. In contrast, in the British Caribbean and some southern North American colonies, enslaved people constituted a majority of the population; a separate class of people distinguished by their status and race with little prospect of moving beyond the permanent, heritable, and debased status of slavery. The scale and scope of slavery in the Americas marked a new turn in the history of Atlantic slavery and can be understood as contributing factors to an epidemic of slave suicide.10 The uncommonly high mortality and morbidity rates of the slave trade also were likely causes of self-destruction by enslaved people. As is well known, the Middle Passage was a site of disease and death. Aboard ship, 9

James Walvin, Africa, the Americas, and the Atlantic Slave Trade (London: Reaktion Books, 2013), 62. 10 All figures are derived from The Trans-Atlantic Slave Trade Database, accessed June 26, 2020, https://www.slavevoyages.org/assessment/estimates. See also Walvin, Africa, the Americas, 58–63, 127–34; and Paul E. Lovejoy, Transformations in Slavery: A History of Slavery in Africa, 3rd ed. (Cambridge: Cambridge University Press, 2011), 1–24; 45–87.

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dying by suicide might have seemed to be a reasonable alternative to painful and lingering deaths from dysentery, smallpox, typhoid, and fevers. For instance, in the wake of a bloody flux that swept through a ship and killed half of the enslaved cargo, crew-members pitched the bodies of the dead and dying overboard; survivors watched and then took the opportunity to jump overboard as well.11 As the studies cited above suggest, suicides were regular events on slave ships. In certain regions of British America, mortality rates appear to have surpassed those of the Middle Passage. Planters in the Caribbean, for instance, expected to lose one-third of newly imported slaves in the first year after their arrival. As one planter put the matter: aside from the mortal dangers of diseases, enslaved people died because they fell into rum cisterns, crushed themselves in sugar mills, and fatally scalded themselves with boiling cane syrup; significant numbers of them also hanged themselves, he added, and “no creature knows why.”12 Historians typically associate high slave mortality rates with the Caribbean, but those of mid-eighteenth-century Virginia and South Carolina appear to rival those figures. A quarter of captive Africans died within the first year of arrival in Virginia, and the odds of death in the Lowcountry were even greater, with thirty percent of newly imported Africans dying within one year of disembarkation. Such high rates of death may have fostered despair among survivors. In Charleston, for instance, traders avoided paying burial fees by throwing overboard the bodies of captives who died awaiting sale; the corpses accumulated in the harbor and marshes surrounding the port city. Perhaps in response to such a grisly scene, one enslaved woman—a “poor pining creature”—hanged herself while waiting to be sold. Just as on the Middle Passage, overwhelming mortality, proximity to the dying, and disregard for customary burial rites may have produced anxiety, despair, and suicidal thoughts in survivors.13 In addition to high mortality, suicide by enslaved people was also closely linked to episodes of revolt. The suicides of captive Africans were themselves perceived as acts of rebellion. When slaves were brought on deck on the Le Rodeur in 1819, three leapt over the side and “many more” made the attempt unsuccessfully. Those who had escaped reportedly 11

Account of J. B. Romaigne (1819) in Slave Ships and Slavin, edited by George Francis Dow (Salem, MA: Marine Research Center, 1927), 30. 12 Edward Littleton, Groans of the Plantations (London: Printed by M. Clark, 1689), 20. 13 Philip D. Morgan, Counterpoint: Black Culture in the Eighteenth-Century Chesapeake and the Lowcountry (Chapel Hill: University of North Carolina Press, 1998), 444–46.

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“[danced] about” among the waves, singing a “song of triumph” in which they were joined by the remaining enslaved men and women on deck. When informed of the “revolt,” the captain identified ringleaders, shot three of them and hanged another three “before the eyes of their comrades.” Hans Sloane reported that slaves understood that death would bring them freedom, and for this reason, they “often cut their own throats.” In the Caribbean and mainland North America as well, some enslaved people who participated in rebellions hanged themselves in the aftermath, robbing the state of its desire to kill them for what it deemed to be treasonous acts.14 In some cases, acts of self-destruction also precipitated or signaled the onset of rebellion. The captain of the Venus noted that a few days after leaving the African coast, one slave leapt overboard in a “fit of passion” and another choked himself during the night. Two suicides in twenty-four hours caused the captain much “uneasiness” because, in them, he saw a “germ of revolt.”15 He was correct in his surmising, later noting that although “every precaution was taken against a rising . . . it finally took place when we least expected it.” If mariners understood suicide to be closely related to insurrection, did other enslaved people as well? Self-destruction by shipboard captives may have similarly signaled—or even deliberately precipitated—slippages in ship surveillance that provided the opportunity for revolt. Moreover, Africans’ self-inflicted deaths pointed toward the crew’s failure to control the human cargo aboard.16 Sexual and physical abuse was routinely used to terrorize enslaved people, and evidence suggests that some killed themselves in response to or 14

Dow, Slave Ships and Slaving, xxx–xxxi (Le Rodeur); and Hans Sloane, A Voyage to the Islands of Madera, Barbados, Nieves, S. Christophers and Jamaica, vol. 1 (London: Printed by B.M. for the author, 1710), xlviii. 15 Captain Theophilus Conneau, A Slaver’s Log Book or 20 Years Residence in Africa, ed. Howard S. Mott (London: Robert Hale Limited, 1977), 208; and Malcolm Cowley, Adventures of an African Slaver: Being a True Account of the Life of Captain Theodore Canot (London: George Routledge, 1928), 264. The accounts disagree in particulars: the former calls the ship the Venus and notes that the suicides made Conneau uneasy; while the latter identifies the vessel as La Estrella and indicates that “the officers” were uneasy. The editor of the 1977 version asserts that it is a more authentic transcription; see Conneau, A Slaver’s Log Book, iii–iv, 208. On Conneau, see Daniel P. Mannix and Malcolm Cowley, Black Cargoes: A History of the Atlantic Slave Trade, 1518–1865 (New York: Viking, 1962), 235, 294. 16 Snyder, Power to Die, 34–35. Henry Laurens to Henry Bright and Co., October 31, 1769, in The Papers of Henry Laurens, vol. 7, eds. George C. Rogers, Jr., David R. Chesnutt, and Peggy J. Clark (Columbia: University of South Carolina Press, 1968), 192.

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to avoid brutality. The captain of the ship Ruby forced one young captive woman into sexual slavery. He became enraged over a minor infraction and beat her so severely that she attempted self-harm. A few days later, three other women who were also destined for rape by the captain, threatened to throw themselves overboard rather than submit. Slaves who attempted to starve themselves on ships were flogged, and the physical brutality only spurred them to redouble their efforts. In 1730, the Sea Surgeon, a guide for medical officers on slave ships, warned that neither “fair means, or foul” could deter enslaved people from starving themselves to death: “they choose to die rather than to be ill-treated.”17 Enslaved people’s mental and emotional states were also cited as reasons for their suicides. Slaves were often described as melancholy and despondent, gloomy and listless, weak and sickly; their physical and mental states were emblematic of one another. One surgeon testified that by the time his ship carrying 602 Africans reached the West Indies, 155 people had died. When queried further, he averred that the greater proportion of these deaths—at least 2:1—was attributable to “melancholy.” Pressed further, he testified that of the ill slaves, those with melancholy had died and those “who had not that melancholy” recovered. He added further that he had “heard them say in their language, that they wished to die.” Or, as he rephrased, their deaths were “owing to their thinking so much of their situation.” Some ill slaves simply refused aid: one woman refused medicine, food, and wine; when asked what she wanted, she reportedly replied, “she wanted nothing but to die.” And she did. Enslaved people endured captivity, forced transport, violence, and separation from families, kin, and community. Moreover, any nascent social bonds that had been formed among captive shipmates on the Middle Passage were fractured upon arrival in the Americas, as captives were sold, endured transshipment to still farther destinations, and suffered renewed social isolation. One witness reported that slaves suffered from “despondency” because they had been torn from their “friends, relation, and country.” And just as onboard ships, once on land, slaves killed themselves individually, serially (one after another), and collectively (en mass) in response to enslavement. For instance, six enslaved men were planting cotton on a small island in the British West Indies. When their overseer left them alone for an evening, he returned the next day to find all six “hanging near together in the woods.”18 In sum, the scale of the 17 Sheila Lambert, ed., House of Commons Sessional Papers of the Eighteenth Century [hereafter HCSP] (Wilmington, DE, 1975), 69:126; and T. Aubrey, M.D., The Sea-Surgeon, or the Guinea Man’s Vade Mecum (John Clarke: London, 1729), 178. 18 HCSP, 73: 277–78.

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trade, high mortality, transshipment, the breaking of social bonds, sexual and physical violence were the prevalent circumstances that fostered an epidemic of slave suicide.19 When we study epidemics in history, we examine not only their precipitating factors but also the prevailing explanations for them. Across the eighteenth-century Anglo-Atlantic slave trade, some observers simply could not fathom the reasons behind slave self-destruction: consider enslaver Edward Littleton’s statement that “no creature knows why” enslaved Africans killed themselves. Mariners, traders, and enslavers alike often attributed suicide to newly imported (rather American-born) enslaved people and suggested that slaves could be socialized out of the practice. Given time, their comments seem to suggest, the apparent epidemic of suicide would disappear on its own. However, since the causes of slave suicide did not abate—forced migration, family separation, rape, sale, and brutality, for instance, were constants across the chronological span of American slavery—it is unlikely that self-destruction by enslaved people became less prevalent. To the contrary, the testimony of multiple slave narratives, along with Frederick Douglass’s remark that “thousands of American slaves” had destroyed themselves, suggests that suicide remained an epidemic among North American born slaves.20 Ex-slave Charles Ball, for instance, argued that self-destruction was “much more frequent among the slaves in the cotton region than is generally supposed,” adding that, based on his own experience of anguish over separation from his family and despair occasioned by domestic sale, he did not “marvel” that the slaves who were “driven to the south” often destroyed themselves. He also flatly stated that suicide by slaves did not violate the “precepts of religion, nor of the laws of God.”21 Rather than disappearing over time, as enslavers argued it would, suicide appears to have become more imaginable and more acceptable to enslaved people. Enslavers also explained slave suicide with reference to African ethnicity. Traders and planters believed that certain African nations were predisposed to revolt and suicide. In 1755, South Carolina merchant Henry Laurens wrote that Igbo slaves were quite “out of repute,” meaning that the prices were low, because great “numbers [of slaves] in every Cargo . . . destroy themselves.” A witness in a slave trade investigation reiterated this idea late in the eighteenth century, noting that slaves from the Igbo country 19 Mannix and Cowley, Black Cargoes, 119–21. HCSP, 72: 274–75, 300; and HCSP, 69: 122. 20 Foner and Taylor, Frederick Douglass, 162 (158–62, inclusive). 21 Ibid., Charles Ball, Slavery in the United States (New York, 1837), 69–70, accessed August 8, 2018, http://docsouth.unc.edu/neh/ballslavery/menu.html.

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were “remarkably high spirited” and “chose suicide because they did not “brook slavery so well as [slaves] from several other countries.” The branding stuck: a nineteenth-century tract described the Igbo as “addicted to suicide.”22 The Igbo were not the only group of Africans to be singled out. Barbot claimed that the Akan were fearless in the face of death and therefore predisposed to suicide. The Sugar Cane: A Poem in Four Books (1764)— reprinted in the United States as late as 1850—counseled planters to avoid the Coromontee because they “chose death before dishonorable bonds.” The verse also advised against purchasing older slaves, who were described as “sullen and unteachable and frequently put an end to their own lives.” Enslavers also developed explanations for suicide based on temperament: they labeled enslaved people as sulky, nostalgic, and stubborn—all traits that, enslavers argued, predisposed slaves to self-destruction. 23 In addition to ethnicity and temperament, observers also cited enslaved people’s spiritual beliefs as explanations for the frequency of suicide. Some enslaved people appear to have believed that death—however it occurred— was the beginning of a journey that would bring spiritual transmigration to Africa. Suicides often occurred in spiritually meaningful environments. Water was a conduit to the spiritual world and a channel of “repatriation” to families, ancestors, and Africa. Souls of the dead were understood to pass over “broad waterscapes,” and woods were associated with ancestors’ spirits who might guide enslaved people’s spiritual returns to Africa. Enslaved people sometimes accompanied their suicides with ritualistic elements necessary to their transmigration. Some slaves put on all of their clothes; others placed food and water nearby; others tied chains or bundles of food around their waists. Collective suicides in South and North Carolina involved ritual preparations that included singing and chanting. Ship captains and slave owners alike believed that Africans sought transmigration to homelands through self-inflicted death; enslavers punished such acts by

22

Henry Laurens to Peter Furnell, September 6, 1755, in The Papers of Henry Laurens, vol. 1, 331; HCSP, 73: 204; and Dr. Collins, Practical Rules for the Management and Medical Treatment of Negro Slaves in the Sugar Colonies (London, 1803), 37. 23 Hair, Jones and Law, eds., Barbot on Guinea, 639–40; James Grainger, “A History of Sugar Cane, from a Poem called Sugar Cane,” Gentleman’s Magazine, October 1764, 487, and later published as The Sugar Cane: A Poem in Four Books (London: Printed for R. and J. Dodsley, 1764), book 6, 129–30. For a nineteenth-century reprinting, see Debow’s Review, Agricultural, Commercial, Industrial Progress and Resources 9, no. 6 (1850): 668.

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decapitating or dismembering corpses, warning survivors that such postmortem desecration would prevent a journey homeward. 24 The belief that self-destruction began the processes of transmigration could be a powerfully positive inducement for enslaved people to take their own lives. Suicide was understood to destroy the body and preserve the soul. While that idea was anathema to those who profited from and owned slaves, evidence suggests that slavery intensified beliefs in the transformational power of death, even when it was self-inflicted. In New England in 1733, for instance, an enslaved New England woman cut open her stomach, exclaiming that she was returning to her own country. In 1707 naturalist and physician, Hans Sloane remarked that because of slaves’ beliefs in spiritual transmigration, they imagined that death would bring freedom and “for this reason often cut their own throats.” Suicide could also provide a resurrection of the self. One enslaved New England woman expressed her belief that death—regardless of whether or not it was self-inflicted—could result in an individual being reborn as the next child into a family. As late as 1823, a Jamaican planter noted that the enslaved people “all” expected that, “after death, they shall first return to their native country, and enjoy again the society of kindred and friends, from whom they have been torn away.” It was this idea, he continued, along with the terrors of seasoning, that “used to prompt numbers, on their first arrival, to acts of suicide.”25 Did slavery in early modern British North American produce an epidemic of suicide among enslaved people? Based on the anecdotal 24 Kevin Dawson, Undercurrents of Power: Aquatic Culture in the African Diaspora (Philadelphia: University of Pennsylvania Press, 2018), 32–33; Mary C. Karasch, Slave Life in Rio de Janeiro, 1808–1850 (Princeton, NJ: Princeton University Press, 1987), 319–20; Stephanie Smallwood, Saltwater Slavery: A Middle Passage from Africa to American Diaspora (Cambridge, MA: Harvard University Press, 2007), 186, 205; Louis A. Pérez, Jr., To Die in Cuba: Suicide and Society (Chapel Hill: University of North Carolina Press, 2005), 37; and John Spencer Bassett, Slavery in the State of North Carolina, (Baltimore, MD: Johns Hopkins University Press, 1899), 92–93. 25 Dawson, Undercurrents of Power, 32–34; Smallwood, Saltwater Slavery, 186; Michael A. Gomez, Exchanging Our Country Marks: The Transformation of African Identities in the Colonial and Antebellum South (Chapel Hill: University of North Carolina Press, 1998), 117–20; William D. Pierson, Black Yankees: The Development of an Afro-American Subculture in Eighteenth-Century New England (Amherst: University of Massachusetts Press, 1988), 75; Sloane, Voyage to the Islands of Madera, 1–48; and John Stewart, A View of the Past and Present State of the Island of Jamaica with Remarks on the Moral and Physical Condition of the Slaves and on the Abolition of Slavery in the Colonies (Edinburgh: Oliver and Boyd, Tweeddale-House, 1823), 280–81.

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evidence examined here, it certainly produced the perception that there was an epidemic of suicide by enslaved people. It must be noted, however, that the enslavers did not cite slavery itself as a cause of this epidemic. Rather, they attributed the epidemic of suicide to enslaved people themselves. Today we might call this “blaming the victim.” Eighteenth-century observers left all kinds of evidence that there was an epidemic of slave suicide, while the enslavers—who largely controlled the narrative of the epidemic until the rise of abolitionism—disarticulated slavery from suicide. Rather than link suicide to the circumstances of captivity, enslavement, labor regimes, physical and sexual violence, and the repeated fracturing of familial and community bonds, enslavers instead blamed suicide on enslaved people themselves—their temperamental propensities, ethnic identities, and spiritual beliefs. Despite this disarticulation, as in the case of any epidemic, enslavers sought to manage and limit the spread of the “disease” of suicide. Traders and planters avoided those groups such as the Igbo or the Akan who were reported to be prone to suicide. Limiting importation might limit the epidemic. In addition, the enslavers attempted to prevent suicide. When slaves tried to starve themselves, ship crews and owners used the speculum oris to open the jaws of the recalcitrant and force them to eat (Fig. 3). Such measures were not routinely successful. When one trader began to forcefeed a slave, he “bit so hard on the ‘mouth screw'” that the mechanism broke. The trader determined that: the slave was so stubborn, “he would rather be dead than eat.” Even children “[took] sulk” and refused sustenance.26 If enslavers could not always physically prevent suicide attempts by enslaved people, they instead sought to instill physical terror as a form of suicide prevention. For instance, when captives jumped overboard, captains hanged and shot some of the survivors and forced others to watch. Similarly, other commanders ordered the bodies of suicides to be tossed to the sharks that followed ships and forced remaining captives to watch the sharks feeding as a means of discouraging any further contemplation of suicide.27

26 Johannes Postma, The Dutch in the Atlantic Slave Trade, 1600–1815, 241; HCSP, 73: 82 (throat cutting), 124 (child); for examples of self-starvation, see also HCSP, 68:125, 73:88, 117, 138, 160, 375. 27 Dow, Slave Ships and Slaving, xxx–xxxi; Dawson, Undercurrents of Power,. 32– 33.

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Figure 3: Speculum Oris, 1786. The speculum oris was used to forcibly feed slaves who refused to eat and drink. According to a merchant who sold the instrument, “slaves were frequently sulky, as to shut their mouths against all sustenance, and this with a determination to die; and it was necessary their mouths should be forced open to throw in nutrient, that they who had purchased them might incur no loss by their death.” Source: Thomas Clarkson, An Essay on the Slavery and Commerce of the Human Species, Particularly the African (1786). This image is reproduced by permission of The Huntington Library, San Marino, California.

Planters followed the lead of ship captains and attempted to manage suicide by manipulating the spiritual beliefs of enslaved people. Planters routinely ordered the post-mortem decapitation of the corpses of self-killing slaves, warning survivors that dismemberment prevented their dead compatriots from returning to Africa to rejoin their ancestors.28 In SaintDomingue, enslavers beheaded or defaced the first Igbo slave who died just after arrival, and in Cuba, owners burned the corpses of suicides. Across the Americas, the heads of suicidal and rebellious slaves were struck from their bodies and displayed on pikes. Some of these practices were consistent with the traditions of Europeans, who also used decapitation and dismemberment to punish traitors and some suicides. In the early modern period, slaves were not the only individuals whose corpses were desecrated; the bodies of traitors to the state and those of some suicides were treated similarly. By the end of the eighteenth century in British North American slave societies, 28

Pierson, “White Cannibals, Black Martyrs,” 154–55.

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however, only the corpses of slaves and occasionally those of white felons were subjected to post-mortem punishment. No evidence suggests that slaves believed their masters or that such dire practices had an effect on enslaved peoples’ suicides.29 Finally, like other epidemics discussed at the SHAPES conferences, information about enslaved people’s suicides was also suppressed. Many across eighteenth-century British America affirmed that slave self-destruction was common if not epidemical, but enslavers in mainland North America denied its existence. In the 1790s, Virginian William Beverley was queried by a House of Commons investigation about the numbers of self-destroying slaves in Virginia. He replied unequivocally that “never one” report of slave suicide had ever reached him. It is certainly possible that Beverley had never read the Virginia Gazette or other British or North American newspapers, gossiped over a coroner’s inquest, or visited any county court in the nearly twenty years that he had lived in the colonies, but that’s pretty unimaginable for a well-born Virginian who planned to enter the law. One slave recalled that when the corpse of a suicide was discovered, his owner ordered his enslaved people to never speak of it. Suicidal slaves reflected poorly on their masters’ reputations, fracturing their images of plantations as bucolic refuges rather than forced labor camps.30 Antislavery activists penned The Dying Negro (1773) for expressly political purposes, and with its publication, the image of the self-murdering slave became a staple of abolitionist print and visual culture. As with other epidemics discussed in this conference, the acknowledgment of an epidemic of slave suicide had to be forced on the public, its recognition driven by the political will of a committed and small band of reformers. Black and white antislavery activists publicized the existence of an epidemic of slave suicides in order to dismantle slavery. The choice of slave suicide was especially relevant in the context of the late eighteenth century for two reasons. First, rising humanitarianism regarded acts of suicide—even those by enslaved people—with sympathy and no longer treated self-destruction as a felony and sin deserving punishment. Second, new developments in 29 Ibid.; Jeffrey R. Watt, From Sin to Insanity: Suicide in Early Modern Europe (Ithaca, NY: Cornell University Press), passim. Michael MacDonald and Terence R. Murphy, Sleepless Souls: Suicide in Early Modern England (Oxford: Clarendon, 1990), 15–23; and Philip J. Schwarz, Slave Laws in Virginia (Athens: University of Georgia Press, 1996), 72–73. 30 Deposition of William Beverley, Lambert, ed., HCSP, 82: 216. For testimony on numbers of slave suicides, see Ibid., 82: 35, 49, 65, 71–74, 85, 196, 204, 211, 229, 230. For testimony that seasoned Africans not at all prone to suicide, see Ibid., 82: 85, 172.

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medical science postulated that enslaved people lacked the mental development to contemplate suicide; at their most extreme, medical authorities claimed that slaves did not have the physical capacity to suffer pain. Accounts like The Dying Negro or Anna used visceral illustrations of the personhood of enslaved people in order to counter the claims of racist medicine. Although white abolitionists fell into racist tropes, their depictions of enslaved peoples’ suicides as the outcome of anguish and suffering were implicitly pleas for their humanity.31 Today researchers study epidemics in relationship to biological causes affecting unsuspecting persons, the choices that lead to the spread of deadly disease, and the social consequences of pandemics. Slave suicide in eighteenth-century British America, however, raises a different question about epidemics. When the context of slavery produces a conscious longing for death and makes suicide more acceptable, can we understand self-killing by enslaved people as an epidemic of choice, as some at this conference have suggested? If so, we must also recognize that it was never a freely made choice. Rather, while often a deliberate decision, death by suicide was a choice made from an egregiously narrow range of possibilities, and, often in the direst of moments. In that sense, it may have been an epidemic of choice, but, at least for enslaved people in the context of British American slave regimes, one in which suicide had not only become more imaginable but also more acceptable.

31 Benjamin Rush. “Observations Intended to Favour the Supposition that the Black Color (as it is called) of the Negroes is Derived from the Leprosy,” Transactions of the American Philosophical Society, vol. 4 (1799), 289–297; and Adam Metcalf Reed, “Mental Death: Slavery, Madness and State Violence in the United States.” (Ph.D. diss., UC Santa Cruz, 2014), 92–149.

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Lambert, Sheila, ed. House of Commons Sessional Papers of the Eighteenth Century. Wilmington, DE, 1975. Littleton, Edward. Groans of the Plantations. London: Printed by M. Clark, 1689. Lloyd’s Evening Post [London], May 1773. Morning Chronicle and London Advertiser, May 28, 1773. Power, Henry and Leonard W. Sedgwick. eds. New Sydenham Society’s Lexicon of Medicine and the Allied Sciences. London: New Sydenham Society, 1882. Accessed July 26, 2020. https://archive.org/stream/newsydenhamsocie02newsuoft#page/562/m ode/2up. Rogers, Jr., George C., David R. Chesnutt, and Peggy J. Clark, eds. The Papers of Henry Laurens. Columbia: University of South Carolina Press, 1968. Rush, Benjamin. “Observations Intended to Favour the Supposition that the Black Color (as it is called) of the Negroes is Derived from the Leprosy” Transactions of the American Philosophical Society 4 (1799). Sloane, Hans. A Voyage to the Islands of Madera, Barbados, Nieves, S. Christophers, and Jamaica. 2 vols. London: Printed by B.M. for the author, 1710. Stewart, John. A View of the Past and Present State of the Island of Jamaica with Remarks on the Moral and Physical Condition of the Slaves and on the Abolition of Slavery in the Colonies. Edinburgh: Oliver and Boyd, Tweeddale-House, 1823. Torrey, Jesse A. A Portraiture of Domestic Slavery in the United States. Philadelphia: Printed by John Bioren, 1817. The Trans-Atlantic Slave Trade Database. Accessed July 26, 2020. http://www.slavevoyages.org/. Virginia Gazette, July 22, 1773.

Secondary Sources Bell, Richard. We Shall Be No More: Suicide and Self-Government in the Newly United States. Cambridge, MA: Harvard University Press, 2012. Carey, Brycchan. British Abolitionism and the Rhetoric of Sensibility: Writing, Sentiment, and Slavery, 1760–1807. New York: Palgrave Macmillian, 2005. Clark, Geoffrey. Betting on Lives: The Culture of Life Insurance in England, 1695–1775. Manchester, UK: Manchester University Press, 1999. Dawson, Kevin. Undercurrents of Power: Aquatic Culture in the African Diaspora. Philadelphia: University of Pennsylvania Press, 2018.

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Eltis, David. The Rise of African Slavery in the Americas. Cambridge: Cambridge University Press, 2000. Gomez, Michael A. Exchanging Our Country Marks: The Transformation of African Identities in the Colonial and Antebellum South. Chapel Hill: University of North Carolina Press, 1998. Gowland, Angus. “The Problem of Early Modern Melancholy.” Past and Present 141 (May 2006), 77-120. Gudmestad, Robert. A Troublesome Commerce: The Transformation of the Interstate Slave Trade. Baton Rouge: Louisiana State University Press, 2003. Hutchinson, Dale H. Disease and Discrimination: Poverty and Pestilence in Colonial Atlantic America. Gainesville: University Press of Florida, 2016. Karasch, Mary C. Slave Life in Rio de Janeiro, 1808–1850. Princeton, NJ: Princeton University Press, 1987. Lovejoy, Paul E. Transformations in Slavery: A History of Slavery in Africa, 3rd ed. New York: Cambridge University Press, 2011. MacDonald, Michael, and Terence R. Murphy. Sleepless Souls: Suicide in Early Modern England. Oxford UK: Clarendon Press, 1990. Mannix, Daniel P., and Malcolm Cowley, Black Cargoes: A History of the Atlantic Slave Trade, 1518–1865. New York: Viking, 1962. Morgan, Philip D. Slave Counterpoint: Black Culture in the EighteenthCentury Chesapeake and the Lowcountry. Chapel Hill: University of North Carolina Press, 1998. Mustakeem, Sowande M. Slavery at Sea: Terror, Sex, and Sickness in the Middle Passage. Champaign-Urbana: University of Illinois Press, 2016. Pargas, Damian Alan. Slavery and Forced Migration in the Antebellum South. New York: Cambridge University Press, 2015. Pérez, Jr., Louis A. To Die in Cuba: Suicide and Society. Chapel Hill: University of North Carolina Press, 2005. Pierson, William D. Black Yankees: The Development of an Afro-American Subculture in Eighteenth-Century New England. Amherst: University of Massachusetts Press, 1988. Pierson, William D. “White Cannibals, Black Martyrs: Fear, Depression, and Religious Faith as Causes of Suicide among New Slaves,” Journal of Negro History 62 (1977): 147–59. Postma, Johannes. The Dutch in the Atlantic Slave Trade, 1600–1815. New York: Cambridge University Press, 1990. Rediker, Marcus. The Slave Ship: A Human History. New York: Viking, 2007.

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Reed, Adam Metcalf. “Mental Death: Slavery, Madness and State Violence in the United States.” Ph.D. diss., UC Santa Cruz, 2014. Rothman, Adam. A Slave Country: American Expansion and the Origins of the Deep South. Cambridge MA: Harvard University Press, 2005. Schwarz, Philip J. Slave Laws in Virginia. Athens: University of Georgia Press, 1996. Smallwood, Stephanie. Saltwater Slavery: A Middle Passage from Africa to American Diaspora. Cambridge MA: Harvard University Press, 2007. Snyder, Terri L. “Suicide, Slavery, and Memory in North America,” Journal of American History, vol. 97, no. 1 (June 2010), 39-62.” Snyder, Terri L. The Power to Die: Slavery and Suicide in British North America. Chicago: University of Chicago Press, 2015. Tadman, Michael. Speculators and Slaves: Masters, Traders, and Slaves in the Old South. Madison: University of Wisconsin Press, 1989. Thornton, John. “Cannibals, Witches, and Slave Traders in the Atlantic World,” William and Mary Quarterly, 3rd ser., 60 (2003): 273–94. Walvin, James. Africa, the Americas, and the Atlantic Slave Trade. London: Reaktion Books, 2013. Watt, Jeffrey R. From Sin to Insanity: Suicide in Early Modern Europe. Ithaca NY: Cornell University Press, 2004.

CHAPTER TWO SUICIDE EPIDEMICS, POST-COLONIAL GOVERNANCE, AND THE IMAGE OF THE RECALCITRANT NATIVE IN OCEANIA EDWARD LOWE

This chapter is about how intervention into epidemics in post-colonial circumstances can be a means of continuing colonial “government at a distance”1 through the formation of translocal networks of expertise dedicated to studying and intervening into these health risks. To demonstrate this process, this chapter focuses on the formation of a network of expertise in the late 1970s and 1980s that emerged to study and intervene into two wellknown suicide epidemics. One in the South Pacific Islands of Samoa and the other in the Micronesian Pacific Islands in the former US Trust Territory of the Pacific Islands (USTTPI), which includes the present-day Republic of the Marshall Islands, Republic of Palau, and the Federated States of Micronesia.2 Based on documentary evidence, the chapter describes the 1

Peter Miller and Rose Nikolas, Governing the Present: Administering Economic, Social and Political Life (Cambridge UK: Polity Press, 2008). 2 Heather Booth, “Pacific Island Suicide in Comparative Perspective,” Journal of Biosocial Science 31, no. 4 (1999): 433–48; John Bowles, “Suicide and Attempted Suicide in Contemporary Western Samoa,” in Culture, Youth and Suicide in the Pacific: Papers from an East-West Center Conference, ed. Francis X. Hezel, Donald H. Rubinstein, and Geoffrey M. White, 15–35. Occasional Paper Series 25, Honolulu: Pacific Islands Studies Program, Center for Asian and Pacific Studies, University of Hawai‘i at MƗnoa. 1985; Francis X. Hezel, “Truk Suicide Epidemic and Social Change,” Human Organization 46, no. 4 (1987): 283–91; Hezel, “Suicide and the Micronesian Family,” The Contemporary Pacific 1, no. 1–2 (1989); Edward Lowe, “Epidemic Suicide in the Context of Modernizing Social Change in Oceania: A Critical Review and Assessment, The Contemporary Assessment 31, no. 1 (2019): 105–38; and Donald H. Rubinstein, “Epidemic Suicide among Micronesian Adolescents,” Social Science and Medicine 17, no. 10 (1983): 657–65.

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formation of this network in three phases. First, non-specialist, expatriate community workers appropriated long-established epidemiological techniques in order to represent the suicide problem in a way that is legible to modern bureaucracies and thereby to establish it as an urgent crisis requiring intervention.3 Second, an expanded network of expertise formed to add academic specialists residing in the former colonial powers of New Zealand and the United States, who aided in the creation of more professional studies of suicide in each region. Third, the academics would then shift from empirical study to theoretical explanation, producing narratives of governance from the distant locales where the academics worked. In part, these narratives blamed the suicide epidemic on the recalcitrance of local peoples to give up their traditional forms of power and self-fashioning and, instead, to embrace the liberal democratic forms of governance and self-fashioning that are common in western societies. These narratives contrast with those that blame modern western institutions and globalizing market processes imposed on places like Samoa and the Micronesian islands by colonial powers for increased suicide.4 It also contrasts with efforts to highlight the value of indigenous cultures as a resource for effectively coping with potentially harmful effects of modernizing social change and globalization.5

Expertise and Government at a Distance This chapter is framed by the theoretical work of Peter Miller and Nikolas Rose on the formation of governmentality in modern liberal democratic societies.6 Their work builds on Bruno Latour’s notion of “action at a distance.”7 Miller and Rose broaden Latour’s notion to become “government at a distance.”8 By that phrase, Miller and Rose mean that the social production of technologies of governance in modern liberal democratic 3 James Scott, Seeing like a State: How Certain Schemes to Improve the Human Condition Have Failed (New Haven CT: Yale University Press, 1998). 4 Edward Lowe, “Social Change and Micronesian Suicide Mortality: A Test of Competing Hypotheses,” Cross-Cultural Research, February 28, 2018, doi.org/10.1177/1069397118759004; and Lowe, “Epidemic Suicide, 105–38. 5 Epeli Hau’ofa, “Our Sea of Islands,” The Contemporary Pacific 6, no. 1 (1994): 148–61; and Sa‘iliemanu Lilomaiava-Doktor, “Beyond ‘Migration’: Samoan Population Movement (Malaga) and the Geography of Social Space (VƗ),” The Contemporary Pacific 2, no.1 (2009): 1–32. 6 Peter Miller and Nikolas Rose, Governing the Present. 7 Bruno Latour, Science in Action. (Milton Keynes: Open University, 1987). 8 Miller and Rose, Governing the Present.

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societies requires the cultivation of expertise, and the granting of authority to recognized experts to define, describe, explain and intervene into the “social problems” they recognize (i.e., crime, poverty, economic development, disease and mental health epidemics, etc.).9 By expertise, Miller and Rose indicate, That complex amalgam of professionals and quasi-professionals, truth claims and technical procedures [that] provide versatile mechanisms for shaping and normalizing ‘private’ enterprise, the ‘private’ firm, the ‘private’ decisions of business people and parents and the self-regulating capacities of ‘private’ selves in ways that are simply not comprehended by the philosophies of politics.10

The cultivation and fielding of expertise is a main feature of contemporary mentalities of government and a central element of government rule in the liberal democratic era. Government at a distance is a notion that enables the linking of “calculations in one place, with actions in another, not through the direct imposition of a form of conduct by force, but through the delicate affiliation of a loose assemblage of agents and agencies into a functioning network.”11 The process of forming expert consensus and forms of expert intervention is not a result of institutional dependencies but on the way members of the network “have come to construe their problems in allied ways.”12 It binds persons, organizations, entities, and locales that “remain differentiated by space, time, and formal boundaries …into a loose, approximate and always mobile indeterminate alignment.”13 In other words, these processes reflect the formation of “expert selves” and networks of expert consensus about how to document, represent, explain, and intervene into the problems that define their areas of expertise as central to modern forms of government. Central to modern forms of governmentality and control are the (1) development of techniques to classify, enumerate, and track diseases of the body, mind, and society; the (2) formulation of moralistic tropes to explain the resulting statistical trends; and the (3) creation of institutions to intervene into and correct those trends that are deemed pathological.14 These techniques for tracking, explaining, and intervening into forms of disease 9

Ibid.; see Ian Hacking, The Timing of Chance (Cambridge: Cambridge University Press, 1990). 10 Miller and Rose, Governing the Present, 33. 11 Ibid., 33–4. 12 Ibid., 34 13 Ibid. 14 Hacking, Taming of Chance.

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form the basis of most modern forms of bureaucratic expertise and been developed since the late 18th century. Suicide, crime, and alcoholism, together with concern over infectious disease, have been the major categories of concern from the start. Changing rates of suicide have been singled out over the past two centuries as a major indicator of societal wellbeing, an indication of both the moral status of society and society’s capacity to promote the overall happiness of its members. Given the preceding, this chapter seeks to understand how the formation of networks of expertise focused on the study of epidemics can serve to reproduce colonial relations in post-colonial circumstances, where former colonial powers can no longer directly impose forms of governance on indigenous peoples. In the next three sections, I will describe the formation of a network of expertise that formed to study suicide epidemics in Samoa and the former USTTPI societies in Micronesia. I will begin with the early efforts by colonial and expatriate community workers to document suicide epidemics in Micronesia and Samoa as epidemiological “facts” that deserve urgent attention and intervention by the colonial and post-colonial state and civil society institutions. Efforts in each of these sites began about the same time, in the middle-to-late 1970s. This period was about a decade and a half after Samoa won political independence from New Zealand in 1962 and about a decade into Micronesians of the USTTPI working toward political independence from the United States that began in the late 1960s.

Expatriate Anxieties: Early Notice of the Suicide Problem In 1976, Fran Hezel, an American Jesuit who had been stationed in the USTTPI since the mid-1960s and the director of the regional Jesuit high school, wrote an article for the Micronesian Independent newspaper titled “Micronesian Hanging Spree.”15 That report represented the efforts of local community workers to bring greater public attention to a suicide epidemic that many had feared had been ongoing for nearly a decade in the region. The report did so in part by representing the crisis through epidemiological statistical procedures. In the article, Fr. Hezel describes how students and staff at the high school worked together to conduct an informal survey among themselves to document all the cases of suicide they had known about during the previous year. They came up with 23 cases. Based on this finding, Fr. Hezel calculated a standardized suicide rate for the USTTPI of 20 per 100,000. This rate was twice as high as had been recorded during an 15 Francis X. Hezel, “Micronesia’s Hanging Spree,” Micronesia Independent, (December 1976).

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earlier period on nearby Guam and the national rate for the United States at that time. Hezel’s article is an example of the appropriation of expert epidemiological techniques by colonial or expatriate community workers to both document and urge public and state intervention into the “suicide problem” that had been a subject of public conversation for some time. The newspaper article makes use of a survey procedure to count the incidence of suicide during the previous year. It converts the results of the survey into statistics that would be legible to bureaucratic workers in a state public health apparatus.16 It also offers compelling, if brief, details of selected cases of suicide that might interest journalists and the public more broadly. The short summaries of cases act to put a human face on the statistical evidence. In addition to statistical and qualitative descriptions, Hezel offered a possible explanation for the high rate of suicide at that time. This explanation was rapid modernization, or the replacement of kin-based community institutions with modern bureaucratic institutions in most domains of life. For Hezel, modernization was driving the disintegration of family and community life throughout Micronesia. Here, he was explicitly drawing on Durkheim’s (1951) theory that higher suicide rates can be caused by social disintegration in contexts of modernizing social change.17 These modernizing changes left young men, who were overwhelmingly the victims of suicide, with little to do and fewer sources of family support than they had in the past. At the same time, enduring cultural values placed these youths firmly under the authority of parents and other family elders. Parents and other elders took notice that their sons or nephews were spending their free time drinking, carousing, and getting into trouble in the village.18 This, in turn, led to constant scolding, which led to youths’ hurt and angry feelings, which all too often led to suicide attempts as a means, Hezel argued at that time, to take revenge against their family’s unjust treatment by shaming them through suicide. In providing this argument, Hezel was repeating parts of explanations that had been in circulation among local leaders, religious clergy, and 16

James Scott, Seeing Like a State. Emile Durkheim, Suicide: A Study in Sociology, trans. John A. Spaulding and George Simpson, ed. George Simpson (Glencoe, IL: Free Press, 1951). Originally published in 1897. 18 Mac Marshall, Weekend Warriors: Alcohol in a Micronesian Culture (Palo Alto, CA: Mayfield Publishing Company, 1979); and Edward Lowe, “Identity, Activity, and the Well-Being of Adolescents and Youths: Lessons from Young People in a Micronesian Society,” Culture, Medicine and Psychiatry 27, no. 2 (2003): 187–219. 17

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colonial workers in the USTTPI for some time. For example, in the memoir of her ethnographic work on the Micronesian island of Pohnpei in 1970, Martha Ward recounts: The suicide rate, particularly among young men, had been climbing not just in Pohnpei but throughout Micronesia; there were reliable vital statistics and serious public health concerns, but no answers. Roger and I attended a funeral service for a teenager [in 1970]; the speakers attached the same complex causality to his suicide as they did for juvenile delinquency— modernization, breakdowns in traditions and in family life, pernicious Western influences, lack of community support systems, personal failings, and a decline of the work ethic.19

The main difference between Fr. Hezel’s account and those circulating in the community where Ward had been working in 1970 was Fr. Hezel’s use of the social scientific literature, specifically Durkheim’s theories. Why was the appropriation of epidemiological techniques by the expatriate community workers needed to motivate intervention into such a well-recognized mental health problem? We gain some insight by examining the material for Samoa. In Samoa, efforts to get the Samoan state and civil society leaders to recognize a suicide epidemic were also underway by the end of the 1970s. As an example of rising concerns among expatriate workers in Samoa at that time, Denis Oliver, a New Zealand citizen sent to Samoa to set up YMCA programs in the late 1970s, wrote the following, I first learned of the suicide problem in Western Samoa when I attended Aggie Grey's birthday party in Apia [the urban center of Samoa] in 1978. My wife and I happened to share a table with another New Zealand couple and during the course of conversation, I mentioned that David didn't appear to be in a party mood. Whereupon he told me that as Magistrate and Coroner there were parts of his job that made him sad. There had been three suicides committed by young people over the previous three weeks and he had felt the sorrow of the parents. As we talked he shared with me his concern. He had written a report of the recent increase in suicides and had sent it upstairs but it had met zero response.20

19 Martha Ward, Nest in the Wind: Adventures in Anthropology on a Tropical Island, 2nd ed. (Long Grove, IL: Waveland Press, 2004), 79. 20 Denis Oliver, “Reducing Suicide in Western Samoa.” in Culture, Youth and Suicide in the Pacific: Papers from an East-West Center Conference, ed. Francis X. Hezel, Donald H. Rubenstein, and Geoffrey M. White, Occasional Papers Series 25 (Honolulu: Pacific Islands Studies Program, Center for Asian and Pacific Studies, University of Hawai’i at Mदnoa, 1985): 74.

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Oliver reports that David’s replacement a year later, also a Coroner on loan from New Zealand, had as little success convincing his superiors to take these anecdotal reports of a raging suicide epidemic seriously as did David. To those, like Oliver, who had been advocating that greater attention from the state and civil-society institutions was needed, it seemed that only “expert” representations of increased suicide rates would be convincing. After three years and no progress, Oliver decided to assume the task of systematically enumerating incidents of suicide throughout Samoa as far back as the official records allowed and used the organization of local YMCA clubs he has set up throughout Samoa to assist in this task. Oliver then asked for and received permission from the YMCA Board of Directors to start a “Suicide Study Group” that included members from the Samoan Health Department, the Justice Department, the Fellowship of Churches, and the YMCA. For the next year (1982), Oliver and a local assistant combed through the Coroner’s court records to identify every case of suicide as well as the basic demographic information about the victims. The results, or “the bare facts,” as Oliver labeled them, were tabulated and released to the Suicide Study Group in Samoa.21 These statistics then allowed the group to support the claim that “the suicide rate in Samoa was by world standards exceedingly high.” Once these facts were published and released to the public, an awareness campaign was designed to get all villages in Samoa to meet, discuss, and find ways to address the suicide problem. In concluding his narrative about how he led the charge to address the suicide problem in Samoa during the early 1980s, Oliver framed his effort as a contest between “new power” and “old power.” He wrote, Nothing happens in human affairs without the creation of new power or the redistribution of old power. Before the new power [of his public awareness campaign] was generated, the old power block [i.e., Samoan parents, Matai [Chief’s] and religious clergy] had made small incremental shifts to accommodate the change in the rate of suicide and so maintain the status quo.22

Here we see the first hint that development experts like Oliver will frame the suicide problem as they had constructed it, in terms of what I call “the recalcitrant native,” which I will discuss further. After leaving in 1983, Oliver would write a book on the principles for democratic forms of economic development based on his experiences in Samoa. Hezel and Oliver’s efforts show how local community workers appropriated methods of epidemiological expertise as a means of making 21 22

Ibid., 76. Ibid., 81

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suicide epidemics in Micronesia and Samoa during the 1970s legible or visible to local state and civil society actors. This then led to the marshaling of local resources to intervene in the crises. But these efforts lacked the active participation of those who held expert credentials and thereby remained a local problem. As such, they had a somewhat wider impact on relevant agents back in the present and former colonial powers of New Zealand and the United States, which had the financial and expert resources on hand to study the problem and intervene more effectively. Seeking and gaining such participation by more distantly located academic experts is the subject of the next section.

The Formation of a Network of Expertise to Study Suicide in the Pacific Islands By 1983, the efforts initiated by Fran Hezel and Denis Oliver (and the Suicide Study Group in Samoa) to make the suicide epidemic in parts of Micronesia and Samoa legible to the local and (post) colonial state actors began to pay off. By the early 1980s, Fr. Hezel joined with a young Ph.D. anthropologist, Donald Rubinstein, who correctly and systematically documented the suicide epidemic from the 1960s throughout Micronesia, using the best epidemiological practices at that time.23 Their work was funded by a National Institute of Mental Health grant funded through the East-West Center at the University of Hawaii in Honolulu. In early March of 1983, the New York Times reprinted an Associated Press report titled, “Micronesia’s Male Suicide Rate Defies Solution” that described their efforts.24 This newspaper article followed the format Hezel had used in his 1976 article, a format that is typical for making social problems legible to bureaucratic experts and the broadly educated public. The article uses epidemiological statistics that Hezel and Rubinstein had calculated to highlight the gravity of the problem. It also provides some case material and expert interpretations given by Hezel and Rubinstein to place the problem in its social and cultural context. It concludes with a discussion of possible interventions. What distinguishes this 1983 New York Times account from the one published in 1976 is that the explanation for suicide shifted to more sensitive local cultural contexts in which the suicide problem in Micronesia took place but was less concerned with processes of modernization described in 23

Rubenstein, “Epidemic Suicide,” 657–65. “Micronesia’s Male Suicide Rate Defies Solution,” New York Times, March 6, 1983.

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Hezel’s 1976 article. In addition, suicide was no longer represented as an act of revenge against family members who the victim believed had treated them wrongly. In this report, the explanation for suicide attempts was framed culturally as a means to repair family relations that had been strained for a considerable period given that more explicit approaches were not culturally appropriate.25 Although it is not clear from the reporting, I suspect that the inclusion of a more nuanced understanding of the local dynamics of suicide was the result of the inclusion of an anthropologist, Dr. Rubinstein, with considerable recent fieldwork experience studying family life in Micronesia at that time.26 The next step was to bring academic and local expertise on the suicide problem and its cultural contextualization for both Micronesia and Samoa together into a single working group. In September 1984, Fr. Hezel, Dr. Rubinstein, and the anthropologist Geoffrey White, who was also a fellow at the East-West Center, hosted a conference in Honolulu that would bring the Micronesia project and the Samoan projects together. This conference represented the first formal instance of the emerging network of expertise dedicated to studying the suicide epidemic in parts of Micronesia and Samoa. The assembled group now included two expatriate mental health professionals assigned to stations in Micronesia and Samoa and several academic researchers, including six anthropologists and two sociologists. One anthropologist, Dr. Rubinstein, was completing a Master of Public Health degree at the University of Hawaii at that time. These academic and mental health experts were in addition to the expatriate NGO workers, Hezel and Oliver. Four of the participants were US, New Zealand, or Australian nationals working in either Micronesia or Samoa. All but one of the academic researchers were based in either Hawaii, the US mainland, or New Zealand at that time. Two of the academics were indigenous to the Pacific islands, although each worked in either the US mainland or New Zealand. In this way, the conference also linked the Micronesian and Samoan contexts with academic expertise in the nations who had once or were currently at that time administering USTTPI Micronesia or Samoa.27 The addition of the academic experts into the network allowed for a more sophisticated statistical representation and description of the suicide 25 Lowe, “Identity, Activity, and Well-Being,” 187–219; Lowe, “Social Change,” and Lowe, “Epidemic Suicide,” 105–38. 26 Donald H. Rubenstein, “Epidemic Suicide,” 657–65. 27 Francis X. Hezel, Donald H. Rubenstein and Geoffrey M. White, eds., Culture, Youth and Suicide in the Pacific: Papers from an East-West Center Conference, Occasional Papers Series 25 (Honolulu: Pacific Islands Studies Program, Center for Asian and Pacific Studies, University of Hawai’i at Mदnoa, 1985).

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epidemics in Samoa and the relevant island groups in Micronesia. These statistical representations were prepared by mental or public health professionals. The final conference report included tables that compared suicide rates for males and females in different age groups, tables that described changes in suicide rates during different historical periods, line graphs that represented the dramatic increase in suicide rates from the late 1960s until 1980, and modest decreases after that time. Bar graphs represented different suicide rates in different island groups, particularly in the diverse Micronesian context.28 The sociologists and anthropologists were also on hand to place the suicide epidemics into established sociological theories of social change and suicide. They further placed them into a regional cultural context of suicide in the Pacific Islands’ indigenous societies.29 The academic reports included discussions of suicide in a cultural context in Samoa and Micronesia, but also in three Melanesian cases, two from the Solomon Islands and one from Highland Papua New Guinea.30 Deferring to these experts, NGO workers like Oliver and Hezel could focus more on intervention efforts in their reports.31 As such, the report documents the formation of a network of expertise as it was defined by Miller and Rose, “that complex amalgam of professionals and quasi-professionals, truth claims and technical procedures” assembled to study the suicide epidemics in Samoa and the USTTPI Micronesian islands.32 28

Ibid. Cluny Macpherson and La’avasa Macpherson, “Suicide in Western Samoa: A Sociological Perspective,” in Culture, Youth and Suicide in the Pacific: Papers from an East-West Center Conference, ed. Francis X. Hexel, Donald Rubenstein and Geoffrey White, 36–73, Occasional Papers Series 25 (Honolulu: Pacific Islands Studies Program, Center for Asian and Pacific Studies, University of Hawai’i at Mदnoa, 1985). 30 Fitz John Porter Poole, “Among the Boughs of the Hanging Tree: Male Suicide among the Bimin-Kuskumin of Papua New Guinea,” in Culture, Youth and Suicide in the Pacific: Papers from an East-West Center Conference, ed. Francis X, Hexel, Donald Rubenstein and Geoffrey White, 152–81. Occasional Papers Series 25 (Honolulu: Pacific Islands Studies Program, Center for Asian and Pacific Studies, University of Hawai’i at Mदnoa, 1985); and David Gegeo and Karen Ann WatsonGegeo, “Patterns of Suicide in West Kwar’ae Malaita, Solomon Islands,” in Culture, Youth and Suicide in the Pacific: Papers from an East-West Center Conference, ed. Francis X, Hexel, Donald H. Rubenstein and Geoffrey M. White, 182–97, Occasional Papers Series 25, (Honolulu: Pacific Islands Studies Program, Center for Asian and Pacific Studies, University of Hawai’i at Mदnoa, 1985). 31 Hezel, Rubenstein, and White, eds., Culture, Youth and Suicide; and Oliver, “Reducing Suicide,” 74-87. 32 Miller and Rose, Governing the Present, 33. 29

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The Honolulu conference in 1984 marked an important shift in the formation of a network of expertise that could enact forms of government at a distance. It used the suicide epidemic to promote much broader political and societal reforms that suited the agendas of the post-colonial states, as opposed to those of local indigenous actors. The earlier efforts by Hezel and Oliver used formal epidemiological techniques to support their efforts to make a suicide epidemic visible to local political and community leaders in Micronesia and Samoa. The results of their early efforts were released to local newspapers or working groups in the USTTPI and Samoa. The report of the Honolulu conference was aimed less at local constituencies and more at academics and policymakers in New Zealand and the United States. As we will see in the next section, once this shift took place, networks’ efforts shifted away from documenting the epidemiological trends over time and toward explanatory narratives and new proposals for governance that might alleviate the problem. What is interesting about these explanatory narratives is who became the target of governance (i.e., who needed to reform their practices) and who was not.

Distant Academic Representations: Suicide and the Recalcitrant Native After the 1984 conference, most of the activity of members of the network became focused on academic and policy work in the post-colonial regional centers in the United States and New Zealand. Fr. Hezel, however, did continue his efforts to both document and direct community programs aimed at trying to ameliorate the suicide problem in Micronesia for the next two decades.33 In Samoa, the effort was led primarily by the Samoan Ministry of Health, which emphasized collecting suicide statistics from hospital records for its annual reporting. After the 1984 conference, some of the first explanatory accounts appeared in the earliest academic work on this topic. I now turn my attention to these accounts and a shift in “governance at a distance.” First, I should present a little context for the way “culture” has been utilized to characterize indigenous peoples in the situation of their coping with modernization and globalization over the past two centuries unfairly. Various tropes involving the culture concept have long been part of the discursive repertoire of people who participate in professional networks of governance, particularly in cases of governing people who are geographically

33

Francis X. Hezel, personal communication, 2008.

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or social-organizationally remote from themselves.34 Two tropes have been particularly enduring. The first is an Enlightenment thesis of the inevitability of civilizational progress as guided by reason over the conservative forces of superstition and tradition. The second, which developed in dialectic with the first, is the Romantic antithesis that emphasizes the importance of a society maintaining its essential cultural spirit in the face of corrupting accompaniments of modernizing social change.35 The Enlightenment framing has been particularly important for those invested in the promotion of modern liberal democratic governance and its associated project of political and economic modernization and globalization. In this view, culture is seen as an obstacle to progress and modernization. As Adam Kuper notes, Culture was invoked when it became necessary to explain why people were clinging to irrational goals and self-destructive strategies. Development projects were defeated by cultural resistance. Democracy crumbled because it was alien to the traditions of a nation. Rational choice theories could not account for what economists despairingly call “stickiness,” entrenched ways of thinking and doing that persist in the face of the most compelling arguments. …Tradition was the refuge of the ignorant and fearful, or the recourse course of the rich and powerful, jealous of any challenge to their established privileges.36

In its schematic form, the Enlightenment framing had been widely adopted in the suicide epidemics in Micronesia and Samoa. It is noteworthy that these studies came about either in the aftermath of political independence from the colonial state (Samoa and New Zealand), or during the process of transition itself (the USTTPI and the United States). These political transformations were accompanied by more intense efforts toward economic modernization, either by the colonial administration or by the post-colonial state. Most of the explanations offered for the sudden increase in suicide drew on these political and economic developments in their explanations. Explanations for modernizing social change and suicide already appeared in an early form in the original newspaper article published by Hezel in 1976. As noted above, Hezel and Rubinstein would develop this line of work further in academic work published in the 1980s and 1990s. Their

34 Adam Kuper, Culture: Anthropological Account; and Kuper, The Reinvention of Primitive Society. 35 Kuper, Culture, Anthropological Account. 36 Ibid., 10.

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more mature arguments can be summarized as follows:37 Modernization programs initiated by the United States in the 1960s increased the ubiquity of modern institutions across a range of domains (schools, government, hospitals, etc.) with greater access to wage labor. These promoted a decline of traditional social organizations at the level of the extended kin group beyond the nuclear family. This led to the expansion of the role of men as fathers, who became the primary caretakers and disciplinarians of postadolescent young men.38 Young men also lost important social supports among the extended kin-group. According to Hezel, “the modern [Micronesian] family must get along without the support roles that other extended family members once played in disciplining the young, in assuaging their hurt feelings, and in serving as intermediaries between parties involved in clashes.”39 Nevertheless, it is claimed this structural shift to modern families was not accompanied by a corresponding shift in the cultural constitution of an appropriately modern and expressive self. Rather than developing a modern, egoistic self that openly expresses feelings of frustration and hurt to one’s parent when the situation demands, Hezel and Rubinstein proposed that youth in Micronesia were vulnerable to suicide because of their ongoing production of selves, as the New York Times reported, Young island men have used withdrawal, such as silence or refusing to eat, to express anger or shame … “[This] is a common strategy employed by [Micronesians] to give vent to strong feelings when it is inappropriate to display these feelings more directly,” Father Hezel said. What has happened over the past 20 years … is that the strategy has turned violent. “Suicide can be considered the extreme form of [culturally sanctioned emotion management] –inflicting the ultimate harm upon oneself in order to save a precious relationship,” Father Hezel said.40

In other words, social institutions had changed, but the culturally informed, psychological habits of indigenous peoples did not. Fr. Hezel holds this view to the present day. In a recent written comment on another 37

Francis X. Hezel, “Truk Suicide Epidemic,” 283–91; Hezel, The New Shape of Old Island Cultures: A Half Century of Social Change in Micronesia (Honolulu: University of Hawaii Press, 2001); Rubenstein, “Epidemic Suicide,” 657–68; Rubenstein, “Suicide in Micronesia and Samoa: A Critique of Explanations,” Pacific Studies 1, no. 1 (1992): 51–75; and Rubenstein, Youth Suicide and Social Change in Micronesia, Occasional Papers 16 (Kagoshima, Japan: Kagoshima University Center for the Pacific Islands, 2002). 38 Hezel, New Shape of Old Island, 20. 39 Ibid. 40 New York Times, “Micronesia’s Male Suicide.”

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article I published,41 Fr. Hezel wrote that if the social changes also accompanied a shift to a sense of self—organized around an ethic of greater personal autonomy—suicide would have been less of a problem in Micronesia. In his comments, Hezel continued that modernizing social change in Micronesia, “certainly does not lead to ‘increased egoism’ in the society—at least not in the theory that I espouse. If it did that, the suicide numbers would drop, since egoism and the independence of spirit that accompanies it inoculates individuals against the bad feelings that occur when a person feels he is cut off from his family.” What we can take away from this argument is that the incomplete transition to a more modern society is blamed for suicide. Furthermore, recalcitrant adherence to local values of family interdependency and sociocentrism is viewed as a major factor increasing suicide. What role the United States policy of rapid modernization from the 1960s through the 1980s might have played in the crisis is not discussed as critically.42 Explanations for the Samoan case that fit the Enlightenment trope are given in the work of New Zealand-based sociologists Cluny and La’avasa Macpherson, both attendees at the 1984 conference.43 Their explanations focus on the frustration of rising aspirations among young adults who are most often the victims of suicide, because their levels of education, opportunities to travel abroad, and exposure to modern lifestyles through globalizing media were much higher than those of previous generations. These frustrations were not only the result of the lack of opportunities for appropriately modern social mobility in an economically stagnant Samoa. They were also a result of conservative traditional leaders, including the matai (‘chiefs’) and clergy, who, according to Macpherson and Macpherson strictly limited the number of these prestigious posts for their own benefit. Finally, like the explanations offered for suicide in Micronesia, blame was placed on Samoan cultural constructions of the self and social relations. Macpherson and Macpherson wrote, Samoan culture prescribes for adolescents a period in which they are expected to serve … not challenge, those who hold power over them. Adolescents are told that service is the path to power…. Since this is almost

41

Lowe, “Social Change.” See Lowe, “Social Change.” and Lowe “Epidemic Suicide,” 105–38. 43 Cluny Macpherson and La’avasa Macpherson, “Towards an Explanation of Recent Trends in Suicide in Western Samoa” Man 22, (1987): 305–30; and MacPherson and Macpherson, The Warm Winds of Change: Globalisation in Contemporary Samoa (Auckland: Auckland University Press, 2009). 42

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In addition, also like Micronesian youths, young adults in Samoa may not openly express anger, frustration, and dissatisfaction when it is directed at the powerful adults whom they must serve. Instead, the suffering young person expresses dissatisfaction through withdrawal, by running away, or in more extreme circumstances acting out in explosive rage. The rage is said to 'leap up' inside the person and take control. In that state people typically lash out, usually at inanimate objects, with fists, knives, paddles and so on. They are watched and eventually the rage is expected to subside. But people will say that a situation can often be seen very clearly in a rage. A number of cases of suicide which we documented occurred during or shortly after a display of rage.45

The Macphersons summarize their model thusly, The young untitled person is offered progressively more education and visions of alternative lifestyles. Samoan society, dominated by older people and traditions, is unable and unwilling to accept some of these expectations or to move to make these attainable … Confronted … with an apparently immovable tradition reflected in councils dominated by those committed to the tradition, attaining those aspirations seems increasingly unlikely. Under these circumstances, the things which have masked a growing alienation on the part of this group of young Samoans are removed and we see more clearly a disaffection which has been growing for some time.46

They sound a rather pessimistic note for the prospect of improvement, If these structural factors are likely to remain intractable for reasons connected with economic linkages between Samoa and the global economy, two possibilities emerge. Youth may adjust their aspirations downwards to levels which are more realistic and reflect some acceptance of available and culturally acceptable means ... Secondly, those who currently control power may accept the need to re-distribute that power and opportunity in ways which accommodate youths' aspirations. Unless one or the other of these occur a continuing high rate of adolescent suicide, or some other form of retreatist adaptation, would seem inevitable.47

44

Macpherson and Macpherson, “Towards an Explanation,” 324. Ibid., 325. 46 Ibid., 326. 47 Ibid., 326–27. 45

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An interesting thesis to be sure. But, by the time their manuscript was in preparation in 1984, the facts on the ground had already proved this thesis unlikely. As Lowe documents, the structural conditions MacPherson and MacPherson (1987) claim to be responsible for the suicide epidemic in Samoa from the mid-1970s until the mid-1980s have persisted up to the present time even as suicide rates declined below the world average through the 1990s and 2000s.48 Specifically, the rising aspirations of young people gained through education, travel, and media, coupled with few opportunities to realize them in the locally-available formal employment sector, have persisted even as the suicide rates decreased sharply in the mid-1980s. Therefore, these structural factors cannot have been responsible for the suicide epidemic in Samoa during that time. Uneven modernization and recalcitrant local leadership were not to blame for Samoa’s suicide epidemic. An increasingly de-regulated global commodity market in an emergent era of neoliberalism is the more likely culprit. More specifically, the suicide epidemic in Samoa was strongly linked to the importation of the herbicide Paraquat, an herbicide invented in 1961 that spread rapidly around the globe as an agricultural weed-killer in the 1960s and 1970s. John Bowles, an Australian contracted in Samoa as a psychiatrist and who was also part of the Suicide Study Group, did the first full statistical analysis of the Suicide epidemiological data that Denis Oliver and his team had collected. In his analyses, Bowles argued that the suicide epidemic was likely the result of a sudden increase in self-poisonings using the highly poisonous herbicide Paraquat. As Bowles documents, Paraquat importations into Samoa began in 1972 at a level of fewer than 5,000 liters and then rose sharply to about 80,000 liters in 1980. The number of Paraquat-related suicide deaths also increased sharply after 1975 when there were just two, increasing to eleven in 1976, and forty in 1981.49 Largely as a result of the efforts of the Suicide Study Group to inform local officials, who then recognized the role that Paraquat had played in the rapid increase of suicide deaths from 1975 to 1980, the Samoan government instituted 48

Lowe, “Epidemic Suicide,” 105–38. John Bowles, “Suicide in Western Samoa: An Example of a Suicide Prevention Program in a Developing Country,” in Preventative Strategies on Suicide, ed. Réne F. W. Diekstra, Walter Gulbinat, Ineke Kienhorst, and Diego de Leo (Leiden: E. J. Brill, 1995), 188: and Bowles “Suicide and Attempted Suicide in Contemporary Western Samoa,” in Culture, Youth and Suicide in the Pacific: Papers from an EastWest Center Conference, ed. Francis X, Hexel, Donald Rubenstein and Geoffrey White, 15–35, Occasional Papers Series 25 (Honolulu: Pacific Islands Studies Program, Center for Asian and Pacific Studies, University of Hawai’i at Mदnoa, 1985). 49

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policies to curb the public availability of Paraquat. After 1980, Paraquat importation declined to less than 25,000 liters in 1983. Deaths related to self-poisonings from Paraquat declined dramatically to a low of five cases in 1984. However, as a result of the lobbying from local business interests, the importation of Paraquat reversed course and increased again to 60,000 liters in 1988, the last year of data available in Bowles.50 Paraquat-related deaths from self-poisonings then again increased to sixteen cases in 1988. Over the course of this period, Paraquat-related poisonings accounted for the great majority of new suicide attempts and deaths. For example, during the peak of the epidemic in 1981, Paraquat poisonings were responsible for 40 of 49 suicide deaths (81.6%) and thirty-four of forty-five non-lethal suicide attempts (75.5%).51 This suggests a causal argument that Paraquat importation and its adoption as a method of intentional self-harm was responsible for most of Samoa’s suicide epidemic from the mid-1970s to the early 1980s.52 What is more, Oliver reported that suicide was not evenly distributed throughout the villages of Samoa as the MacPhersons’ theoretical speculations suggest. Oliver reported in the 1984 conference that 261 of 360 (72.5%) villages in Samoa had not reported a case of suicide since 1966 (nearly two decades earlier).53 Indeed, just nineteen villages accounted for half of the total of suicides between 1966 and 1981; many of these were near the urban center of Apia. This pattern suggests that the suicide “epidemic” in Samoa was spatially limited to a small number of villages. It may also reflect the diffusion of a new and particularly lethal means of committing acts of self-harm to “protest” the perceived injustice associated with the actions of one’s elders, as described earlier. Poisoning as a method of intentional self-harm aimed at the expression of protest when one is in an emotionally-intense conflict with family members is a widely-documented, although rare, practice in Samoa and elsewhere in Polynesia. Bowles reports that eighty-three of ninety-four (88%) recorded suicide attempts and deaths in 1981 were self-poisonings.54 Poisoning may be chosen as a means of selfharm because the victim knows that there is a possibility that the amount of poison ingested will be non-lethal. Victims may believe that the family can come to their aid or address the conflict that has motivated the act of self-

50

Ibid. Ibid., 199. 52 Ibid., 198. 53 Oliver, ‘Reducing Suicide,” 76. 54 Bowles, “Suicide in Western Samoa,” 99. 51

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harm.55 However, unlike poisons that had been available in earlier times, Paraquat is particularly lethal and a very small amount can be deadly.56 So, if young people in those villages most affected began to adopt Paraquat as a means of protest self-harm as it became increasingly available, its much greater lethality would cause a sudden epidemic in deaths from these acts of self-harm. The structural arguments fare no better in the Micronesian case. Lowe found that variation in suicide rates among eighty municipalities of the Federated States of Micronesia is best explained by the way local communities participated in the consumption of commodities that signify western lifestyles in order to pursue local, competitive, status-enhancing practices. Many that are historically enduring and not well explained by indices of uneven economic modernization such as the mismatch between levels of educational achievement and the levels of formal employment.57 It was the way the United States’ post-colonial development policies fueled increased participation of local actors in globalizing commodity markets, locally meaningful to those actors responsible for much of the suicide epidemic in the Micronesian region. Poisonings do not play a significant role in the Micronesian case, however, underscoring the importance of the careful study of the emergence of epidemics as an outcome of diverse local-global articulations. The preceding shows that as the work of this network of expertise shifted from the local communities in Micronesia and Samoa to academic centers in the United States and New Zealand, the emphasis also shifted to discussions of “the recalcitrant native.” This trope was deployed by researchers as a main feature of their explanations for the suicide epidemics in Micronesia and Samoa in the 1970s and 1980s. One of the main problems with this narrative is that it quickly collapses under the weight of empirical scrutiny as the summary of previously published work reviewed above documents. But, empirically testing the assertions made by distantly located academic experts was probably never the point. Rather, the epidemics themselves became sites for the construction of new forms of expertise and the articulation of new forms of governmentality in the post-colonial era Samoa and the former USTTPI Micronesian societies. These forms of governmentality seem to have had the effect of privileging American and New Zealander values and priorities for modernization, reinscribing a relationship of dependency and subordination for local peoples that were struggling with an ongoing behavioral health crisis. 55

Ibid. 173–206. Ibid. 57 Lowe, “Social Change.” 56

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Conclusion The main aim of this chapter was to show how the expert study of and intervention into epidemics in post-colonial circumstances can be a way of continuing colonial relations as “government at a distance,” even after political independence. After summarizing the approach to governmentality by Miller and Rose (2008), the chapter described the formation of a network of professionals and quasi-professionals that was dedicated to better understanding and intervening into suicide epidemics in the Pacific islands and parts of Micronesia and Samoa. One of the interesting findings of this chapter is that early work by local foreign nationals and expatriates working in the Micronesian USTTPI and in Samoa emphasized the appropriation of expert techniques for the epidemiological study and statistical representation of suicide. In effect, to make an apparent suicide epidemic legible to the local modern bureaucracies and thereby to establish it as an urgent crisis requiring intervention. In the later phase of the network’s formation, however, work was undertaken primarily by academic specialists and shifted to distant sites in the United States and New Zealand. In the academic work, explanatory accounts at that time emphasized the responsibility of recalcitrant local peoples for the suicide crisis. These responsible local peoples were blamed for stubbornly maintaining traditional forms of authority or traditional styles of self-management rather than embracing economic and political modernization schemes. These schemes privilege formal educational achievement as a pathway to employment in formal labor markets within a liberal modern polity. As an alternative, Lowe argues that “it would be more useful to examine a wider range of processes associated with globalization and modernization that can worsen vulnerabilities and strengthen resiliencies in different contexts.”58 One particularly important alternative site for investigation is to roles that globalizing industrial commodity markets, globalizing finance schemes, and forms of neoliberal governance can play in making local populations more vulnerable. These alternatives can also ally themselves with recent efforts to highlight the value of indigenous cultures as a resource for effectively coping with potentially harmful effects of modernizing social change and globalization.59 One hopes that studies of how networks of expertise that form to study epidemics can perpetuate forms of post-colonial governance at a distance will promote greater reflexive awareness among social scientists, policy 58

Lowe, “Epidemic Suicide,” 127. Hau’ofa, “Our Sea of Islands,” 148–61; and Lilomaiava-Doktor, “Beyond ‘Migration,’” 1–32. 59

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makers, and local actors. With greater reflexivity, we may be more careful about our complicity in ongoing forms of colonial domination and more open-minded with further productive explanations for worsened mental health and possible pathways of intervening into them, including those from indigenous perspectives. As a final note, I do not intend by this argument to imply that the critical study of networks of expertise is itself part of some larger process where the networks of bureaucratic expertise are inherently self-corrective. In my view, it is the tendency of spatially distributed bureaucracies to behave conservatively and defensively in order to reproduce their practices over time, thereby avoiding calls for selfassessment or the welcoming in of critical voices from the outside.60 My argument is intended to speak more to the resurgent interest in the anthropology of modernity.61 This line of thought seeks to understand how modern spatially dispersed bureaucracies act to construct the public understanding of epidemics, and other social problems of public concern, in ways that may not reflect local realities but instead serve larger, distant bureaucratic interests. Such critique is less directed at encouraging modern bureaucratic institutional actors and their networks of expertise toward reform and more toward promoting a dialog with local actors who seek alternatives to the understandings of the pressing problems they confront from distant institutions.

Bibliography Booth, Heather. “Pacific Island Suicide in Comparative Perspective.” Journal of Biosocial Science 31, no. 4 (1999): 433–48. Bowles, John. “Suicide and Attempted Suicide in Contemporary Western Samoa.” In Culture, Youth and Suicide in the Pacific: Papers from an East-West Center Conference, Edited by Francis X. Hezel, Donald H. Rubinstein, and Geoffrey M. White, 15–35. Occasional Paper Series 25. Honolulu: Pacific Islands Studies Program, Center for Asian and Pacific Studies. University of Hawai‘i at MƗnoa, 1985. Bowles, John. “Suicide in Western Samoa: An Example of a Suicide Prevention Program in a Developing Country.” In Preventative Strategies on Suicide, Edited by Réne F. W. Diekstra, Walter Gulbinat, Ineke Kienhorst, and Diego de Leo, 173–206. Leiden: E. J. Brill, 1995. 60 See David Graeber, The Utopia of Rules (Brooklyn: Melville House Publishing, 2015); and Miller and Rose, Governing the Present; and Scott, Seeing like a State. 61 Didier Fassin, ed., At the Heart of the State: The Moral World of Institutions (Chicago: University of Chicago Press, 2015).

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Durkeim, Émile. Suicide: A Study in Sociology. Translated by John A Spaulding and George Simpson. Edited by George Simpson. Glencoe, IL: Free Press, 1951. Originally published in 1897. Fassin, Didier, ed. At the Heart of the State: The Moral World of Institutions. Chicago: University of Chicago Press, 2015. Gegeo, David, and Karen Ann Watson-Gegeo. “Patterns of Suicide in West Kwara‘ae, Malaita, Solomon Islands.” In Culture, Youth and Suicide in the Pacific: Papers from an East-West Center Conference, Edited by Francis X. Hezel, Donald H. Rubinstein, and Geoffrey M. White, 182– 97. Occasional Paper Series 25. Honolulu: Pacific Islands Studies Program. Center for Asian and Pacific Studies. University of Hawai‘i at MƗnoa. 1985. Graber, David. The Utopia of Rules. Brooklyn, NY: Melville House, 2015. Hacking, Ian. The Taming of Chance. Cambridge: Cambridge University Press, 1990. Hau‘ofa, Epeli. “Our Sea of Islands.” The Contemporary Pacific 6, no. 1 (1994): 148–61. Hezel, Francis X., Donald H. Rubinstein, and Geoffrey M. White, eds. Culture, Youth and Suicide in the Pacific: Papers from an East-West Center Conference. Occasional Paper Series 25. Honolulu: Pacific Islands Studies Program. Center for Asian and Pacific Studies. University of Hawai‘i at MƗnoa, 1985. Hezel, Francis X. Micronesia’s Hanging Spree. Micronesian Independent, 31 (December 1976). Hexel, Francis X. The New Shape of Old Island Cultures: A Half-Century of Social Change in Micronesia. Honolulu: University of Hawaii Press, 2001. Hezel, Francis X. Suicide and the Micronesian Family. The Contemporary Pacific 1, no. 1–2 (1989): 43–74. Hezel, Francis X. “Truk Suicide Epidemic and Social Change.” Human Organization 46, no. 4 (1987): 283–91. Kuper, Adam. Culture: The Anthropologists Account. Cambridge MA: Harvard University Press, 1999. Kuper, Adam. The Reinvention of Primitive Society: Transformations of a Myth. Second edition. London: Routledge, 2005. Latour, Bruno. Science in Action. Milton Keynes: Open University Press, 1987. Lilomaiava-Doktor, Sa‘iliemanu “Beyond ‘Migration’: Samoan Population Movement (Malaga) and the Geography of Social Space (VƗ).” The Contemporary Pacific 21, no. 1 (2009): 1–32.

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Lowe, Edward. “Epidemic Suicide in the Context of Modernizing Social Change in Oceania: A Critical Review and Assessment.” The Contemporary Pacific 31, no. 1 (2019): 105–38. Lowe, Edward. “Identity, Activity, and the Well-Being of Adolescents and Youths: Lessons from Young People in a Micronesian Society.” Culture, Medicine and Psychiatry 27, no. 2 (2003): 187–219. Lowe, Edward. “Social Change and Micronesian Suicide Mortality: A Test of Competing Hypotheses.” Cross-Cultural Research. Accessed February 28, 2018. doi.org/10.1177/1069397118759004. Macpherson, Cluny, and La‘avasa Macpherson. “Suicide in Western Samoa: A Sociological Perspective.” In Culture, Youth and Suicide in the Pacific: Papers from an East-West Center Conference, Edited by Francis X. Hezel, Donald H. Rubinstein, and Geoffrey M. White, 36– 73. Occasional Paper Series 25. Honolulu: Pacific Islands Studies Program. Center for Asian and Pacific Studies. University of Hawai‘i at MƗnoa, 1985. Macpherson, Cluny and La’avasa Macpherson. “Towards an Explanation of Recent Trends in Suicide in Western Samoa.” Man 22 (1987): 305–30. Macpherson, Cluny and La’avasa Macpherson. The Warm Winds of Change: Globalisation in Contemporary SƗmoa. Auckland: Auckland University Press, 2009. Marshall, Mac. Weekend Warriors: Alcohol in a Micronesian Culture. Palo Alto, CA: Mayfield, 1979. Miller, Peter and Niklas Rose. Governing the Present: Administering Economic, Social and Political Life. Malden MA: Polity Press, 2008. New York Times. “Micronesia’s Male Suicide Rate Defies Solution.” March 6 1983. Oliver, Denis. “Reducing Suicide in Western Samoa.” In Culture, Youth and Suicide in the Pacific: Papers from an East-West Center Conference. Edited by Francis X. Hezel, Donald H. Rubinstein, and Geoffrey M. White, 74–87. Occasional Paper Series 25. Honolulu: Pacific Islands Studies Program. Center for Asian and Pacific Studies. University of Hawai‘i at MƗnoa, 1985. Poole, Fitz John Porter. “Among the Boughs of the Hanging Tree: Male Suicide among the Bimin-Kuskusmin of Papua New Guinea.” In Culture, Youth and Suicide in the Pacific: Papers from an East-West Center Conference, Edited by Francis X. Hezel, Donald H. Rubinstein, and Geoffrey M. White, 152–81. Occasional Paper Series 25. Honolulu: Pacific Islands Studies Program. Center for Asian and Pacific Studies. University of Hawai‘i at MƗnoa, 1985.

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Rubinstein, Donald H. “Epidemic Suicide among ’Micronesian’ Adolescents.” Social Science and Medicine 17, no. 10 (1983): 657–65. Rubinstein, Donald H. “Suicide in Micronesia and Samoa: A Critique of Explanations.” Pacific Studies 15, no. 1 (1992): 51–75. Rubinstein, Donald H. Youth Suicide and Social Change in Micronesia. Occasional Papers 36. Kagoshima, Japan: Kagoshima University Research Center for the Pacific Islands, 2002. Scott, James. Seeing Like a State: How Certain Schemes to Improve the Human Condition Have Failed. New Haven CT: Yale University Press, 1998. Ward, Martha. Nest in the Wind: Adventures in Anthropology on a Tropical Island. 2nd ed. Long Grove, IL: Waveland Press, 2004.

CHAPTER THREE LEPROSY CONTROL IN IMPERIAL JAPAN MICHAEL WEINER

Confinement and Criminalization Spread across Japan is a state-run system of thirteen leprosaria, which houses nearly 1,600 people. Nearly half continue to use aliases to protect their families from discrimination, while others have had no contact with their families for decades. The Aisei-en, which once housed 2,000 inmates, is typical of these facilities. Located on the small island of Nagashima and connected to the mainland by the “Bridge to Humanity,” its charnel house contains the unclaimed ashes of 3,600 former inmates. The Aisei-en is currently home to 204 individuals, whose average age is eighty-five. Most have spent more than six decades within this institution. The trajectory of their lives and deaths was shaped by laws introduced in 1907, 1931, and 1953 that mandated the involuntary confinement of all persons diagnosed with Raibyǀ (Leprosy). It was not until 1996 that the Diet finally repealed these laws. The objective of this chapter is to analyze how public policies toward and the treatment of Hansen’s disease sufferers were shaped within the context of Japan’s rise as an imperial power. Japan’s initial leprosy prevention policy was promulgated in 1907. It held doctors legally responsible for notifying the police in the case of a diagnosis of leprosy and gave them the responsibility for overseeing the isolation and disinfection of sufferers who had homes and families. But the law was primarily concerned with itinerant lepers and required their confinement at public expense in five regional leprosaria established in 1909. Its passage owed much to the international medical discourse on leprosy that emerged after G. A. Hansen identified Mycobacterium leprae as the causal agent. Later attempts to disassociate Hansen’s disease from the historical stigma attached to leprosy have continued to encounter resistance,

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particularly in areas of South and Southeast Asia, and Africa where the disease remains prevalent.1 Moreover, while the new terminology implied connotations of a progressive modernity, Hansen himself was an advocate of compulsory isolation of lepers and associated confinement policies with patriotism.2 During the decades that followed, Hansen’s prescription exerted enormous influence on generations of leprologists in Japan. Underlying the ensuing debates that incorporated the medical “best practice” were preexisting understandings of leprosy in Japan reinforced by social Darwinism and eugenics. From this coalescence of the traditional and the modern, the state created a legal framework based upon involuntary lifetime confinement. At the end of the nineteenth century, science carried immense social authority. This was paralleled by a growing number of academics, journalists, and doctors who introduced Darwinian analogies into public health discourse. However, the journey to the deliberate manipulation of human populations was by no means straightforward. Moreover, when enthusiasm for more assertive public health policies among the colonial powers did coalesce, it was driven in equal measure by social, political, and economic anxieties and advances in scientific or epidemiological knowledge.3 Comparable phenomena can be found in Japan, where the creation of an empire was a scientific project, while science itself served the interests of the imperial project. Initially, state polices were focused on sanitation, public health, and measures to improve the capacities of the Japanese population. The physician bureaucrat, Nagayo Sensai, who was instrumental in the creation of national institutions governing health management, coined the term eisei (hygiene) in 1872. In the same year, Nagayo established the Central Sanitary Bureau within the Ministry of Education, thus creating the first national archival resource providing data [updated every two years] on the “national body.” In 1874, the Central Hygiene Bureau was incorporated within the Home Ministry, as one of

1

Alicia Cruz, “Special Rapporteur on the Elimination of Discrimination on Persons Affected by Leprosy and Their Family Members, to Mark World Leprosy Day.” United Nations Humans Rights High Commissioner. Accessed January 28, 2018. http://ohchr.org/EN/Issues/Leprosy/Pages/LeprosyIndex.aspx. 2 Rod Edmond, Leprosy and Empire; A Medical and Cultural History, (Cambridge: Cambridge University Press, 2006) 103; and Eunjung Kim, “Cultural Rehabilitation: Hansen’s Disease, Gender and Disability in Korea,” Wagadu 4, (2007): 132–51. 3 Kathryn Tanaka, “Contested Histories and Happiness: Leprosy Literature in Japan,” Health, Culture and Society 5 no.1 (2013): 99–118.

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seven principal departments.4 Advances in the treatment of infectious diseases also accelerated a shift in focus among public health officials towards the treatment and control of both acute and chronic diseases. Health reforms designed to improve the Japanese race were ultimately extended to public sanitation, nutrition, personal hygiene, gender relations, and reproductive behavior. The chronically ill, particularly those afflicted with tuberculosis, leprosy, mental and venereal disease, were targeted as potential sources of both physical and social infection. This was readily apparent in the treatment of leprosy, as established in the Leprosy Prevention Law (LPL) of 1907.

A Disease Apart: Leprosy and Leprosy Control in Japan References to rai, as one of a number of skin diseases endemic to Japan, can be found as early as the eighth century, though its prevalence remains unknown.5 Under the influence of Buddhism, rai came to be generally understood as a form of gǀbyǀ (karmic disease), or punishment for crimes— committed in a previous lifetime. Rai no mono (lepers) appeared as a distinct category in contemporary civil codes, subject to official regulation and social marginalization.6 Yokoi Kiyoshi has argued that rai was also understood as a disease of the “unclean” wherein physical deformity was a manifestation of moral corruption.7 Yet, while sanctifying discrimination, on the one hand, Buddhism also invoked compassion and charity for lepers. The thirteenth-century Buddhist priest Nichiren understood rai as physical evidence of the imminent expiation of karmic sin and called upon his followers to embrace sufferers. His contemporary, the physician priest Kajiwara Shǀzen identified twelve variants of the disease, only four of

4

Christopher Aldous and Akihito Suzuki, Reforming Public Health in Occupied Japan, 1945–1952: Alien Prescriptions? (London: Routledge, 2012), 6, 19, 21–27, 32; Ann Jannetta, The Vaccinators: Smallpox, Medical Knowledge and the ‘Opening’ of Japan, (Stanford, CA: Stanford University Press, 2007), 174–76; and William Johnston, The Modern Epidemic; A History of Tuberculosis in Japan, (Cambridge, MA: Harvard University Press, 1995), 167–81. 5 Kiyomitsu Kanai, Chûsei no Raija to Sabetsu, (Tokyo: Iwata Shoin, 2003), 16. 6 Ibid., 14–17; Johnston, Modern Epidemic, 117–20; and T. Niunoya, ”Chûsei no Hinin to “Rai” Sabetsu,” in Hansenbyô: Haijo, Sabetsu, Kakuri no Rekishi, eds., Okiura Kazuteru and Tokunaga, Susumu (Tokyo: Iwanami Shoten, 2001), 80–87. 7 Susan Burns, “From Leper Villages to Leprosaria: Public Health, Nationalism and the Culture of Exclusion in Japan,” in Isolation: Places and Practices of Exclusion, eds. Carolyn Strange and Alison Bashford (London: Routledge, 2003), 106.

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which were karmic in origin and therefore untreatable.8 Thus, while rai was broadly understood as karmic in origin, this association did not imply shared definitions or forms of the treatment of rai. During the late Medieval and early Modern eras, special shelters attached to Buddhist Temples like that at Kitayama Juhachikenko in Nara provided housing for lepers. Lepers who were attached to these facilities possessed the right to beg for alms, and the sites themselves were open to the public. The intention was not to provide medical treatment but to facilitate salvation for lepers and for those whose charity supported the institution. Lepers were encouraged to engage in prayer and acts of penance to expiate the sins that had produced their condition.9 The Tokugawa Period (1603–1867) was characterized by the emergence of autonomous leper communities known as monoyoshi. Members were permitted to collect alms on specified days, reflecting the belief that acts of charity and compassion would be rewarded with good fortune. Many, perhaps the majority of lepers remained with their families and contributed to the household income through begging. Pilgrimages to hot springs, due to their assumed curative properties, were also common.10 Contemporary accounts also suggest both continuity and change in attitudes during this period. Influenced by Chinese medical practices, leprosy was gradually associated with unwholesome behavior leading to a poisoning of the blood. This association encouraged a more generalized belief that once “bad blood” had formed, it assumed a hereditary character. Thus, leprosy came to be understood as reflecting both karmic sins and a disease of the family or bloodline.11 Given the decentralized nature of the Tokugawa rule, there was considerable diversity in terms of attitudes and segregation. In certain feudal domains, lepers were assigned the status of rai mibun and often placed under the control of local eta (outcast) headmen, giving rise to the belief that eta were more likely to contract leprosy.12 As a precursor to the public policies adopted during the twentieth century, Katakura Katsuryô, a respected physician and author of A New Text on Syphilis and Leprosy 8 Andrew Edmund Goble, Confluences of Medicine in Medieval Japan (Honolulu: University of Hawaii Press, 2011), 15–20, 68–87. 9 Kanai, Chûsei no Raija to Sabetsu, 53, 56, 63–64, 69–70; and Niunoya, ‘Chûsei no Hinin to “Rai” Sabetsu, 78–79. 10 Justice Research Organization of the Japan Law Foundation (JRO), Final Report of the Verification Committee Concerning Hansen’s Disease Problem. (Tokyo, 2005), 13–17. 11 Duncan Rynjken Williams, The Other Side of Zen; A Social History of Sǀtǀ Zen Buddhism in Tokugawa Japan (Princeton NJ: Princeton University Press, 2005), 29– 30, 108–10. 12 JRO, Final Report, 17–22.

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(1786), condoned the existence of segregated leper villages as a means of avoiding dangerous marriages.13 Most monoyoshi communities did not survive the social and political transformation of the early Meiji period. Many disappeared quite quickly or were supplanted by more modern institutions, while others survived, only to become targeted by those committed to more “progressive” forms of confinement. An 1872 ordinance prohibiting the collection of alms, for example, precipitated the demise of the Kyoto community, and the gradual disappearance of traditional forms of isolation would encourage direct intervention by the central government.14 The Yôkuin, established in Tokyo in 1873, was designed to provide housing for the growing population of abandoned children, the infirmed (including lepers), and the insane, all of whom were regarded as “dirtying” the streets and creating an unfavorable impression among Westerners. The first modern leprosy facility, the Kihai Byǀin (Kihai Hospital) was founded in 1875. Its founder, Gotǀ Masafumi, regularly published on the causes and treatment of leprosy and provided empirical evidence of the infectiousness of leprosy.15 In 1885, at the invitation of the Hawaiian Board of Health, his son was invited to introduce the Gotǀ Treatment Regime, which involved reliance on a variety of herbal medications and immersions. However, Gotǀ Masanao’s understanding was also shaped by the perceived relationship between civilization and health. Writing in the Sei-I Kai Medical Journal in 1888, Gotǀ defined leprosy as “an endemic, contagious, chronic, malignant, constitutional, hereditary disease, whose origins could be found in the ‘immoral condition of a people,’ and a ‘lack of civilization.’”16 This understanding of leprosy as a medical, social, and political problem was confirmed at the First International Leprosy Conference in Berlin in 1897, at which the imperial powers endorsed the systematic isolation of lepers in their colonial territories. This not only distinguished modern leprosy prevention policies from a European past characterized by superstition, but also identified leprosy as a marker of cultural inferiority.17 13

Burns, “Leper Villages to Leprosaria,” 107. Ibid., 107–13. 15 JRO, Final Report, 18. 16 Kerri A. Inglis, “Cure the Dread Disease:19th Century Attempts to Treat Leprosy in the Hawaiian Islands,” The Hawaiian Journal of History 43, (2009): 106, 108, 118–19. 17 Edmond, Leprosy and Empire, 19; J. N. Hays, The Burdens of Disease; Epidemics and Human Response in Western History, (New Brunswick, NJ: Rutgers University Press, 1998), 20–29; and Luke Demaitre, Leprosy in Premodern Medicine; A Malady of the Whole Body, (Baltimore, MD: Johns Hopkins University Press, 2007), 102, 125, 259–69. 14

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Until about 1895, the public health administration, under the aegis of the Home Ministry, had been primarily concerned either with raising general levels of hygiene or with the policing and prevention of acute infectious diseases like cholera and smallpox. By contrast, the treatment of leprosy had been left to private, mainly missionary hospitals, like the Kaishun Hospital in Kumamoto Prefecture founded by Hanna Ridell. But, the establishment of five missionary-affiliated leprosaria between 1888 and 1906 and the consequent appearance in the English language press (e.g., New York Tribune, Japan Weekly Mail) of articles detailing the prevalence of leprosy in Japan provoked a heightened sense of urgency.18 Politicians were particularly distressed by the fact that Westerners exploited the higher incidence of certain “stigmatized” diseases as evidence of backwardness and lack of civilization.19 For a nation that had emerged victorious from the Sino-Japanese War (1894–1895) and had successfully negotiated an end to the humiliation of the Unequal Treaties, the presence of tens of thousands of lepers was regarded as a national disgrace.20 Subsequent debates incorporated not only medical or epidemiological knowledge but also questions of national identity and preexisting understandings of leprosy. The public health system that took form during this period thus reflected a growing association between the health of the nation and its geopolitical status. Without aggressive intervention by the state, it was argued, the existence of the unfit would provoke a gradual deterioration in the overall capacities of the Japanese race. The Infectious Disease Prevention Law (IDPL) of 1897 targeted eight acute infectious diseases (cholera, dysentery, typhoid, smallpox, typhus, scarlet fever, diphtheria, and black plague) for government action, and the infected were to be segregated from the healthy population. Nevertheless, when confronted by a rising crescendo of demands for the isolation of lepers, the government demurred. In fact, the Home Ministry cautioned that a distinction had to be made between acute infectious diseases (e.g., smallpox) that required isolation, and chronic infectious diseases that did not.21 In other words, the government was not only aware of this important distinction but knew that there was no medical justification for the confinement of leprosy sufferers Nonetheless, in 1900, the Ministry published the results of a national survey of lepers. Its conclusions reinforced commonsense understandings 18

Yutaka Fujino, “Inochi” no Kindaishi: “Minzoku Jôka” no nan no moto ni Hakugai sareta Hansenbyô Kanja, (Kyoto: Kamogawa Shuppan, 2001), 39. 19 Edmond, Leprosy and Empire, 80–86, 99, 110–12. 20 Fujino, “Inochi” no Kindaishi, 39; Yutaka Fujino, Hansenbyǀ to Sengo Minshushugi, (Tokyo: Iwanami Shoten, 2006), 7. 21 Ibid., 4.

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that associated leprosy with family bloodlines and suggested epidemic levels of leprosy. According to the survey, there were 30,359 sufferers and 19,907 households whose lineage contained leprosy, with another 990,930 people associated with such bloodlines. The figure of one million lepers rapidly came to dominate public discourse after 1900.22 Demands for stricter controls emanated from various quarters. Diet member, Nemoto Tadashi, lamented that the existence of 50,000 furǀ rai kanja (homeless lepers) undermined kokka no taimen (national prestige). Others emphasized the threat posed by “hidden” or unmarked bearers of the leprosy lineage,23 while an editorial in the Tokyo Nichinichi Shimbum expressed concern that when it came to leprosy control, Japan was comparable to India. More generalized fears of leprosy were reinforced by fictionalized accounts like Takahashi Oden Monogatari (“Tales of Oden Takahashi”), which first appeared in 1879. A 1921 iteration of the story by Suzuki Seizaburǀ reinforced the popular association of leprosy with the former outcast population.24 In March 1902, the debate was renewed when the Director of the Gunma Medical Association not only likened leprosy to the Black Plague but also associated it with an absence of civilization.25 In an article entitled, “One Million Leprosy Patients,” the Yomiuri Shimbun collapsed the distinction between hereditary transmission and infection to emphasize the threat posed by bearers of the leprosy lineage in the food and drink industry. It was these hidden, unmarked lepers, concluded the Yomiuri, who were responsible for spreading this “poison.”26 While the government regarded the confinement of one million Japanese as an economic impossibility, others invoked the Tokugawa practice of social exclusion of lepers as worthy of emulation. Mitsuda Kensuke, later hailed as Japan’s Albert Schweitzer for his work with lepers, not only recommended prohibitions on sufferers entering professions that involved interaction with the public but access to virtually all public spaces.27 Drawing upon his experiences at the Tokyo Yôkuin, Mitsuda warned of the incipient threat posed by the hidden leper, “the one who is not a beggar, but works on a ship, or preparing food and drink or something else, and there is the barber whose parents are lepers and the woman whose 22

Yutaka Fujino, Nihon fashizumu to iryǀ: Hansenbyǀ wo meguru jisshǀteki kenkynj, (Tokyo: Iwanami Shoten, 1993), 12. 23JRO, Final Report, 53; Fujino, “Inochi” no Kindaishi, 38–40; and Sawano, Raisha no Sei; Bunmei Kaika no Joken toshiteno (Tokyo: Seikyusha, 1994), 47. 24 JRO, Final Report, 18. 25 Fujino, “Inochi” no Kindaishi ,40. 26 Burns, “Leper Villages to Leprosaria,” 108–10. 27 Sawano, Raisha no Sei, 92; Fujino, “Inochi” no Kindaishi ,46, 48.

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husband is a leper who works serving food and drink.”28 As would be revealed a century later, Mitsuda’s decades long preeminence in the field of leprosy control was, however, grounded in eugenics rather than legitimate scientific investigation.29 Mitsuda’s elevation of past practices as “natural” was shared by many of his contemporaries. Writing in the prestigious Kyoto Newspaper of Medicine and Public Health, Sawa Riichiro described Japan as “the most leprous country in the world,” and prescribed the thirteenth-century Jûhachikenko as a source of indigenous inspiration.30 While the practices advocated by Mitsuda and Sawa were hardly comparable to the Buddhist temple shelters of the medieval period, appeals to tradition were extremely powerful. Within this new eugenics informed discourse that conjoined the past with contemporary narratives of progress and civilization, the leper would retain the stigmata of pollution and immorality but was denied the compassion that had characterized earlier practices. Mitsuda’s recommendations were incorporated in the LPL of 1907 (effective from 1909), under which doctors were legally responsible for notifying the police in the case of a diagnosis of leprosy, and the police were responsible for overseeing the isolation and disinfection of sufferers. Japan was divided into five regions, with a sanatorium located in each. Due to budgetary constraints, however, the capacity of this national network was 1,100, representing less than four percent of an estimated 30,000 leprosy sufferers. In addition, the financial burden of staffing and maintaining the sanatoria was delegated to individual prefectures.31 The fact that homeless lepers were the initial targets of absolute segregation had enormous implications for future care. Since they were regarded as possessing the requisite skills, many sanatoria directors and virtually all staff were recruited from among the pool of former police officers.32 Difficulty in the recruitment and retention of labor also increased reliance on inmate labor, ranging from cleaning and patient care to construction. In 1915, under the direction of its new director, Mitsuda Kensuke, the Tama Zenshǀ-en (Sanatorium) began offering rewards to young men who

28

Burns, “Leper Villages to Leprosaria,” 109–10. Fumiyo Hataya, Sabetsu to Hansenbyǀ: “Hiiragi no Kakine” wa ima mo, (Tokyo: Heibonsha, 2006), 176–77; and Waka Hirokawa, Kindai Nihon no Hansenbyǀ Mondai to Chiiki Shakai (Osaka: Osaka Daigaku Shuppankai, 2011), 23, 245–49. 30 Burns, “Leper Villages to Leprosaria,” 110. 31 Fujino, “Inochi” no Kindaishi, 49–51. 32 JRO, Final Report, 21. 29

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agreed to voluntary sterilization.33 When sterilization (male and female) failed to prevent conception, abortions were carried out and the fetuses were stored in formalin.34 Upon arrival and usually under police escort, all personal belongings were confiscated. Regardless of gender or age, inmates were issued identical sets of institutional clothing, making them more visible to the outside world, while effacing individuality. In later years, “belongings” came to include cash, in place of which inmates were issued institutional scrip that could only be used in the leprosarium canteen. Rooms were modeled on those commonly found in prisons, as were the punishments meted for infractions of the rules. By 1916, sanatoria directors were empowered to (a) reduce the daily food allowance, (b) confine or imprison recalcitrant inmates in small box-like cells for up to sixty days.35 In the same year, a Health and Hygiene Study Committee was established within the Home Ministry. Its conclusions, enacted in 1921, called for the expansion of existing facilities and the creation of a national sanatorium based upon the principle of absolute segregation. The influence of eugenics was apparent in official discourse throughout the 1920s and 1930s. In 1926, Takano Rokuro, the director of the Prevention Division within the Hygiene Bureau, described leprosy control as a form of minzoku jǀka (racial purification). Following criticisms of Japan at the Third International Leprosy Conference (1923) in an article published in the same year, Mitsuda, Kensuke reiterated that absolute segregation of lepers and the eradication of the disease were essential to the preservation of the purity of Japan’s bloodline.36 In 1930, the Health Bureau of the Ministry proposed a “Twenty-Year Program” designed to eradicate leprosy. This master plan was predicated on the assumption that all remaining (10,000) lepers would be incarcerated within ten years, and that they could be expected to die off within a further decade.37 In the 1930s, prefectural governments were encouraged to promote Muraiken Undǀ (Leprosy Free Campaigns), the objective of which was the identification, incarceration, and effective elimination of all lepers.38 33

Hirokawa Waka, Kindai Nihon no Hansenbyô Mondai to Chiiki Shakai, Osaka Daigaku Shuppankai (Hirokawa, 2011), 16; and Yutaka Fujino, Hansenbyǀ to Sengo Minshushugi (Tokyo: Iwanami Shoten, 2006), 11–17. 34 JRO, Final Report, 64–67; and Hataya, Sabetsu to Hansenbyǀ, 196–97. 35 Fujino, “Inochi” no Kindaishi, 68–70, 299–301; and Sawano, Raisha no Sei, 151–58. 36 Fujino, “Inochi” no Kindaishi, 92–93; and JRO, Final Report, 121. 37 Ibid., 82–83, 126; and Ibid., 21–22. 38 Yutaka Fujino, Nihon Fashizumu to Yusei Shisǀ (Kyoto: Kamogawa Shuppan, 2002), 156; and Hataya, Sabetsu to Hansenbyǀ, 185–86.

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To garner public support for segregation, the Ministry of Home Affairs established the Leprosy Prevention Association (LPA) in 1930. In recognition of the support provided by the imperial family, June 25 the birthday of the then empress was selected as “Leprosy Prevention Day.”39 In subsequent years, the weeks before and after June 25 were marked by the distribution of pamphlets, film screenings, and public lectures all of which were designed to encourage support for official policies. Although never fully enforced, under the revised LPL (1931), all leprosy sufferers were subject to transportation to the leprosaria.40 Guidelines issued through the Ministry of Welfare reiterated a national policy of leprosy eradication through absolute segregation.41 As institutional capacity expanded and the anti-leprosy campaigns intensified, the number of patients increased. Patients were sent to leprosaria within a state-operated network stretching from Aomori in the north to Okinawa in the south. By the late 1930s, recalcitrants, including politically active patients, were transported to “special wards” at the Kuryu Rakusen sanatorium (Gunma Prefecture), which was equipped with punishment cells. The death rate among inmates was approximately twenty percent.42 Leprosy specialists like Mitsuda Kensuke dominated mainstream publications in the form of official reports and publications in journals and newspapers. Leprosaria directors also encouraged writing as both a form of therapy and as a means of highlighting the benefits of isolation though patient output was subject to rigorous censorship until the 1950s. However, patients did make significant contributions to the leprosy literature (later Hansen’s disease literature). These took the form of journals, haiku and tanka poetry, novels, and short stories. Unlike the former, which provided justifications for state policies, patient literature often spoke to the trauma of incarceration, separation from family and friends, and the experience of living with leprosy. In this sense, their writings are better understood, as Arai Yuki has argued, the Literature of Quarantine.43 Literary luminaries such as Kawabata Yasunari and Yosano Akiko promoted the publication of 39

Fujino, “Inochi” no Kindaishi, 132–34. Sawano, Raisha no Sei, 119–27; Hirokawa, Kindai Nihon, 119–21; and Kazeteru Okiura and Susumu Tokunaga, eds., Hansenbyǀ: Haijǀ, Sabetsu, Kakuri no Rekishi, (Tokyo: Iwanami Shoten, 2001), 45–47. 41 JRO, Final Report, 47–48; and Fujino, “Inochi” no Kindaishi, 129–30. 42 JRO, Final Report, 23; Fujino, “Inochi” no Kindaishi, 298–301; and Sawano, Raisha no Sei, 151–58. 43 Kathryn M. Tanaka, “‘Life’s First Night’ and the Treatment of Hansen’s Disease in Japan, A Translation and Introduction to Hôjô Tamio’s Novela,” The Asia-Pacific Journal, Japan Focus 13 (Issue 4), no. 1 (2015): 1-36. 40

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the writings of patients, as was the case in the publication in 1936 of Hôjô Tamio’s account of institutional life “Inochi no Shoya” (Life’s First Night). Although fictional, the experience of Hǀjǀ’s protagonist Oda during his first night of institutionalization was a composite drawn from the real-life experiences of sufferers.44 Compulsory sterilization of leprosy sufferers was neither condoned nor prohibited under contemporary legal codes but had regularly been carried out on a de facto basis by sanatoria doctors. In 1930, Diet members, Chnjma Okimaru and Arakawa Gorǀ proposed an expanded definition of “hereditary” that would include not only lepers and those suffering from venereal diseases but social undesirables, including congenital criminals, alcoholics and those of a “morbid” or “impulsive” character. This was rejected by the Ministry of Health and Welfare and the National Eugenic Law of 1940, which provided for the sterilization of individuals suffering from specific hereditary diseases, while excluding leprosy patients from this procedure.45 Nonetheless, compulsory sterilization of leprosy patients at state-operated leprosaria not only continued throughout the Pacific War but also was finally legalized under Ynjsei Hogohǀ, the Eugenic Protection Law (EPL) of 1948.46 The explicit purpose of the law was “to prevent the birth of eugenically inferior offspring and to protect the health and life of the mother.” While Allied Occupation officials broadly supported the legislation,47 those sections related to compulsory sterilization were criticized on both scientific and legal grounds. Some argued that the legislation was unconstitutional since it did not include the right to appeal through the courts. Alfred Oppler, chief of the Courts and Law Division, Government Section of SCAP (Supreme Commander Allied Powers), unfavorably compared the proposed law with the sterilization policies of the

44

Ibid.; and Burns, “From Leper Villages to Leprosaria,” 191–211. Fujino, “Inochi” no Kindaishi, 278–81; and Yôko Matsubara, “The Enactment of Japan’s Sterilization Laws in the 1940s: A Prelude to Postwar Eugenic Policy,” Historia Scientiarum: The International Journal of the History of Science Society of Japan 8, no. 2 (1998): 187–201. 46 Sawano, Raisha no Sei, 90; JRO, Final Report, 23–24, 53–55; Fujino, “Inochi” no Kindaishi, 112–13, 278–79; Yutaka Fujino, Nihon Fashizumu To Yusei Shisǀ (Kyoto: Kamogawa Shuppan, 2002), 324–30; and Hataya, Sabetsu to Hansenbyǀ, 196–97. 47 Deborah Oakley “American-Japanese Interaction in the Development of Population Policy in Japan, 1945–1952,” Population and Development Review, 4, no. 4 (1978): 617–43. 45

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Third Reich.48 Ultimately, however, and perhaps due to the prevalence of eugenic laws that permitted involuntary sterilization in certain US states (particularly California), such voices did not prevent the passage of the EPL.49

Leprosy Treatment and Control within the Japanese Empire Identical, though often more coercive, policies were extended to Taiwan, Korea, and elsewhere within the empire.50 In 1901, six years after the annexation of Taiwan, Aoki Taiyû, a physician working at the Taihoku (Taipei) Hospital, reported that leprosy in Taiwan had reached epidemic levels. Estimates were as high as 28,800, with the majority being highly contagious. Aoki recommended the immediate establishment of leprosaria, both for compulsory segregation of lepers and for laboratory studies. During the first two decades of colonial rule, plans for building leprosaria were proposed by Japanese doctors on several occasions and were supported by some Japanese and Taiwanese social elites. But the response of the colonial administration to the leprosy “crisis” was highly selective and reflected the project of transforming Taiwan into an environment suitable for Japanese emigration. The result was that the diffusion of modern medical and sanitary facilities was largely confined to areas of Japanese settlement. Encouraged by Mitsuda Kensuke the Government General began planning for the compulsory segregation of lepers. Budgetary constraints led to the abandonment of initial plans to develop three leper settlements. The budget for an Isolation Hospital was approved in 1927, and the Leprosy Prevention Law of Taiwan was introduced two years later.51 The Rakusei-in (Happy Life Leprosarium) was not opened until December 1930. While estimates of the Taiwanese leper population during this period ranged from just under 1,100 to more than 20,000, this facility could only accommodate one hundred permanent patients and a further fifty outpatients. Reflecting the views of the mainland specialists, Kamikawa 48 Norikazu Chiba, “Allied Forces GHQ Criticized Eugenics Bill as More Problematic than Nazi Law,” Mainichi Newspapers, accessed July 26, 2018, https://mainichi.jp/english/articles/20180624/p2a/00m/0na/001000c. 49 Edwin Black, War against the Weak: Eugenics and America’s Campaign to Create a Master Race, (New York: Four Walls Eight Windows, 2003), 385–409. 50 Fujino, “Sensǀ to Hansenbyǀ,” 167–86; and JRO, Final Report, 134–38. 51 Wen-Ji Wang, “‘Laying out a Model Village’: George Gushue-Taylor and Missionary Leprosy Work in Colonial Taiwan,” East Asian Science, Technology and Society 1, no. 1 (December, 2007): 113–15.

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Yutaka, director of the Happy Life Leprosarium, anticipated the eradication of leprosy through a rigorously enforced policy of confinement and segregation.52

Korea In 1909, one year before the annexation of Korea, R. M. Wilson established the first of three missionary hospitals for lepers in Kwangju. In 1910, there were an estimated 15,000–20,000 leprosy patients, found mainly in the southern parts of the peninsula. Determined to limit Christian influence in Korea, the Government General gradually assumed responsibility for the management of leprosy. In 1916, it opened the Chahye Pyǂngwǂn (Mercy Hospital) as a precursor to the Sorokdo (Sorok Island) Leprosarium. Under its then (1933) director, Suho Masasue, Sorokdo was greatly expanded until it was home to an estimated 6,000 lepers.53 Involuntary sterilization and abortion, physical abuse, and punishment cells modeled on those in Japan were incorporated into the regime. Forced labor was also deployed for both the expansion of facilities and the construction of a statue of Suho, before which inmates were expected to pray.54 In 1942, Suho was assassinated by a patient because of the deteriorating conditions at the institution and the mistreatment of inmates.55 By 1935, the year in which the Chosǂn Leprosy Prevention Act was promulgated, the Government General was well on its way to establishing its pre-eminence in the area of leprosy control. By duplicating the mainland experience, the colonial authorities reinforced their superiority over Koreans and missionaries alike. In implementing its policies, including compulsory sterilization, the colonial administration was indirectly assisted by indigenous images of lepers as cannibals, which coexisted with the official discourse that emphasized the infectious and the hereditary nature of the disease. Between 1920 and 1931, for example, the Tonga Ilbo published twenty-one articles detailing the gruesome practices of lepers.56

52

Ibid., 123–25. Takio, Chǀsen Hansenbyǀ-shi: Nihon Shokuminchi-ka no Sorokuto, (Tokyo: Miraisha, 2001), 46–49. 54 JRO, Final Report, 131–32. 55 Takio, Chǀsen Hansenbyǀ-shi, 266. 56 Kim, “Cultural Rehabilitation,” 136–42. 53Eiji

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Postscript Lifetime confinement of leprosy sufferers was enforced within Japan at a time when leprosy was understood as a highly contagious disease. Moreover, compulsory confinement was maintained long after it became known that isolation was unnecessary in the majority of cases.57 Preservation of the leprosaria did provide patients with limited social and medical support, but continued to deprive them of fundamental human rights. On the other hand, the LPL as the most authoritative statement on the disease reinforced existing social stigmas associated with leprosy. It also reduced the likelihood of patients’ reintegration into society. In 1947, the “Special Wards” were closed, only to be replaced by a Leprosy Prison adjacent to the Kikuchi Keifu sanatorium in 1953.58 Moreover, between 1948 and 1996, when the LPL was finally repealed, an estimated 1,500 sterilizations and nearly 8,000 involuntary abortions were performed. As a consequence of nearly a century of legal segregation and mistreatment, a total of 16,475 involuntary sterilizations had been carried out, the last having taken place in 1992.59 The most effective treatment for leprosy patients, the sulfone drug Promin, was introduced to Japan in 1946. Although its benefits were reported to the Congress of the Japan Leprosy Association (JLA), leprosaria directors argued that the possibility of relapse precluded universal application. In fact, influential leprologists like Mitsuda, who advised on early postwar policy discussions, exploited residual popular fears as a means of retaining the current regime and defending their own reputations.60 Challenging these expert opinions, leprosy patients organized the Federation of National Leprosarium Patients (FNLP) in an effort to obtain political support for improved treatment. The Diet ultimately approved a budget for the purchase and distribution of sulfones to state-run leprosaria, and, in 1951, an initial group of thirty-five recipients of Promin treatment was discharged as a result of improvement in their conditions. Such positive measures, however, did not signal an end to the policy of segregation. In the same year, the Health and Welfare Committee of the House of Councilors received expert testimony from renowned leprologists, Mitsuda Kensuke 57

JRO, Final Report, 119–21. Fujino, “Inochi” no Kindaishi, 499; and JRO, Final Report, 33–36. 59 Fujino, “Inochi” no Kindaishi, 480–82; and Mari Yamaguchi, “Victims Begin to Talk about Japan's Sterilization Program,” AP News, December 18, 1997, https://www.apnews.com/1fefa5a14516efe9ab18763d9a8c9c46, 1–3. 60 JRO, Final Report, 29, 49–50, 83–87; and Burns, “Leper Villages to Leprosaria,” 113. 58

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and Hayashi Yoshinobu (the current President of the JLA). Hayashi emphasized the threat of infection still posed by an estimated 15,000 leprosy sufferers, 9,000 of whom remained institutionalized. He recommended an expansion of the existing system to accommodate the remaining 6,000. Mitsuda also reiterated the necessity of confinement, coupled with sterilization, to prevent the spread of the disease.61 The Ministry of Health and Welfare (MHW) representative concurred with these assessments but advocated expanded research into the disease and the implementation of public awareness programs. He opposed the release of patients on the grounds that their deformities and disabilities would not only constrain their daily lives but would make them unacceptable in society.62 A cabinet bill to revise the LPL was submitted to the Diet for consideration in 1953. Although referred to as a revision, key elements of the 1931 law remained unaffected. Yamaguchi Masayoshi, Director of the Public Health Bureau within the MHW, expressed confidence in confinement, adding that compulsory institutionalization should be warranted by law but only as a last resort. Yamaguchi further argued that both the discharge of patients whose isolation was no longer necessary and the issuance of temporary leave should be left to the discretion of individual leprosaria directors.63 The FNLP unsuccessfully argued that the proposed legislation, though less draconian than its predecessor, emphasized social protection from leprosy at the expense of patients’ rights. In essence, the revised LPL of 1953 retained a legal basis for the compulsory isolation of leprosy patients, and invested leprosaria directors with near absolute authority over the lives of patients.64 In response to criticisms voiced by patients and their supporters, a further nine supplementary resolutions were adopted. These included provisions for living stipends and patient work, improvement in living conditions, promotion of research, and installation of rehabilitation facilities. In fact, the Ministry did initiate programs for patient rehabilitation but remained committed to expanding existing institutional capacity. In 1956, the Ministry produced a “tentative” standard for patient discharge, but this was clearly not intended to “expedite” protocols. In practice, an estimated 500 patients were admitted or readmitted to leprosaria that year, while fewer than one hundred were 61 Hataya, Sabetsu to Hansenbyǀ, 93, 175–76; and Tony Gould, A Disease Apart: Leprosy in the Modern World (New York: St Martin’s Press, 2005), 368. 62 Hajime Sato and Janet E. Frantz, “Termination of the Leprosy Isolation Policy in the US and Japan: Science, Policy Changes and the Garbage Can Model,” BMC International Health and Human Rights 5, no. 3, (2005): 5. 63 Fujino, Sensõ to Hansenbyǀ, 132–38. 64 JRO, Final Report, 29–30.

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discharged.65 In contrast to mainland policies, in 1961, the Okinawan legislature, while under US occupation, passed the Hansen's Disease Prevention Act. This authorized the Chief Executive not only to advise the hospitalization of leprosy patients but also to order the discharge of improved patients.66 Encouraged by both the example set by Okinawa and internationally sanctioned approaches that favored outpatient treatment rather than confinement, the FNLP restated its demand for further revision of the LPL, charging that the social stigma and discrimination associated with leprosy had been fostered by laws that required enforced confinement. In 1963, the FNLP submitted a petition for the revision of the law. Rather than directly addressing revision, the Diet referred the matter to the MHW. Ministry officials argued that the LPL legitimized compulsory isolation of leprosy patients and that this, in turn, confirmed the legal basis for the government's responsibility to provide sufferers with medical care and a comfortable living environment. Therefore, this revision of the law might result in the elimination of the leprosaria, making it impossible for the patients to receive public support. Similarly, reliance on outpatient treatment rather than inpatient isolation could produce the same loss of state support.67 Ministerial obfuscations were indirectly confirmed by the results of a 1965 survey, which revealed that 84% of current leprosaria residents had expressed themselves to be either unwilling or unable to be fully discharged. During the 1970s, leprosaria directors gradually relaxed treatment guidelines, and outpatient treatment was expanded on an informal basis. However, given that many sufferers had spent their lives in a dependent institutional environment, patients often shared the view of administrators that revision of the LPL could endanger or eliminate entitlements.68 In 1976, the Federation of Leprosarium Directors (FLD) drafted a revision to the LPL, which incorporated specific discharge codes, and then submitted it to patients for their consideration. The FNLP objected on the grounds that the adoption of specific discharge codes could result in the compulsory discharge of patients, and focused its activities on compensation for lowwage patient labor and the consequences of compulsory segregation. In fact, it was not until 1984 that the FNLP established a committee to consider a revision of the LPL.

65

Sato and Frantz, “Termination of Leprosy Isolation Policy,” 5. JRO, Final Report, 128–30. 67 Ibid., 44–47. 68 Miwako Hosoda, “Hansen’s Disease Recoverers as Agents of Change: A Case Study in Japan,” Lepra Review 81, (2010): 11. 66

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Given the patients’ ambivalence toward the potential closure of the leprosaria, the FLD concluded that the sanatoria should not be abruptly closed since many residents were already too old to leave. In the intervening years, the MHW had also responded more positively by improving living conditions in leprosaria and increasing staffing levels and government subsidies. Similarly, reliance on patient labor was gradually reduced and made more rewarding or replaced by rehabilitative programs. On the other hand, patients were repeatedly warned that entitlements could be threatened if revisions to the LPL were hastily implemented. Moreover, many patients who had been incarcerated for decades had become institutionally dependent on the leprosaria. They genuinely feared to lose their privileges. Others justified the continuation of their special status as compensation for the egregious treatment they had endured at the hands of the state.69 With the appointment of ƿtani Fujio as Director General of the Tǀfu Kyǀkai, a foundation that had been established in 1952,70 obstacles to reform began to dissolve. A retired senior official within the MHW, Õtani also served as the Chairman of the Advisory Council on Public Health in the same Ministry. The FNLP consulted him on its draft petition of the LPL and, in 1992, the Federation filed a petition with the MHW. While many patients remained ambivalent about the revision, Õtani offered the reassurance that their homes (leprosaria) would be maintained.71 One year later, the Tǀfu Kyǀkai was officially consulted by the Ministry on leprosy prevention policies. A committee was subsequently established and composed of leprologists, lawyers, media representatives, ministerial officials, and patients presided over by Õtani. In an effort to re-educate the public, Õtani was also instrumental in establishing the Takamatsu Memorial Hansen’s Disease Museum in Tokyo (1993), where he hosted a series of symposia critical of Japan’s Hansen’s disease policies.72 In 1994, at the 67th Congress of the JLA, ƿtani successfully argued that the existing LPL lacked scientific foundation, violated patients’ human rights, and should be abolished. In 1995, the MHW established an internal panel of experts to consider the abolition of the LPL. Chaired by ƿtani, the panel subsequently recommended abolishing the LPL, a continued provision of public support for existing patients, and the use of the term "Hansen's Disease" in place of "Leprosy" in all future laws. In 1996, the Diet passed the Act to Abolish the LPL. It also outlined the government's 69

JRO, Final Report, 42–47, 87–89, 108–12. Ibid., 42. 71 Sato and Frantz, “Termination of Leprosy Isolation Policy,” 6. 72 Fujio ƿtani, When the Walls Crumble; The Emancipation of Persons Affected by Hansen's Disease in Japan (Tokyo: Tǀfu Kyǀkai, 1998), 166–67. 70

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responsibility to provide patients with continuous medical and social services, provided that they could either leave or remain at the leprosaria and guaranteed that those who decided to return to the leprosaria after their discharge could be readmitted.73 At that time, there were 5,413 patients in leprosaria, whose average length of stay was more than forty years and whose average age was seventy-two years. Only six patients actually left their leprosaria in the following two years, and as of February 2009, there were 2,609 patients (average age over eighty) still living in thirteen leprosaria in Japan. In May 2001, the Kumamoto District Court (Hansen’s Disease Government Liability Lawsuit) ruled that the LPL had been unconstitutional and ordered the government to provide compensation for patients who had been incarcerated under that law. Under the terms of the Act on Payment of Compensation to Inmates of Hansen’s Disease Sanatoria (2001), the government agreed to pay between US$40,000 and $100,000 to each of 2,000 plaintiffs. Payments were sent to both leprosaria inmates and their families.74 In 2007, the Prince Takamatsu Memorial Museum was renamed as the National Hansen's Disease Museum. Located in Higashimurayama outside Tokyo, the museum is adjacent to the Tama Zensho-en (Sanatorium), at which Mitsuda Kensuke once served as director. The site contains three permanent exhibition halls and a library, and the mission of the museum is to: promote awareness of leprosy; represent and preserve the history of leprosy in Japan; exhibit what persons affected by leprosy have achieved; help restore the sufferer’s dignity; demonstrate the importance of human rights; and commit to ending prejudice and discrimination. In 2008, a new law was enacted to extend social welfare services and restore the honor of Hansen’s Disease sufferers (Act No. 82 2008:1–12) and, since 2009, June 22 has been designated as the annual “Day of Restoration of Honor and Remembrance of Victims of the Hansen’s Disease Prevention Act.” In April 2009, the Diet passed the Basic Law on the Promotion of Issues Related to Hansen’s disease. The objectives are: (a) to protect the rights of people affected by leprosy in Japan; (b) to facilitate their full integration into society; and (c) to encourage patients to find better ways to make the

73

Sato and Frantz, “Termination of Leprosy Isolation Policy,” 5. Atsushi Suzuki, “The Campaign to Seek Compensation for Japan’s Policy of Isolating Hansen’s Disease Sufferers” (report, 16th Congress of the International Association of Democratic Lawyers, Paris, 2005), 1–6; and Jonathan Watts, “Japanese Leprosy Patients Receive Official Apology,” The Lancet 357, no. 9270 (2001): 1774, https:// doi:10.1016/s0140-6736(00)04945-x). 74

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leprosaria accessible for education and communication with the general public.75 Certain parallels can be found in legal responses to claims made by former colonial subjects. In October 2005, a three-judge panel of the Tokyo District Court upheld a lawsuit filed by twenty-five Taiwanese leprosy sufferers who had endured compulsory segregation during the colonial period. Yet, on the same day, a second panel of the Tokyo District Court rejected similar claims from 117 Koreans on the grounds that the 2001 ruling did not specifically include inmates of leprosaria located outside of Japan.76 In 2006, the 2001 compensation agreement was revised to allow for the processing of claims made by former colonial subjects who had been incarcerated in leprosaria in Taiwan, Korea, and on the Micronesian islands of Yap, Palau, Saipan, and Jaluit.77 The Ministry of Health Labor and Welfare has posted an online application for former colonial inmates (in English). Applicants may also telephone the Ministry, but calls are only accepted in Japanese. During the past decade, further initiatives, both public and private, have been introduced to “normalize” the lives of patients and address the history of leprosy and its treatment, but after a century of criminalization and confinement, the evidence thus far suggests that re-education and acceptance will be no easy task. In 2016, for example, family members of former Hansen’s disease patients initiated a class-action lawsuit against the Japanese government, claiming they had suffered discrimination in marriage, housing, employment, and education as a consequence of officially sanctioned policies of segregation.78 In addition to financial compensation, the nearly six hundred plaintiffs have requested the publication of a formal apology from the government. In June 2019, the Kumamoto District Court ruled in favor of plaintiffs and ordered the government to pay damages to the families of former leprosy patients. The Abe government subsequently announced that it would not appeal, and under the “Act on Payments of Compensation for Family Members of Former Hansen’s Disease Patients,” enacted in December 2019, the 75

International Federation of Anti-Leprosy Associations, Japan: Law on the Promotion of Issues Related to Hansen’s Disease (Geneva: ILEP, 2009), 1–3. 76 Jeff Kingston, “Compensating Colonial Lepers, Slave Laborers and Hibakusha: Troubling Legacies and Evolving Standards of Postcolonial Justice in Japan, Japan Focus 3, no. 11 (2005): 1–2. 77 Kim Min-kyung, "13 Years of Cooperative Struggle by S. Korean and Japanese Lawyers," The Hankyoreh, January 29, 2017, http://english.hani.co.kr/arti/english_edition/e_national/780508.html. 78 Mainichi Shimbun, Allied Forces, 1–2.

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government extended eligibility to the relatives of former patients in Okinawa during the American Occupation, as well as in Korea and Taiwan prior to the Second World War.79

Bibliography Aldous, Christopher, and Akihito Suzuki. Reforming Public Health in Occupied Japan, 1945-52: Alien Prescriptions? London: Routledge, 2012. Black, Edwin. War Against the Weak: Eugenics and America's Campaign to Create a Master Race. New York: Four Walls Eight Windows, 2003. Burns, Susan. “From Leper Villages to Leprosaria: Public Health, Nationalism and the Culture of Exclusion in Japan.” In Isolation: Places and Practices of Exclusion, edited by Alison Bashford and Carolyn Strange, 97-110. London: Routledge, 2003. Chiba, Norikazu. “Allied Forces GHQ Criticized Eugenics Bill as More Problematic than Nazi Law.” Mainichi Newspapers, June 24, 2018. Accessed July 26, 2018. https://mainichi.jp/english/articles/20180624/p2a/00m/0na/001000c. Demaitre, Luke. Leprosy in Premodern Medicine: A Malady of the Whole Body. Baltimore, MD: The Johns Hopkins University Press, 2007. Edmond, Rod. Leprosy and Empire: A Medical and Cultural History. Cambridge: Cambridge University Press, 2006. Fujino, Yutaka. Hansenbyǀ to Sengo Minshushugi. Tokyo: Iwanami Shoten, 2006. Fujino, Yutaka. Nihon Fashizumu to Yusei Shisǀ. Kyoto: Kamogawa Shuppan, 2002. Fujino, Yutaka. “Inochi” no Kindaishi: “Minzoku Jôka” no nan no moto ni Hakugai sareta Hansenbyô Kanja. Kyoto: Kamogawa Shuppan, 2001. Fujino, Yutaka. Nihon fashizumu to iryǀ: Hansenbyǀ wo meguru jisshǀteki kenkynj. Tokyo: Iwanami Shoten, 1993.

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Library of Congress Law, “Japan: New Law Enacted to Compensate Family Members of Former Hansen’s Disease (Leprosy) Patients” December 18, 2019 https://www.loc.gov/law/foreign-news/article/japan-new-law-enacted-tocompensate-family-members-of-former-hansens-disease-leprosy-patients/; Kyodo News, “Japan lawmaker OK plan to compensate kin of former leprosy patients,” October 24, 2019, https://english.kyodonews.net/news/2019/10/7673e1c52735japan-lawmakers-ok-plan-to-compensate-kin-of-former-leprosy-patients.html.

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Goble, Andrew E. Confluences of Medicine in Medieval Japan: Buddhist Healing, Chinese Knowledge, Islamic Formulas, and Wounds of War. Honolulu: University of Hawaii Press, 2011. Gould, Tony. A Disease Apart: Leprosy in the Modern World. New York: St. Martin's Press, 2005. Hataya, Fumiyo. Sabetsu to Hansenbyǀ: “Hiiragi no Kakine” wa ima mo. Tokyo: Heibonsha, 2006. Hays, J. N. The Burdens of Disease: Epidemics and Human Response in Western History. Brunswick, NJ: Rutgers University Press, 1998. Hirokawa, Waka. Kindai Nihon no Hansenbyǀ Mondai to Chiiki Shakai. Osaka: Osaka Daigaku Shuppankai, 2011. Hosoda, Miwako. “Hansen’s Disease Recoverers as Agents of Change: A Case Study in Japan.” Lepra Review 81, no. 1 (March 2010), 5-16. https://www.ncbi.nlm.nih.gov/pubmed/20496565. Inglis, Kerri A. “‘Cure the dread disease’: 19th Century Attempts to Treat Leprosy in the Hawaiian Islands.” Hawaiian Journal of History 43 (2009), 101-124. http://hdl.handle.net/10524/12241. International Federation of Anti-Leprosy Associations. Japan: Law on the Promotion of Issues Related to Hansen’s Disease. Geneva: ILEP, 2009. Jannetta, Ann. The Vaccinators: Smallpox, Medical Knowledge, and the ‘Opening’ of Japan. Stanford, CA: Stanford University Press, 2007. Johnston, William. The Modern Epidemic: A History of Tuberculosis in Japan. Cambridge, MA: Harvard University Asia Center, 1995. Kanai, Kiyomitsu. Chûsei no Raija to Sabetsu. Tokyo: Iwata Shoin, 2003. Kim, Eunjung. “Cultural Rehabilitation: Hansen’s Disease, Gender and Disability in Korea.” Wagadu 4: Intersecting Gender and Disability Perspectives in Rethinking Postcolonial Identities 4 (August 2007), 108124. Kingston, Jeff. “Compensating Colonial Lepers, Slave Laborers and Hibakusha: Troubling Legacies and Evolving Standards of Postcolonial Justice in Japan.” Japan Focus 3, no. 11 (November 2005). https://apjjf.org/-Jeff-Kingston/1579/article.html. Kyodo News. “Japan lawmaker OK plan to compensate kin of former leprosy patients,” October 24, 2019, https://english.kyodonews.net/news/2019/10/7673e1c52735-japanlawmakers-ok-plan-to-compensate-kin-of-former-leprosypatients.html.

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Library of Congress Law. “Japan: New Law Enacted to Compensate Family Members of Former Hansen’s Disease (Leprosy) Patients” December 18, 2019, https://www.loc.gov/law/foreign-news/article/japan-new-lawenacted-to-compensate-family-members-of-former-hansens-diseaseleprosy-patients/ Matsubara, Yoko. “The Enactment of Japan’s Sterilization Laws in the 1940s: A Prelude to Postwar Eugenic Policy.” Historia Scientiarum: The International Journal of the History of Science Society of Japan 8, no. 2 (December 1998), 187-201. http://hdl.handle.net/10822/534242. Min-kyung, Kim. “13 years of cooperative struggle by S. Korean and Japanese lawyers.” Hankyoreh, January 29, 2017. http://english.hani.co.kr/arti/english_edition/e_national/780508.html. Niunoya, Tetsuichi. “Chûsei no Hinin to “Rai” Sabetsu.” In Hansenbyô: Haijo, Sabetsu, Kakuri no Rekishi, edited by Kazuteru Okiura and Susumu Tokunaga, 80-87. Tokyo: Iwanami Shoten, 2001. Oakley, Deborah. “American-Japanese Interaction in the Development of Population Policy in Japan, 1945-52.” Population and Development Review 4, no. 4 (December 1978), 617-643. doi:10.2307/1971729. Okamoto, Takuya. “Leprosy patients' relatives seek damages, apology for discrimination.” Kyodo News, June 11, 2018. https://english.kyodonews.net/news/2018/06/243e88de9663-featureleprosy-patients-relatives-seek-damages-apology-fordiscrimination.html. Sato, Hajime, and Janet E. Frantz. “Termination of the leprosy isolation policy in the US and Japan: Science, policy changes, and the garbage can model.” BMC International Health and Human Rights 5, no. 3 (March 2005). https://doi:10.1186/1472-698x-5-3. Sawano, Masaki. Raisha no Sei; Bunmei Kaika no Joken toshiteno. Tokyo: Seikyusha, 1994. “Special Rapporteur on the Elimination of Discrimination on Persons Affected by Leprosy and Their Family Members, to Mark World Leprosy Day.” The Office of the High Commissioner for Human Rights. Accessed January 28, 2018. http://ohchr.org/EN/Issues/Leprosy/Pages/LeprosyIndex.asp. Suzuki, Atsushi. The Campaign to Seek Compensation for Japan’s Policy of Isolating Hansen’s Disease Sufferers. Paris: 16th Congress of the International Association of Democratic Lawyers, 2005. http://iadllaw.org/files/The%20Campaign%20to%20Seek%20Compen sation%20for%20Japan's%20Policy%20of%20Isolating%20Hansen's %20Disease%20Sufferers_0.pdf.

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Takio, Eiji. Chǀsen Hansenbyǀ-shi: Nihon Shokuminchi-ka no Sorokuto. Tokyo: Miraisha, 2001. Tanaka, Kathryn M. "Contested Histories and Happiness: Leprosy literature in Japan." Health, Culture and Society 5, no. 1 (2013), 99-118. doi:10.5195/hcs.2013.133. Tanaka, Kathryn M. “‘Life’s First Night’ and the Treatment of Hansen’s Disease in Japan, A Translation and Introduction to Hôjô Tamio’s Novela.” The Asia-Pacific Journal, Japan Focus 13 (Issue 4), no. 1, (2015). Verification Committee Concerning Hansen’s Disease Problem. Final Report of the Verification Committee Concerning Hansen’s Disease Problem. Justice Research Organization of the Japan Law Foundation, 2005. https://www.mhlw.go.jp/english/policy/health/01/pdf/01.pdf. Hirokawa Waka, Kindai Nihon no Hansenbyô Mondai to Chiiki Shakai, Osaka Daigaku Shuppankai. Hirokawa: 2011. Wang, Wen-Ji. “’Laying out a Model Village’: George Gushue-Taylor and Missionary Leprosy Work in Colonial Taiwan.” East Asian Science, Technology and Society 1, no. 1 (December 2007), 111-133. Watts, Jonathan. “Japanese leprosy patients receive official apology.” The Lancet 357, no. 9270 (June 2001), 1774. doi:10.1016/s0140-6736(00)04945-x. Williams, Duncan R. The Other Side of Zen: A Social History of Sǀtǀ Zen Buddhism in Tokugawa Japan. Princeton NJ: Princeton University Press, 2005. Yamaguchi, Mari. “Victims begin to talk about Japan’s sterilization program.” Associated Press, December 18, 1997. https://www.apnews.com/1fefa5a14516efe9ab18763d9a8c9c46. ƿtani, Fujio. The Walls Crumble: The Emancipation of Persons Affected by Hansen's Disease in Japan. Tokyo: Tofu Kyokai Association, 1998.

CHAPTER FOUR EPIDEMICS OF INEQUITY: CHALLENGING THE RACIAL PREDISPOSITION HYPOTHESIS ANDREA PATTERSON

In the early years of the twentieth century, popular theories from newly emerging academic disciplines lent a distinctly scientific aura to preexisting racial views in the American South. Scientific theories were informed by a white supremacist worldview, and most experts agreed that innate physiological and biological differences separated the races. In this context, widespread disease and frequent outbreaks of epidemics became not only a matter of life and death but also served as an ideological battleground. Disproportionately high morbidity and mortality rates among black people were viewed as a consequence of inherent racial deficiencies. Much of the scholarship in the new field of anthropology, dedicated to the “study of primitive races of mankind,” as well as scientific advances in evolutionary biology, genetics, and pathology promoted rather than deterred racist beliefs and practices, and therefore most in the medical establishment believed that rendered any attempt to ameliorate this situation as futile.1 While the scientific and medical community blamed the dire state of black health on biological inferiority, advances in microbiology, and 1

NOTE: This chapter is a revised and updated version of a previously published journal article entitled “Germs and Jim Crow: The Impact of Microbiology on Public Health Policies in Progressive Era American South.” Andrea Patterson, Journal of the History of Biology 42, no. 3 (2009), 529-559. Throughout this paper, I deliberately use the term “black people.” During the time period covered in my work the black community referred to themselves as “blacks,” “Africans,” “colored Americans,” “Afro-American,” “Negros,” or “New Negro,” each bearing a specific cultural and historic connotation. At that time, “Negro” and “New Negro” had become the preferred terms, but their use has since the Civil Rights Era become derogatory.

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particularly, the development of the germ theory, gradually led to the improvement of black health. In an era of deepening scientific racism, ironically, germ theory stirred a variety of responses from the traditional scientific and public health community. Most of these responses, which were sporadic and limited, were motivated by sheer self–interest in order to protect the health of white people at the first sign of an epidemic. Nonetheless, the eventual outcome for southern black people was positive, as it prompted public health measures that addressed and ameliorated their endemic suffering. In this essay, I will discuss how physicians, politicians, and public health officials justified the utter lack of medical care given to black people by invoking scientific theories that supported the medicalization of racism. Secondly, I will examine how an increased understanding of the germ theory and disease-causing microorganisms challenged the racial predisposition hypothesis and transformed southern medical care, leading to the development of public health services that began to include black people. While the germ theory hardly brought an end to scientific or medical racism, it did, in an era of Jim Crow discrimination and inequity, initiate some remedies to the precarious state of black health and instigated a steady decline in death and infection rates in the black community. Finally, I will illustrate how disease prevention and medical treatment, despite the real fear of epidemics, remained closely connected to issues of racial inequity in the Progressive Era American South. Many of the public health initiatives proved biased and inadequate as a result.

“The Rapid Dying Out of the Negro is Natural” The poor health and medical care of southern black people during the Progressive Era was a direct consequence of racial discrimination. Health conditions for the black population had worsened since the end of Reconstruction. Rather than attributing the decline to social, economic, and political factors that had created a highly structured racial caste society in the South, scholars relied on biological determinism. They maintained that differences between the races in regards to health, as well as social and economic disparities, arose from inherited inborn distinctions, making society a mirror of biology. The triumphs of nineteenth-century science had created unshaken confidence in the accuracy of science, and the application of “sound” scientific theories to preexisting cultural and social prejudices

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promoted a medicalization of racism, where science increasingly had “to be understood as a social phenomenon.”2 When the scientific and medical community looked for empirical evidence to justify their claims of black biological inferiority, they needed to look no farther than mortality and morbidity rates that reached epidemic proportions. In 1890, black mortality in the five largest southern cities averaged 35.2 per thousand, compared to 19.6 for white people. While conditions improved slowly but steadily, the black mortality rate in 1930 remained almost two-thirds higher, with a life expectancy of fifty-four years for white men compared to forty years for black men. Likewise, infant mortality consistently decreased from 579.8 per thousand in 1890 to 110.8 in 1930. Throughout the entire period, however, it constituted an alarming number and proved nearly twice as high as the infant death rate of white people.3 The general conditions of health in the black community appear even more perilous when placed in the context of the various diseases afflicting black people during this period. The death rate for waterborne diseases, such as cholera, typhoid, and dysentery, together with whooping cough and puerperal difficulties, was approximately twice that of white people. Respiratory diseases like pneumonia, bronchitis, and influenza caused two and a half times more deaths, and acute nephritis, malaria, and pellagra were three to eleven times more devastating for the black community. In addition, 2

Stephen J. Gould, The Mismeasure of Man (New York: W. W. Norton, 1996), 52, 55–57; Lee D. Baker, From Surgery to Negro: Anthropology and the Construction of Race,1896–1954 (Berkeley CA: Berkeley University Press, 1998). Baker considers this period a defining moment in the history of both racial formation and university-based anthropology. He argues that the Supreme Court decision Plessey vs. Ferguson which delegated black people into separate and most often inferior institutions, found its justification in the insistence that anthropology “offers a positive basis for legislation, politics and education as applied to a given ethnic group;” Robert N. Proctor, Racial Hygiene Medicine under the Nazis (Cambridge, MA: Harvard University Press, 1988). Proctor argues that the social Darwinism of the late nineteenth century in America and Europe eventually gave rise to theories of racial hygiene. See Proctor, Racial Hygiene for social, political, and economic conditions of black people during what Litwack calls “the nadir of black life”; see Leon F. Litwack, Trouble in Mind: Black Southerners in the Age of Jim Crow (New York: Knopf, 1999); and Comer V. Woodward, Origins of the New South 1877– 1913, (Baton Rouge: Louisiana State University Press, 1971). 3 Thomas N. Chase, “Mortality among Negroes in Cities,” Conference for the Study of Negro Problems 1 (1903): 8; Bureau of the Census, Vital Statistics Rates in the United States, 1900–1943, (Washington DC : Government Printing Office, 1943), 150; and W. E. B. Du Bois, “Health and Physique of the Negro American,” Conference for the Study of the Negro Problems 11 (1906): 72.

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black people suffered a disproportional burden from heart and kidney disease, venereal diseases, and parasites such as hookworms.4 Among all the diseases, the most prevalent and devastating was tuberculosis. Over fifty percent of the urban black population became infected with the disease at one time or another while growing up. In 1906, one of every six deaths resulted from tuberculosis, and it claimed five out of seven lives between the ages of eighteen and twenty-eight. Even though the death toll from tuberculosis began to decrease after 1920, it remained two to three times higher than that of white people. As tuberculosis underwent a steady decline, heart diseases such as endocarditis, myocarditis, angina pectoris, and diseases of the coronary arteries increased at an alarming rate and soon became the second-largest threat to black health. The third major killer of southern black people was associated with childbearing and infancy. While maternal mortality was not nearly approaching the death rate connected with tuberculosis or heart disease, infant deaths, as evidenced in the mortality statistics, were rampant.5 This picture of endemic disease that characterized the general condition of black health in the late nineteenth and early twentieth centuries led many to conclude that the disease-causing factors were racial rather than social or economic. White supremacists used it as an argument for the alleged inferiority of the black race and maintained that, in a matter of time, “the disease-ridden Negro” would lose the struggle for survival and become extinct. They cited the gradual decrease of the black population from twenty percent of the total population in the 1820s to fewer than ten percent in 1920 to support their contention of “the rapid dying out of the Negroes.” Indeed, many southern cities reported a death rate that was greater than the birth rate in 1912. For example, in Jefferson City, Missouri, ninety more black people died than were born in February alone, and the black population had decreased gradually for the last decade. This phenomenon, repeated in other cities throughout the South, prompted the southern medical fraternity to propose, “One sure and easy way of solving the race problem would be to huddle all the Negroes into our cities.” In this scheme, the biological inferiority of black people would inevitably lead to their “complete race extinction in this country.”6 4

W. E. B. Du Bois, ed., The Crisis, 1910–1934, 40, no. 2 (February 1933): 31. Du Bois, “Health and Physique,” 87–88. 6 Du Bois, Crisis 36, 3 (March 1929): 84, 97; The Tuskegee Institute News Clippings File, 1912, reel 1, Chattanooga News, July 20, 1912, 566; Ibid., 573 (Jefferson Tribune, Jul. 6, 1912); Reel 4, 1915, 199; for more on the social role of science see Hamilton Cravens, The Triumph of Evolution: American Scientists and the Hereditary-Environment Controversy 1900–1941 (Philadelphia: Pennsylvania 5

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Due to the scientific and social views of most whites who conceived of black people as disease-ridden because of their alleged biological and moral inferiority, few efforts were made to curb disease in the black community. Crisis, the official organ of the NAACP, published a discussion of the black health problem among six southern lawyers in Atlanta, which was indicative of the public attitude pervasive in the South. These lawyers perceived the ill health of black people as a blessing rather than a predicament, and one suggested in explicitly social Darwinist terms that the “Negro problem was working itself out in a satisfactory way without further legislation.” He argued that tuberculosis and pulmonary diseases would reduce black people “to inconsiderable numbers” until they eventually became extinct. They further expressed their hope that “the increased use of cocaine among the Negroes would greatly hasten this result,” and voiced their disappointment over the state’s decision to abolish the sale of liquor, as it could have accelerated the extinction of black people. Social Darwinists even faulted charity organizations for providing health services, “because these efforts only contributed to the artificial preservation of the weak.” This attitude was clearly demonstrated by Montgomery health officials who, confronted with the vital statistics report of 1910, when black mortality was over twice that of white mortality, declared that “the heavy death rate among blacks is natural.”7 During the early decades of the 20th century, some diseases were considered almost exclusively racial, such as syphilis, sickle cell, and polio. Black people were portrayed as members of a “notoriously syphilis-soaked race” who lacked “stamina and resisting power;” sickle cell was used as a marker for racial identity; and the fact that “the complex and delicate bodies” of white people were afflicted with polio to a much greater degree than black people led many to conclude that the “primitive” races seemed

University Press, 1978), 11. Craven maintains that much of the appeal of the new experimental biology was the notion that “one could observe nature at work.” Quantifiable data such as vital statistics were interpreted as evolution in progress and scientists “proclaimed that they had unlocked the secrets to a science of social control.” 7 Du Bois, Crisis 1, 6 (April 1911), 23; Clippings, Reel 1, 1912, 566 (Chattanooga News, July 20, 1912); Clippings, Reel 1, 1911, 251 (Montgomery Advertiser, March 3, 1911); Baker, Savage to Negro, 28. For further discussion of the application of evolutionary methodology to the study of man and the notion of “natural extinction” see John S. Haller, Outcasts from Evolution: Scientific Attitudes of Racial Inferiority, 1859–1900 (Urbana: Illinois University Press, 1971); and Thomas F. Gossett, The History of an Idea in America (New York: Oxford University Press, 1997).

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less susceptible to this disease than the “civilized” descendants of Northern Europe.8 The majority of black physicians and civil rights leaders were outraged by reports like these and initiated a civil rights fight on the health care front, attempting to stem the tide of racialized medicine by pointing out the apparent environmental factors contributing to the poor health of black people, such as discrimination and poverty. W.E.B. Du Bois created a new dialogue on race with his research program at Atlanta University. Franz Boas, who had an immense influence on Du Bois, challenged the prevailing views of racial inferiority in both anthropology and society, fragmenting the nascent discipline by assuming an egalitarian position and explaining human differences in terms of cultural conditioning.9 8

James H. Jones, Bad Blood: The Tuskegee Syphilis Experiment (New York: Free Press, 1993), 29. Jones’ book provides an excellent discussion on racialized medicine and pathology due to the continued confusion over what role biology, culture, and environment played in the contraction of disease. For further discussion on sickle cell and the assigning of racial identity, see Melbourne Tapper, In the Blood: Sickle Cell Anemia and the Politics of Race (Philadelphia: Pennsylvania University Press, 1999). For a discussion on polio cases that were not diagnosed as a result of medical racism, neglect and inadequately trained black physicians, thus skewing the health statistics, see Naomi Rogers, “Race and the Politics of Polio: Warm Springs, Tuskegee, and the March of Dimes,” American Journal of Public Health 97, no. 5 (2007): 784–92. For further evidence on inherited differences in black people that were used to justify slavery in the 19th century see Gould, Mismeasure of Man, 101–103; For contemporary views of racial differences in medicine see Ta-Nehisi Coates and Sora Song, “Suspicious Minds,” Time, 2005, 36; and Richard David and James Collins Jr., “Disparities in Infant Mortality: What’s Genetics Got To Do with It?,” American Journal of Public Health 97, no. 7 (2007): 1191–97. Disparities between white and black people are often seen because of genetic differences, fueling a reinvention of the concept of genetic “race,” while continuing to ignore that health statistics primarily take into account ethnicity rather than social class and the fact that minorities in the United States continue to receive lower-quality health care than white people. 9 Baker, Savage to Negro, 119, 121–24; George W. Stocking Jr., Race, Culture, and Evolution: Essays in the History of Anthropology (New York: Free Press, 1968), 306–07; see also Stocking, The Shaping of American Anthropology, 1883–1891: A Franz Boas Reader (New York: Basic Books, 1974) for a discussion on Boas’ influence on black leadership that helped construct a concept of racial equality and cultural relativity, contrasting with those evolutionist notions. Boas’ impact, however, was limited within science and the public in general at that time due to the extent that racism dictated social relations, and because the new emphasis on cultural anthropology by Boas was viewed as unscientific. See a detailed discussion on the substantial resistance to Boas, supported by influential capitalists, such as Carnegie and Gilder, who had the financial resources to control the media and articulate

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Dr. Charles V. Roman, a black physician and former head of the National Medical Association, called on doctors, lawyers, and teachers to “battle with the AVATARS of prejudice who have entered the arena of public discussion to serve Caste and Discrimination under the banner of Medicine.” Noting severe discrepancies in public resources allotted to white and black people in Nashville, Tennessee, he established that “Conduct and Conditions, Not Race are the Determining Factors in Disease and Death, Nature is Impartial as well as inexorable.” According to the records, the white community enjoyed more than ninety-three percent of the public parks and all the playgrounds, while the black community had none. Likewise, the majority of the 180 miles of paved streets and 98 miles of public sewers were available only to the “favored” population. Considering that typhoid and malaria were more prevalent in regions without sewer systems, it was “not unreasonable to suspect that agencies other than race may account for the difference in mortality rate.” Segregation policies confined the majority of black people to “the worst alleys in the world.” In Jackson Ward, the black section of Richmond, Virginia, black people were “piled upon each other like rats in a trap.” They had to live in blind alleys where houses in the back could only be accessed by walking through someone else’s house in the front. Instead of playgrounds or parks, a public refuse dump and “a crematory for diseased, dead and putrefying animals” added to the unsanitary and unhealthy living conditions, making “the undertaker the most popular businessman and the gravedigger the most over-worked individual in our community.” Jackson Ward illustrated the working of segregation, in which “colored people are by law actually murdered that the separation of the races may be an unqualified success.” Other examples can be drawn from communities throughout the South.10 notions of racial inferiority, Baker, Savage to Negro, 148–50. Nevertheless, Boas eventually succeeded in creating a paradigmatic shift in the discipline; Ibid., 100; Stocking, Race, Culture, and Evolution, 306; and Elizan Barkan, The Retreat of Scientific Racism: Changing Concepts of Race in Britain and the United States between World Wars (Cambridge, MA: Harvard University Press, 1991), 67. 10 This statement is taken from an address to the National Medical Association at Raleigh, North Carolina, Clippings, Reel 2, 1914, 947–48 (National Baptist Union Review, Sep. 19, 1914); Du Bois, “Health and Physique,” 89–90; Crisis 8, 6 (October 1914), 277–78; Du Bois frequently used the Atlanta University Publications and Crisis, both of which he edited, as forums to voice his concerns about black health. See Edward H. Beardsley, A History of Neglect: Health Care for Blacks and Mill Workers in the Twentieth-Century South (Knoxville: Tennessee University Press, 1987), 12–13, 28–29. Beardsley argues that racism and segregation in the South “held blacks to the very bottom rungs,” when compared to poor white and northern black people.

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“Germs Know No Color Line” Only the advances in microbiology, and in particular the notion that disease-causing microorganisms did not differentiate among their victims, led to the gradual development of public health services that addressed and improved the ill health of black people in the South to some extent. Concern for white health could no longer ignore black health, and fear of epidemics and contagious disease urged some action out of sheer self-interest. Such was the case in Louisiana, where Senator Huey Long proudly claimed, “Whites have decided nigras have got to have public health care. Got to give ‘em clinics and hospitals. Got to keep ‘em healthy. That’s fair and it’s good sense. I said to them: ‘you wouldn’t want a colored woman…watching over your children if she had pyorrhea, would you?’” The idea that “disease germs know no color line” meant that health improvement in the South increasingly became an interrelated rather than a race problem. Consequently, both white and black leaders made frequent use of the slogan in order to force action. Economic concerns, due to the continuous ill health of much of the South’s labor force, also contributed to a growing health concern for its black population. The southern progressive movement was instrumental in the initiation of health reforms, the passage of sanitary laws, and the establishment of hospitals, laboratories, and state boards of health. Cleanup and Better Babies campaigns, midwife control, and the Rockefeller Sanitary Commission for the Eradication of Hookworm were some of the initiatives launched in an effort to improve southern health across the color line. Black morbidity and alleged ignorance were “liabilities and dangers” to all. Amidst the realization that “Jim Crow laws do not hold for germs of measles, tuberculosis, pneumonia, and typhoid” and do not follow rules of segregation, the lives of black and white people increasingly overlapped, especially in matters of health.11

11

Du Bois, Crisis 42, 2 (Feb. 1935), 52; Ibid., 36, 3 (March 1929), 84; see Todd L. Savitt and James Harvey Young, eds., Disease and Distinctiveness in the American South (Knoxville: Tennessee University Press, 1988), for a discussion of how the advent of the germ theory, an improving economy, and the southern progressive movement initiated health reforms that resulted in sanitary campaigns, hospitals, sanitaria, bacterial laboratories, and boards of health. By 1913, every state in the South had some form of health agency. The discovery of insect carriers for malaria (1898) and yellow fever (1899), together with the diagnosis of hookworm disease (1902) and pellagra (1906), spurred efforts to control and eradicate conditions responsible for those ailments.

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Figure 1. “Germs Know No Color Line.” Atlanta Constitution, February 4, 1914.

Demands increased for action that included black people in public health. The Virginian-Pilot appealed to the municipalities throughout the State, and the South in general, to apply one standard of sanitation in residential sections regardless of race. Atlanta’s Constitution claimed, “The

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careless or ignorant Negro…is likely to nullify the scrupulous sanitary safeguards with which the white man surrounds his home and his business establishment” until there is one, strictly enforced, sanitary law for “high and humble, Peachtree and Peters Street.” Prominent Atlanta businessmen found out that “no man liveth to himself, nor dieth, either,” when they lost family members to smallpox and diphtheria. Incidents like these emphasized the importance of a black facility for contagious diseases, because “as we owe the Negro himself something in the way of protecting him from his ignorance, we owe a graver duty to the white population.” Edwin R. Embree, president of the Julius Rosenwald Fund, reiterated the notion that germs were the “original democrats” and demanded that attention be paid to diseases affecting all Americans.12 Epidemic disease thrust the South into the national limelight and stigmatized the region, and persistent notions of southern deficiency and backwardness irritated southern politicians and businessmen. In the 1920s, Joseph Goldberger, who had established that pellagra was caused by the southern diet, appealed to the United States Public Health Service for national assistance to aid the region and prevent famine, yet southern leaders vehemently denied that hunger existed and consequently refused any northern aid. Dr. Elton S. Osborne of Savannah claimed the condition was due to ignorance and not poverty. The Washington Herald echoed this view, suggesting that the proper remedy came not from northern funds but “in dissemination of common every-day horse sense, and knowledge as to how to live and what to eat.” These defenses had a distinctly racial edge. For instance, hog and hominy, staples of the black diet, which “no selfrespecting weevil will eat” were said to be at the bottom of the southern health problem. Others even suggested southern superiority in matters of health and blamed black people for the picture of morbidity that haunted the 12

Clippings, Reel 2, 1914, 946 (Virginia Pilot, Nov. 28, 1914); Reel 2, 1914, 910 (Atlanta Constitution, Jun. 28, 1914); Reel 2, 1914, 916 (Atlanta Constitution, Feb. 3, 1914); Reel 2, 1914, 229 (Richmond Times Dispatch, Nov. 21, 1914); Crisis 36, 3 (March 1929), 84, 97; also see above, FN9; Carnegie and Gilder used financial resources to control the media and articulate notions of racial inferiority; despite their charitable support of black people, northern philanthropists maintained their racial bias and support for the eugenics movement. Johnson writes on southern white resistance to northern funding for black people in Elna C. Green, ed. Before the New Deal: Social Welfare in the South, 1830–1930 (Athens: Georgia University Press, 1999), 168–69. The southern reform movements generally were intended for white people only. Southerners even refused northern aid if it included black people, thereby sacrificing and risking improvement of overall social and economic conditions. The only exception to this was when assistance was deemed necessary in order to save white lives.

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South and relegated it to an inferior station. The Montgomery Advertiser angrily disputed a report stating that women in Ohio were fifty percent healthier than typical southern women. It charged that the study took into account the total population, including “the Negroes who since the war have become an unhealthy race,” and requested a comparison between the white mortality rates only, of northerners and southerners, convinced that “southern white people will get the best of it.”13 As much as southerners loathed the fact, they became increasingly dependent on assistance from northern philanthropies and the federal government. The Rockefeller Sanitary Commission, dedicated to the control of hookworms, served as an incentive for the establishment of numerous county health departments. While it failed to eradicate hookworms in the South, it helped create a network of state and local public health agencies and propelled state expenditures by eighty-one percent between 1910 and 1914. Charles Wardell Stiles, the zoologist who brought to national attention the prevalence of hookworms in the South in 1902, argued that the apparent greater immunity to the disease in black people made them “better carriers and spreaders,” and concluded that “the white man owes it to his own race that he lend a helping hand to improve the sanitary surroundings of the Negro.”14 Though black people were charged as culprits for hookworm disease, the degree to which they were examined and treated remains debatable. No black doctor was ever employed with the organization. White agents in the field, trained to work predominantly amid white communities, were illadapted to overcome racial stereotypes, as evidenced in a leaflet distributed among Mississippi planters. The Negro cannot be interested in, nor can they readily understand the situation. They cannot be reached through regular channels, yet unless they are reached, treated, and cured, they will continue to infect the soil and perpetuate the disease among the whites. So, for self-protection, every PLANTER WHO HAS NEGRO TENANTS, EVERY PERSON HAVING NEGRO SERVANTS, EVERY COMMUNITY HAVING NEGRO

13

Savitt, Disease and Distinctiveness, 14, 17; Clippings, Reel 13, 1921, 342 (Atlanta Constitution, Aug. 28, 1921); Reel 2, 1913, 163 (Montgomery Advertiser); Pellagra results from niacin/tryptophan deficiency and can cause dermatitis, severe damage to digestive tract and nervous system; more on southern resistance to public health services, see William A. Link, The Paradox of Southern Progressivism 1880–1930 (Chapel Hill: North Carolina University Press, 1992). 14 John Ettling, The Germ of Laziness: Rockefeller Philanthropy and Public Health in the New South (Cambridge: Harvard University Press, 1981).

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FAMILIES LIVING NEAR THEM, should induce these Negroes to seek treatment at once.15

In the age of Jim Crow segregation, forced integration in terms of public health had clear limitations. The cautious approach of the Commission, intended to avoid racial strife and open antagonism of southern white people, hampered the extent to which black people would benefit, especially considering that the treatment with Thymol and Epsom salts was relatively complicated and potentially lethal. In addition, unless hookworm disease was attacked at its source, by preventing soil contamination through an extensive privy construction program, recurrence of infection was very likely. The city of Atlanta, Georgia, serves as another example where fear of “democratic germs” encouraged action, but the half-heartedness of the effort also limited its success. Forty percent of its population relied on openbacked privies, attracting flies that spread intestinal diseases and typhoid fever. Naturally, the poor and predominantly black neighborhoods were mostly in want of modern sanitary facilities. Surface wells, usually polluted by human feces, supplied most of the water. Drainage of the elevated white residential districts created unbelievable filthy conditions. Wastes piled up in small stagnant streams and foul-smelling pools in backyards and alleys, providing hazardous breeding grounds for malaria-bearing mosquitoes. Atlanta had no sewage treatment facilities until 1910, and raw sewage of some 80,000 people was dumped into small streams in close proximity to 15

Ibid., 172–75, 220–21. The quote can be found in its entirety in Ettling’s excellent book on the Rockefeller’s Sanitary Commission and Northern Philanthropy in the South; Ettling discusses articles published in the Mc Clure’s Magazine “The Vampire of the South,” and The World’s Work “The Health Menace of Alien Races” that clearly reveal how southern whites perceived hookworm disease as “act of treachery” on the part of black people, calling attention to their “sanitary sins” and the “damage that has been done to the white people of the South by the diseases brought by this alien race.” Ettling further reports that there is little evidence that the Commission worked specifically in black communities. While the Commission “offered quiet encouragement” to extend the campaign to black schools and communities, it also “invoked the principle of nonintervention when called upon to employ the financial clout of the Sanitary Commission to force work toward that end.” For more on similar strategies employed by social welfare progressives to avoid racial confrontation, see Elizabeth Lasch-Quinn, Black Neighbors, Race, and the Limits of Reform in the American Settlement House Movements, 1890–1945 (Chapel Hill: North Carolina University Press, 1993) and Elna C. Green, This Business of Relief: Confronting Poverty in a Southern City, 1740–1940 (Athens: Georgia University Press, 2003).

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black residential areas, being both offensive and unhealthy. The city exceeded the national mortality rate by forty-seven percent.16 In 1909, the Atlanta Constitution reported that frequent outbreaks of epidemics not only endangered the health of its white population but also jeopardized Atlanta’s prosperity that largely depended on tourism and business investments. The disease germ knows no color or race line, no class distinction and has little respect for distance, when it can fasten on a human carrier. To purge the Negro of disease, is not so much a kindness to the Negro himself as it is a matter of sheer self-preservation to the white man, Philanthropy doesn’t enter into this battle of life and death; grim, primitive self-interest, the conservation of the health of the white race is the controlling factor. If the people of the south expect to fight a winning war with the death rate, they must recognize this as the fundamental principle in the campaign.

As a result, the city issued a $3,000,000 bond issue to improve the city’s water supply and sewer system, a measure that resulted in a seventy percent reduction of the typhoid death rate. Unfortunately, the measure did not affect most of the inexpensive rental properties, largely occupied by black people, and thousands did not profit fully from the sanitary reforms because they were poor and black. Three years later, the Constitution still complained that Atlanta financed sanitary measures in the more privileged neighborhoods and business sections while neglecting those areas where the germs came from.17 While some of the measures aimed at black people were no doubt beneficial, limited as they were, other examples of new health regulations took the form of persecution. For example, a candidate for mayor of Atlanta called for the creation of a municipal servants’ bureau. It would cooperate with the city health board to protect our “little women [who] are made to suffer and worry and fret their souls out trying to handle incompetent worthless, diseased and irresponsible Negroes.” In addition to vouching for the good health of black servants, the bureau would collect records of the servants’ character, work performance, and be responsible for detecting “worthless and diseased” servants and ordering them out of town. Servants suffering from tuberculosis or a certain “filthy blood disease,” as well as those found irresponsible or stealing, would be deemed vagrants. The 16 Stuart Galishoff. “Germs Know No Color Line: Black Health and Public Policy in Atlanta, 1900–1918.” Journal of the History of Medicine and Allied Sciences 40 (1985): 22–41. 17 Ibid., 29–30, 33, 40–41; Atlanta Constitution (March 17, 1912), Sec. F, 4, (January 01, 1914), 6; and Clippings, Reel 1, 1912, 563 (Atlanta Constitution, Sep. 1, 1912).

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proposed measure met with the enthusiastic approval of lawyers, city officials, doctors, and Atlanta’s “delicate and frail” women and was hailed as “an absolute and positive means of treating the servant question.” The city of Mobile, Alabama, along with numerous cities throughout the South, began to register washerwomen through the office of the City Health and Sanitary Department, issuing health certificates to those who passed a rigorous medical examination. The measure there was prompted by a smallpox outbreak, in which a wealthy citizen contracted the disease through his clothes washed by an infected black woman.18 Black people themselves were eager to point out that “no section is immune from danger if any section is neglected and left to suffer the ravages of preventable disease.” In order to force some action, black leaders played on white fears and frequently reminded officials that improving black living conditions was “of vital concern to the well-being of the white people,” because germs did not recognize segregation. If for no other motive than self-interest, white- people should provide their black tenants with “decent houses.” A three-year-old black boy in Lynchburg, Virginia, became violently ill with typhoid fever after drinking contaminated well water. He was forced to drink it because the city had turned off the family’s water supply for an unpaid water bill. City health officials then worried that “for the sake of a few dollars water bill,” an epidemic may have started and “white residents of the city would be equally in danger of infection.”19 Instilling anxiety over indiscriminate and contagious disease germs certainly had the potential to spur much-needed action, but also served to foster racist ideology by characterizing black people as notoriously diseased or ignorant. Addressing a convention of teachers in Montgomery, Dr. J. A. Kenny, a renowned leader of the black medical community and first director of the John A. Andrew Memorial Hospital at Tuskegee Institute, warned white people of their black neighbors, because “ignorance and indifference of one had an effect upon the general health of the other.” Similarly, Dr. Charles H. Johnson, a black physician in Atlanta, appealed to the selfinterest of the white community, because “Negroes living in or near the highest class of residential sections menace the lives of both races by their 18

Du Bois, Crisis 8, 1 (May 1914), 30–31; Clippings, Reel 1, 1912, 571 (Atlanta Constitution, Sep. 15, 1912); Reel 2, 1914, 932 (Montgomery Advertiser, Jan. 27, 1914); Hickey argues that the ideal of a “democratized language of equality” in response to disease germs that didn’t recognize the color line and necessitated healthcare for both black and white people, was contradicted by the white fears of black women as “agents of contagion” and their “conception of washerwomen as dangerous and ignorant,” see Green, Before New Deal, 187. 19 Clippings, Reel 20, 1924, 600, 604, 609.

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ignorance and violation of the ordinary laws of sanitation.” Some in the black community vehemently denounced these attempts to blame “ignorant” black people for white sickness. P. Samuel, a pastor in Philadelphia, insisted that this “slavish, cringing and begging” to ensure better homes and health “to serve the whites” was intolerable. Instead, black people should demand decent housing as their undeniable right as citizens. He asserted that some seemed all too willing to surrender their human rights to secure charity and “humiliating favors,” because prejudice had placed them in the worst possible position.20 Notwithstanding these warranted concerns, for this tactic no doubt furthered beliefs in racial inferiority, it also increased recognition that highly contagious diseases could only be curbed effectively by aggressively attacking its spread among both communities. This proved especially true for one of the most prevalent and devastating diseases: tuberculosis. Public health efforts were successful in reducing its overall death rate, yet they also demonstrate the complexity of the problems involved in southern public health projects. Steps taken by the Anti-Tuberculosis Association were compromised by racial discrimination, economic inequity, and lack of cooperation between white and black citizens. Cities across the South solicited the support of black civic and religious organizations to educate black families in a systematic cleanup campaign to guard against the spread of tuberculosis. Sanitation inspectors visited homes, encouraged ventilation, removal of unsanitary conditions, regular disinfecting with lime, and gave explicit instructions for bodily hygiene and diet. Yet how fragile these cooperative efforts sometimes turned out became evident in a Louisville, Kentucky, incident where a black sanitary inspector, Dr. J. C. Colbert, had fumigated the home of a white citizen. The owner, irate over this “disloyalty” and “lack of harmony,” demanded the immediate dismissal of the black sanitary inspector. The episode prompted the mayor to write letters to both the Board of Safety and health officer, insisting that black inspectors were appointed solely to work among black people. Public health projects could only be successful in the South if they maintained the color line.21 Montgomery, Alabama, one of the pioneer cities of the South, employed a black nurse in 1908. A Fresh Air Camp was added in 1912, with nine cabins for white and five for black patients, even though the majority of tubercular patients came from the black community. The possibility of 20

Clippings, Reel 2, 1913, 165 (Montgomery Advertiser, Apr. 7, 1913); Reel 1, 1912, 573 (Atlanta Constitution, Sep. 15, 1912); and Reel 11, 1920, 550 (Letter to the Editor of the Public Ledger, Feb. 7, 1920). 21 Galishoff, “Germs Know No Color,” 28; and Clippings, Reel 8, 1918, 499 (Louisville News, Apr. 6, 1918).

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treatment, however, depended not only on availability but also on the ability to afford it. The Anti-Tuberculosis League demanded that “Negroes must aid or forfeit” their admission. Black people were charged with “indifference” and called to either provide financial support or “find some other treatment among their race.” Even though the League emphasized that it regretted such action and meant no discrimination, it apparently ignored the fact that such decisions resulted in the continued contraction of the disease by both white and black populations.22 This combination of discrimination and neglect impeded the struggle against contagious diseases and was responsible for the continued racial health disparities. Racial segregation made a dual health system necessary and contributed to the cost of southern public health agencies. Black people had little or no access to white hospitals and access to few and often deficient black hospitals. Atlanta, for instance, desperately needed hospitals for both black and white patients in 1919. The few existing facilities were, as reported in Crisis, “hopelessly inadequate and inefficient,” and this pertained to a greater degree to “colored people.” The City Hospital prevented black physicians from entering the building, forcing black patients to leave their regular doctor behind, and delivering them instead to “a physician certainly less interested.” Du Bois stressed the racial factor dictating hospital policy. An improvement “with regard to air, sleep, food, clothes and medical attention, and even increased income will not entirely settle our problem of sickness and death, so long as race discrimination continues.” He reported that “even for those of us who are able to pay, hospital doors are today half-closed in our faces.”23 Inequality condemned black people to ill health. Infant death, a major killer in the black community, was linked to a significant degree to unsanitary water supply, thereby starting epidemics such as infantile cholera, dysentery, and typhoid fever. Infantile cholera was responsible for more deaths than any other children’s disease and especially feared, because “perfectly healthy children may carry the germs and give the disease to other children who are less hardy.” Health reforms affected a gradual decline once they began to include black children. For instance, in 1913, the Infant Welfare Association in Birmingham, Alabama, was organized to campaign against the intolerable death rate of babies in that city. It launched a sixmonth program providing a white visiting nurse, obstetric services in the homes, and instructions in baby care and food. The nurse focused on prevention, referring patients who required treatment to hospitals. Only one 22

Clippings, Reel 1, 1912, 569–70 (Montgomery Advertiser); Reel 2, 1914, 939 (Montgomery Advertiser, June 27, 1914). 23 Du Bois, Crisis 18, 2 (Apr. 1919), 90–91; and Ibid., 40, 2 (Feb. 1933), 44.

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of the hospitals admitted black children, however, and consequently was continuously overcrowded.24 In subsequent years, the “Better Babies” campaign drew attention to the plight of black mothers and infants and resulted in numerous measures such as the appropriation of funding for free baby clinics in Topeka, Kansas. The clinics were held twice a week in a city building, and mothers were encouraged to have their babies examined every week. Because of the racial dynamics of southern society, these clinics did not always run smoothly. White nurses were not likely to suppress their prejudice and condescension in their conduct with black mothers and children. One nurse described six black babies that had come to her care as “some of the cutest pickaninnies you ever saw.” In a similar program in Maryland, black mothers refused to cooperate with the nurses, because they were afraid to have their babies weighed. The child welfare committee accused them of a “distinct lack of patriotism,” providing some insight into the motivation on the side of white health care professionals, who often reluctantly attempted to improve black health in order to curtail the spread of disease to the white population. Black mothers were urged to “be as interested in the welfare of their babies as white mothers are,” implying that black mothers were to blame for the high infant morbidity and spread of disease. The health of black mothers and infants might have been of particular concern to white people, considering the widespread custom of employing black wet nurses for white infants. The notion that “protection of the black [wet] nurse may save its white charge” shows how closely “shared” public health was tied to white self-interest.25

Conclusion This concept of “shared” public health reinforced local, state, and federal efforts to improve sanitation and hygiene and reduced the frequency of cholera, dysentery, tuberculosis, typhoid fever, measles, and scarlet fever epidemics. The death rate from infectious diseases, at sixty percent in the 24

Clippings, Reel 2 (1914), 920 (Montgomery Advertiser, May 28, 1914); and Reel 4 (1915), 204. 25 Clippings, Reel 7 (1918), 898, 891 (Jackson Mississippi News, Sep. 5, 1918); more on the dynamics between professional health care providers, midwives and mothers, who had to submit to the authority under the “threat of punishment should there be resistance,” see Fraser (1998); more on social workers whose ability to reach black people was compromised by the fact that they clearly held racial stereotypes such as the belief in the “white burden” to help “inferior” black people, see Lily Hammond (2008) and Gordon (1991). Gordon notes that white people viewed all black people, irrespective of their class, as poor and uneducated.

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early 1900s for the total population in the South, experienced a sharp decline for both white and black people. Most notable, deaths from tuberculosis dropped from over twenty percent to six percent by 1930. Yellow fever, malaria, hookworm, and pellagra—largely responsible for stigmatizing the American South as an unhealthy region—had nearly disappeared by the 1950s. Success in black communities, though, lagged behind. The social and cultural context of Jim Crow affected therapeutic control as public health responses to the dismal state of black health ranged from indifference and inaction to inadequate and often racially motivated efforts to curb disease.26 Rather than attacking the core causes of endemic disease among black people, such as poverty, neglect and discrimination, the medical community, informed by a white supremacist worldview and supported by anthropologists, geneticists, pathologists, and evolutionary biologists, blamed “physiological and moral inferiority” for the dire state of black health. The passive attitude of the city, state, and federal authorities combined with black powerlessness magnified the black health dilemma. Mortality and morbidity were higher in the South than in the North, and southern black people were measurably worse off than even poor white people. Segregation policies required a costly dual health care system that proved especially devastating to black people who were relegated to substandard facilities and negligent care. Many in both the lay and medical community considered black people as physically distinct and predisposed to disease. Some linked excessive morbidity to their alleged immorality. And social Darwinists viewed it as proof for gradual extinction, claiming that the black “race” was “unfit.” Still, at a time when scientific racism backed neglect and even entertained hopes of extinction, public health policies for black people and, as a consequence, the health of southern black communities made unprecedented advances during the Progressive Era. Among the newly developing scientific disciplines, microbiology alone challenged the racial predisposition hypothesis and provided scientific support for the inevitability of addressing the ill health of black people, prompting measures by foundations and public health services that gradually affected a steady decline in the mortality rates. Infant mortality, for instance, 26 Bernard Guyer, Mary Anne Freedman, Donna M. Strobino, and Edward J. Sondik, “Annual Summary of Vital Statistics: Trends in the Health of Americans during the 20th Century,” Pediatrics 106, no. 6 (2000): 1307–17; Forrest E. Linder and Robert D. Grove, “Vital Statics Rates in the United States 1900–1940.” Federal Security Agency United States Public Health Service, National Office of Vital Statistics. Washington, DC: United States Government Printing Office, 1947. Vital Statistics Report 1900–1940.

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decreased from fifty-eight percent in 1890 to eleven percent in 1925. Amidst fear of contagion and concern for white health, epidemic diseases proved a powerful force in transforming health care. The environment increasingly began to play a part in the attribution of disease, rather than anatomy and heredity alone. However, persistent prejudice and a continued belief in racially distinct physiology and pathology overshadowed the positive impact the “democratic germ theory” could have had in regards to black health.27 Today we observe a renewed scientific legitimacy of racial differences, albeit carefully disguised under the beneficial cloak of “personalized medicine” or “gene therapy.” With the completion of the Human Genome Project in 2003 and the beginning of genomic medicine and pharmacogenetics, medical research aims at finding a “race drug” for heart disease or a “preterm birth gene” to explain racial differences in infant death. More than a century after the decision was made to control epidemics by extending public health care to black people, a decision that improved black health through the Progressive and into the Civil Rights Era, black Americans still experience disparities in health and health care. Indeed, they are at a significantly higher risk for almost all diseases, including a higher death rate and shorter survival rate for all cancers combined. According to a government health report in 2016, they constitute the leading group in both infant and adult mortality statistics, and black men are six times and women an astounding eighteen times more likely to die from HIV/AIDS than their white counterparts. This, however, does not support the popular and convenient conclusion of biological (“racial”) differences. Rather, it shows that prevention and treatment continue to be connected to issues of racial discrimination. In the United States, “race” (not socioeconomics or minority status) remains to be the most commonly used variable in health research. A recent study shows that racial disparities in mortality rates decreased by thirty-six percent for infectious diseases, and by fifty-five percent for all diseases combined if adjusted for family income and education. It is easy to dismiss the claims of early twentieth-century scientists as pseudo-scientific. Yet, unrelenting preoccupation with racial differences, in both research and therapeutic control, seems eerily reminiscent of a past when “bad genes” were always seen as the culprits, even in communicable diseases. A biological notion of race and the persistent belief in racial predisposition to disease seem to be contradicted by the rapid improvement black health experienced when public health policies and resources were directed accordingly.28 27

Bureau of the Census, “Vital Statistics,” 150. African Americans make up 14% of the population, but account for 34% of TB and 45% of HIV/AIDS cases in the US. Centers for Disease Control and Prevention, 28

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Bibliography Baker, Lee D. From Savage to Negro: Anthropology and the Construction of Race, 1896–1954. Berkeley CA: Berkeley University Press, 1998. Baptiste-Roberts, Kesha, Tiffany L. Gary, Gloria L. Beckles, Edward W. Gregg, Michelle Owens, Deborah Porterfield, and Michael Engelgau. “Family History of Diabetes, Awareness of Risk Factors, and Health Behaviors among African Americans.” American Journal of Public Health 97, no. 5 (2007): 907–13. Barkan, Elazar. The Retreat of Scientific Racism: Changing Concepts of Race in Britain and the United States between the World Wars. Cambridge MA: Harvard University Press, 1992. Beardsley, Edward H. A History of Neglect: Health Care for Blacks and Mill Workers in the Twentieth-Century South. Knoxville: Tennessee University Press, 1987. Bureau of the Census. Vital Statistics Rates in the United States, 1900– 1940. Washington, DC: Government Printing Office, 1943. Centers for Disease Control and Prevention. “Health Disparities in HIV/AIDS, Viral Hepatitis, STDs, and TB.” U.S. Department of Health & Human Services, 2016. Accessed June 22, 2018. https://www.cdc.gov/nchhstp/healthdisparities/africanamericans.html. Chase, Thomas N. “Mortality Among Negroes in Cities.” Conference for the Study of the Negro Problems. Atlanta University Press 1 (1903). Coates, Ta-Nehisi Paul, and Sora Song. “Suspicious Minds.” Time 1166, no. 1 (2005): 36. Cravens, Hamilton. The Triumph of Evolution: American Scientists and the Heredity-Environment Controversy 1900–1941. Philadelphia: Pennsylvania University Press, 1978.

“Health Disparities in HIV/AIDS, Viral Hepatitis, STDs and TB,” U.S. Department of Health & Human Services, 2016. Accessed June 22, 2018. https://www.cdc.gov/nchhstp/healthdisparities/africanamericans.html; Bijou Hunt and Steve Whitman, “Black: White Health Disparities in the United States and Chicago: 1900–2010,” Journal of Racial and Ethnic Health Disparities 2 (2015): 93–100. The gap in health disparities widened across eight (out of seventeen) health indicators, and in six significantly—particularly heart disease and diabetes; David and Collins, “Disparities in Infant Mortality,” 1195; CDC, “HIV Surveillance Report: Diagnoses of HIV Infection in the United States and Dependent Areas, 2016,” v.28. Table 3a, 2017. Accessed May 29, 2019. http://www.cdc.gov/hiv/pdf/library/reports/surveillance/cdc-hiv-surveillancereport-2016-vol-28.pdf.

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David, Richard, and James Collins, Jr. “Disparities in Infant Mortality: What’s Genetics Got to Do with It?” American Journal of Public Health 97, no. 7 (2007): 1191–1197. Du Bois, W. E. B. ed. The Crisis 1910–1934. Baltimore, MD: Official Organ of the National Association for the Advancement of Colored People (NAACP). Du Bois, W. E. B. “Health and Physique of the Negro American.” Conference for the Study of the Negro Problems. Atlanta University Press 11 (1906): 272–76. Ettling, John. The Germ of Laziness: Rockefeller Philanthropy and Public Health in the New South. Cambridge MA: Harvard University Press, 1981. Fraser, Gertrude J. African American Midwifery in the South. Cambridge MA: Harvard University Press, 1998. Galishoff, Stuart. “Germs Know No Color Line: Black Health and Public Policy in Atlanta, 1900–1918.” Journal of the History of Medicine and Allied Sciences 40 (1985): 22–41. Gordon, Linda. “Black and White Visions of Welfare: Women’s Welfare Activism, 1890–1945.” Journal of American History 78, no. 2 (1991): 559–90. Gossett, Thomas F. Race: The History of an Idea in America. New York: Oxford University Press, 1997. Gould, Stephen J. The Mismeasure of Man. New York: W. W. Norton, 1996. Green, Elna C. ed. Before the New Deal: Social Welfare in the South, 1830– 1930. Athens: Georgia University Press, 1999. Green, Elna C. This Business of Relief: Confronting Poverty in a Southern City, 1740–1940. Athens: Georgia University Press, 2003. Guyer, Bernard, Mary Anne Freedman, Donna M. Strobino, and Edward Jay Sondik. Annual Summary of Vital Statistics: Trends in the Health of Americans during the 20th Century." Pediatrics 106, no. 6 (2000): 1307–17. Haller, John S., Jr. Outcasts from Evolution: Scientific Attitudes of Racial Inferiority, 1859–1900. Urbana: Illinois University Press, 1971. Hammond, Lily Hardy. In Black and White: An Interpretation of the South.: Georgia University Press, 2008. Hunt, Bijou, and Steve Whitman. “Black: White Health Disparities in the United States and Chicago: 1990–2010.” Journal of Racial and Ethnic Health Disparities 2 (2015): 93–100. Jones, James H. Bad Blood: The Tuskegee Syphilis Experiment. New York: Free Press, 1993.

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Lasch-Quinn, Elisabeth. Black Neighbors, Race, and the Limits of Reform in the American Settlement House Movements, 1890–1945. Chapel Hill: North Carolina University Press, 1993. Linder, Forrest E., and Robert D. Grove. “Vital Statistics Rates in the United States 1900–1940.” Federal Security Agency, United States Public Health Service, National Office of Vital Statistics. Washington, DC: United States Government Printing Office, 1947. Link, William A. The Paradox of Southern Progressivism 1880–1930. Chapel Hill: North Carolina University Press, 1992. Link, William A. ed. The Rebuilding of Old Commonwealths and Other Documents of Social Reform in the Progressive Era South. Boston: Bedford Book Press/St. Martin’s, 1996. Litwack, Leon F. Trouble in Mind: Black Southerners in the Age of Jim Crow. New York: Knopf, 1999. Proctor, Robert N. Racial Hygiene Medicine Under the Nazis. Cambridge MA: Harvard University Press, 1988. Richardus, Jan H., and Anton E Kunst. “Black-White Differences in Infectious Disease Mortality in the United States August.” American Journal of Public Health 91, no. 8 (2001): 1251–53. Rogers, Naomi. “Race and the Politics of Polio: Warm Springs, Tuskegee, and the March of Dimes.” American Journal of Public Health 97, no. 5 (2007): 784–92. Savitt, Todd L., and James Harvey Young, eds. Disease and Distinctiveness in the American South. Knoxville: Tennessee University Press, 1988. Stocking, George W., Jr. Race, Culture, and Evolution: Essays in the History of Anthropology. New York: Free Press, 1968. Stocking, George W., Jr. The Shaping of American Anthropology, 1883– 1911: A Franz Boas Reader. New York: Basic Books, 1974. Tapper, Melbourne. In the Blood: Sickle Cell Anemia and the Politics of Race. Philadelphia: Pennsylvania University Press, 1999. The Tuskegee Institute News Clippings File [microform, 252 microfilm reels]. National Historical Publications and Records Commission. John W. Kitchens (Project Director). 1976. Tuskegee, Alabama. Division of Behavioral Science Research, Carver Research Foundation, Tuskegee Institute. Sanford, NC: Microfilming Corp. of America. Woodward, Comer V. Origins of the New South 1877–1913, Baton Rouge: Louisiana State University Press, 1971.

CHAPTER FIVE EPIDEMICS AS COMPLEX SYSTEMS: SEXUAL MEANINGS AND HIV AMONG LATINO GAY AND BISEXUAL MEN JORGE FONTDEVILA

Introduction The AIDS pandemic is closing its fourth decade since the human immunodeficiency virus (HIV) was first identified in the 1980s. Significant advances have been developed to curb the disease since, but the pandemic continues to expand among vulnerable populations with no efficient vaccine or cure in sight.1 Although behavioral and biomedical interventions against HIV have saved many lives and are undoubtedly necessary, by themselves they have proven insufficient to counter the sociocultural complexities that relentlessly drive the epidemic.2 In this respect, the HIV/AIDS epidemic constitutes a prototypical example of a complex system with emergent

1

Steven G. Deeks, Sharon R. Lewin, Anna Laura Ross, et al., “International AIDS Society Scientific Strategy: Towards an HIV Cure 2016,” Nature Medicine 22, no.8 (2016): 839–50; Powel Kazanjian, “The AIDS Pandemic in Historical Perspective,” Journal of the History of Medicine and Allied Sciences 69, no.3 (2012): 351–82; and UNAIDS, “Fact Sheet–Latest Global and Regional Statistics on the Status of the AIDS Epidemic,” accessed July 1, 2018, http://www.unaids.org/en/resources/documents/2017/UNAIDS_FactSheet. 2 Judith D. Auerbach, Justin O. Parkhurst, and Carlos F. Cáceres. “Addressing Social Drivers of HIV/AIDS for the Long-term Response: Conceptual and Methodological Considerations,” supplement, Global Public Health 6, no. 3 (2011): 1–17; Thomas J. Coates, Linda Richter, and Carlos Cáceres, “Behavioural Strategies to Reduce HIV Transmission: How to Make Them Work Better,” Lancet 372, no. 9639 (2008):669–84; and Susan Kippax and Niamh Stephenson. “Prevention through the Lens of a Social Public Health,” American Journal of Public Health 102, no. 5 (2012): 780–99.

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properties produced by the interactions of many component parts at multiple levels, including individual, group, and population levels.3 Complex systems show sensitivity to initial conditions and sudden “phase” transitions that in the case of complex epidemics rapidly and unexpectedly shift the spread and morbidity of the disease. These systems typically include nonlinear causal relations and feedback loops that go beyond linear chains of events, with elements in a sequence affecting other elements in the sequence before and after them. For instance, the introduction of a biomedical intervention to treat one sexually transmitted infection (STI) may have unintended consequences and reinforce the spread of other STIs in the system.4 Thus in certain sexual contexts among men who have sex with men (MSM), introducing antiretroviral therapy (ART) may have positive effects on reducing HIV viral load but negative effects on the spread of other STIs. A kind of ART “treatment optimism” among some men may develop that increases STI incidence by relaxing condom use and even creates suboptimal ART adherence.5 In turn, increases in STI incidence—syphilis or gonorrhea, for example—feedback into the system via genital mucosae damage as tissue inflammation precipitates CD4 T-cell recruitment and viral density shedding reactivates HIV infectivity levels.6 3

Sevgi O. Aral, Jami S. Leichliter, and James F. Blanchard, “Overview: The Role of Emergent Properties of Complex Systems in the Epidemiology and Prevention of Sexually Transmitted Infections including HIV Infection,” supplement, Sexually Transmitted Infections 86, no. S3 (2010): iii1–iii3. 4 Aral et al.,“Overview: Role of Emergent Properties,” iii1–iii3; James F Blanchard and Sevgi O. Aral, “Emergent Properties and Structural Patterns in Sexually Transmitted Infection and HIV Research,” Sexually Transmitted Infections 86, no. 3 (2010): iii4–iii9. 5 Aaron J. Blashill, C. Andres Bedoya, Kenneth H. Mayer, Conall O’Cleirigh, Megan M. Pinkston, Jocelyn E. Remmert, Matthew J. Mimiaga, et al., “Psychosocial Syndemics Are Additively Associated with Worse ART Adherence in HIV-Infected Individuals,” AIDS and Behavior 19 (2015): 981–86; M. Reul Friedman, Ron Stall, Anthony J. Silvestre, Chongyi Wei, Steve Shoptaw, Amy Herrick, Pamela J. Surkan, et al., “Effects of Syndemics on HIV Viral Load and Medication Adherence in the Multicentre AIDS Cohort Study,” AIDS 29 (2015): 1087–96; and Sheldon R. Morris, and Susan J. Little, “MSM: Resurgent Epidemics,” Current Opinion in HIV and AIDS 6 (2011): 326–32. 6 Centers for Disease Control and Prevention (CDC), 2017a. “STDS and HIV– CDC Fact Sheet,” accessed July 1, 2018, https://www.cdc.gov/std/hiv/stdfact-std-hiv. htm; Jennifer Jain, Glenn-Milo Santos, Susan Scheer, Steve Gibson, Pierre-Cédric Crouch, Robert Kohn, Walter Chang, et al., “Rates and Correlates of Syphilis Reinfection in Men Who Have Sex with Men,” LGBT Health 4, no. 3 (2017): 233– 36; and Seth C. Kalichman, Chauncey Cherry, Denise White, Mich’l Jones, and Moira Kalichman, “The Achilles’ Heel of HIV Treatment for Prevention: History of

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In short, behavioral and biomedical interventions—condom and ART—in certain contexts become part of complex dynamics that do not necessarily follow linear causality but interact nonlinearly with unintended effects in feedback chains.

Syndemics, Stigma, and HIV/AIDS To capture some of these complex emergent interactions between two or more epidemics—for instance, HIV and syphilis—a syndemics theoretical framework has been applied recently in HIV research.7 Syndemics refers to the synergistic interaction of coexisting epidemics or epidemiological factors that result in an excess burden of disease in a population. Each epidemic by itself produces lesser additive effects on a population than when interacting together by clustering their comorbidities. A syndemics framework incorporates the synergistic effects of co-infecting pathogens affecting HIV transmission (as explained above regarding STIs interaction) but also, most significantly, looks beyond biology to show that diseases do not exist in a sociocultural vacuum. Ultimately, social and cultural factors can be much more instrumental to the burden of disease of a population than the disease’s causal pathogens. In the case of HIV transmission among MSM, mounting research shows strong synergistic effects of intertwining psychosocial epidemics—violence, substance use, childhood sexual abuse, depression—producing excess burden of HIV in this population.8 In this line, a syndemics framework Sexually Transmitted Coinfections among People Living with HIV/AIDS Receiving Antiretroviral Therapies,” Journal of the International Association of Physicians in AIDS Care 10, no. 6 (2011): 365–72. 7 Merrill Singer, Introduction to Syndemics: A Critical Systems Approach to Public and Community Health (San Francisco: Jossey-Bass, 2009); and Merrill Singer, and Scott Clair, “Syndemics and Public Health: Reconceptualizing Disease in Bio-Social Context,” Medical Anthropology Quarterly 17, no. 4 (2003): 423–41. 8 Ron Stall, Thomas C. Mills, John Williamson, Trevor Hart, Greg Greenwood, Jay Paul, Lance Pollack, et al., “Association of Co-occurring Psychosocial Health Problems and Increased Vulnerability to HIV/AIDS among Urban Men Who Have Sex with Men,” American Journal of Public Health 93, no. 6 (2003): 939–42; Ron Stall, Mark Friedman, and Joseph A. Catania, “Interacting Epidemics and Gay Men's Health: A Theory of Syndemic Production among Urban Gay Men,” in Unequal Opportunity: Health Disparities Affecting Gay and Bisexual Men in the United States, ed. by R. J. Wolitski, R. Stall, and R. O. Valdiserri (New York: Oxford University Press, 2007), 251–74; and Barry D. Adam, Trevor A. Hart, Jack Mohr, Todd Coleman, and Julia Vernon, “HIV-related Syndemic Pathways and Risk Subjectivities among Gay and Bisexual Men: A Qualitative Investigation,” Culture,

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strongly points to the social dimensions and conditions that affect population health and “suggests the need for a biosocial reconception of disease.”9 Moreover, a syndemics framework examines not just proximal psychosocial epidemics—depression and substance use interactions leading to HIV risk, for example—that synergistically create an excess burden of disease in a population. It looks also to the distal social determinants of health that drive and shape the more proximal factors. Social determinants of health are defined by social processes and forces linked to unequal symbolic and material resources that affect diseases through multiple pathways and mechanisms. Social processes and forces include, among others, stigma and discrimination (racism, homophobia, life stressors, lack of opportunity) and poverty (overcrowding, malnutrition, lack of health care). Among the most important social determinants of health, stigma and discrimination are considered fundamental causes of disease because they are linked to prestige evaluations and access to resources that significantly affect a population’s health and perpetuate health disparities.10 As a fundamental cause of disease, stigma is involved in the structural reproduction of inequality and exclusion among groups. Stigma is often compounded as when HIV-related stigma intersects with sexual stigma due to homophobia. The stigma against sexual and gender minorities in particular significantly drives the HIV/AIDS epidemic, including symbolic and material barriers to HIV disclosure, testing, treatment, and care, as well Health, and Sexuality 19, no. 11 (2017); 1254–67. Also see Alexander C. Tsai, “Syndemics: A Theory in Search of Data or Data in Search of a Theory?” Social Science and Medicine 206 (2018): 117–122 for a constructive critique of syndemics research where he argues that the operationalization of multiple co-occurring psychosocial epidemics as “sum score” to show HIV excess burden fails to specify the actual mechanisms involved, whether mutually causal, serially causal, or synergistically interacting epidemics. 9 Singer and Clair, “Syndemics and Public Health,” 423–41; and Singer et al., 941– 50. 10 Centers for Disease Control and Prevention (CDC), 2016. “Stigma and Discrimination,” accessed July 1, 2018, https://www.cdc.gov/msmhealth/stigma-anddiscrimination.htm; Hazel D. Dean and Kevin A. Fenton, “Addressing Social Determinants of Health in the Prevention and Control of HIV/AIDS, Viral Hepatitis, Sexually Transmitted Infections, and Tuberculosis,” supplement, Public Health Reports 125, no. S4 (2010): S1–S5; Mark L. Hatzenbuehler, Bruce G. Link and Jo C. Phelan, “Stigma as a Fundamental Cause of Population Health Inequalities,” American Journal of Public Health 103, no.5 (2013): 813–85; and Bruce G. Link,. and Joe C. Phelan, “Social Conditions as Fundamental Causes of Disease,” Journal of Health and Social Behavior 35 (1995): 80–94.

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as family rejection and job or housing denials. In this respect, it is important to conceptualize stigma not simply as direct individual-level “discrediting attributes” or “spoiled identities” but as part of broader mechanisms of power and control in a society that perpetuate health disparities.11 Typically, HIV-related stigma is based on unfounded fears of contagion, illness, and death. It has been shown—especially when compounded with the stigma of same-sex sexualities—to negatively affect HIV preventive behaviors like condom use, testing, care-seeking behaviors, ART adherence behaviors, quality of care, and overall perceptions and treatment of people living with HIV/AIDS by communities, families, and partners.12 In short, stigma as a fundamental cause of disease affects through different pathways a wide range of health-related behaviors linked to prevention, treatment, and care of HIV/AIDS.

Latino Gay and Bisexual Men It is within these unequal syndemic contexts of stigma and discrimination that MSM remains the population most affected by HIV/AIDS in the United States. In 2014 alone MSM (including gay-identified, bisexual, and other men who have sex with men) represented an estimated 2% of the male US 11 Erving Goffman, Stigma: Notes on the Management of Spoiled Identity, (New York: Simon & Schuster, 1986); Link and Phelan, “Stigma as Fundamental Cause, 813–85; and Richard Parker and Peter Aggleton, “HIV and AIDS-related Stigma and Discrimination: A Conceptual Framework and Implications for Action,” Social Science and Medicine 57 (2003): 13–24. 12 Lisanne Brown, Kate Macintyre, and Lea Trujillo, “Interventions to Reduce HIV/AIDS Stigma: What Have We Learned?” AIDS Education and Prevention 15, no. 1 (2003): 49–69; Valerie A. Earnshaw, and Stephenie Chaudoir, “From Conceptualizing to Measuring HIV Stigma: A Review of HIV Stigma Mechanism Measures,” AIDS and Behavior 13 (2009): 1160–77: Miriam Heijnders and Suzanne Van Der Meij, “The Fight against Stigma: An Overview of Stigma-reduction Strategies and Interventions,” Psychology, Health, & Medicine 11, no. 3 (2006): 353–63; Bronwen Lichtenstein, Social Stigma and Sexual Epidemics: Dangerous Dynamics. (Boulder, Colorado: Lynne Rienner, 2012); Lichtenstein, “Stigma as a Barrier to Treatment of Sexually Transmitted Infection in the American Deep South: Issues of Race, Gender and Poverty,” Social Science & Medicine 57 (2003): 2435– 45; Anish P. Mahajan, Jennifer N. Sayles, Vishal A. Patel, Robert H. Remien, Sharif R. Sawires, Daniel J. Ortiz, Greg Szekeres, et al., “Stigma in the HIV/AIDS Epidemic: A Review of the Literature and Recommendations for the Way Forward,” supplement, AIDS 22, S2 (2008): S67–S79; and Sohini Sengupta, Bahby Banks, Dan Jonas, Margaret S. Miles, and Giselle C. Smith, “HIV Interventions to Reduce HIV/AIDS Stigma: A Systematic Review,” AIDS and Behavior 15 (2011): 1075– 87.

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population but accounted for 70% of all new infections. Moreover, HIV disproportionately affects Latino and African American MSM, which points to broader historical processes of racial/ethnic stigma and discrimination. Thus in 2015 Latinos, in general, represented 18% of the US population but accounted for 24% of all new HIV diagnoses. In addition, from 2010 to 2014 HIV infections declined 11% among white MSM but increased 14% among Latino MSM.13 These health disparities are significant and call for further social-behavioral research to better understand the HIV prevention and care needs of a diverse Latino MSM population. In this connection, it is worth noting that to understand the HIV/AIDS syndemic complexity of a vulnerable population requires first deep cultural knowledge and immersion in the lived worlds of those affected by the epidemic. Qualitative and ethnographic methods are in this respect indispensable as the first point of entry to begin unpacking such complexity. These methods are ideally suited to deliver deep interpretive insights on micro-level mechanisms and pathways that can then be used to model larger-scale epidemiological processes through agent-based, network, or path analysis techniques, among others.14 Ultimately it is through triangulation of data from multiple sources and emergent levels—biological, individual, group, population—that we can tackle HIV/AIDS syndemic complexity and design efficient combination prevention strategies.15 13 Centers for Disease Control and Prevention (CDC), 2017b. “HIV among Gay and Bisexual Men,” accessed July 1, 2018, https://www.cdc.gov/hiv/group/msm/index. html.; Ibid.; and Centers for Disease Control and Prevention (CDC), 2017c, “HIV among Hispanics/Latinos,” accessed July 1, 2018, https://www.cdc.gov/hiv/group/racialethnic/hispaniclatinos/index.html. 14 Auerbach, et al., “Addressing Social Drivers,” 1–17; Paul Gaist, and Michael J. Stirratt, “The Roles of Behavioral and Social Science Research in the Fight against HIV/AIDS: A Functional Framework,” Journal of Acquired Immune Deficiency Syndrome 75 (2017): 371–81; and Tsai, “Syndemics: Theory in Search of Data,” 117–22. 15UNAIDS, “Combination HIV Prevention: Tailoring and Coordinating Biomedical, Behavioural and Structural Strategies to Reduce New HIV Infections,” accessed July 1, 2018, http://www.unaids.org/en/resources/documents/2010/20101006_ JC2007_Combination_Prevention_paper; Michael Quinn Patton, “Enhancing the Quality and Credibility of Qualitative Analysis,” pt: 1, Health Services Research 34, no. 5 (1999): 1189–1208. The push to address the complexities of the HIV/AIDS epidemic by including social determinants and socio-structural levels in prevention efforts has been defined by UNAIDS as “combination prevention” or “the strategic, coordinated use of different classes of prevention activities—biomedical, behavioral, and structural—to design interventions that operate on multiple levels (e.g., individual, relationship, community, societal) and respond to the specific needs of relevant

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From the outset, it is important to clarify that “Latino MSM” is a heuristic category based simply on the mode of transmission without much ontological validity. As other scholars have noted, MSM is an umbrella term used in epidemiology that tends to uncritically obscure the diversity of sexual orientations and identities that emerge from the lived experiences of sexual and gender minorities.16 Overlooking this great heterogeneity has detrimental consequences in the design of targeted HIV prevention interventions and health promotion messages for specific MSM groups. In the case of Latino MSM, it is important to highlight their sexual diversity to recognize that they do not constitute a monolithic group.17 It is to this diversity of Latino MSM experiences producing distinct meanings in contexts where HIV transmission may occur that I turn now. audiences and documented modes of HIV transmission” UNAIDS, “Combination HIV Prevention,” 9. 16 Richard Parker, Peter Aggleton, and Amaya G. Perez-Brumer, “The Trouble with ‘Categories’: Rethinking Men Who Have Sex with Men, Transgender and their Equivalents in HIV Prevention and Health Promotion,” Global Public Health 11, no. 7–8 (2016): 819–23; and Rebecca M. Young and Ilan H. Meyer, “The Trouble with ‘MSM’ and ‘WSW’: Erasure of the Sexual-Minority Person in Public Health Discourse,” American Journal of Public Health 95, no. 7 (2005): 1144–49. 17 Héctor Carrillo and Jorge Fontdevila. “Border Crossings and Shifting Sexualities among Mexican Gay Immigrant Men: Beyond Monolithic Conceptions,” Sexualities 17 (2014): 919–38. They explain that historically the study of Latino/Latin American homosexuality was influenced by a highly gendered model known as the pasivo/activo model, where men who have sex with men were classified into two rigid types: anal-receptive “pasivo” men (often stigmatized as effeminate), and anal-insertive “activo” men (often self-identified as heterosexual). The pasivo/activo model became essentialized in the literature as the only one to describe Latino/Latin American homosexualities. Eventually it was challenged by research that highlighted the recent adoption of contemporary interpretations of gay identity in Latin American countries. This new model of contemporary gay identities in Latin America has also been criticized as reductionist and challenged on two fronts. On the one hand, there is a third form—besides gendered or gay—of samesex practices that was found to also co-exist in Latin America, historically with gendered forms but more recently with global contemporary gay identities. This form labeled homosocial or homoerotic involves sexual encounters between nongay-identified men that occur without the gendered interpretations of the pasivo/activo model. On the other hand, new research challenges treating all these patterns—gendered, gay, homosocial—as incompatible discrete categories, and finds various contexts in which individuals adapt to various interpretations, blendings, and even move back and forth across categories. These flexibilities have been captured by the concept of sexual hybridity. Héctor Carrillo, Pathways of Desire: The Sexual Migration of Mexican Gay Men, (Chicago: University of Chicago Press, 2017).

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Three Meaning Systems in Context In this essay, based on qualitative and ethnographic research among Latino MSM in southern California, I show that within the unequal contexts of sexual and HIV-related stigma, different interpretations and meanings during sex have different implications for HIV transmission. I examine the meanings these Latino men attach to their same-sex sexual encounters—and to their sexualities more generally—to shed light on how such meanings may lead to unintended risky behaviors within broader HIV/AIDS syndemic frameworks. I thus analyze in depth the specific meanings and interpretations that are part of the production of causal pathways by which HIV can be transmitted within the larger context of stigma as a fundamental cause of disease. To achieve this goal, I draw on a selection of findings from three qualitative studies that I conducted among Latino MSM in southern California: First, from the Trayectos study among Mexican gay and bisexual men who migrated to San Diego, California, I examine the HIV implications of the meaning of silence as signaling trust during sexual exchanges with local men. Second, from the Contextos study among non-gay identified Latino men who have sex with men and women in Orange County, California, I show how sex with men—in contrast to women—signifies a liminal and transgressive space. This space is less normatively regulated and often HIV riskier. Finally, from the Stigma study among young Latino gay men in Orange County, California, I explore how a recent biomedical intervention—pre-exposure prophylaxis (PrEP)—attains stigmatizing meanings of sexual promiscuity with detrimental implications for HIV prevention. By examining findings from these three qualitative studies, I intend to show the analytical relevance of focusing first on “meaning in context” to understand how HIV can be transmitted through different pathways within larger syndemic frameworks. I then conclude by contrasting these meaning systems within the larger syndemic context of stigma and HIV. I turn now to the meaning of silence as signaling trust during sex.

Silence during Sex Meaning Trust Based on data from the Trayectos Study, I find that some Mexican gay and bisexual immigrant men upon arrival in San Diego may encounter local sexual networks informed by very different expectations regarding HIV

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disclosure.18 Their interpretations before migration—especially if their places of origin were rural areas and they had not experienced modern gay life in Mexico—may lead them to trust that US casual partners who do not disclose HIV status during sex are HIV negative. Thus, “silence” during sex regarding HIV disclosure for some recent immigrant men who are HIV negative or do not know their HIV status often means HIV-negative serosorting.19

Reducing HIV Uncertainty To illustrate some of these HIV dilemmas of serosorting and protection during sex, in the following vignette, Heriberto, a 21-year-old man originally from Durango, Mexico, who met his same-sex partner at a porn theatre, explains: We undressed and I realized the guy had a nice body … I didn’t have condoms handy … I was hesitant whether to penetrate him or not … First, because I didn’t know whether he was “top” or “bottom.” And so I said to myself, ‘What shall I do?’

18

Jorge Fontdevila, “Framing Dilemmas during Sex: A Micro-sociological Approach to HIV Risk,” Social Theory and Health 7, no. 3 (2009): 241–263; and Héctor Carrillo, Jorge Fontdevila, Jaweer Brown, and Walter Gómez, Risk across Borders: Sexual Contexts and HIV Prevention Challenges among Mexican Gay and Bisexual Immigrant Men, (San Francisco: University of California, Center for AIDS Prevention Studies, 2008). Data that I present here were collected as part of the larger ethnographic Trayectos Study—led by Dr. Héctor Carrillo (NIH R01HD042919)—which explored contexts of HIV risk among self-identified gay and bisexual Mexican men who migrated to San Diego, California. For comparison purposes, the larger study also included data collected from US-born Latino and non-Latino gay men who had engaged in sex with Mexican-born men. Participants were recruited between 2003 and 2005, and to be eligible they were at least 18, had migrated to or worked in the US within the past 10 years, and had engaged in sex with men in the past 6 months. For this analysis I selected a purposive subsample of Mexican men who were HIV seronegative or untested (but assumed they were negative), and who in their in-depth interviews produced an account of unprotected anal sex with a casual partner. Twenty-one participants met both sampling conditions. They were on average 29.7 (sd=5.7) years old, most had high school (n=11) or college (n=6) degrees, and were either formally or informally employed (n=20) in the service and retail sectors. Passages were translated into English by the author. All participants’ names are pseudonyms. 19 HIV-negative serosorting means that two HIV-negative men decide to have sex without condom protection because they trust both are negative.

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Note that like many participants facing similar dilemmas of unprotected penetration, Heriberto here poses the phenomenological, metacommunicative question of “What is going on here?” by asking to himself “What shall I do?” regarding HIV risks.20 Heriberto continues: Then we started with oral sex first, oral sex with caresses and everything. And then … to find out whether [sex partners] are “top” or “bottom” I often stick my finger [in their anus] … and if they push away then it means they don’t like it. If they don’t say anything, then yes [they like it]. So then I did it, I stuck my finger, and he didn’t say anything, he only moaned with pleasure … [Then] I positioned myself and began teasing him with my penis [as if penetrating] … waiting for his response. He didn’t say anything … that is, he didn’t say: “put on a condom” or anything. And I was so horny that I recall that I simply put some lube on me and him, and I penetrated him without a condom.

In this vignette, Heriberto—who has never been HIV tested but assumes he is negative—is at first hesitant to penetrate his sex partner without a condom. At some juncture of their sexual ritual, he attempts to reduce HIV uncertainty by teasing his sex partner with his erect penis, waiting for a response. In other words, he “indexes” permission to engage in unprotected anal intercourse expecting his partner’s consent. He is concerned about the risks involved, but since his partner “didn’t say anything,” he proceeds to penetrate. The lack of condom request is the green light to trust that it is likely safe to penetrate without protection. Though he is not explicit about his assumptions in this vignette, Heriberto expresses great concern about HIV infection throughout the entire interview. It is unlikely he thought his partner was “knowingly” HIV positive. In other words, he trusted his partner would have disclosed or requested condoms had he been HIV positive. This assumption was common among many recent immigrant gay and bisexual men.

HIV Stigma and Individual Responsibility In many sexualized spaces and networks among gay men in the US— bathhouses, sex parties, internet, public sex environments (e.g., parks, beaches, porn bookstores) among others—it is often mutually understood 20

Note that Heriberto asks “what shall I do?” first in direct relation to a dilemma of “sex-role” coordination that gay men may encounter during casual sex. In response to this dilemma, as shown in the following vignette, he reduces sex-role uncertainty by using his tactic of “fingering” partners to determine their role preference, whether “top” (anal insertive) or “bottom” (anal receptive).

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that the moral responsibility of HIV disclosure or condom request does not fall on the HIV-positive sex partner. Rather, it falls on any individual who freely enters the sexual exchange with the ultimate preference to remain HIV safe.21 In these contractual sexual arenas, HIV non-disclosure and “silence” regarding protection is part of a discourse of individual responsibility that often signals sex between HIV-positive partners (HIV-positive serosorting). In contrast, recent gay and bisexual immigrant men who are newly introduced to US sexualized spaces may interpret “silence” regarding protection as having sex with an HIV-negative partner (HIV-negative serosorting). In other words, two distinct meaning systems circulate that can bypass each other during sexual exchanges between local and migrant sexual networks. Needless to say, this interactional miscommunication on the meaning of “silence” has implications for HIV transmission, given that ultimately protection is not used. To illustrate this discourse of individual responsibility, Austin, a 54year-old HIV-positive white man, explicitly said in his interview that he did not want to infect anyone, but he also clarified that: If someone’s in the bathhouse, I usually don’t tell them that I’m HIV. Okay. And my thinking—either correct or incorrect—is that they're there and they're taking as much of a risk as I'm taking and they must be aware of the risk … I think anybody who's very sexually active, if I meet you in a bathhouse you probably … or if I were to meet you in the park, meet you where there's only the possibility of sex going on … most likely you're probably HIV positive. That is my assumption.

21 Barry D. Adam, ‘Infectious Behaviour: Imputing Subjectivity to HIV Transmission,” Social Theory and Health 4 (2006): 168–79; Ronald Bayer, “AIDS Prevention–Sexual Ethics and Responsibility,” The New England Journal of Medicine 334 (1996): 1540–42; David M. Halperin, What Do Gay Men Want: An Essay on Sex, Risk, and Subjectivity (Ann Arbor: University of Michigan Press, 2007); Robert Klitzman and Ronald Bayer, Mortal Secrets: Truth and Lies in the Age of AIDS (Baltimore, MD: Johns Hopkins University Press, 2003); Claudine Offer, Olga Grinstead, Ellen Goldstein, Edward Mamary, Nicholas Alvarado, Jason Euren, and William J. Woods, “Responsibility for HIV Prevention: Patterns of Attribution among HIV-seropositive Gay and Bisexual Men,” AIDS Education and Prevention 19, no. 1 (2007): 24–35; and Richard J. Wolitski and Caroline J. Bailey, “It Takes Two to Tango: HIV-Positive Gay and Bisexual Men’s Beliefs about their Responsibility to Protect Others from HIV infection. in HIV+ Sex: The Psychological and Interpersonal Dynamics of HIV Seropositive Gay and Bisexual Men’s Relationships, edited by P. N. Halkitis, C. Gómez, and R. Wolitski (Washington, DC: American Psychological Association, 2005) 147–62.

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Although most HIV-positive men disclose their status, a significant number of HIV-positive gay men resist stigma and rejection by “reclaiming” such discourses of individual responsibility that avoid HIV disclosure. Such discourses have been theorized as the empowering response to the entrenched stigma and rejection that HIV-positive men endure in the context of the ongoing epidemic.22 Moreover, such discourses of individual responsibility during sex show strong elective affinities with globalized neoliberal constructions of contemporary gay masculinities as risk-taking and self-sufficient selves.23 In short, it is this empowering reaction to HIV stigma by HIV-positive men in sexualized spaces that paradoxically may create the contexts of HIV transmission where recent Mexican gay and bisexual men may find themselves unaware of the rules of the game. In the process of adjusting to gay life in the US, immigrant men may unwittingly follow trusting assumptions in sexual situations where discourses of individual responsibility have become dominant. In this regard, at least half of the Mexican gay and bisexual immigrant men of this analysis participated in spaces linked to sexual networks where discourses of HIV non-disclosure circulated unabated. I have argued elsewhere that selves are inherently inconsistent during sexual interaction and that they juggle multiple motivations.24 Despite their strong HIV protection intentions, individuals at certain junctures of their sexual interactions often feel more accountable to their face-to-face ritualized framings—such as communicating trust or performing masculinity—than to their long-term health goals of avoiding infection by using condoms. In the context of these powerful performative framings during sex, many gay and bisexual immigrant men who trusted their sex partners’ “silence” to mean HIV-negative serosorting would have required stronger persuasion by their partners to engage in unprotected sex had they 22

Ibid. To clarify, here I use the concept of “discourse of individual responsibility” as it is used in the HIV research literature to convey the contractual ethics of a sexual marketplace that is governed by the principle of “buyer beware.” See Adam, “Infectious Behaviour,” 168–179. The concept assigns responsibility to the individual who decides to have unprotected sex and who must bear the (HIV) risks without blaming his sex partner. The concept does not imply in any case that HIVnegative men have the moral “responsibility” to avoid having sex with HIV positive men. 23 Barry D. Adam, “Neoliberalism, Masculinity, and HIV Risk,” Sexuality Research and Social Policy 13 (2016): 321–29. 24 Jorge Fontdevila, “Phenomenologies of the Akratic Self: Masculinity, Regrets, and HIV among Men on Methadone,” Journal of Urban Health 83, no. 4 (2006): 586–601; and Fontdevila, “Framing Dilemmas,” 241–63.

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known that sexualized spaces were informed by discourses of individual responsibility with few altruistic expectations.

Sex with Men Meaning Liminality I now turn to findings from the Contextos Study among Latino behaviorally bisexual men in Orange County, California, to explain another meaning system—sex with men as signifying liminal transgression—that within broader contexts of sexual stigma has implications for HIV transmission.25 Bisexuality is one of the most unstable categories in contemporary constructions of sexuality.26 Ever since heterosexual/homosexual binary classifications were instituted in Victorian times, the modern “heterosexualization” of desire—in particular of masculine desire—has been contingent on the “erasure” of bisexuality as a stable category.27 In fact, male bisexuality in modern times is often stigmatized by both heterosexual and gay-identified men. Yet some men can still negotiate their 25

Jorge Fontdevila, “Heteronormativity or Homoeroticism? Contexts of HIV Risk among Non-gay Identified Latino Men Who Have Sex with Men and Women,” Presented at the XIX International AIDS Conference, July 22–27, Washington, DC., 2012; and Jorge Fontdevila, “Productive Pleasures across Binary Regimes: Phenomenologies of Bisexual Desires among Latino Men,” Sexualities, published ahead of print, April 5, 2019, https://doi.org/10.1177/1363460719839915. Data that I present here are from the Contextos Study, a qualitative in-depth interview study that I conducted in 2010 among 20 Latino non-gay identified men who have sex with men and women in Orange County, California. To be eligible participants were at least 18, had engaged in sex with men and women in the past 12 months, and selfidentified as being of Latin or Hispanic origin. In addition to their sexual histories, participants provided two recent “event” narratives of unprotected sex (one of vaginal or anal sex with a female sex partner, and another of anal sex with a male sex partner). Passages were translated into English by the author. All participants’ names are pseudonyms. Participants were on average 39 (range 25-48), most (n=15) did not have a high school degree, and almost half (n=9) did not have permanent jobs (e.g., day laborer). Those who worked were employed in the service and construction sectors. Most (n=15) were born in Mexico; others in Guatemala, Honduras, Peru, and the US. Many (n=8) were currently married or had been married to a woman in the past. The majority (n=12) self-identified as bisexual. The rest reported a variety of heterosexual-oriented identities, including derecho [straight] (n=3), heterosexual (n=2), normal (n=2), and hombre [man] (n=1). 26 Steven Angelides, A History of Bisexuality (Chicago: University of Chicago Press, 2001). 27 Judith Butler, Gender Trouble: Feminism and the Subversion of Identity (New York: Routledge, 1990); and Thomas W. Laqueur, Making Sex: Body and Gender from the Greeks to Freud (Cambridge, MA: Harvard University Press, 1990).

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bisexual desires in productive ways without undermining their sense of masculinity and sexual agency. In this analysis, I show how a group of bisexual men—Latino men who have sex with men and women—learn to navigate modern “binary regimes” of gender and sexuality. Based on their sexual narratives, I find that the “rules of the game” regarding seeking sex across genders are interactionally very different. Cruising rituals and sexual practices with women—in contrast to men—involve more interactional effort and higher levels of ritualized masculine “self” impression management, “courtship” material resources, and moral respect.

Cruising Rituals across Gender Participants reported that seeking sex across genders was interactionally very different, involving distinct venues and spaces in southern California. They met male sex partners at porn bookstores, via magazine ads, internet sites, gyms, friends’ networks, house parties, parks, and on the streets. To illustrate a typical cruising ritual between men, in this vignette Julian, a 46year-old Latino man from Santa Ana, California, describes a sexual encounter with a man at a porn bookstore: There is little booths, and say it was you, you walked in a booth, and go, ‘hey, what’s up,’ ‘hey, what’s up, come here’… by that time everybody already has their pants down or [are] jacking it off … and then usually whoever is going to go down on you, goes down on you, you know, …‘do you want to fuck?’

Another example of a male cruising ritual is described by Ulises, a 41-yearold man from a rancho in Morelos, Mexico, who met a married man at a hotel: I met him through a magazine [ad] … that said ‘married man seeking similar for fun.’ … Then I dialed the number … [He answered] ‘I am married … but I like to be penetrated.’ We got to the hotel … and he told me ‘you know that what I like is to give oral sex and … be penetrated.’

Regarding female cruising rituals, participants met female sex partners through friends’ networks, bailes (Latino dance clubs), house parties, local neighborhoods, church, and on the streets. Claudio, a 43-year-old man from a rancho near Toluca, Mexico, illustrates a quite typical cruising ritual with women at a baile to have casual sex:

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Interaction Ritual Demands Female cruising rituals are thus different from male rituals. The former require more step-wise work and hence are interactionally more demanding. Claudio best conveys a widespread theme that obtaining sex with women involves significant impression management. He eloquently indicates, “There are rules” to follow: Because I wanted a woman, [had] desires, right, before going to the casino, I went to the gym, to run, to get fit … I also bought nice clothes to look good …, cologne, so that there are rules … I mean, you have to follow them if you want to have sex, you have to be presentable … women pay attention to detail. There are many women that … [when] you undress … and [if your] toenails look long and like filthy … they decide better not to have sex.

It is important to highlight that these participants—except for one—never patronized gay bars or venues. In fact, most had never been to institutionalized gay spaces and did not intersect with “commodified” gay subcultures. Because of this, these bisexual men never experienced the type of “presentation of self” pressures that gay-identified men typically do. Beyond the ritual pressures to cruise women, a number of participants also expressed that in general, it was easier to please a man sexually than a woman. For instance, Nestor, a 41-year-old man from a town in Orange County, indicated: I guess it depends on your skill, to me it’s easier to please a man sexually, to make a man orgasm, it’s easier to do that than [to] a woman, I mean, how many women fake orgasms before, and you haven’t really made them orgasm… Men, it’s obvious when a man has an orgasm, and I think it’s just a lot easier, to complete the mission [laughs], and then women want… feelings and emotions, and all that stuff, you know, guys is just, like let’s do it and go.

Moreover, most participants also reported that women—in contrast to men—tend to be more careful about protection during sex and typically

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request condoms. According to Claudio, for example, his female casual partners may not carry condoms but will definitely request them, and even ask to drive by a drugstore to buy them before going to a hotel. Possibly women also requested condoms due to pregnancy concerns, but participants in this study never articulated such a rationale. Most participants simply reported that male partners take more HIV risks than female partners. Ulises, for example, illustrates this theme that male partners are riskier. After ejaculating inside his male partner’s mouth, he pondered: And right away I started thinking that there are risks involved if I were to have sexual relations with him ... and with a woman, no, because women are hundred percent … cautious. She does not do anything unless it is with protection. So I feel safer being with a woman than with a man. For my next encounter with a man, I would have to be more careful than … with a woman also … but [with] her, I am sure that a woman takes more care of herself.

Ulises claims that women always say “no condoms, no sex” whereas men always find excuses not to use condoms, and thus it is harder to bring them up. In short, women brought to the sexual performance an extra layer of interactional demands by requesting condoms. In addition to female sex partners requesting condoms, participants gave other reasons why sex with men is riskier. Julian, for instance, explains that it is easier to use condoms with a woman because with a man he gets too aroused and forgets to use them. For Mauro, a 41-year-old man from Minatitlán, Mexico, it is the opposite reason. He finds using condoms with a man more difficult because he does not feel as much arousal or physical sensation, and so he is often reluctant to use them and miss the opportunity. In his own words: With a condom on [inside a man] you cannot feel… when you penetrate a woman with a condom you feel almost the same [than without a condom]. I do not know why … perhaps because it gets wetter, they produce more liquids, lubricate more, it feels a bit more natural than with a man … because … the anus is … yes, it gets wet, but for the most part, it’s dry … it only gets wet if you use lubricant, right?

Nestor also reports that women always want to use condoms, but in his case, it is harder for him to use condoms with male partners because he typically has sex with men in the context of drug euphoria, mostly methamphetamine. Another reason why it is harder to use condoms with men comes from Gerardo, a 25-year-old man from Mexico City, who indicates that anal sex is rougher than vaginal sex. He explains that anal sex is tighter, with more pressure, and so he has a harder time maintaining an

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erection with a condom inside a male partner. Finally, in contrast to the widespread theme that it is harder to use condoms with men, one participant Alfredo, a 26-year-old man from a small town near Acapulco, Mexico, reports the opposite. For him, it is harder to put on a condom with a woman because of la calentura [strong arousal] he feels with women, but easier with a male partner because “already with a man, I imagine … that because you have in your mind that he can be infected with AIDS, right? So then one uses protection.” In short, participants offered different (sometimes opposite) reasons why sex with men is riskier. Thus, condoms are harder to use with men because (1) one is too aroused by men and forgets, (2) not aroused enough and would diminish sensation, (3) sex with men takes place in the context of drug euphoria, or (4) it is harder to maintain a physical erection given that anal sex is tighter or drier than vaginal sex. The HIV prevention implication of this qualitative analysis sheds light on the complex range of sexual scenarios and motivations that need to be considered.

Resource Ritual Demands In addition to interaction ritual demands (cruising, pleasing sexually, and condom requests), many participants reported that having sex with a woman requires spending money or resources. Ronaldo, a 27-year-old man from a municipality in Guerrero, Mexico, near Acapulco, says that he used to go out with a female partner. Lately, he does not see her in part because he does not have a job: “I am a man who feels shame … I am not without shame. I am a person that if I like to go out with a woman, it is because I will pay for the expenses out of my pocket, to take her out, so she feels secure about who she is going out with.” In relation to male partners being less materially costly than females. Ulises also says: With men, it’s easier … I search in the newspaper and I talk to them on the phone, and they tell me where [to meet]… a man is easy … he doesn’t charge you, and provides for everything, pays for the hotel, he gives you food, he buys anything you want … as long as you give him sex.

Santiago, a 48-year-old man from a town in Honduras who engaged in same-sex behavior to obtain money, also captures this theme of resource demands in relation to female cruising or sexual rituals. He explains that lately, he has not had sex with women because he does not have financial resources, and for him, resources are “part of the courtship” of women:

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I haven’t been financially well enough to visit my female friends … Because I don’t like to go empty-handed, I like to invite them to places … even if it is out to eat …because, as I told you, I don’t pay them … but it’s part of the courtship …and so it’s different when you are wooing someone … because you want to invite her to dinner, to dance, and when everything is, so to speak, ripe, you mention the issue [having sex] … you go home and prepare everything.

Often lacking resources to court or date women also means not having enough money to pay for a female sex worker. In this context, a number of men opt to have sex with gay men who are freely available and can be cruised on the streets. To illustrate this, Alfredo states that he would have preferred to have sex with a woman instead of a guy but “because they had paid me very little [at his day-laborer job], I did not have enough money [for a female sex worker].” Hence, he decided to have casual sex with a man he met on the street who did not charge money. In some instances, the lack of resources occurs after having spent all one’s money inviting female casual partners to drink at local bars. When the money runs out and sex with these women did not occur, some participants will go to public parks or spaces where men seek men at no cost.

Moral Ritual Demands Finally, some participants expressed the belief that women—in contrast to men—have special moral standing, and thus certain sexual behaviors or interactions are inappropriate with women. In this sense, women involve moral demands that men do not. To illustrate these moral demands, Domingo, a 39-year-old man from Mexico City who identifies as bisexual and likes men and women equally, explains that online chat rooms are ultimately disrespectful to women: The only [difference] I have regarding women is that I don’t treat women, in the same way, I treat men … It’s like I have much more respect for women … I am much more careful, I’m afraid to ask them to do things, or to do things the way I’d like them … With a man, I feel at ease to tell him … [With a woman] I am afraid to offend her, not to do it right … A woman is of great value to me … I cannot talk sex to women in [online] chats … to a man, yes, not sure why … I’d rather go to a night club, dance, and meet [women] there … [online chats] are very disrespectful to them [women].

Some participants who identified as heterosexual also reported this moral standing of women that comes with respect. Narciso, a 32-year-old man from Acapulco, Mexico, mentions that he and his friends back in

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Mexico never gossiped about their sex with women because women “deserve respect.” In contrast, they would laugh and joke about their sex with maricones [derogatory for gay men]. Asked why they never joked about sex with women, Narciso remarks: Oh, no, not with women … I have never liked to talk that way about a woman because I believe [a woman] is something worthy of respect, right? … that’s my way of thinking … when I am with a woman I don’t tell my friends what I did with her in bed, whether I made her get in a certain position or this other, or that I tongued her there, those things I never tell my friends … [About maricones] I would at times tell [my friends] … it’s like it’s funny [giggles], so they would ask me and they have also experienced the same, that they have been with another person like that, and they tell me the other day this and that … that he gave me some mamadas [oral sex], and we laugh, but as I was telling you, whatever I do with women that, no … that I never tell any of them [friends]. 28

In a related vein, the patriarchal double standard of “good/bad” women was articulated by many participants. Some admired their wives or girlfriends for being “respectful homemakers” or “God-fearing.” Hernan, a 40-year-old man from a town in Michoacán, Mexico, praised his wife for being “very much of a woman… a homemaker, respectful, quehacerosa [devoted to housework], very tidy.” Ezequiel, a 35-year-old man from a town in Michoacán, Mexico, says that besides his girlfriend’s pretty looks what caught his attention was that she was a “family woman, a quiet woman, who has fear of God.” Julian found his girlfriend in church and was very explicit about the fact that “when I like a girl … she has to be, like, I don’t want no hooker hood rat [implying sexually available], or something like that, I want someone normal, you know.”

28 This vignette opens a window into highly gendered same-sex cultures in Mexico where disclosure of same-sex acts among male peers (albeit in scripted “activo” ways) does not threaten and even reproduces heteronormative masculine constructions, see Carrillo and Fontdevila, “Border Crossings,” 931. It is beyond this essay’s scope to explore the different types of bisexualities found in my analysis. Most participants had negotiated their bisexual desires in productive ways without experiencing internal conflict. Half (n=10) practiced homoerotic desires, including mutual kissing and anal role play, departing from the strict “activo” heterogendered experience illustrated by Narciso.

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Liminal Spaces and HIV Based on these findings, I argue that for these Latino bisexual men sexual acts with women are “burdened with an excess of significance”29 that is not experienced when they have sex with men. Such burdens also involve the high-stake demands of hetero-masculine presentations of self vis-à-vis female partners.30 Obtaining sex with women requires highly ritualized yet fragile phenomenological performances—at the interactional, resource, and moral level—where “breaches” may happen at any juncture. This asymmetry in female ritual demands is the pragmatic expression of institutionalized gender discourses of “proper” femininity that circulate unabated and are heavily regulated at the normative and moral level. Within the broader discursive orders of gender, therefore, acquiring sex with women involves interactional work that is more reflexive and stepwise. It is constructed upon complex polythetic structures of action with higher demands for fine-tuned timings and inner durées in phenomenological parlance.31 In contrast, obtaining sex with men is less demanding for these bisexual men who also desire men. It involves less reflexive stepwise actions, including more routinized “flash-like” actions that are not as regulated by normative discourses. In short, sex with men requires less polythetic complexity in accomplishing sexual success. For those participants who strongly intersect with inequalities of class and who lack resources, same-sex practices are also part of a pleasure economy that is readily accessible and less costly. In this light, I argue that same-sex practices for these bisexual men are transgressive spaces where, albeit stigmatized, they experience strong liminality. These liminal spaces produce same-sex pleasures that are less 29

Gayle S. Rubin, “Thinking Sex: Notes for a Radical Theory of the Politics of Sexuality” in Pleasure and Danger: Exploring Female Sexuality, ed. by C. S. Vance (New York: HarperCollins, 1992), 279. 30 Similarly, Héctor Carrillo and Amanda Hoffman, “From MSM to Heteroflexibilities: Non-exclusive Straight Male Identities and their Implications for HIV Prevention and Health Promotion.” Global Public Health 11, no. 7–8 (2016), 931, find in their sample of non-exclusive straight-identified men that some participants justify their sex with other men partly as “a desire for having a space in which they can seek relief from the pressures of being a man—at least in terms of conventional or hegemonic masculinities... [These] participants feel that finding a respite from the burdens of masculinity requires secrecy, and moreover, they view such secrecy as exciting and erotic.” Also see Fontdevila, “Phenomenologies of Akratic Self,” 586– 601. 31Alfred Schutz, The Phenomenology of the Social World. (Evanston, IL: Northwestern University Press, 1967).

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normatively regulated than different-sex pleasures—from less impression management demands and condom interruptions, less pressure to provide sexual pleasure to partners, to less moral and resource burdens. In this sense, these spaces challenge conventional binary classifications of identity politics, such as being “gay” or “heterosexual.” More than identity, for these men sex with other men, attains a liminal site of transgression that resists binary definitions and is highly productive of pleasure. This has strong implications for HIV transmission because liminal spaces involving minimal cognitive steps for sexual accomplishment are some of the hardest interactional contexts where partners can introduce or request condoms.

PrEP Meaning Promiscuous Sex Finally, from my recent qualitative focus group research among gayidentified (mostly) Latino young men, I present findings of yet another meaning system—pre-exposure prophylaxis (PrEP) as a signifier of sexual promiscuity.32 These findings are significant because they reveal the existence of stigma mechanisms at work within biomedical interventions among this population. PrEP involves HIV-negative individuals taking one pill made of an antiretroviral combination (in this case) to prevent HIV infection. Clinical trials have shown that when taken consistently, one pill daily reduces the risk of HIV infection by up to 92%.33 Typically, PrEP is 32

Data that I present here are from the Stigma Study, Jorge Fontdevila, “Stigmarelated Barriers to HIV Prevention and Care among MSM in Orange County.” Research Grant #355216, California State University, Fullerton, CA, 2016. A qualitative study of 5 focus groups among 24 gay-identified men that I conducted in 2017 in Orange County, California, on changing definitions of safe sex in the era of biomedical interventions. To be eligible, participants were at least 18 and had engaged in sex with men in the past 12 months. Participants discussed how safe sex had changed in recent years, biomedical knowledge, how biomedical interventions had changed intimate relations between HIV positive and negative men, impact of sexual media digital applications, and attitudes toward PrEP, among other topics. Passages are translated into English by the author. All participants’ names are pseudonyms. Participants were on average 28 (range 19-40), most had high school (n=15) or college (n=6) degrees, and were employed (n=23) in the service and construction sectors. Most were born in Mexico (n=20) or in the US of Mexican descent (n=2). One was born in Nicaragua and another in Vietnam. Most were HIV negative (n=20), and of those, 4 were taking PrEP. 33 Centers for Disease Control and Prevention (CDC). 2018. “Pre-Exposure Prophylaxis (PrEP)” accessed July 1, 2018, https://www.cdc.gov/hiv/risk/prep/ index.html; and Robert M Grant, Javier R. Lama, Peter L. Anderson, Vanessa McMahan, Albert Y. Liu, LorenaVargas et al. 2010, “Pre-exposure Chemoprophylaxis

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prescribed to supplement condom use as an extra layer of protection to HIVnegative individuals in serodiscordant intimate relationships or that have multiple sex partners of unknown serostatus. Recent research shows, however, that many MSM on PrEP are not using condoms during sex.34 Ever since it was commercialized as the brand name Truvada in 2012, PrEP has been at the center of heated debates on the relative significance of biomedical versus behavioral and social dimensions of HIV prevention. It exemplifies the tension in prevention research between efficacy (clinical trial “pure” conditions) and effectiveness (the “real world” conditions under which biomedical interventions can actually reduce HIV). From a sociological perspective, no single mechanism can ever explain efficacyeffectiveness relations across different populations given that any biomedical intervention is also a behavioral intervention—including issues of access, adherence, and symbolic interpretations—embedded in particular sociocultural contexts. Thus, while in some social contexts PrEP’s efficacy may translate into real-world effectiveness by sustained decreases of HIV infection. However, in other syndemic contexts, various social and behavioral mechanisms may undo its effectiveness, including prevention optimism, risk compensation (e.g., more sex partners, more sexual acts) due to less perceived risks, inconsistent adherence, increases in other STIs, or other structural mechanisms, such as stigma.35 for HIV Prevention in Men Who Have Sex with Men,” The New England Journal of Medicine 363, no. 27 (2010): 2587–99. 34 Yea-Hung Chen, Jonathan M. Snowden, Willi McFarland, and H. Fisher Raymond, “Pre-exposure Prophylaxis (PrEP) Use, Seroadaptation, and Sexual Behavior Among Men Who Have Sex with Men, San Francisco, 2004–2014.” AIDS and Behavior 20 (2016): 2791–97; and Martin Holt, Toby Lea, Limin Mao, Johann Kolstee, Iryna Zablotska, and Tim Duck et al., “Community-level Changes in Condom Use and Uptake of HIV Pre-exposure Prophylaxis by Gay and Bisexual Men in Melbourne and Sydney, Australia: Results of Repeated Behavioural Surveillance in 2013–2017,” Lancet HIV (forthcoming) https://doi.org/10.1016/S2352-3018(18)30072-9, accessed July 4, 2018, https://www.thelancet.com/journals/lanhiv/article/PIIS2352-3018(18)30072-9/ fulltext. 35Jared M. Baeten, and Robert Grant, “Use of Antiretrovirals for HIV Prevention: What Do We Know and What Don’t We Know?” Current HIV/AIDS Reports 10, no. 2 (2013): 142–51; James D. Campbell, Jeffrey H. Herbst, Robert T. Koppenhaver, and Dawn K. Smith, “Antiretroviral Prophylaxis for Sexual and Injection Drug Use Acquisition of HIV,” American Journal of Preventive Medicine 44, no. S1–S2 (2013): S63–S69; Martin Holt, and Dean A. Murphy, “Individual Versus Community-Level Risk Compensation Following Preexposure Prophylaxis of HIV,” American Journal of Public Health 107, no. 10 (2017): 1568–71; Linda J. Koenig, Cynthia Lyles, and Dawn K. Smith, “Adherence to Antiretroviral

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Moreover, PrEP is also part of the concept of pharmaceutical citizenship defined as the “biomedical promise of demarginalization.”36 Together with treatment as prevention (TasP) strategies among HIV-positive individuals37 PrEP can also be “framed as having the power to remove marginality and empower stigmatized and disadvantaged people to re-enter society and regain their full citizenship status.”38 In fact, PrEP bridges dimensions of pharmaceutical and sexual citizenship, enabling HIV-negative individuals to regain control of their sexuality without fear of infection. In this context, some current debates—what has been called the “PrEP wars”—are not too different from debates beginning in the mid-twentieth century over birth control for women. These debates involved issues of cost, safety, health risks associated with long term use, and licentious impacts on sexual behavior. The latter often is driven by moralities that traditionally perceive non-reproductive sexual pleasure as taboo, sinful, or self-destructive.39 It is in the context of these debates that I find among a sample of young Latino gay men that the meanings many attach to PrEP are part of broader sociocultural dynamics of sexual and HIV stigma. Most focus group participants were quite knowledgeable of these new biomedical interventions and concurred that safe sex definitions—traditionally about consistent condom use for anal sex—have changed considerably since the advent of Medications for HIV Pre-Exposure Prophylaxis: Lessons Learned from Trials and Treatment Studies,” American Journal of Preventive Medicine 44, no. S1–S2 (2013): S91–S98; and Eric T. Roberts and Derrick D. Matthews, “HIV and Chemoprophylaxis, the Importance of Considering Social Structures alongside Biomedical and Behavioral Intervention,” Social Science and Medicine 75 (2012):1555–61. 36 Stefan Ecks, “Pharmaceutical Citizenship: Antidepressant Marketing and the Promise of Demarginalization in India,” Anthropology & Medicine 12, no. 3 (2015): 239–54. 37Treatment as prevention (TasP) involves HIV-positive individuals taking antiretroviral medication as soon as possible after HIV diagnosis to reduce their HIV viral load in blood to undetectable levels. This strategy prevents HIV transmission to others. 38 Asha Persson, “‘The World Has Changed’: Pharmaceutical Citizenship and the Reimagining of Serodiscordant Sexuality among Couples with Mixed HIV Status in Australia,” Sociology of Health and Illness 28, no. 3 (2016): 381. 39 Judith D. Auerbach and Trevor A. Hoppe, “Beyond ‘Getting Drugs into Bodies’: Social Science Perspectives on Pre-Exposure Prophylaxis for HIV,” supplement, Journal of the International AIDS Society 18, no. S3 (2015): S1–S5; Julie E. Myers and Kent A. Sepkowitz, “A Pill for HIV Prevention: Déjà Vu All Over Again?” Clinical Infectious Diseases 56, no. 11 (2013): 1604–12; and Kane Race, “Reluctant Objects: Sexual Pleasure as a Problem for HIV Biomedical Prevention,” GLQ: A Journal of Lesbian and Gay Studies 22, no. 1 (2015): 1–31.

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PrEP and TasP. Many participants across groups discussed that—though HIV stigma was still pervasive—biomedical interventions had to some degree brought HIV-positive and HIV-negative men closer together. At least they had reduced reluctance to date or fall in love with an HIV-positive man. For many participants, PrEP had been a positive addition to their prevention toolkit since it allowed having sex without HIV infection worries. For instance, Juan, a 29-year-old Latino man, who was taking PrEP illustrates this empowering effect at the intersection of pharmacological and sexual citizenship: For me, PrEP was a liberation, that is, [on PrEP] sex is much safer, you lose fear, you can explore your own sexuality because you know that if you are taking it … or the other person is taking the way it’s supposed to … it’s a liberation.

However, the expression “double-edged sword” and related dualities came up frequently in discussions of PrEP. Many participants felt that PrEP was, on the one hand, empowering, but on the other, it also brought negative consequences, including more STIs and more sex with multiple partners. Thus, Jorge, a 29-year-old Latino man indicates, “PrEP is one of the best inventions of late in terms of HIV protection, but I believe people are letting their guard down regarding fighting other diseases—because many people are not using condoms.” In this light, a common theme across all focus groups was the notion that PrEP was a “perfect excuse to have sex without [condom] protection.” Related to this was the widespread finding that someone taking PrEP was perceived as engaging in promiscuous casual sex, often stigmatized for that reason by his peers. This is captured by the emic tropes puta [whore] and putear [to whore around] expressed in this exchange between two young Latino participants in their 20s: 40 Gonzalo: Some people have asked [my friend]: Why do you want to go on PrEP if you only want to be with your [HIV negative] partner? … automatically they call him puta … [they think] he wants to sleep around … There are people who prefer not to disclose publicly they are on PrEP because others may think he is a puta. Jorge: Nowadays a synonym of PrEP is that you want to putear … so that you want to andar de puta [sleep around] without the risks. So now, the definition of PrEP is mostly puta.

40

Interestingly the equivalent English derogatory expression “Truvada whore” that circulates in Anglo American gay circles was only known by a few participants. Most had just heard the expressions puta and putear in Spanish.

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Other emic expressions linking PrEP to promiscuous sex that participants across groups mentioned—and had heard friends or acquaintances use— were: andar de pito suelto [to walk around with your penis loose] or andar de cabrones [to walk around looking for sex/out on the prowl]. In short, PrEP with all its empowering value brought also much negative stigmatizing to users because of its sexualized assumptions. As Rodrigo, a 27-year-old Latino man put it and others in the group agreed, “The person on PrEP is always accused of being very promiscuous.” Using a pharmacological analogy, in this case, related to mental health stigma, one participant insightfully framed this empowering/stigmatizing duality by comparing PrEP to Prozac: If you are taking Prozac, there are so many assumptions for Prozac too. So it is a good thing you are taking Prozac, but it also can be perceived as a bad thing that you are taking Prozac. It is the same thing with PrEP.

This stigmatizing labeling has serious implications for HIV prevention because men on PrEP can feel reluctant to disclose to others that they are taking it. Those who are indecisive about getting on PrEP may also feel reluctant to request it. When asked what may prevent men from taking PrEP, besides access and lack of medical insurance, Pedro, a 30-year-old Latino man, said that “simply that if you see so much negativity [then] one is guided by what people say […].” He further explained that this was especially the case if the people creating such negativity were also very influential in the community or in social media platforms such as Facebook and online videos. Other participants mentioned that gossip about who is on PrEP circulates in the night scene and clubs as well, especially when someone is seen interacting with HIV prevention outreach workers outside the clubs. Some participants explicitly indicated they were careful not to disclose they were taking PrEP among certain friends or to post it on Facebook: “I believe that [disclosing] among [close] friends perhaps yes, but no, one has to be also careful about who you tell, so to not be burdened by their stigma.” In this connection, Hernán, a 28-year-old Latino man who is part of a health promotion activist group, captures well these stigma challenges circulating in the Latino gay community. In his own words: Honestly, in our ambiente [scene], our gay world is very cruel … it is one of the cruelest worlds that can exist because there is a lot of jealousy … lots of discrimination against ourselves. There is quite a bit of mala lengua [bad mouthing/gossip] in that people [think that] if they see you at a clinic taking a test, it’s because you are already HIV positive. So you can’t just go and request information in any place … Not long ago we launched a PrEP

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campaign via Facebook. We, as a group, received responses by gay men from the outside, people we knew … comments that were very ugly and harsh. But we didn’t care, because what we want is to educate the Latino community, not just gay men … to [educate] all those people who can be reached by our message.

When I asked Hernán whether they knew who had made those comments, he responded: Yes, we knew where they were coming from … [The comments] would ask how it was possible that we were promoting PrEP when all of them [gay men] were such putas. Then we replied that one thing has nothing to do with the other. If you are puta and you are on PrEP, it’s because you take care of yourself, but if you are puta and have no information, that’s because you are an ignorant who doesn’t love and take care of yourself … So I posted something back that said: ‘people who love and take care of themselves, who respect themselves, need not be a saint.’ No one is saintly here … in the gay world, some of us are cabroncitos [always on the prowl], but just because you are on PrEP it doesn’t mean that you are of the worst kind, it means that you love and take care of yourself.

These findings are significant because they show that biomedical interventions—such as PrEP—do not fall in a cultural vacuum but become embedded in meaning systems with potential HIV implications.41 We know that in the course of prevention and treatment interventions, community stigma and secrecy have detrimental consequences with regard to motivations for consistent adherence and regular access. In the case of this vulnerable population of young Latino gay men, sexual stigma itself circulates and is internalized in ways that can be counterproductive to PrEP’s effectiveness. The syndemic implication of this analysis brings contextual complexity to the biomedicalization of HIV prevention by shedding light on the fragile translation mechanisms that can exist between clinical efficacy and real-world effectiveness. To date, the epidemiological

41 Patrick D Herron, “Ethical Implications of Social Stigma Associated with the Promotion and Use of Pre-Exposure Prophylaxis for HIV Prevention,” LGBT Health 3, no. 2 (2016): 103–108; Katrina Kubicek, Cesar Arauz-Cuadra, and Michele D. Kipke, “Attitudes and Perceptions of Biomedical HIV Prevention Methods: Voices from Young Men Who Have Sex with Men,” Archives of Sexual Behavior 44 (2015): 487–97; Matt G Mutchler, Bryce McDavitt, Mansur A. Ghani, Kelsey Nogg, Terrell J.A. Winder, and Juliana K. Soto, “Getting PrEPared for HIV Prevention Navigation: Young Black Gay Men Talk about HIV Prevention in the Biomedical Era,” AIDS Patient Care and STDs 29, no. 9 (2015): 490–502.

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consequences of the biomedicalization of HIV prevention via PrEP and TasP remain uncertain.42

Conclusion Based on rich qualitative data, in this essay I have shown how three different systems of meaning in context—silence during sex as serosorting trust, same-sex practice as liminal space, and PrEP as promiscuous sex— can have significant implications for HIV transmission among a diverse Latino MSM population. First, among recent Mexican gay and bisexual immigrant men, HIV can be transmitted when there is miscommunication about the meaning of silence and trust surrounding HIV disclosure during sex. For some recent immigrant men, silence during sex may signal that their sex partner can be trusted to disclose if he is HIV positive. For local gay men in sexualized spaces, silence during sex signals the opposite, that is, the individual responsibility of a contractual sexual arena regarding HIV self-protection. Second, among Latino behaviorally bisexual men, HIV can be transmitted when they enter liminal spaces with other men to have transgressive sex that feels less normatively regulated and involves fewer interactional, resource, and moral ritual demands. This sexual context renders liminal spaces highly productive of pleasure but also less reflexive and cognitive about HIV protection. Finally, among young Latino gay men, HIV transmission may not be effectively prevented if these men become reluctant to access, openly disclose among peers, or consistently take a biomedical intervention such as PrEP because it has become symbolically associated with promiscuous sexualities in the community. It is worth emphasizing that each one of these meaning systems—trust, liminality, and promiscuity—can be theorized from a syndemics framework to be the “on-the-ground” performative expression of stigma as a social determinant of disease—including sexual and HIV-related stigma. In this light, these meaning systems and interpretations should be seen as constituting the various micro and meso-level pathways and mechanisms through which stigma as a fundamental cause of disease becomes actualized and drives HIV. Thus, “silence signaling trust” becomes a mechanism of HIV transmission when it articulates with long-standing sexual and HIV stigma against HIV-positive gay men who avoid and resist such compounded stigma through the discourse of individual responsibility. “Same-sex practices as liminal space” can become another mechanism of 42

Vinh-Kim Nguyen, Nathalie Bajos, Françoise Dubois-Arber, Jeffrey O’Malley, and Catherine M. Pirkle, “Remedicalizing an Epidemic: From HIV Treatment as Prevention to HIV Treatment is Prevention,” AIDS 25 (2011): 291–93.

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HIV transmission because of its embeddedness in unstable categories of bisexual desires that resist cognitive framings and are strongly stigmatized in modern binary constructions of sexuality. Same-sex desires among these bisexual men act as transgressive semiotic counterpoints to heavy regulatory discourses of heterosexual sex. “PrEP as promiscuous sex” may become part of a mechanism that undermines biomedical effectiveness if it becomes entrenched in interpretations ultimately rooted in traditional belief systems that stigmatize homoerotic desires and non-reproductive sex as sinful and self-destructive. In short, all of these meaning systems point to larger societal processes of sexual and disease stigma at work. In this post-ART era, HIV is increasingly considered a chronic and manageable disease. As a result, people may show less commitment to safe sex than in the early decades of the epidemic. Following recent trends to remedicalize HIV prevention via biomedical interventions (PrEP, TasP), some may even think that we have finally found the “magic bullet” against HIV.43 However, it is worth noting that even among MSM living with diagnosed HIV, only 61% achieve viral suppression.44 This fact alone reveals deep-rooted structural barriers to care and treatment in the US. Moreover, among those who take ART even in affluent populations, studies find that on average only 62% of people take their medication as prescribed.45 Thus biomedical prevention strategies by themselves—which let us not forget are behavioral strategies as well—are unlikely to offer more than partial effectiveness. The reality is that HIV/AIDS continues to expand among vulnerable populations around the world. In this light, we should never lose sight that HIV/AIDS is an insidiously complex syndemic that thrives on the fault lines of social stigma and inequality. It does this through multiple emerging levels and nonlinear interactions. Prevention strategies must target such complexity at all levels to be effective—biomedical, behavioral, cultural, structural. In this essay, I have shown that a crucial point of entry to tackle such complexity is ethnographic and qualitative knowledge of the contextual meanings of vulnerable populations and how meanings shape risky behaviors. The lessons learned are that a “one-model-fits-all” approach 43

Nguyen et al., “Remedicalizing an Epidemic,” 291–93. Centers for Disease Control and Prevention (CDC). 2017d. “HIV Care Outcomes among Men Who Have Sex with Men with Diagnosed HIV Infection—United States 2015,” Accessed July 1, 2018. (https://www.cdc.gov/mmwr/volumes/66/wr/mm6637a2.htm?s_cid=mm6637a2_e. 45 Carmen Ortego, Tania B. Huedo-Medina, Javier Llorca, et al. “Adherence to Highly Active Antiretroviral Therapy (HAART): A Meta-analysis.” AIDS and Behavior 15 (2011): 1381–96. 44

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will have limited success in addressing the HIV prevention and care needs of a diverse group of Latino gay and bisexual men.

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Sengupta, Sohini, Bahby Banks, Dan Jonas, Margaret S. Miles, and Giselle C. Smith. “HIV Interventions to Reduce HIV/AIDS Stigma: A Systematic Review.” AIDS and Behavior 15 (2011): 1075–87. Singer, Merrill. Introduction to Syndemics: A Critical Systems Approach to Public and Community Health. San Francisco: Jossey-Bass 2009. Singer, Merrill, Nicola Bulled, Bayla Ostrach, and Emily Mendenhall. “Syndemics and the Biosocial Concept of Health.” Lancet 389 (2017): 941–50. Singer, Merrill and Scott Clair. “Syndemics and Public Health: Reconceptualizing Disease in Bio-Social Context.” Medical Anthropology Quarterly 17, no. 4 (2003): 423–41. Stall, Ron, Mark Friedman, and Joseph A. Catania. “Interacting Epidemics and Gay Men's Health: A Theory of Syndemic Production among Urban Gay Men.” In Unequal Opportunity: Health Disparities Affecting Gay and Bisexual Men in the United States, Edited by R. J. Wolitski, R. Stall, and R. O. Valdiserri, 251–74. New York: Oxford University Press, 2007. Stall, Ron, Thomas C. Mills, John Williamson, Trevor Hart, Greg Greenwood, Jay Paul, Lance Pollack, Diane Binson, Dennis Osmond, and Joseph A. Catania. 2003. “Association of Co-occurring Psychosocial Health Problems and Increased Vulnerability to HIV/AIDS among Urban Men Who Have Sex with Men.” American Journal of Public Health 93, no. 6 (2003): 939–42. Tsai, Alexander C. “Syndemics: A Theory in Search of Data or Data in Search of a Theory?” Social Science and Medicine 206 (2018): 117–22. UNAIDS. 2010. “Combination HIV Prevention: Tailoring and Coordinating Biomedical, Behavioural and Structural Strategies to Reduce New HIV Infections.” Accessed July 1, 2018. http://www.unaids.org/en/resources/documents/2010/20101006_JC200 7_Combination_Prevention_paper. UNAIDS. 2017. “Fact Sheet–Latest Global and Regional Statistics on the Status of the AIDS Epidemic.” Accessed July 1, 2018. http://www.unaids.org/en/resources/documents/2017/UNAIDS_FactSh eet. Wolitski, Richard J. and Caroline J. Bailey. “It Takes Two to Tango: HIVPositive Gay and Bisexual Men’s Beliefs about Their Responsibility to Protect Others from HIV Infection. In HIV+ Sex: The Psychological and Interpersonal Dynamics of HIV Seropositive Gay and Bisexual Men’s Relationships, Edited by P. N. Halkitis, C. Gómez, and R. Wolitski 147– 162. Washington, DC: American Psychological Association, 2005.

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Young, Rebecca M. and Ilan H. Meyer. “The Trouble with ‘MSM’ and ‘WSW’: Erasure of the Sexual-Minority Person in Public Health Discourse.” American Journal of Public Health 95, no. 7 (2005): 1144– 49.

CHAPTER SIX A PICTURE IS WORTH A 1000 LIVED EXPERIENCES OF ILLNESS: PHOTOVOICE AS AN EMANCIPATORY APPROACH TO PUBLIC HEALTH AND HIV RESEARCH MICHELLE TETI AND AMY SLATON

HIV/AIDS persists as a public health problem in the United States (US) and globally despite medical advances in testing and treatment over the course of the last 30 years.1 HIV testing enables people to learn that they have the virus and seek medical care. Effective Pre-exposure Prophylaxis (PrEP) to prevent HIV, as well as effective Antiretroviral Therapy (ART) to contain and slow the progression of the virus, are available and have the potential to medically reframe HIV from an acute and life-threatening disease to a chronic and manageable illness.2 Yet, 14% of those infected with HIV are unaware they are infected,3 uptake of PrEP has been slow, and around half of the people living with HIV are not accessing care and/or sustaining treatment at adequate levels to protect their own health or limit HIV transmission to others.4 Closer to the onset of the HIV epidemic in the US, Jonathan Mann, an HIV World Health Organization leader, stated, “vulnerability to HIV 1

Centers for Disease Control and Prevention, CDC, “HIV/AIDS in the United States,” https://www.cdc.gov/hiv/statistics/overview/ataglance.html. 2 Centers for Disease Control and Prevention, CDC, “Pre-Exposure Prophylaxis (PrEP),” https://www.cdc.gov/hiv/risk/prep/index.html.; and “HIV Treatment,” https://www.cdc.gov/actagainstaids/campaigns/hivtreatmentworks/stayincare/treat ment.html. 3 Centers for Disease Control and Prevention, CDC, “Estimated HIV Incidence and Prevalence in the United States, 2010–2015,” https://www.cdc.gov/hiv/pdf/library/ reports/surveillance/cdc-hiv-surveillance-supplemental-report-vol-23-1.pdf. 4 Ibid.

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reflects the extent to which people are, or are not, capable of making free and informed decisions about their health.”5 He went on to predict that those who face societal marginalization, discrimination, and stigma would consistently face the most significant HIV burden. As predicted, in 2020, HIV affects socially vulnerable populations, like racial and ethnic minorities, the poor, and men who have sex with men, at crisis levels.6 As a result, the US National HIV/AIDS Strategy outlines AIDS-related public health goals such as reducing new HIV infections, increasing access to HIV care and treatment, and reducing health disparities. Scholars and researchers from a diverse set of disciplines study and raise solutions to eradicate HIV/AIDS. The public health approach to HIV/AIDS is the focal point of this chapter. Considering the disappointing impacts of strategies to eradicate HIV, particularly among marginalized populations, we reflect in this chapter on the methods and metrics that public health scholars use to understand HIV/AIDS. We propose that existing approaches to generate HIV/AIDS solutions can inadvertently sustain the marginality of people with HIV and reinforce the social structures (racism, sexism, and poverty) that allow HIV to thrive. In particular, we propose that the way that we define the problem of and effective solutions for HIV/AIDS is essential to addressing HIV/AIDS and its harm to socially vulnerable populations. We aim to show how less conventional ideas about what constitutes valuable knowledge about HIV/AIDS and who defines it can augment the intended emancipatory power of public health. To demonstrate our argument, we will first describe the emancipatory intent of the discipline of public health. Then we will address how, despite good intentions, public health scholars and programs fall short of such emancipation. This results from their inability to engage in reflexivity about or act on, the positionality, expertise, and power of “best practice” methods and models. We consider such reflexivity to be an epistemic commitment that is necessary, if not sufficient, for the address of powerful structural forces like racism, or subsequent entrenched disciplinary traditions (which are influenced by such structural forces). Next, we will describe what is at stake if we value only narrow forms of HIV knowledge, such as that emerging from familiar medical and health sectors. As a counter to conventional forms of knowledge circulating in public health research, we will introduce the concept of community-based participatory research 5

Jonathan M. Mann, “Human Rights and Aids: The Future of the Pandemic,” in Health and Human Rights, A Reader, ed. Jonathan M. Mann, S. Gruskin, M. A. Grodin, and G. J. Annas (New York: Routledge, 1999). 6 CDC, “Estimated HIV Incidence.”

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(CBPR) and one CBPR method, in particular, Photovoice. Using examples from Dr. Teti’s research, we will provide cases in which Photovoice serves to prioritize an alternate form of HIV knowledge and expertise, and what we can learn from this knowledge. Finally, we will discuss the implications of our observations, including how to use them to support the well-being of people with HIV and limit its transmission.

Public Health and Emancipation As a discipline, public health is committed to promoting and protecting the health of people and communities.7 Public health is prospective and focuses on disease prevention and health promotion. A focus on the collective good and the link between health and basic rights (over individual wants and needs) ground the discipline in an emancipatory and social justice (versus a market justice) orientation.8 Similarly, a Social Determinants of Health approach guides the work of public health actors. This approach purports that people’s health is a product of the conditions in which they live, grow, and work; that political, social, and economic forces shape these conditions; and that the attainment of basic needs and rights are necessary for people to be healthy amid these conditions.9 Health promotion, theoretically, is a process of enabling people to increase control over their circumstances, which can improve their health. To achieve a state of wellness, health promotion researchers and practitioners agree, people need to be able to cope with and/or address the social determinants of health.10 Public health, then, is widely agreed to be a tool for health equity and social justice.11 Despite this emancipatory rhetoric, however, sometimes public health actors are not able to follow through on their social justice intent in health promotion interventions. Conventional epistemic commitments of public health, such as the traditional epidemiologic models of studying behavior, enable researchers to position communities and offer associated solutions 7

American Public Health Association, APHA, “What Is Public Health?” https://www.apha.org/what-is-public-health. 8 Mary Jane Schneider, Introduction to Public Health (Burlington, MA: Jones and Bartlett Learning, 2017). 9 World Health Organization, WHO, “About Social Determinants of Health,” http://www.who.int/social_determinants/sdh_definition/en/. 10 World Health Organization, WHO, “The Ottawa Charter for Health Promotion,” Adopted November 21, 1986, http://www.who.int/healthpromotion/conferences/ previous/ottawa/en/. 11 WHO, “About Social Determinants.”

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that can constrain emancipation.12 Such commitments follow long-standing traditions of medicine and research. Adhering to existing (i.e., status-quo) traditions and models can discourage researchers’ reflections about power and privilege that enact particular expectations and standards regarding public health practice. Overt statements of ideology or political strategy are well understood by many people to express ideas about social power and privilege, of more or less socially transformative character, but these ideas can also be expressed in elements of research design or in notions of rigorous science. For example, the public health approach to solving problems customarily includes a five-step process of using epidemiology—or the science of public health.13 The five steps are (1) define the problem; (2) identify the risk factors; (3) develop and test interventions to address the problem; (4) implement the interventions; and (5) evaluate the interventions. Thus, public health solutions arise from research findings and are evidencebased.14 The most rigorous and thus, “valuable,” evidence, or the evidence that drives solutions, results from specific forms of privileged science (e.g., randomized controlled trials) and scientific outcomes (e.g., statistically significant quantitative findings of difference between intervention options).15 The challenge with this way of defining valuable evidence, however, is that the factors that allow people to achieve control over their circumstances (i.e., health promotion) cannot always be measured by a trial or in numerical terms. This approach to research may obscure significant social patterns of disease occurrence. Epidemiologists acknowledge that there are multiple risk factors for illness, modeled by a “web of causation.”16 Theoretically, the web is in line with the Social Determinants of Health approach, acknowledging that illnesses have many drivers. Nancy Krieger posits, the shift from the individual to the web paradigm is still heavily tied to an individual model of disease understanding, even though the web theoretically supports a complex array of disease contributors.17 For example, public health scholars 12 Robin Bunton and Jane Wills. “25 Years of Critical Public Health.” Critical Public

Health 14, no. 2 (2004): 79–80. 13 Schneider, Introduction to Public Health. 14 Ibid. 15 Department of Health and Human Services, “Evidence-Based Clinical and Public Health: Generating and Applying the Evidence,” https:// www.healthypeople.gov/sites/default/files/EvidenceBasedClinicalPH2010.pdf. 16 Nancy N. Krieger, “Epidemiology and the Web of Causation: Has Anyone Seen the Spider?” [In eng]. Social Science Medicine 39, no. 7 (Oct 1994): 887–903. 17 Ibid.

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rarely question how factors become part of the web and as a result, the web tests selective and predetermined risk factors. The social aspects of health (e.g., poverty, discrimination) are very clearly presented by leading public health doctrines as driving forces of illness. Yet, they are much more difficult to study in randomized trials and capture via statistically significant results (e.g., the gold standard for evidence-based outcomes) than are lifestyle or biological factors. Thus, they are often ironically left behind by the public health approach to solving problems, despite public health’s social determinants mission.18 As a result, our public health interventions and solutions focus mainly on individual action while calls for attention to the social determinants of health remain unanswered. Krieger concludes that: “The field of epidemiology today suffers from the absence of not only a clearly articulated and comprehensive epidemiologic theory [that drives decision making about interventions], but it seems, even the awareness that it lacks such a theory.”19 We contend, then, that social normativities pervade public health research methods and findings and that it cannot be otherwise; only those views of nature (that is, of disease, of organisms, or of any other objects of scientific attention) that conform to researchers’ social understandings will be legible to researchers. These may be understandings that conform to socially conservative outlooks, such as the notion that people who classify as obese are responsible for their illness. These may also be socially liberal outlooks that are simply unable to grasp the needs and priorities of vulnerable people. People with a specific illness condition, such as people with intellectual disabilities, for example, are a labeled group. Many social meanings about them exist and are ingrained in our way of thinking about them.20 These meanings and assumptions make it hard to know the backgrounds of others without further exploration of lived experiences. The problem with not questioning our outlooks, or the origins of our research inquiries and methods themselves, is that the answers to those questions can reveal important points of opportunity to reframe issues from different perspectives. Such perspectives are likely to emerge when researchers systematically seek to understand the experiences of those outside familiar expert circles. This method can ultimately improve the reach and impact of our public health programming to address the social determinants that researchers and practitioners agree are causing harm. It is from such a 18

Ibid. Ibid. 20 Ashley Taylor, “Knowledge Citizens? Intellectual Disability and the Production of Social Meanings within Educational Research,” Harvard Educational Review 88, no. 1 (2018): 1–25 19

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reconfiguration that social change, such as improved public health, may derive.

AIDS as a Biological, Social, Political, and Cultural Illness If we aim to consider seriously the experiences of the subjects of public health interventions in formulating PH research, the example of HIV/AIDS can be instructive. People living with HIV/AIDS (PLWH) have long framed themselves as experts and demanded a place at the table regarding HIV prevention and care. HIV/AIDS as a topic of public health and medical research comprises a wide array of social determinants, and PLWH has made clear that medical and public health expertise elide many such determinants. Their activities highlight the socially contingent character of science and ways that “non-scientists” may reframe both the aims of science and what will count as rigor. ACT UP protestors have questioned the worth of HIV science and the expertise of scientists since the beginning of the epidemic, with calls such as “We are here to show defiance for what Harvard calls science” and “Is the pursuit of elegant science leading to the destruction of our community?”21 Seeking access to developing drugs and greater resources for research on AIDS, protestors made clear that prevailing science on the illness was limited by social and political context. As Fee and Krieger state, “AIDS is at once a social and biological disorder; its course cannot be understood or altered without attention to its social and political context.”22 HIV/AIDS is transmitted predominantly via (homosexual) sex and drug use–actions that are subject to moral, philosophical, and religious judgment; and that are socially enacted. When scientists first reported AIDS cases, the illness was recognized to be both mysterious and deadly. AIDS evoked, and continues to evoke fear, even as scientific knowledge and treatments have developed significantly in recent years. What is more, it affected and continues to affect the sub-groups of the US population subjected to stigma and discrimination prior to HIV.23 If current rates persist, for example, the Center for Disease Control and Prevention (CDC) projects that approximately one in 20 Black men, one in 48 Black women, and one in two Black gay and bisexual men will receive 21

AIDS Coalition to Unleash Power, ACT UP, http://www.actupny.org/. Elizabeth Fee and Nancy Krieger. “Understanding Aids: Historical Interpretations and the Limits of Biomedical Individualism.” [In eng]. American Journal of Public Health 83, no. 10 (Oct 1993): 1477–86. 23 Paul Farmer, Aids and Accusation: Haiti and the Geography of Blame. (Los Angeles: University of California Press, 1992). 22

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a diagnosis of HIV during their lifetimes.24 The braiding of fear with preexisting forms of stigma has supported formulations of blame associated with HIV/AIDS. Given that HIV “risk groups” such as gay men and/or African Americans face preexisting discrimination, risk groups for HIV can easily become groups of people that others hold responsible for the existence or spread of the virus.25 ACT UP, by extreme contrast, sought to integrate “risk groups” into the scientific address of HIV/AIDS. In his exploration of the study of HIV, Epstein summarizes the diverse communities of people with interest in HIV solutions.26 Inside a large and often floodlit arena with a diffuse and porous perimeter, an eclectic assortment of actors has sought to assert and assess credible knowledge about AIDS: biomedical researchers and healthcare professionals of different stripes; activists, advocacy groups, and people with AIDS or HIV infection; health educators and social scientists; politicians and public health officials; government agencies and advisory committees; pharmaceutical and biotechnology companies; writers, journalists and the institutions of the mainstream and alternative media. What we know about AIDS is the product of this elaborate, often heated, and sometimes peculiar complex of interactions.

Epstein stresses for us the varied interest groups that contribute to circulating knowledge regarding HIV/AIDS. We can follow the changing character of this knowledge as stakeholders—define and redefine its features, responding to one another’s delineations of HIV/AIDS rather than to a single, stable object of attention.

What Is at Stake? We in Public Health fields routinely develop initiatives, research programs, and subsequent interventions complete with assumptions and answers to problems that people living with HIV are not themselves posing solutions. When public health scholars and researchers try to “objectively know”27 HIV/AIDS and define unbiased HIV experts, we miss opportunities to 24 Centers for Disease Control and Prevention, CDC, “HIV/AIDS among African Americans,” Centers for Disease Control and Prevention, https://www.cdc.gov/ nchhstp/newsroom/docs/factsheets/cdc-hiv-aa-508.pdf. 25 Fee and Krieger, “Understanding Aids.” 1477–86. 26 Steven Epstein, Impure Science: Aids, Activism, and the Politics of Knowledge (Los Angeles: University of California Press, 1996). 27 Fee and Krieger, “Understanding Aids.” 1477–86.

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understand and address the social production and presentation of an illness, this illness. The multiple and complex social determinants of a public health challenge are hidden by narrowed presumptions of HIV as a singular, and singularly experienced, natural entity. For instance, current research initiatives are designed to improve the HIV Care Continuum, to improve specific testing, care, and treatment metrics. The United Nations 90-90-90 plan aims by 2020, for 90% of all people living with HIV to know their HIV status; 90% of all people with diagnosed HIV infection to receive sustained antiretroviral therapy; and 90% of all people receiving antiretroviral therapy to experience HIV viral suppression.28 The assumption here is that people want to and can increase testing, care, and treatment because, “logically,” we can address HIV with these tools. As Bourgois notes, however, when we follow the numbers (e.g., those that show we need to increase the HIV Care Continuum) we can miss the social conditions and power relations that shape, albeit invisibly, the numbers.29 For instance, Baggaley points out the 90-90-90 goal erases the complexity for the most vulnerable groups, like non-white injection drug users who lack multiple resources to connect to HIV testing and care.30 Likewise, although public health research indicates that condom use and/or medication adherence can prevent new cases of HIV,31 this kind of researcher logic often becomes illogical amid people’s daily lives. Sobo, for instance, found that among low-income, urban, African American women, their sexual decisions were not driven by their desires for safe sex. Instead, a desire to protect their self-esteem and self-protective narratives of monogamy and “healthy” intimate relationships drove their sexual decisions, which did not include condom use.32 Teti, Bowleg, and Lloyd33 28

UNAIDS, “90-90-90: An Ambitious Treatment Target to Help End the Aids Epidemic,”http://www.unaids.org/sites/default/files/media_asset/90-90-90_en.pdf.; and Philippe Bourgois, “The Mystery of Marijuana: Science and the U.S. War on Drugs,” Substance Use and Misuse 43, no. 3-4 (2008): 581–83. 29 Peter Bourgois, “The Moral Economies of Homeless Heroin Addicts: Confronting Ethnography, HIV Risk, and Everyday Violence in San Francisco Shooting Encampments,” Substance Use and Misuse 33, no. 11 (1998): 2323–51. 30 Rachel Baggaley, Shona Dalal, Cheryl Johnson, Virginia Macdonald, Ioannis Mameletzis, Michelle Rodolph, Carmen Figueroa, et al., “Beyond the 90-90-90: Refocusing HIV Prevention as Part of the Global HIV Response.” [In eng]. Journal of the International AIDS Society 19, no. 1 (2016): 21348. 31 CDC, “Estimated HIV Incidence.” 32 Elisa J. Sobo, Choosing Unsafe Sex (Philadelphia: University of Pennsylvania Press, 1995). 33 Michelle Teti, Lisa Bowleg, and Linda Lloyd. “‘Pain on Top of Pain, Hurtness on Top of Hurtness’: Social Discrimination, Psychological Well-Being, and Sexual

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found that HIV positive women prioritized their physical safety, which sometimes meant having (unsafe) sex for purposes of gaining shelter or avoiding physical violence. Teti, Koegler, and Enriquez (in review) found that low-income people of color with HIV who were not taking their lifesaving medicines reported an average of 27 major life barriers during a sixweek-period. Barriers included addiction, severe mental distress, grief, disability, eviction, car accidents, homelessness, and hunger. Taking their HIV medicine rarely appeared in their top 10 priorities. Others questioned the value of the medicine and reported challenges trusting the authority figures (e.g., physicians) prescribing the regimens. The lives and needs of people with HIV must be considered or we run the risk of delivering public health research-based messages that are, as Bourgois noted, “sanitary admonitions.” Such admonitions are ignored or serve to further lead PLWH to blame themselves for their condition.34

Community-Based Participatory Research If we want to facilitate empowerment (and ultimately improve wellbeing) among the recipients of public health interventions, we need to acknowledge that, as researchers, we hold power in multiple ways. We have the power to choose our methods, some of which, as the above examples illustrate, can obfuscate the experiences of those we study. Below we interrogate community-based participatory research (CBPR) as an approach that may help us generate solutions that are grounded in the lives of people with HIV. This participatory approach can reveal the complex social determinants of illness that position public health as a social justice discipline. CBPR is a partnership approach to research that prioritizes the input and guidance of the people whose lives are being studied and affected by the research outcomes. The aim of CBPR develops out of the interaction and mutual understanding between research and practice. Both sides benefit from the research process. Bergold and Thomas point out that CBPR “enables co-researchers to step back cognitively from familiar routines, forms of interaction, and power relationships in order to fundamentally question and rethink established interpretations of situations and

Risk among Women Living with HIV/AIDS.” Inernational Journal of Sexual Health 22, no. 4 (2010): 205–18. 34 Bourgois, “The Mystery of Marijuana,” 581–83.

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strategies.”35 Torre, Stoudt, Manoff, and Fine call participatory research a “bold innovation” in the production and ownership of critical inquiry by and for communities under siege. It is cooperative science, and “challenges the hegemony of elite interests as the dominant lens of science and insists on social inquiry theorized, practiced, and collectively owned by and for communities enduring state violence.”36 CBPR interrupts the ignorance that keeps us from acknowledging and really seeing social injustices. It also helps to build relationships and understanding by which we can challenge our ignorances versus ignoring them. Nine key principles guide CBPR. 1. CBPR promotes collaborative and equitable partnerships in all research phases and involves an empowering and power-sharing process. 2. CBPR recognizes the community as a unit of identity. 3. CBPR builds on strengths and resources within the community. 4. CBPR facilitates co-learning and capacity building among all partners. 5. CBPR for health focuses on problems of relevance to the local community using an ecological approach (e.g., someone's broader context) that attends to multiple determinants of health and disease. 6. CBPR balances research and action for the mutual benefit of all partners. 7. CBPR disseminates findings and knowledge gained to the broader community and involves all partners in the dissemination process. 8. CBPR promotes a long-term process and commitment to sustainability. 9. Involves systems development using a cyclical and iterative process. Chavez, Wallerstein, and Duran,37 explain CBPR as a dance between researchers and community members. This analogy captures the varied and 35 Jarg Bergold and Stefan Thomas, “Participatory Research Methods: A Methodological Approach in Motion,” Forum: Qualitative Social Research 13, no.1 (2012): Art. #30. 36 N. E. Torre, B. G. Stoudt, E. Manoff, and M. Fine., “Critical Participatory Action Research on State Violence: Bearing Wit(H)Ness across Faultlines of Power, Privilege, and Dispossession” in Sage Handbook of Qualitative Research 5e, ed. N. K. Denzin and S. L. Lincoln (London: Sage Publications, 2017). 37 Vivian Chavez, Bonnie Duran,. Quinton E. Baker, Magdalena M. Avila, and Nina Wallerstein. “The Dance of Race and Privilege in Community Based Participatory Research.” Chap. 4 in Community Based Participatory Research for Health, edited by N. Wallerstein and M. Minkler, ( San Francisco: Jossey Bass, 2003): 81–97.

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sometimes contradictory aspects of dancing as both awkward and exciting, free and controlled, or communicative and silent. It is, however, a partnership, where the knowledge and skills of both sides are important to the overall equation. Given that power imbalance is in the researchers’ favor, they often have to learn to value and listen to what community members have to say, for any hope that such an unbalanced situation produces authentic information. Although while community members are “experts” on their life situations, researchers are “experts” on the researcher process. The outcome is a project that merges both perspectives and contributions. Some traditional (non-CBPR) researchers view CBPR as more of a strategy for exploration than a valuable research method, critiquing CBPR as divorced from traditional evidence-based research guidelines. Those guidelines themselves, however, embody power relations. Stoudt, Fox, and Fine38 assert that CBPR “challenges the illusion of separate lives [of researchers and participants] by reconnecting empirically, politically, and emotionally the haves and have nots, in the praxis of science and in the objects and products of our research.” We agree with Stoudt, Fox, and Fine that this “radical rethinking of science” is a potential means to “interrupt injustice,” allowing researchers to create new justice-focused frames.

Photovoice Photovoice is a CBPR method that enables people to identify, share, and address their lived experiences through photography and discussions of their own photographs.39 Those organizing Photovoice interventions enable participants to take photographs and facilitate conversations among the photographers and between photographers and target audiences, including those who may provide new resources and services to participants. The use of Photovoice in public health originated with Wang and her colleagues’ efforts to understand the everyday health experiences of Chinese women through participant-generated images.40 Wang and colleagues described three goals of using Photovoice: to enable participants to record their community strengths, to promote critical dialogue and knowledge about 38 Brett G. Stoudt, Michelle Fine, and Madeline. Fox. “Contesting Privilege with Critical Participatory Action Research.” Journal of Social Issues 68, no. 1 (2012): 178–93. 39 Caroline Wang, “Photovoice: A Participatory Action Research Strategy Applied to Women's Health,” Journal of Women's Health 8, no. 2 (1999): 185–92. 40 Caroline Wang and Mary Ann Burris, “Empowerment through Photo Novella: Portraits of Participation,” Health Education Quarterly 2, no. 2 (1994): 171–186.

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personal and community issues through the discussion of images, and to reach policymakers via these images. The Photovoice method relies on the ability of an image to act as a concrete starting point for shared conversations and interpretations, draw attention, motivate dialogue, and present stories across diverse levels of participant language and literacy.41 Photovoice also allows participants’ ideas and values to drive the research process and findings. Liebenberg describes Photovoice as a way to honor the voices of participants alongside those of researchers.42 As researchers, do we not impose our perceived reality of the other right from the start of our research, in the questions we pose to participants? How do we raise the voices of our participants above our own from the beginning of the research process?

This “honoring” strikes us as constituting the reconnection that Stoudt, Fox, and Fine seek. The theoretical basis of Photovoice includes three related concepts: empowerment education for critical consciousness, feminist theory, and documentary photography. These foundations share common assumptions about the importance of participants’ voices.43 Photovoice empowers individuals to understand and critically discuss the contextual issues that affect their health and well-being by focusing on and portraying participants’ experiences. This approach of collecting knowledge that is grounded in experience enables participants to collectively communicate their shared concerns/needs/visions to each other and to those with the authority to allocate resources towards creating the needed change.44 From a feminist approach, Photovoice promotes the value of women’s and other unrepresented groups’ experiences. Photovoice fosters conditions in which underrepresented groups are able to influence action.45 Finally, in contrast to considerable documentary photography, Photovoice puts cameras in the hands of participants (not professional photographers) and trains them to capture and use their own experiences to gain insights about their lives and inform decision-making processes in their communities. When project participants record their lived experiences and tell their stories, they are “often imaginative and observant” in ways that provide more richness to the researcher’s data.46 41

Stoudt, et al., “Contesting Privilege,” 178–93; and Wang, “Photovoice,” 185–92. Linda Liebenberg, “The Visual Image as Discussion Point: Increasing Validity in Boundary Crossing Research.” Qualitative Health Research 9 (2009): 441–67. 43 Stoudt, et al., “Contesting Privilege,” 178–93. 44 Ibid. 45 Ibid.; and Wang, “Photovoice,” 185–92. 46 Wang, “Empowerment Through Photo Novella,” 177. 42

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Original Photovoice methods (via Wang and colleagues) included a set of procedures to gather data and translate research findings into action and practice. As a first step, projects included the identification of both a target audience–—who could help put participants’ ideas into action—and a group of interested photo-takers. Participants would then undergo a camera tutorial, a photo-ethics training, and an introduction to the Photovoice method. A cycle of photo taking, discussion, and sharing followed. Discussions were guided by the “SHOWeD technique”: What do you See here? What is really Happening here? How does this relate to Our Lives? Why does the situation or concern exist? What can we Do about it? The facilitators and participants then worked together to share their photos and stories with policymakers via slide shows or exhibits. These exhibits can educate communities and inform new practices or policies. Participants, with rewritten narratives about their lives with HIV, can gain advocacy skills and networks.47 As a CBPR method, Photovoice procedures are aligned with the collaborative goals of CBPR. For instance, participants help drive the research questions and findings by taking photos that constitute the core of the project. Thus, Photovoice participants can generate new questions and answers to health problems.48 Researchers learn in-depth information about the issues presented, and participants acquire photography skills and learn from sharing strategies with one another. Given power and control over the research questions and answers, participants are also more inclined to share their assets and solutions and not simply their challenges or barriers.49 Photographs and the subsequent shared discussions about solutions for issues presented in the photographs can lead to immediate change and action. Dissemination via photo exhibits can allow the findings to reach diverse audiences.50 CBPR approaches overall encourage researchers to formulate questions, choose methods, and identify significant findings in a more collaborative and open-ended manner than many other investigative methods, each step informing the others. Photovoice is such a research technique, deriving from a justice-oriented researcher perspective, effectively decentering the researcher’s experiences and any pre-existing research questions to allow consideration of participant perspectives. 47

Wang, “Photovoice,” 185–92. Wang, “Empowerment through Photo Novella,” 171–86. 49 Michelle Teti, Latrice Pinchon, Allison Kabel, Rose Farnan, and Diane Binson, “Taking Pictures to Take Control: Photovoice as a Tool to Facilitate Empowerment among Poor and Racial/Ethnic Minority Women with HIV,” Journal of the Association of Nurses in AIDS Care 24, no. 6 (2013): 539–53. 50 Stoudt, et al., “Contesting Privilege,” 178–93; and Wang, “Photovoice,” 185–92. 48

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Case Examples from Picturing New Possibilities with Women with HIV/AIDS With the aim of establishing solidarity with PLWH, Dr. Teti incorporated Photovoice in the design of research on women’s health and intervention needs. Her choice to do so arose from her experience leading public health interventions in which participant’s perspectives were not merely set aside, but actively obscured by public health project goals. Dr. Teti’s use of qualitative methods had previously brought unexpected data to the fore: Bringing diverse experiences to researchers’ attention. Photovoice as a creative, visual activity opened the range of participant expressions still further, encouraging affective and aesthetic self-expression. These formed the basis for what we believe is a particularly indeterminate and cooperative form of public health engagement. Dr. Teti had led a public health intervention for women with HIV that was intended to help women practice safer sex and disclose their HIV status to their sexual partners, in an effort to decrease HIV transmission.51 The group-level intervention introduced concepts of safe sex and healthy relationships and focused on giving women the skills to use and negotiate condoms and talk about their HIV status with others. During the intervention groups, however, the women expressed the challenges of these particular goals. Despite the researchers and interventionists’ best intentions, the intervention was demeaning. Women understood the importance of safer sex and disclosure, and understood how to use condoms and talk to others, but faced significant life barriers to accomplishing these goals. Challenges included a range of difficulties that took away women’s control over their lives and health decisions, such as poverty, violence, and homelessness. The challenges also rendered HIV as low on their survival priority list. These findings were not isolated to Dr. Teti’s work. Several other critical HIV scholars’ also pointed out that interventions were not necessarily in line with women’s daily life experiences and could be causing more harm (by demeaning women, etc.) than good.52 These conversations marked the beginning of what would become a Photovoice project, “Picturing New Possibilities.” Instead of learning how 51 Teti, Michelle, Lisa Bowleg, Russell Cole, Linda Lloyd, Susan Rubinstein, Susan Spencer, Erika Aaron, et al. “A Mixed Methods Evaluation of the Effect of the Protect and Respect Intervention on the Condom Use and Disclosure Practices of Women Living with HIV/AIDS.” [In eng]. AIDS and Behavior 14, no. 3 (2010): 567–79. 52 Bourgois, “Moral Economies,” 2323–51.

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to use condoms, women with HIV indicated that they wanted opportunities to talk about their lives and tell their stories of HIV. In doing so, they wanted to share strategies about their health challenges. In other words, they wanted strategies to emerge naturally as they supported each other with examples from their own lives, rather than being offered solutions (e.g., use condoms, disclose their HIV status) to problems that they were not even identifying. Photovoice did not fill in details to experts’ definitions of health or risk, but opened up unfamiliar outcomes: The women’s valuations of health provided new ways of understanding their lives and needed solutions that were previously hidden. Dr. Teti decided to use Photovoice to meet these requests (e.g., a space for conversation) and to learn more about 30 women’s health and intervention needs. The majority of the women were poor. Over half (n=18) of the women reported earning less than $10,000 a year, five women reported earning between $10,001–20,000 a year, two women reported earning $20,001–30,000 a year, and five women chose not to report their annual income. Most of the participants identified their race/ethnicity as Black (n=25), three identified as White, and two as “Other.” On average, the participants were living with HIV for 11 years (6 months to 17 years). Dr. Teti and the women sought to find out, if interventions that focused on condoms or disclosure were not helpful to women living with HIV, what was? As typical to Photovoice projects, the project included picture taking, discussions, and exhibits. The women planned and chose the exhibit location and their preferred target audience, based on whom they wanted to hear and understand their stories. The exhibit influenced action regarding HIV-related policies and practices by disseminating experiences to audiences who could use the information, advocating for housing, media opportunities, safer neighborhoods, and the acquisition of a community garden and housing for one woman. These immediate experiences of participants comprised one set of project outcomes. Another set of outcomes resulted from Dr. Teti’s role and expertise as a qualitative analyst. Both sets of outcomes were equally important. Dr. Teti analyzed the project sessions and photographs (processes described in detail elsewhere)53 to identify themes and patterns in women’s stories that could result in lessons learned, practice suggestions, and directions for future research. To provide an example of how women shared their lives through Photovoice, we present here a summary of one of 53 Michelle Teti, Bryana French, Loida Bonney, and Marguerita Lightfoot, “I Created Something New with Something That Had Died”: Photo-Narratives of Positive Transformation among Women with HIV,” AIDS and Behavior 19, no. 7 (2015): 1275–87. Published online: January 20, 2015.

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the key themes: life transformations. Photovoice made visible a number of experiences, positive and potentially positive, that is not always captured by conventional public health assessments of HIV, and that countered the disempowering assumptions behind the HIV label. Below we discuss three aspects of the transformation theme, health, self-acceptance, and purpose.

Health Transformations Women commonly described HIV as a journey. Becoming and feeling healthier was often a key aspect of that experience. Despite being at different points in their lives with HIV (1 to 22 years), it was common for participants to capture positive progression regarding their health. Women defined “healthier” in regards to overcoming depression, anxiety, isolation, substance abuse, negative relationships, physical illness, and lack of engagement in HIV care or medication adherence. Adal provided an example of using images to describe an overall health transformation. She shared two pictures of her church. In the first picture, the church was dilapidated and boarded. In the second picture, the church was in the process of being rebuilt. She explained, “This [old church] reminds me of me. My body got weak and needed re-sewing ... The new church is the new me.” She further explained that when she was first diagnosed with HIV the doctors gave her “6 months to live.” She weighed less than 40 pounds and had to be “carried around like a baby.” Eventually, she “got up and tried to walk, and said she is now “running.” Cadence shared a picture of a long road to describe her “road to recovery.” She said, “I was 38 years old and I was slowly killing myself doing crack cocaine. When they [doctors] told me I was HIV positive I thought ‘I’m already dead so what’s the difference?’” Her daughter, however, helped to redirect her and Cadence had what she described as an epiphany about self-care. I decided that after all of the years trying to die, I’ve got a potential death sentence, but do I really want to die? I thought “No.” HIV saved my life ... It clicked that if I wanted to live I had to do something different. I packed up and I moved. I left the drugs alone and haven’t taken drugs since. I’m nine years clean ... I learned that I can live with HIV.

Dani, 57 years old and living with HIV for 17 years, admitted that she struggled to take medicine until her friend died, which was her “turning point.” She showed the group two self-portraits of herself with her plants. In the first picture, the plants were wilted and brown. In the second photo,

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the plants were vibrant and healthy. She compared the plants’ health to her own: I wouldn’t take medicine for seven years ... I wouldn’t come to the doctors. I was just giving up. I said, “The meds ain’t going to do it.” But, one day, my [friend] got sick. It woke me up ... It was like [feeding] my plants a miracle drug. When I took that medicine, everything—my color, my pigment, my skin—came back ... I thank God that I took the pills because, if I didn’t, I’d probably be wilted like the plants, my life going down. But, I came back. I just said, “I’m going to grow … Bring myself back to life.”

Embracing Self-Acceptance Another common transformation was towards acceptance of self. For example, collectively, the participants described accepting their diagnosis, believing that they could live with or survive HIV, creating a life and an identity beyond HIV, and understanding how to challenge or manage HIV stigma—others and their own. Moving past denial was a major aspect of this transformation. Marley, who was living with HIV for 17 years, described an initial “internal stigma.” She could not accept that she was HIV positive. She shared a self-portrait to describe her journey towards feeling “free.” [I] “kept [having HIV] inside of me for so many years and then finally, I [decided], I’m going to talk out about it, and when I talked out about it, I felt liberated, I was free.” [I became] comfortable with [HIV] in my own skin … I’ve chosen not to be ashamed in my life ... I’m free to be whoever I want to be. I tell people, “I’m grateful for [HIV]. I truly am.” It’s like living a whole new life ... HIV really made me know who I was overall … I believe that HIV has freed me to be.

Tianna also struggled with HIV stigma. Living with HIV for eight years, she described how she wanted to tell more friends and family members about her HIV status, but “wasn’t there yet.” To explain this visually, she shared a photograph of wires, tangled and attempting to connect with each other. She said she was taking baby steps. She shared several pictures, including this flower growing out of a rock (Fig. 1), to explain that with her artwork and her life with HIV, she “created something new with something that had died,” and that she was looking forward to “growth” and how “life will find a way” despite HIV and HIV stigma.

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Figure 1. Tianna’s photo of a flower.

Some women used images to describe how they accepted and now wanted to move beyond HIV. As one participant put it, “I’m not HIV anymore. It’s not ‘my everything.’ It is part of me and it’s becoming kind of more in the background of my life.” Rani shared a picture of herself walking through the city, and said this picture helped her to feel just “like everybody else.”

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Purpose One final example indicates that women wanted to elaborate on how their lives gained purpose and recognized that they could be successful and achieve their goals despite illness. Anna said that taking pictures Made me focus on what I can do instead of running into a brick wall all the time. It let me focus and gave me courage … It gives me a positive thought about things I can do in my life and not be down and out and stressed and depressed.

She addressed multiple challenges in her life with the camera. One was the lack of safety in her neighborhood. She took photographs of an unsafe area with empty buildings, leading a neighborhood effort to get the buildings torn down. In its place, the city agreed to construct a community garden (Fig. 2).

Figure 2. Anna`s photo of the community garden

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Anna describes this process below: Kids walk past that building [points to an image of the dilapidated building] to go to school and it's been about four, five little girls snatched behind that building and raped. There were protestors in the neighborhood about that building. I was walking with them because they need to tear them down. Because ain't no point in them sitting there and all they do is just leave them there … There's a lot of kids down on the corners waiting on their school buses. I'm signing the papers and everything to get them torn down.

Reflecting on the image of the cleared out lot (Fig. 3) after the building came down, she further commented: I like looking at this picture [of the new lot] because it lets me know that I can do something and I can actually complete it and feel good about it...Even though I’m going through the things that I’m going through. I am strong enough to continue to go farther and do things. I been going to school online and they going to help me get a building for my homeless shelter. I’m thinking about doing a beauty salon and a daycare. I just been going around, taking pictures of different buildings that’s leasing and stuff, to pick which one I really want to be--once I graduate, they going to help me put the down payment on the building

Figure 3. Anna’s photo of a cleared lot

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What Do We Gain When We Count Women’s Photos as Valuable Knowledge? Presenting women with the task of sharing their lives with HIV visually resulted in several insights about women’s experiences and needs. Women chose the focus of their responses and highlighted their strengths. They were able to reframe the picture or narrative of their story with HIV away from a singular lens of illness. When applied to programming, this information suggested that women want more opportunities to develop their skills, and to be put in fewer situations in which they are expected to dwell on their risks. This means changing the current perspective of interventions from, “How can we stop women from engaging in specific behaviors?” to, “How can we help women continue to engage in actions that support their lives?” Doing so may result in interventions that respond to women’s needs and as a result, lead to increases in safe behaviors and medication practices, which ultimately decrease the impact and transmission of HIV. Women also made meaning of their illness via the Photovoice process and expressed that this was a powerful and important experience. It suggests women may benefit from having opportunities to search for meaning in the course of their illness, and that meaning could increase their motivation to make healthier decisions that will protect their health and limit HIV transmission (e.g., “HIV saved my life”). Of course, not all of the women described HIV as a lifesaver. Still, however, this was an important counternarrative to popular culture and media descriptions (which are shared by research and interventions!) of HIV as something terrible to navigate. Other women pointed out that HIV was not a major aspect of their lives. In some cases, women faced greater challenges than HIV (such as Anna’s example of violence in her neighborhood). Other women accepted HIV as part of their lives and did not want to dwell on it anymore. In fact, they wanted to share and show other aspects of their lives. This suggests that women may be more receptive to programs and interventions that address the woman as a whole and do not focus solely on HIV outcomes or behaviors that are assumed to matter to women. The images and stories insist that we envision women as whole beings, not just through the lens of HIV. As researchers and practitioners, we remain open to viewing women’s self-defined problems and successes. If interventions resonate with how women with HIV define themselves, their content may also be more relevant to women. Relevant content and messaging will likely produce interventions that work hand in hand with women’s expertise to help women engage in safe and healthy practices that will protect individual and public health.

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Limitations of Community Research This is all meant to be an effort of research-as-solidarity, but solidarity is not easily achieved, not a matter of sentiment alone. Structural and institutional conditions continue to determine distributions of authority and well-being even as researchers seek collaborative relations with participants.54 There are certainly limits to CBPR and Photovoice along these lines. Ideally, CBPR includes a process by which all partners have an important and equal input into how a project is organized. Ideally, both researchers and community members have decision-making power. Such collaboration is a fragile balance, however, and difficult to obtain given the power imbalances between researchers and community members. CBPR can be uncomfortable and challenging to navigate. Stoudt, Fox, and Fine55 note that collaboration can deepen the scars of oppression. Researchers must acknowledge the significant space between activist scholarship and the attainment of social justice. They point out that “Scholars have a debt to engage with justice movements in HUMBLE solidarity to contribute what we know, knowing well we are ‘ignorant’ of course as a consequence of our privilege and to build new imaginings together.” If this is not done correctly, the same old oppressive power structures are replicated and repeated. Images also have their own particular ethical challenges. We need to explore if the images make participants vulnerable, recording their outlooks and experiences in permanent formats with unpredictable distribution and exposure. We need to recognize that images have an internal story and an external narrative, the interpretation that others who view the photos will place on the photo. Will this story reinforce stereotypes? Guillemin and Drew56 state, image production and showing are not a neutral exercise. Images do not speak a thousand words as much as they welcome a thousand interpretations. Given that the power of the image comes from showing and sharing it, participants also need to clearly understand what they are consenting to and how the images will be used now and in the future. Careful conversations about privacy and ownership need to occur. Without these caveats, the work can be damaging.

54 David Roediger, “Making Solidarity Uneasy: Cautions on a Keyword from Black Lives Matter to the Past,” https://www.versobooks.com/blogs/3313-david-roedigermaking-solidarity-uneasy-cautions-on-a-keyword-from-black-lives-matter-to-thepast. 55 Stoudt, et al., “Contesting Privilege,” 178–93. 56 Marilys Guillemin and Sarah Drew, “Questions of Process in ParticipantGenerated Visual Methodologies,” Visual Studies 25, no. 2 (2010): 175–88.

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Moving Forward An additional limitation of Photovoice is that it may be an actionoriented method, but the path from photo research to actual action can nonetheless be slow and uncertain. Participants may or may not realize their place in this path and expect immediate change. However, the slow and even meandering path from Photovoice encounters to practical or policy changes can be a source of opportunity. If the hegemonic role of science, public health institutions, and familiar forms of expertise in contemporary social relations are thoroughly decentered, as we believe happens in the course of Photovoice encounters, stubborn inequities that have not budged under familiar progressive address may give way. That decentering can only happen when less traditional methods are admitted into mainstream public health research practices and given legitimacy. Conventional public health research can unintentionally reproduce inequitable social relations by sidelining the social character of illness and casting social structural conditions such as race, gender, or socioeconomic discrimination as beyond the purview of public health intervention. In some ways, simply acknowledging those forms of discrimination can lead to a more just and inclusive sort of public health research by adding complexity to causal understandings of illness and health. Public health initiatives in support of those with HIV/AIDS have turned to this more contextual approach. But, the definitions of what counts as illness and health, as we have shown, can themselves lead to interventions ill-fitted to people’s needs. These definitions can only come into question when the boundaries of expertise are expanded to include those whom interventions are intended to support, an expansion that Photovoice and other CBPR methods enable. For public health to reach its emancipatory promise, it must promote non-traditional forms of public health in which formulations of the problem itself emerge as part of the research.

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Farmer, Paul. AIDS and Accusation: Haiti and the Geography of Blame. Los Angeles: University of California Press, 1992. Fee, Elizabeth, and Nancy Krieger. “Understanding Aids: Historical Interpretations and the Limits of Biomedical Individualism.” [In eng]. American Journal of Public Health 83, no. 10 (Oct 1993): 1477–86. Guillemin, Marilyn, and Sarah Drew. “Questions of Process in ParticipantGenerated Visual Methodologies.” Visual Studies 25, no. 2 (2010): 175– 88. Krieger, Nancy. “Epidemiology and the Web of Causation: Has Anyone Seen the Spider?” [In eng]. Social Science Medicine 39, no. 7 (Oct 1994): 887–903. Liebenberg, Linda. “The Visual Image as Discussion Point: Increasing Validity in Boundary Crossing Research.” Qualitative Health Research 9 (2009): 441–67. Mann, Jonathan. “Human Rights and Aids: The Future of the Pandemic.” In Health and Human Rights, A Reader, edited by Jonathan Mann, Sofia Gruskin, Michael A. Grodin and George. J. Annas, 216–26. New York: Routledge, 1999. Patrick, Rudy, David Forrest, Gabriel Cardenas, Jenevieve Opoku, Manya Magnus, Gregory Phillips, Alan Greenberg, Lisa Metsch, Michael Kharfen, Marlene LaLota, and Irene Kuo. “Awareness, Willingness, and Use of Pre-Exposure Prophylaxis among Men Who Have Sex with Men in Washington, DC and Miami-Dade County, Fl: National HIV Behavioral Surveillance, 2011 and 2014.” [In eng]. supplement. Journal of Acquired Immune Deficiency Syndrome 75 no. S3 (July 1, 2017): S375–S82. Roediger, David. “Making Solidarity Uneasy: Cautions on a Keyword from Black Lives Matter to the Past.” https://www.versobooks.com/ blogs/3313-david-roediger-making-solidarity-uneasy-cautions-on-akeyword-from-black-lives-matter-to-the-past. Schneider, Mary Jane. Introduction to Public Health. Burlington, MA: Jones and Bartlett Learning, 2017. Sobo, Elisa J. Choosing Unsafe Sex. Philadelphia: University of Pennsylvania Press, 1995. Stoudt, Brett. E., Michelle Fine, and Madeline Fox. “Contesting Privilege with Critical Participatory Action Research.” Journal of Social Issues 68, no. 1 (2012): 178–93. Taylor, Ashley. “Knowledge Citizens? Intellectual Disability and the Production of Social Meanings within Educational Research.” Harvard Educational Review 88, no. 1 (2018): 1–25.

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Teti, Michelle, Lisa Bowleg, Russell Cole, Linda Lloyd, Susan Rubinstein, Susan Spencer, Erika Aaron, Ann Ricksecker, Zekarias Berhane and Marta Gold. “A Mixed Methods Evaluation of the Effect of the Protect and Respect Intervention on the Condom Use and Disclosure Practices of Women Living with HIV/AIDS.” [In eng]. AIDS and Behavior 14, no. 3 (2010): 567–79. Teti, Michelle, Bryana French, Loida Bonney, and Marguerita Lightfoot. “I Created Something New with Something That Had Died”: PhotoNarratives of Positive Transformation among Women with HIV.” AIDS and Behavior 19, no. 7 (2015): 1275–87. Published online: January 20, 2015. Teti, Michelle, Lisa Bowleg, and Linda Lloyd. “'Pain on Top of Pain, Hurtness on Top of Hurtness’: Social Discrimination, Psychological Well-Being, and Sexual Risk among Women Living with HIV/AIDS.” International Journal of Sexual Health 22, no. 4 (2010): 205–18. Teti, Michelle, Latrice Pichon, Allison Kabel, Rose Farnan, and Diane Binson. “Taking Pictures to Take Control: Photovoice as a Tool to Facilitate Empowerment among Poor and Racial/Ethnic Minority Women with HIV.” Journal of the Association of Nurses in AIDS Care 24, no. 6 (2013): 539–53. Torre, N. E., B. G. Stoudt, E. Manoff, and M. Fine. “Critical Participatory Action Research on State Violence: Bearing Wit(H)Ness across Faultlines of Power, Privilege, and Dispossession.” In Sage Handbook of Qualitative Research 5e, edited by Norman K. Denzin and Yvonna S. Lincoln. London: Sage Publications, 2017. UNAIDS. “90-90-90: An Ambitious Treatment Target to Help End the Aids Epidemic.” http://www.unaids.org/sites/default/files/media_asset/9090-90_en.pdf. Wang, Caroline. “Photovoice: A Participatory Action Research Strategy Applied to Women's Health.” [In eng]. Journal of Women's Health 8, no. 2 (March 1999): 185–92. Wang, Caroline, and Mary Ann Burris. “Empowerment through Photo Novella: Portraits of Participation.” Health Education Quarterly 2, no. 2 (1994): 171–86. World Health Organization.WHO. “About Social Determinants of Health.” http://www.who.int/social_determinants/sdh_definition/en/. World Health Organization. WHO. “The Ottawa Charter for Health Promotion.” Adopted November 21, 1986. http://www.who.int/healthpromotion/conferences/previous/ottawa/en/.

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Abbreviations PREP: ART: PLWH: CBPR:

pre-exposure prophylaxis antiretroviral therapy people living with HIV/AIDS community-based participatory research

Immemorial: The Poetics of AIDS

Figure 1. Rudy Lemcke, still from Where the Buffalo Roam, 2007, video. See the video at https://vimeo.com/126862428.

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Figure 2. Rudy Lemcke, Are You Sleeping, 1987, graphite on paper.

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Figure 3. Rudy Lemcke, Untitled Installation for Breathing, 1979, installation view, Contemporary Arts Center, New Orleans.

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Figure 4. Rudy Lemcke, Iscador, 1989, graphite on Fabriano Roma paper

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Figure 5. Rudy Lemcke, Foscarnet, 1989, graphite on Fabriano Roma paper

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Figure 6. Group Material, AIDS Timeline, installation view, Whitney Biennial, 1990.

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Figure 7. Rudy Lemcke, Glinda, 1988, acrylic on canvas.

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Figure 8. Rink, untitled photograph of pedestrians outside Star Pharmacy, San Francisco, 1982.

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Figure 9. Rudy Lemcke, Cinders, 1996, mixed media, obituaries from Bay Area Reporter newspaper, oil, beeswax on canvas.

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Figure 10. Rudy Lemcke, detail of Cinders, 1996.

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Figure 11. Rink, Immemorial, 1992, documentation of performance at de Young Museum in San Francisco for Day Without Art.

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Figure 12. Rudy Lemcke, Immemorial, 1996, documentation of performance at de Young Museum for Day Without Art.

Figure 13. Rudy Lemcke, still from Immemorial, 2005, 10 min, single channel video.

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Figure 14. Rudy Lemcke, Shadow puppet for The Uninvited, 2003.

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Figure 15. Rudy Lemcke, still from The Uninvited, 2003, 13 min., single channel video. See the video at https://vimeo.com/121104881.

Figure 16. Rudy Lemcke, still from (Orpheus) The Poetics of Finitude, 2014, 7 min., single channel video.

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Figure 17. Rudy Lemcke, New World, 2017, de Young Museum.

PART II: THE SHAPE AND SHAPING OF EPIDEMICS IN WEBS OF MATTER

CHAPTER SEVEN FOUR TURNING POINTS IN THE TREATMENT OF HIV/AIDS JOHN E. LESCH

The discovery, development, and implementation of effective drug treatments for HIV infection and AIDS-related conditions have changed the course of the disease. So much so, that medicinal drugs and drug treatments are usually close to the center of any account of the global AIDS epidemic. Even before physicians understood the viral etiology of AIDS, they attempted to treat their patients’ immune deficiencies, cancers, and infections with both established and experimental medicines. AIDS activists devoted much of their energy to demands that greater resources be put into the search for new drug treatments, to efforts to ease the regulatory path of new drugs, and to the organization of networks of information and distribution that would supply drugs—officially approved or not—to people with AIDS. Once the pharmaceutical industry perceived the extent of the epidemic, it became heavily engaged in the search for new treatments. Most dramatically, beginning in the mid-1990s, the introduction of combination drug therapies that included protease inhibitors or non-nucleoside reverse transcriptase inhibitors added to the already available drugs of the reverse transcriptase class, converted HIV infection from a death sentence to a chronic illness for many of those who had access to the new treatments. Although it is not a cure and problems remain, drug treatment of HIV infection is one of the undoubted success stories of late twentieth and early twenty-first century medicine.1 1 There is now extensive literature on the history of the epidemic. Several important treatments are, in chronological order of first publication, Randy Shilts, And the Band Played On: Politics, People, and the AIDS Epidemic (New York: St. Martin’s Griffin, 2007. 20th anniversary edition. First published 1987); Mirko D. Grmek, History of AIDS: Emergence and Origin of a Modern Pandemic (Princeton NJ: Princeton University Press, 1990). Originally published as Histoire du sida: Début et origine d’une pandémie actuelle, Paris: Éditions Payot, 1989); Steven Epstein,

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Much of the evolution of drug treatment for HIV infection and AIDSrelated conditions occurred in the first decade and a half of the epidemic, from the first published reports of what were eventually recognized as cases of AIDS in 1981 to the initial availability of combination therapy that included protease inhibitors or non-nucleoside reverse transcriptase inhibitors in 1996. Within this period, the evolution of drug therapy was marked by four distinct turning points. Two of these at least will be immediately recognizable to those familiar with the broad contours of the AIDS epidemic. The other two have been less visible as distinct stages, although some of their constituent parts will be familiar. The first and one of the less visible turning points occurred with the initial engagement of researchers in investigations on drug therapies from 1982 to 1985. This phase began before the identification of a specific virus as the cause of AIDS and was characterized by initiatives taken by small teams of researchers in government and academic laboratories and hospital clinics. A second and well-recognized turning point came with the finding in 1986–1987 that a nucleoside analog, azidothymidine or AZT (generic name: zidovudine) had a clinically significant effect on HIV infection. The product of a collaboration between a small research team within the National Institutes of Health and a pharmaceutical company’s research division, AZT, as it came to be widely known, raised optimism about the possibilities of drug therapy for AIDS and set investigators on a quest for other nucleoside analogs of equal or superior therapeutic potential.2 By the time that AZT appeared on the scene a third turning point was beginning to take shape, one that was consolidated by the early 1990s. This was due to the effective management of the opportunistic infections that brought suffering and death to many of those whose immune systems had been compromised by HIV infection. Less easily recognizable as a distinct stage in part due to the plurality of conditions, drugs, and research actors involved, and their overlapping but unsynchronized chronologies, the convergent effect is nevertheless unmistakable. People with AIDS were living longer and had a better quality of life than they had in the earliest years of the epidemic. Finally, most recognizable as a turning point because most dramatic, and because it is foundational for subsequent therapy of HIV infection, is the introduction of combined therapies including protease Impure Science: AIDS, Activism, and the Politics of Knowledge (Berkeley: University of California Press, 1996); and Victoria A. Harden, AIDS at 30: A History (Washington, DC: Potomac Books, 2012). 2 On the initial engagement of researchers, see below. On AZT, see Linda J. Wastila and Louis Lasagna, “The History of Zidovudine (AZT),” Journal of Clinical Research and Pharmacoepidemiology, 4 (1990): 25–37; and below.

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inhibitors or non-nucleoside reverse transcriptase inhibitors beginning in 1996. In this, pharmaceutical companies working both separately and cooperatively played a leading role.3 These changes in the first fifteen years of the epidemic, in turn, drew upon substantial resources of knowledge and experience that antedated the AIDS epidemic by years or decades, or that appeared contemporaneously with the AIDS epidemic but independently of it. The researchers who first sought drug treatments for AIDS made use of, and in some cases were themselves involved in, research of the 1970s and early 1980s on viral causation of cancers and efforts to find antiviral or even specifically antiretroviral drug therapies for cancer. AZT was first synthesized in the 1960s as a potential cancer drug. Viewed in a larger frame, both this synthesis and AZT’s subsequent development as an antiretroviral in the AIDS epidemic must be seen as extensions of an antimetabolite research program that began in the 1940s and was most closely associated with Burroughs Wellcome researchers, George H. Hitchings and Gertrude B. Elion.4 Several of the drugs that played key roles in the management of opportunistic infections also emerged from the antimetabolite program or closely related research, including co-trimoxazole (trade names: Bactrim, Septra) for treatment or prevention of pneumocystis carinii pneumonia (PCP), and acyclovir for the treatment of herpes infections. Others, such as isoniazid, used in the prevention or treatment of tuberculosis, long antedated the AIDS epidemic. The mid-1990s breakthrough that finally succeeded in making HIV infection a chronic condition depended not only on the introduction of protease inhibitors and non-nucleoside reverse transcriptase inhibitors, but also crucially on the turn to combination drug therapy,

3 Luc Montagnier, Virus: The Co-discoverer of HIV Tracks Its Rampage and Charts the Future, trans. Stephen Sartarelli (New York and London: W. W. Norton & Company, 2000. Original French edition, Des virus et des hommes, 1994), 152–56; Ronald Bayer and Gerald M. Oppenheimer, AIDS Doctors: Voices from the Epidemic (Oxford and New York: Oxford University Press, 2000), 119–125; and Martin Delaney, “The Development of Combination Therapies for HIV Infection,” AIDS Research and Human Retroviruses 26, no. 5 (2010): 501–09. 4 Montagnier, Virus, 152–56. On the origins and early history of the antimetabolite research program, see Thibaut Serviant-Fine, Une approche rationnelle de la chimiothérapie: histoire des antimétabolites (1935–1955), Histoire, Philosophie et Sociologie des Sciences, (Thèse de Doctorat, Université de Lyon, 2016), NNT: 2016 LYSE1271. On AZT and the antimetabolite program, see below.

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preexisting models for which were available in longstanding treatment regimens for tuberculosis, cancer, and other diseases.5

The Engagement of Researchers We now think of HIV/AIDS as a vast medical, political, and humanitarian problem, with numerous ramifications in global public health. It takes some effort of historical imagination to recall a time, prior to mid-1981, when it had no existence in the minds of researchers, or even in the minds of those we now know were already infected with HIV. How did medical researchers become engaged with AIDS in the first place? When they did turn to AIDS, what resources did they bring to bear on the new disease? One way to answer this question is to take a brief look at three drug treatments that were tried early in the AIDS epidemic. The stories of alpha interferon, HPA-23, and suramin show how researchers began to redirect medical knowledge and practice to engage with the new disease. They also demonstrate that the trajectory toward the control of a new, fearsome epidemic disease was hardly a straight line or without major setbacks: two of the three drugs were failures, and the third was only modestly successful.

Alpha Interferon and the Arrival of AIDS In 1980, interferon was thought to herald a promising new approach to cancer therapy. Interferon was a protein, eventually, a class of proteins, naturally produced by the human body in response to viral infection or other stimuli. Research revealed it to be a modulator of the immune system, either inhibiting or enhancing the immune response. By 1980, it had already been the subject of several decades of laboratory and clinical study.6 In the late 1950s and 1960s, interferon was hailed as a potential “antiviral penicillin,” a compound “that would do for viral diseases what antibiotics had done for bacterial infections.” These expectations were not met. A new phase in interferon’s history began in the 1970s as a few investigators began to perceive its potential in cancer therapy. Foremost among these was Mathilde Krim, a medical researcher at Memorial Sloan Kettering Cancer Center in New York. Interferon’s rise to potential miracle 5

David Greenwood, Antimicrobial Drugs: Chronicle of a Twentieth Century Medical Triumph (Oxford and New York: Oxford University Press, 2008), 170–79, 252–56, 375–77; and Delaney, “Development of Combination Therapies,” 501–09. 6 On the history of interferon see especially Toine Pieters, Interferon: The Science and Selling of a Miracle Drug, (London and New York: Routledge, 2005).

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drug status owed in part to the tireless efforts of Krim, who organized conferences to promote its study and sought funds for research.7 It was also boosted by its close fit with other trends. As a naturally occurring, and therefore presumably nontoxic product of the human body, interferon seemed to have an advantage over the conventional cancer therapies of surgery, radiation, and chemotherapy. As a product of the recombinant DNA techniques of the new industrial genetic engineering, interferon carried the aura of path-breaking science and technology.8 Then came AIDS. In 1981, in the course of a clinical trial of interferon open to “patients with advanced cancer who had failed to respond to conventional treatments,” a young, gay male patient with Kaposi’s sarcoma was referred to Krim’s group for treatment. Kaposi’s sarcoma, a rare and slowly progressing cancer of the blood vessels previously found mainly among men older than 60, was turning up with increasing frequency among gay men in their twenties and thirties. It was one of the earliest and most visible manifestations of AIDS. So much so, that the new and mysterious disease was often referred to as “the gay cancer.”9 Krim’s patient responded to treatment and from 1981 to 1983, Sloan Kettering ran a clinical trial of interferon. Other trials of interferon in Kaposi’s sarcoma were undertaken at San Francisco General Hospital by Paul Volberding and his colleagues, and at UCLA, beginning in 1982. Results of these trials were mixed. Tumor regression was noted in about forty percent of patients, but there was no boost to the immune system, and toxicities, including fever, malaise, and myalgias, were significant.10 7

Ibid., 1–90 (quote on 1), 110–11, 122–23, 128, 144–50. Mathilde Krim reviewed the status of interferon treatment of cancer as of 1980 in “Towards Tumor Therapy with Interferons, Part I. Interferons: Production and Properties,” Blood 55, no. 5 (May 1980): 711–21; and idem.; “Towards Tumor Therapy with Interferons, Part II. Interferons: in Vivo Effects,” Blood 55, no. 6 (June 1980): 875–84. 8 Pieters, Interferon, 134, 143, 146-147. The promise of interferon was spotlighted in media coverage. See e.g. the Time magazine cover story, “The big IF in cancer: will the natural drug interferon fulfill its early promise?” Time 113, No. 13 (March 31, 1980): 60-66. 9 Susan E. Krown et al., “Recombinant Leucocyte A Interferon in Kaposi’s Sarcoma,” Annals of the New York Academy of Sciences 437 (1984): 431–38 (quotes on 431). On Kaposi’s sarcoma see Mirko Grmek, History of AIDS, 6–10, 111–14. 10 Krown et al., “Recombinant Leucocyte,” 431–38; Paul Volberding et al., “Alpha Interferon Therapy of Kaposi’s Sarcoma,” Annals of the New York Academy of Sciences 437 (1984): 439–46; Paul Volberding et al., “Interferon and Interleukin-2 Therapy of Kaposi’s Sarcoma,” Advances in Experimental Biology and Medicine 187 (1985): 151–57; and Jerome E. Groopman et al., “Recombinant Alpha-2

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In the end, interferon did not have the hoped-for effect on AIDS. It did retain a modest place in treatment and— for a time at least—gave a measure of hope to physicians and patients.

HPA-23 A new vista was opened for therapy by the discovery of a retrovirus associated with AIDS by Luc Montagnier, Françoise Barré-Sinoussi, and their colleagues at the Pasteur Institute in Paris, in 1983. Called the lymphadenopathy-associated virus (LAV) by the French investigators, the same virus was isolated by Robert Gallo and his team at the National Cancer Institute and called human T-cell lymphotropic virus-III (HTLV-III) on the initial view that it was a new member of a class of retroviruses already under investigation at NCI. At around the same time at UCSF, Jay Levy also isolated the virus and named it AIDS-associated retrovirus (ARV). Eventually, it would be called the human immunodeficiency virus, or HIV, the name that was made official in 1986. By whatever name the new virus, presumed to be the cause of AIDS, provided an obvious target for therapeutic research.11 The French were positioned to respond quickly. For more than a decade, researchers at the Pasteur Institute in Paris, working in collaboration with investigators at other Paris institutions and with American and Japanese researchers, looked for chemical agents with activity against cancer-causing viruses, including retroviruses involved in animal cancers such as mouse leukemia and sarcomas. The central focus of this research was a group of mineral compounds known as heteropolyanions or HPA. By the late 1970s, one of these compounds, ammonium 21-tungsto-9-antimoniate, or HPA-23, was recognized as having the strongest in vivo activity against cancer retroviruses.12 By 1982, the first AIDS cases had appeared in France. Interferon Therapy for Kaposi’s Sarcoma Associated with the Acquired Immunodeficiency Syndrome,” Annals of Internal Medicine 100 (1984): 671–76. 11 Grmek, History of AIDS, 47–70; and Harden, AIDS at 30, 39–70. 12 On this research program see e.g. Dharam V. Ablashi et al., “Effects of 5-Tungsto2-Antimoniate in Oncogenic DNA and RNA Virus Cell Systems,” European Journal of Cancer 13, no. 7 (July 1977): 713–20; M. Hervé et al., “Correlation between Structure of Polyoxotungstates and Their Inhibitory Activity on Polymerases,” Biochemical and Biophysical Research Communications 16, no. 1 (October 14, 1983): 222–29; and Katsuhiko Ono et al., “Inhibition of DNA Polymerase Activity by Ammonium 21-Tungsto-9-Antimoniate (HPA-23),” Nucleic Acids Symposium Series 15 (Oxford and Washington, DC: IRL Press, 1984), 169–72.

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Montagnier’s group set aside other research to focus exclusively on the possible retroviral causation of AIDS. As Montagnier later recalled, “We had the necessary technology and training to move on from cancer retroviruses to AIDS retroviruses.” The transition from one line of research to the other was evidently a smooth one, and Montagnier recorded his early findings in the search for an AIDS retrovirus in the same red notebook he had been using since 1977 in his search for retroviruses in human cancers. So a little later, it was an obvious step for the Pasteur Institute researchers to ask if HPA-23 would also inhibit a key enzyme of the AIDS virus, its reverse transcriptase that acted to convert viral RNA to DNA, which could be integrated into the infected cell’s DNA.13 In the summer of 1983, the Pasteur Institute researchers began treating a handful of LAV (i.e., HIV) positive patients with HPA-23. In a letter published in The Lancet in February 1985, they claimed a reduction of LAV (HIV) replication and clinical improvement in all of these patients.14 By mid-1984, several months before the Lancet publication, interest in HPA-23 was already rising in both France and the United States. News of the promise of HPA-23 spread informally on what Randy Shilts has called “the AIDS grapevine” or “gay medical grapevine.”15 One of the Americans who heard about HPA-23 through this informal network was the film star, Rock Hudson. First diagnosed with AIDS in June 1984, Hudson was under the care of UCLA physician Michael Gottlieb. Gottlieb, who was in contact with the French researchers, arranged for Hudson to be treated. Hudson arrived in Paris in September, where he began treatments with HPA-23.16 Hudson’s health continued to deteriorate. Rumors circulated that Hudson, an icon of American cinematic masculinity, was gay. On July 30, 1985, Michael Gottlieb was authorized by Hudson to make the dramatic announcement that he was “being evaluated and treated for the complications of Acquired Immune Deficiency Syndrome.” Hudson died on October 2, 1985.17 The publicity surrounding Hudson’s illness and treatment marked a turning point in the public visibility of AIDS; but by this time, the French

13

Montagnier, Virus, 38–41, 47–48, 51. Rozenbaum et al., “Antimoniotungstate (HPA-23) Treatment of Three Patients with AIDS and One with Prodrome,” The Lancet 325, no. 8426 (February 23, 1985): 450–51. 15 Shilts, And the Band Played On, 474–75, 494–96. 16 Ibid., 474–76. 17 Ibid., 577–82. 14

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investigators seemed to have lost their enthusiasm for HPA-23 and were advising patients to try other drugs.18 The Americans had not given up. American researchers organized an open-label, multi-center clinical trial to determine the tolerance of HPA-23 in AIDS patients. Study findings were not published until September 1988. Investigators found that HPA-23 was reasonably well tolerated, but produced no changes in immune system function and no significant clinical improvement. HPA-23 disappeared from the radar of AIDS treatment research.19

Suramin By the time Rock Hudson’s AIDS diagnosis was announced in July 1985, American investigators were conducting the first U.S. national study of an experimental anti-HIV drug. The drug was suramin, and the initiative for its study came from a small group at the National Cancer Institute, led by Samuel Broder. Following isolation of the AIDS virus, one member of Broder’s team, Hiroaki Mitsuya, had developed a highly sensitive test for in vitro activity of compounds against the virus.20 Broder’s group initially selected suramin for testing because, in 1979, a Belgian researcher, Erik De Clercq, had shown it to be a strong inhibitor of 18

Ibid., 562, 578–82, 585. Bruce L. Moskovitz and the HPA-23 Cooperative Study Group, “Clinical Trial of Tolerance of HPA-23 in Patients with Acquired Immune Deficiency Syndrome,” Antimicrobial Agents Chemotherapy 32, no. 9 (September 1988): 1300–03. 20 Hiroaki Mitsuya et al., “Suramin Protection of T cells in Vitro against Infectivity and Cytopathic Effect of HTLV-III,” Science, vol. 226 (October 12, 1984): 172–74; R. Yarchoan et al., “Implications of the Discovery of HTLV-III for the Treatment of AIDS,” supplement, Cancer Research, vol. 45 (September 1985): 4685S–88S; Bruce D. Cheson et al., “Suramin Therapy in AIDS and Related Disorders: Report of the U. S. Suramin Working Group,” Journal of the American Medical Association 258, no. 10 (September 11, 1987): 1347–51; On the Broder group at the National Cancer Institute see Harden, AIDS at 30, 129–32; and Robert Yarchoan, “Oral History,” interview by Victoria A. Harden and Caroline Hannaway, In Their Own Words: NIH Researchers Recall the Early Years of AIDS, Oral History Project, April 30,1998 (http://history.nih.gov/NIHInOwnWords/). Section on Search for Treatments, Transcripts, paginated 1–37. The 1984 paper by Mitsuya et al. cited above was the first on AIDS treatment to be published in Science; See Ruth M. Kuhlstad, “Publishing AIDS Papers in the Early 1980s,” in AIDS and the Public Debate: Historical and Contemporary Perspectives, ed. Caroline Hannaway, Victoria A. Harden, and John Parascadola (Washington, DC: IOS Press, 1995), 107– 23, (notes 118 and 48). 19

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the reverse transcriptase of mouse and bird tumor retroviruses. Suramin had another great advantage in the eyes of NCI researchers. It had perhaps the longest medical pedigree of any of the compounds being screened for activity against HIV. A complex aromatic urea derivative first synthesized by chemists at the Bayer company in Germany in 1916, it was first dubbed Bayer 205 by the company, and later renamed Germanin. Bayer 205 was found to be an effective treatment for sleeping sickness, a trypanosomal disease transmitted by the tsetse fly, and of considerable human and economic importance in French and British colonies in Africa. In 1945, a Belgian doctor working in what was then the Belgian Congo (now the Democratic Republic of the Congo) discovered that suramin was capable of curing another serious disease of tropical Africa, onchocerciasis or river blindness, caused by the parasitic worm Onchocerca volvulus.21 Suramin—the generic name for the drug came into use in the 1930s— had a long record of clinical use. It did not need to be reviewed by the Food and Drug Administration, and it was available in sufficient quantities. It showed marked anti-HIV activity in vitro. In other words, it seemed an almost ideal candidate for AIDS clinical trials. Broder’s group began organizing a national, multi-center trial of suramin in AIDS and related disorders in August 1984. Over the next two years, 98 patients in six states participated in the trial, located in eight research units in addition to the NCI group. Despite suramin’s initial promise and years of hard work, the results were disappointing. The final report, published in 1987, found that viral suppression occurred in 40 percent of those receiving the drug. At the same time, investigators found no improvement in immune response, no clinical improvement, and significant toxicity. They concluded, “Suramin as currently administered cannot be recommended as effective therapy for AIDS.”22 One point that emerges clearly from these three cases is the importance of prior research on cancer therapy. From 1981 to 1985, there was a 21 Erik De Clercq, “Suramin: a Potent Inhibitor of the Reverse Transcriptase of RNA Tumor Viruses,” Cancer Letters 8 (1979): 9–22; Mitsuya et al., “Suramin Protection of T Cells in Vitro.” On the development and early use of suramin, and its significance as a major advance in the therapy of trypanosomiasis in the 1920s, see Greenwood, Antimicrobial Drugs (ref. 5), 272—77, 332; On the chemical background to the development of suramin and its relation to dye chemistry, see F. L. Rose, “Origin and Rise of the Synthetic Drugs,” in Chemistry in the Service of Medicine, ed. F. N. L. Poynter (London: Pitman Medical Publishing Company, 1963), 179–97 (on 185–89). 22 Cheson et al., “Suramin Therapy in AIDS and Related Disorders: Report of the U.S. Suramin Working Group.” Journal of the American Medical Association 258, no. 10 (September 11, 1987):1347–51.

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transition from a framing of the new disease as a cancer, with a focus on Kaposi’s sarcoma, to a framing of the disease as a viral infection causing immune system damage. The early cancer framing is reflected in, among other things, the location of the research in departments of oncology, such as that at San Francisco General Hospital, cancer research centers such as the Pasteur Institute’s Department of Viral Oncology or Sloan Kettering in New York, and the National Cancer Institute. These cases also show that there was an underlying continuity in the transition. The idea of viral causation—specifically retroviral causation— of cancers that was prominent in the 1970s and early 1980s, plus the early visibility of a cancer, Kaposi’s sarcoma, in the AIDS epidemic, smoothed the way from antiviral therapy as cancer therapy to antiviral therapy as AIDS therapy. Drugs whose antiviral activity had won them a place in experimental cancer treatment, like HPA-23, could be repurposed as possible treatments for HIV. So too could drugs with long histories unrelated to cancer treatment, like suramin, if they were found to have antiretroviral activity. Moreover, an anticancer drug such as alpha interferon, which came with both antiviral and immune-modulating credentials, might seem most promising of all. Implicit in the first point is a second one: by repurposing existing drugs, whether originally targeted at cancer or at tropical diseases, investigators were able to move quickly into AIDS treatment research. As Samuel Broder later said of suramin: I can tell you that the work we have done here (at The National Cancer Institute) does derive a lot indirectly from the commitment that was made in studying one drug. Suramin started many things going. Basically, I feel that many other drugs that are now being developed [this quote is from 1988] are indirectly related to the fact that we finally were able to get together and try something. Suramin was the first drug that looked like it could be administered, and adequate supplies were available. The drug had a 60-year experience of being given to people and basically, it could be started immediately.23

Third, in the early years of the AIDS epidemic, when large-scale federal funding was not yet available and when the pharmaceutical industry was not yet fully engaged, a disproportionate role was played by the leaders of small research units or hospital departments who were able to take the initiative to quickly redirect resources to respond to the new disease. 23

Charles Linebarger, “Tragedy at San Francisco General. Suramin: The Broken Promise of a Cure for AIDS,” San Francisco: The Magazine 2, no. 7 (July-August, 1988): 48–52, 126–28 (on 128).

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Finally, in all three cases—alpha interferon, HPA-23, and suramin—the experimental drug was eagerly embraced by those who had conditions associated with AIDS or were found to be infected with the virus. In all three cases, expectations were disappointed. None of these failures diminished the expectations of eventual success, and with each failure, hope was transferred to the next experimental treatment.

Recognition of a Path to Rational Drug Design By the time the suramin episode ended in 1986, researchers were focusing on another antiretroviral compound that would open a new direction for drug discovery in the AIDS epidemic. This was AZT, short for azidothymidine (generic name: zidovudine; original trade name: Retrovir), the first nucleoside reverse transcriptase inhibitor. On September 19, 1986, about seven months into a Phase II clinical trial of AZT, an independent Data and Safety Monitoring Board determined that those patients receiving AZT had a significantly higher survival rate than those on placebos. They also had fewer opportunistic infections, had gained weight, and had improved immune response. The clinical trial was suspended on ethical grounds. Steps were taken to make AZT available to AIDS patients. FDA approval followed on March 19, 1987. AZT became the first antiretroviral drug to gain official sanction and to enter medical practice for the treatment of HIV infections. It also set a new direction for research on antiretroviral drugs.24 This much is familiar from most accounts of the AIDS epidemic, but what was AZT, and where did it come from? A short version of the story— and the one that is usually given—is that it was first synthesized as a potential cancer drug in the 1960s, but failed in cancer treatment. In 1974, a German researcher, Wolfram Ostertag, reported that azidothymidine and another thymidine analog, bromodeoxyuridine, inhibited replication of a cancer-causing retrovirus in cultured mouse cells. Since retroviruses were then unknown in humans, Ostertag’s finding drew little attention. Azidothymidine then sat on the shelves at the pharmaceutical company Burroughs Wellcome, where it was tried as an antibacterial, again without success. Then in the 1980s, when Samuel Broder’s group at NCI was

24

Wastila and Lasagna, “The History of Zidovudine (AZT),” 25–37; Walter Sneader, Drug Discovery: A History (Chichester UK: John Wiley & Sons, 2005), 260–61; and Greenwood, Antimicrobial Drugs, 378–79.

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looking for compounds to screen against the AIDS virus, Burroughs Wellcome sent them AZT.25 It proved active in the test tube, so clinical trials were arranged. Success came quickly, and in the context of an exploding AIDS epidemic—by the end of 1986, 28,712 cases of AIDS and 24,559 deaths had been reported in the United States—and with rising AIDS activism, AZT won rapid FDA approval and was made available to doctors and patients.26 What is usually not included in AZT’s early history is the broader and longer-term research program that prompted both the original synthesis of the drug in 1964 and the continuing interest in it on the part of Burroughs Wellcome. For that, we need to look to the 1940s and the beginnings of what has been called the antimetabolite concept in medicinal drug research.27 The original, and we might say the paradigm case for the antimetabolite concept was the explanation of the mechanism of action of the sulfa drugs or sulfonamides. Preceding penicillin by about ten years, the sulfonamides were the first effective drug therapies for streptococcal infections such as puerperal fever, and also for bacterial pneumonia, gonorrhea, bacillary dysentery, meningitis, and other bacterial infections. Clinically they were enormously successful, but researchers were at first frustrated by their inability to explain how the sulfa drugs worked.28 Then, in 1940, two British researchers, Paul Fildes and Donald Woods, proposed an explanation based on the concept of competitive inhibition. They argued that because sulfanilamide—one of the first and most effective of the sulfonamides—closely resembles an essential bacterial nutrient, paraaminobenzoic acid, it could compete with the latter as a substrate for the bacterial enzyme that usually acted on the nutrient. In so doing, sulfanilamide prevents the bacterium’s growth and reproduction. Unable to increase in numbers, the invading bacteria are then destroyed by the defenses of the human or animal host.29 25Wastila and Lasagna, “The History of Zidovudine (AZT),” 26–27; Sneader, Drug Discovery, 260–61; and Greenwood, Antimicrobial Drugs, 378–79. 26 The Foundation for AIDS Research, “Thirty Years of HIV/AIDS: Snapshots of an Epidemic,” accessed July 30, 2018, www.amfar.org/thirty-years-of-hiv/aidssnapshots-of-an-epidemic/. 27 The need for a broader historical context is recognized by Walter Sneader, who places the AZT story in his chapter on antimetabolites. See Sneader, Drug Discovery, 248–68. 28 On the sulfa drugs, see John E. Lesch, The First Miracle Drugs: How the Sulfa Drugs Transformed Medicine (New York: Oxford University Press, 2007). 29 Ibid., 251–68, Woods-Fildes theory and its background.

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The Woods-Fildes theory, as it came to be known, explained the activity of the sulfa drugs against bacterial infections. This was an important result, but it applied to just this class of drugs. In the 1940s, Fildes and other researchers moved from this particular finding to the concept of antimetabolite. In its most general form, the antimetabolite concept states that a compound chemically similar to a compound needed by a cell or organism can interfere with the cell or organism’s use of the needed compound, and thereby prevent normal functioning or growth. So stated, the antimetabolite idea had potential applications far beyond the realm of sulfa drugs or even bacterial chemotherapy. Chemical compounds could be sought that resembled known essential metabolites, then tested in the laboratory or clinic as potential drug candidates.30 One of the formulators of the antimetabolite concept was George Hitchings, a biochemist at the Wellcome Research Laboratories in Tuckahoe, New York. From the 1940s to the 1980s, Hitchings and his collaborators, notably chemist Gertrude Elion, achieved great success in pursuing a research program based on the antimetabolite idea. Over the four decades from the 1940s to the 1980s, it yielded effective drugs for use in a remarkable variety of conditions, including cancer, gout, organ transplantation, malaria, and bacterial and viral infections.31 Other researchers also took up the antimetabolite approach. One of these was Jerome Horwitz, an organic chemist working at the Detroit Institute for Cancer Research. In the 1960s, Horwitz synthesized a number of nucleoside analogs, or what he called “fraudulent nucleosides,” hoping to find one or more that would interfere with the nucleic acid synthesis in cancer cells. Among these was azidothymidine or AZT. None of them worked, including AZT. Horwitz abandoned the search, and it is at this point that the conventional story of AZT begins.32 30

Ibid., 263–65; and Sneader, Drug Discovery, 248. John E. Lesch, “Chemotherapy by Design,” in A Master of Science History: Essays in Honor of Charles Coulston Gillispie, ed. Jed Z. Buchwald. Archimedes: New Studies in the History and Philosophy of Science and Technology, vol. 30 (New York: Springer, 2012): 275–95; and Serviant-Fine, Une approche rationnelle de la chimiothérapie, 181–227. 32 Sneader, Drug Discovery, 260; Greenwood, Antimicrobial Drugs, 378–379; and Woo, “Jerome Horwitz Dies at 93; Developed Potent Anti-AIDS Drug AZT,” Los Angeles Times, September 27, 2012; Woo’s obituary of Horwitz, in common with those authored by others, made no reference to the prior background of antimetabolite research; See e.g. Paul Vitello, “Jerome Horwitz, AZT Creator, Dies at 93,” New York Times, September 20, 2012; and Emily Langer, “Researcher Jerome P. Horwitz, 93, Created AZT, the First Approved Treatment for HIV/AIDS,” Washington Post, September 19, 2012. 31

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AZT, or azidothymidine, is an analog of the natural nucleoside thymidine, which is itself a compound of the pyrimidine base thymine and the sugar deoxyribose. Taken up by the retroviral enzyme reverse transcriptase, it blocks the synthesis of viral DNA and thus the replication of HIV.33 The approval, introduction, and use of AZT as a treatment for HIV infection raised important and controversial issues around drug regulation and pricing, toxicities, and risk. These require separate treatment. What should be added here is that in addition to its status as a product of a decadeslong antimetabolite research program, AZT also became the prototype for the first generation of officially approved antiretroviral drugs, the nucleoside reverse transcriptase inhibitors.34 Around the time that AZT was found to be active against HIV in laboratory tests, Broder’s group at NCI decided to look at other nucleoside analogs. In addition to AZT, several of these had been synthesized in the 1960s by Horwitz or others, and most could be ordered from chemical or pharmaceutical companies. Mitsuya found that a number of them were active against HIV in vitro.35 One of the first nucleoside analogs to be developed at NCI was zalcitabine (dideoxycytidine, ddC), which had been synthesized by Horwitz and his colleagues in 1967. Clinical trials began by early 1987. Broder’s group found ddC to be very active against HIV in patients, but also that it had notable toxicity and was less likely than AZT to support the immune system. NCI licensed ddC to Hoffmann-La Roche, and it gained FDA approval in 1992. In 1987, laboratory tests by Broder’s group showed that another nucleoside analog, didanosine (dideoxyinosine, ddI) was active against HIV. Prepared from another nucleoside analog that was first synthesized by Roland Robbins in 1964, didanosine underwent clinical testing beginning in 1988. Bristol-Myers Squibb assisted NCI with clinical trials, and ddI won FDA approval in 1991.36 Other reverse transcriptase inhibitors followed in the 1990s and early 2000s. A table of antiretroviral drugs published in 2008 listed eight NRTIs approved in the United States since the introduction of AZT in 1987. These drugs had problems with toxicity, and they soon encountered viral resistance when used alone. Nevertheless, their introduction and use 33

Sneader, Drug Discovery, 261. Wastila and Lasagna, “The History of Zidovudine (AZT),” 25–37; and Epstein, Impure Science, esp. 181–329. 35 Yarchoan, “Oral History,” 27, 29; Sneader, Drug Discovery, 261–62; Greenwood, Antimicrobial Drugs, 378–79; and Montagnier, Virus, 159. 36 Yarchoan, “Oral History,” 29–30; Sneader, Drug Discovery, 261–62; and Greenwood, Antimicrobial Drugs, 379–80. 34

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demonstrated the value of targeting specific stages of the viral reproductive cycle. From the mid-1990s forward, they remained essential components of the combination therapies that changed the course of the AIDS epidemic.37

Prevention and Control of Opportunistic Infections The therapeutic impact of the nucleoside reverse transcriptase inhibitors, when given by themselves, was limited. The next breakthrough in antiretroviral drugs would not come until the mid-1990s. Meanwhile, the toll of HIV infection in suffering and death was climbing. By the end of 1992, the year in which a third NRTI was given FDA approval, 254,147 cases of AIDS had been reported in the United States, with 194,476 deaths. In America’s gay communities, and among IV drug users, the epidemic was reaching staggering proportions.38 Fortunately, a third, less visible turning point in treatment intervened between the two major ones involving antiretroviral drugs. This was the mobilization of existing drug therapies to treat or prevent the opportunistic infections associated with HIV and AIDS. HIV attacks the immune system. The resulting compromise or suppression of the immune system makes the HIV positive person vulnerable to infections that would otherwise be kept at bay. In the 1980s and early 1990s, absent the availability of drugs that would effectively suppress or eliminate HIV, doctors did their best to prevent, eliminate, or manage these AIDSrelated conditions. In doing so, they frequently turned to drugs whose origin had nothing to do with HIV or AIDS. The opportunistic infections faced by people with AIDS and their physicians were numerous and varied. They included, most prominently, pneumocystis carinii pneumonia (PCP, now called pneumocystis jirovecii), a condition sometimes observed in immune-compromised individuals but otherwise rare prior to the AIDS epidemic. In addition, commonly occurring in approximately forty percent of severely immunosuppressed AIDS 37

The table is in Greenwood, Antimicrobial Drugs, 380. “Thirty Years of HIV/AIDS.” For an analysis of HIV/AIDS mortality in the U.S. 1987–2015 according to age, sex, geographical region, and race/ethnicity, see National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention, “Mortality Slide Series through 2015,” accessed August 14, 2018, https://www.cdc.gov/hiv/pdf/library/slidesets/cdc-hiv-mortality.pdf. For detailed historical data on HIV/AIDS epidemiology in the U.S., 1982–2015, see the CDC HIV Surveillance Reports Archive, accessed August 14, 2018, https://www.cdc.gov/hiv/libraryreports/hiv-surveillance-archive.html#specialarchive. 38

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patients was disseminated mycobacterium avium complex (MAC), a bacterial infection that typically affected multiple organs. Equally frequent were cytomegalovirus (CMV) infections, which in the form of CMV retinitis could lead to blindness if untreated. Less common but also serious if untreated was cryptococcal meningitis, a fungal infection of tissues covering the brain and spinal cord. A key challenge facing physicians in the early years of the epidemic was to identify, differentiate, and diagnose these and other conditions afflicting their patients with AIDS.39 Most conspicuous among the opportunistic infections in numbers of cases, morbidity, and mortality was PCP. A lung infection caused by an organism originally thought to be a protozoon but later classified as a fungus, PCP eventually appeared in more than fifty percent of AIDS patients. In the early years of the epidemic, a person who survived an initial attack of PCP could expect to die of later attacks, probably within twelve months. The first published cases of what was later called AIDS were of gay men with PCP.40 Prior to the AIDS epidemic, regimens to treat or prevent PCP had been developed for immunocompromised populations such as those with leukemia or undergoing organ transplants. The drugs pentamidine, and cotrimoxazole were both considered effective, with co-trimoxazole as the usual medicine of choice. Pentamidine was a diamidine originally tried in the 1940s as a treatment for sleeping sickness. Co-trimoxazole, usually referred to by the trade names Bactrim or Septra, was a combination of trimethoprim, a nucleoside analog that came out of the Hitchings-Elion antimetabolite research program, and the sulfonamide sulfamethoxazole.41 In the early years of the epidemic, AIDS patients with PCP might be treated with either intravenous pentamidine or with co-trimoxazole. 39

Mark A. Jacobson, personal communication, May 10–11, 2018; Bayer and Oppenheimer, AIDS Doctors, 12–18, 64–69; Greenwood, Antimicrobial Drugs, 361–62; and Montagnier, Virus, 153–56. Montagnier mentions several other opportunistic infections associated with AIDS, including toxoplasmosis, candidiasis, shingles, leukoplakia, tuberculosis, lymphomas, and Kaposi’s sarcoma (the latter two viewed as viral in origin). 40 Bayer and Oppenheimer, AIDS Doctors, 121–22; Montagnier, Virus, 153; Mark A. Jacobson, personal communication, May 10, 2018; “Pneumocystis pneumonia— Los Angeles,” Morbidity and Mortality Weekly Report, June 5, 1981, 250–52. 41 Bayer and Oppenheimer, AIDS Doctors, 122; Greenwood, Antimicrobial Drugs, 282–83; Peter S. Arno and Karyn L. Feiden, Against the Odds: The Story of AIDS Drug Development, Politics & Profits (New York: HarperCollins Publishers, Inc., 1992), 85; and Mark A. Jacobson, personal communication, May 10–11, 2018. On trimethoprim and co-trimoxazole see Greenwood, Antimicrobial Drugs, 254–56; and Lesch, “Chemotherapy by Design,” 289–90.

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Medical opinions differed at first on the prophylactic use of co-trimoxazole, and it was not until 1988 that a clinical trial was published that gave scientific support to this practice. By that time, community-based clinical trials were underway on the use of aerosolized pentamidine as a treatment or preventive measure, on the view that localization of the drug in the lungs would minimize the drug’s systemic toxicity. Aerosolized pentamidine won FDA approval in 1989, but problems of cost, the difficulty of administration, side effects, and occasional extrapulmonary pneumocystis disease with this approach soon gave the advantage to co-trimoxazole in clinical practice.42 By the late 1980s, treatment and prophylaxis of PCP had become part of standard medical care for people with AIDS, with significant impact on morbidity and mortality. Joined to parallel developments in the management of other opportunistic infections, treatment and prevention of PCP led to marked improvements in length and quality of life for those who were HIV positive. The average life expectancy for those with full-blown AIDS increased from eight months in 1981 to a little less than three years in 1994. Physicians who had struggled with the bewildering manifestations of AIDS in the early years regained some sense of control if not yet mastery. Some observers saw in these events the first steps toward the conversion of AIDS from an inexorably fatal disease to a manageable chronic illness.43 From the mid-1980s to the early 1990s, an important shift occurred in the treatment and prevention of AIDS-related conditions. As the example of PCP indicates, this change came primarily not from new drugs arising from AIDS-focused research, but from the organization of prevention and treatment around drugs from other sources repurposed for the new crisis.

Protease Inhibitors and Combination Therapy The real conversion of HIV infection to a chronic condition had to wait for the next breakthrough in antiretroviral drugs. This came with the introduction of the protease inhibitors and non-nucleoside reverse 42

Bayer and Oppenheimer, AIDS Doctors, 122–23; Mark A. Jacobson, personal communication, May 10–11, 2018; M. A. Fischl, “Safety and Efficacy of Sulfamethoxazole and Trimethoprim Chemoprophylaxis for Pneumocystis Carinii Pneumonia in AIDS,” Journal of the American Medical Association, 259 (February 26, 1988): 1185–89; Arno and Feiden, Against the Odds, 83–96, 114–18; and Montagnier, Virus, 154–55. 43 Montagnier, Virus, 152–55; Bayer and Oppenheimer, AIDS Doctors, 124–25; Arno and Feiden, Against the Odds, 20; and AIDS: The Making of a Chronic Disease, ed. Elizabeth Fee and Daniel M. Fox (Berkeley: University of California Press, 1992), 4–5.

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transcriptase inhibitors beginning in the mid-1990s and their incorporation into combination therapies with nucleoside reverse transcriptase inhibitors. As the name indicates, the protease inhibitors interfere with the enzyme protease, which plays a key role in the replication cycle of HIV, at a distinct and later stage from reverse transcriptase. The non-nucleoside reverse transcriptase inhibitors block the conversion of viral RNA to DNA by attaching to the active site of the reverse transcriptase.44 The possibility of intervention at the stage of protease activity was perceived early. Already in 1986, scientists at two pharmaceutical companies, Merck and Hoffmann La Roche, began a search for inhibitors of the protease enzyme. Other companies joined the search. The research benefited from a recently improved understanding of the three-dimensional structure of the active enzyme, and the use of computational chemistry. In the early 1990s, three protease inhibitors were being tested: indinavir from Merck, saquinavir from Hoffmann La Roche, and ritonavir from Abbott Laboratories.45 Each of these compounds by itself has a powerful inhibiting action on HIV replication. It soon became clear, though, that used alone each one presented serious problems. Most important, the protease inhibitors—like the reverse transcriptase inhibitors before them—soon encountered viral resistance. A decisive step came with the recognition that the protease inhibitors might be more effective and durable if they were used in combination with a distinct group of antiretrovirals, namely the reverse transcriptase inhibitors.46 The turn to combination therapy was a natural extension of an approach to drug treatment that long antedated the protease inhibitors and even the AIDS epidemic. One of the earliest and strongest endorsements of the promise of combination therapy in the treatment of HIV infection came from Harvard researcher Martin Hirsch. Speaking at a conference in November 1985, Hirsch pointed out that diseases for which synergistic drug combinations were already a fact included enterococcal endocarditis, cryptococcal meningitis, and tuberculosis. He also referred to successful

44

Montagnier, Virus, 160–65; Greenwood, Antimicrobial Drugs, 379–80; Victoria A. Johnson, “New Developments in Antiretroviral Drug Therapy for HIV-1 Infections,” AIDS Clinical Review 1995/1996, ed. Paul Volberding and Mark A. Jacobson (New York: Marcel Dekker, Inc, 1996), 305–46 (esp. 332–36); and Mark A. Jacobson, personal communication, June 6, 2018. 45 Montagnier, Virus, 161–2; Delaney, “Development of Combination Therapy,” 503–04. 46 Ibid., 504 ; Yarchoan Oral History, 32–33.

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combination therapies of herpes infections and cancer. The implication was clear: treatment of HIV might find success by following the same path.47 When, in late 1986, Samuel Broder’s group at NCI began looking at NRTIs other than AZT, “there was,” Robert Yarchoan recalled, “initially not so much the idea of combining drugs. We just hoped the next one was going to be better.” It soon became evident that each drug by itself had limited activity. They also saw several positive reasons to try drug combinations. The example of the combination therapy of cancer suggested that combining drugs with different toxicities could allow lower doses of each to be used, with greater anti-tumor activity. Two different drugs used together might have synergy. The example of combination therapy for tuberculosis since the 1950s suggested that two different drugs used together might slow the development of viral resistance. In a trial in which they compared using AZT and ddI simultaneously versus alternating them, they found that subjects did much better if the drugs were given simultaneously at half dosage than if they were alternated at full dose. They hypothesized that the drugs were acting on different cell populations.48 Speaking at the International AIDS Conference in Montreal in 1989, Broder described the evolution of successful combination therapy for childhood acute lymphoblastic leukemia and predicted that HIV treatment would also improve as new drugs made possible new combination therapies.49 The early 1990s witnessed a rapid expansion of combination therapy studies, driven in part by the increasing presence and role of the pharmaceutical industry in AIDS drug research. Between 1991 and 1995, more than twenty significant combination therapy trials were completed or in progress, with three-drug combinations increasingly favored.50 In 1995, the Inter-Company Collaboration for AIDS Drug Development (ICC), a group of pharmaceutical companies, announced the creation of a master protocol for combination therapy. Like Hirsch’s statement of ten years earlier and Broder’s statement of six years earlier, the ICC looked to the past as the model. The ICC wrote that its protocol “builds upon historical work with combination chemotherapy that resulted in treatments to successfully control chronic immunosuppressive, infectious, or malignant

47 Martin S. Hirsch, “Prospects for Chemotherapy of Retroviruses,” in Antiviral Chemotherapy: New Directions for Clinical Application and Research, ed. John Mills and Lawrence Corey (New York: Elsevier, 1986), 111–17 (on 115). 48 Yarchoan, “Oral History,” 30–32. 49 Delaney, “Development of Combination Therapies,” 503. 50 Ibid., 503–04.

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diseases, such as tuberculosis, leprosy, childhood acute lymphoblastic leukemia, and Hodgkin’s lymphoma.”51 The most dramatic news came a year later. At the Eleventh International Conference on AIDS in Vancouver (1996), several research groups reported on the success of recent clinical studies of combination antiretroviral therapies. Combinations included two nucleoside reverse transcriptase inhibitors taken together or joined with a non-nucleoside reverse transcriptase inhibitor, or one or two nucleoside reverse transcriptase inhibitors joined with a protease inhibitor. A panel convened by the International AIDS Society USA proposed revised therapeutic guidelines that took into account findings on combination therapy as well as recent improvements in the quantitative measurement of HIV RNA. Toward the end of the conference, Martin Markowitz of the Aaron Diamond AIDS Research Center in New York presented striking results with a combination therapy comprised of the nucleoside reverse transcriptase inhibitors AZT and 3TC and the protease inhibitor ritonavir and raised the possibility of the eradication of HIV infection. Many questions remained to be resolved, but there was no doubt in the minds of conference participants that the therapy of HIV infection had taken an important turn.52 What followed is well known. For many of those with access to it, in particular those who had not received any prior treatment and thus had HIV strains with no underlying resistance to any component of the three-drug regimens, the new combination therapy durably suppressed the virus. Viral load dropped. Symptoms of HIV infection and frequency of opportunistic infections declined precipitously, as did mortality from AIDS. People with advanced disease seemingly came back from the dead, in what became known as the “Lazarus effect.” In the decade and a half following the introduction of combination therapy, life expectancy at age 20 increased sharply for those infected with HIV in Europe and North America, while

51

Ibid., 504. Montagnier, Virus, 163; Kevin M. De Cock et al., “Summary of Track B: Clinical Science,” in One World. One Hope. Proceedings of the XI International Conference on AIDS, Vancouver, Canada, July 7–12, 1996, supplement, AIDS 103 (December 1996): S1–S133 (on S107–S113); Charles C. J. Carpenter et al., “Antiretroviral Therapy for HIV Infection in 1996: Recommendations of an International Panel,” Journal of the American Medical Association 276, no.2 (July 10, 1996): 146–54; Milo Gibaldi, “The Eleventh International Conference on AIDS: Cautious Celebration in Vancouver,” Journal of Clinical Pharmacology 37, no. 1 (January 1997): 20–24; and David Brown, “AIDS Therapy Faces a Turning Point,” Washington Post special report, July 12, 1996. 52

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still falling short of that of uninfected individuals with comparable access to health care. The AIDS epidemic entered a new phase.53

Conclusion While the far-reaching impact on mortality and life expectancy for those who were HIV-infected came only with the availability of combination therapies from the mid-1990s, each of the turning points considered here marked an important stage in research and development on drug treatment, and each contributed to the therapeutic success that was eventually achieved. At each major turning point in treatment between 1981 and 1996, specific knowledge and practices from the past, and in some cases contemporary knowledge and practices developed independently of AIDS, proved decisive in advancing the therapy of HIV/AIDS. The initial engagement of researchers was facilitated by earlier cancer research and by preexisting drugs like interferon, HPA-23, and suramin. A decades-old research program based on the antimetabolite concept guided recognition of a path to rational drug design. Prevention and control of opportunistic infections drew on an armamentarium of powerful drugs developed for the most part before AIDS came on the scene. The successful combination therapies introduced in 1996 drew on prior models of combination therapies for tuberculosis, cancer, and other diseases, as well as on a decade of thought and trials focused on antiretroviral drugs. These four turning points also illustrate a long-term trend in the trajectory of treatment research—from the prominence of small modestly funded research teams that had the flexibility to move quickly to respond to the new disease in the beginning of the period—to large-scale more heavily

53

Delaney, “The development of combination therapy for HIV infections,” 501; Mark A. Jacobson, personal communication, May 10-11, 2018. On mortality trends see “Mortality Slide Series through 2015”; and Centers for Disease Control, “HIV and AIDS—United States, 1981-2000,” MMWR 50 (21) (June 1, 2001): 430-434. On changes in life expectancy see The Antiretroviral Therapy Cohort Collaboration, “Life expectancy of individuals on combination antiretroviral therapy in highincome countries: a collaborative analysis of 14 cohort studies,” The Lancet 372 (no. 9635) (July 26, 2008): 293-299; and Julia L. Marcus et al., “Narrowing the gap in life expectancy between HIV-infected and HIV-uninfected individuals with access to care,” Journal of Acquired Immune Deficiency Syndrome 73, no. 1 (September 1, 2016): 39-46.

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funded research programs led especially by the pharmaceutical industry toward the end of the period. AIDS appeared on the scene at a historical moment when multiple resources supplied by the prior history of medical science could be brought to bear on the development of treatments. Without the prior existence of this knowledge and experience neither the pressures exerted by a rising AIDS activism nor the presence of a powerful and well-supported network of academic, government, and pharmaceutical industry institutions would have been sufficient to yield effective drug therapies for HIV/AIDS in the first decade and a half of the epidemic.

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Vitello, Paul. “Jerome Horwitz, AZT Creator, Dies at 93.” New York Times, September 20, 2012. Volberding, Paul, Ruben Valero, John Rothman, Gayling Gee. “Alpha Interferon Therapy of Kaposi’s Sarcoma.” Annals of the New York Academy of Sciences 437 (1984): 439–46. Volberding, Paul, C. B. Wofsy, and D. I. Abrams. “Interferon and Interleukin-2 Therapy of Kaposi’s Sarcoma.” Advances in Experimental Biology and Medicine 187 (1985): 151–57. Wastila, Linda J., and Louis Lasagna. “The History of Zidovudine (AZT).” Journal of Clinical Research and Pharmacoepidemiology 4 (1990): 25– 37. Woo, Elaine. “Jerome Horwitz Dies at 93; Developed Potent Anti-AIDS Drug AZT.” Los Angeles Times, September 27, 2012. Yarchoan, R., H. Mitsuya, S. Matsushita, and S. Broder. “Implications of the Discovery of HTLV-III for the Treatment of AIDS,” supplement, Cancer Research 45 (September 1985): 4685S–88S. Yarchoan, Robert. “Oral History,” Interview by Victoria A. Harden and Caroline Hannaway. In Their Own Words: NIH Researchers Recall the Early Years of AIDS, April 30, 1998, http://history.nih.gov/NIHInOwnWords/.

CHAPTER EIGHT “DAMAGE CONTROL” AND THE HIV/AIDS EPIDEMIC IN HENAN CHINA XIAOXING LIU

Introduction On the eve of the World AIDS Day in 2016, Qian Liu, the author of Death in Blood War: Field Report on HIV/AIDS in Henan China, posted an article online, “Henan AIDS incident, the truth must be revealed.” In this article, she states, “The truth about the AIDS epidemic in Henan has never been truly disclosed.” She recounts the many travesties suffered by Henan AIDS patients and their families, and in doing so draws attention to the public health incident that would later devolve into a devastating humanitarian disaster. In part, this severity rests on the fact that although twenty years have passed since the first group of infected patients fell ill and began dying, the Henan AIDS epidemic continues to linger. As the works of Qian Liu and Yaojie Gao (the first Chinese AIDS activist) repeatedly proclaim, the disaster in Henan remains as undisclosed as it is unfinished. It is not over, and more remains to be said precisely because the provincial government has done much damage control to prevent those who know the truth from speaking out. This article aims to echo such sentiments and to support the political efforts of the activists. Although epidemics are obviously medical issues, their prevention and treatment are also always matters of political and social responsibility. The AIDS epidemic in Henan is no exception to this rule. As a disease, it has to do with pathogens, illness, medicine, treatment, and death. As a social and political issue, questions concerning how a government and its people should and have responded to health crises also cannot be avoided. In the case of Henan, the provincial and local governments’ corruption, deception, and ineffectual responses to the AIDS epidemic remain one of the most painful reminders of this inseparability between medicine and politics. Considering that tens of thousands of people

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are now dead, families have been destroyed, and villages withered, the present paper argues that the events of the Henan blood disaster indicate the urgency with which China’s political system must be reformed. To ensure that responses to future epidemics and other disasters are successful, policy and organizational changes at the level of local government will be especially necessary.

AIDS in the Age of Global Health No past effort to combat disease captures the promise of medicine and global health like the worldwide response to AIDS.1 After the initial shock of its discovery, the efforts of doctors, scientists, and health workers, who mobilized to fight against this deadly disease, constitute an important achievement in the recent history of medical innovation. As Luke Messac and Krishna Prabhu note: In the space of thirty years, scientists identified the pathogen and developed the necessary tools to turn what had been a death sentence into a manageable chronic disease. This is modern medicine at its best.2

More promising still is the fact that it is not only patients from the global North who benefit from the outcomes. In addition, reduced drug prices and increased government and NGO funding initiatives have allowed patients in poorer countries to receive treatment as well. Indicative of this wider international commitment to eliminating AIDS, President George W. Bush, as leader of the world’s then undisputed financial hegemon, proposed a sweeping new plan of action during his January 28, 2003 State of the Union Address: AIDS can be prevented. Antiretroviral drugs can extend life for many years … Seldom has history offered a greater opportunity to do so much for so many … I ask the Congress to commit $15 billion over the next five years, including nearly $10 billion in new money, to turn the tide against AIDS in the most afflicted nations of Africa and the Caribbean.3

1 Luke Messac and Prabhu Krishna, “Redefining the Possible: The Global AIDS Response,” in Reimagining Global Health: An Introduction, ed. Paul Farmer et al., (Berkeley and Los Angeles: University of California Press, 2013), 5. 2 Ibid. 3 George W. Bush, “State of the Union Address,” Washington Post, January 28, 2003, http://www.washingtonpost.com/wp-srv/onpolitics/transcripts/bushtext_ 012803.html.

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When pathogens develop and invade human bodies, we might not be able to avoid this invasion, but if we respond quickly with the resources and technology available, it is possible to control or reduce the damage. In this process, governments and its officials play a significant role, as did President Bush, in implementing policies, allocating resources, and mobilizing trained personnel to respond to a given health crisis.

AIDS in Henan Province, China Commenting on AIDS in Henan Province, Joan Kaufman et al. point out, “This is a mode of infection particular to China that has devastated entire villages, creating a large number of AIDS victims who acquired HIV not through known high risk stigmatized behaviors such as drug use, prostitution, or homosexual activity.”4 Instead, the cause is institutionally based and stems from the local government’s own organization of largescale plasma donations and sales, often referred to as a “plasma economy.” The rationale behind its initial implementation was that such a project would be “good for both the country and the donors.” However, these alluded to benefits solely financial in nature. At a time when China was transitioning to a regulated market economy, the prioritization of lucrative social projects led to growing public and private interests in the sale of blood. A popular slogan at the time was “Get rich quickly, donating blood is an honorable thing to do!”5 It quickly became a campaign that swept across many counties in the province. In particular, individuals with low education levels and little capital were desperate to sell their plasma as a means of survival; for the state, it offered a chance to recoup these costs and generate revenue through the development of engineered products, such as human albumin and immunoglobulin. To support the so-called plasma economy, a whole series of official plasma stations and blood collectors were required to facilitate the operation. How are paid blood donors infected with HIV? In addition to poor disinfection of equipment and poor sanitation, returning blood cells to the donors is the fatal route of infection. The blood station harvests only plasma, 4

Joan Kaufman, Arthur Kleinman, and Tony Saich, eds., AIDS and Social Policy in China, (Cambridge, MA: Harvard University Asia Center, 2006), 11. 5 Qian Liu ี೒, “Henan aizi shijian, zhenxiang bixu dabai—xiezai 2016 nian shijie aizibing ri qianxi” Ἑ༡Ⱅ⁠஦௳㸪┿┦ᚲ桢⤎䙤—෗ᅾ2016ᖺୡ⏺Ⱅ⁠⑓᪥๓ ኤ [Henan AIDS incident, the truth must be revealed—Written on the eve of 2016 World AIDS Day], (Human Rights in China ୰ᅜே㜪, (accessed November 10, 2016), https://www.hrichina.org/chs/zhong-guo-ren-quan-shuang-zhou-kan/liuqian-he-nan-ai-zi-bing-shi-jian-zhen-xiang-bi-xu-da-bai-xie.

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not blood cells. Normally, this is done individually, and blood is drawn from one donor. After plasma is extracted by centrifugation, the blood cells left will be put back into the person’s body. In the Henan case, so many villagers rushed to sell their blood that the blood stations were not able to handle the amount of work, but they were unwilling to reject the profits brought by the donors. As a result, they did something transgressive. During this process, blood from several donors of the same blood type was placed together into the centrifuge to extract plasma. Then the blood cells were washed and injected back into the blood donors. Therefore, as long as there was one HIV-infected person in that group, most of the other people would likely become infected also. As a result of this erroneous operation, HIV spread rapidly.6 Henan’s plasma traveled to the country’s six major biological product institutes,7 all affiliated with the China National Biotechnology Group Company (CNBG) established in 1989. As the largest supplier of domestic biological products, CNBG exported goods to 32 countries and throughout China.8 As a result, many people living with HIV/AIDS in Beijing, Shanghai, and other places have iatrogenic roots in Henan. For a certain commission, doctors would even encourage patients to have a blood transfusion, whether it was necessary or not, which prompted more people to be infected.9 Thus, at the same time as international initiatives to fight the disease were proposed and approved, hundreds of thousands of despairing peasants were quietly dying in Henan. It is much too late to reverse this unsettling irony, nonetheless, I will briefly attempt to illustrate the reality suffered by the people there.

6

Ibid. Qian Liu ี೒, Xueshang—Zhongguo Henan HIV/AIDS Baogao ⾑㭮—୰ᅜἙ༡ HIV/AIDS㊌␱ [Death in Blood War: Field Report on HIV/AIDS in Henan China], (Taipei: Tonsan Pub., 2012), 247. 8 Baike Baidu ⓒᗘⓒ⛉, Zhongguo Shengwu Jishu Jituan Gongsi୰ᅜ⏕≀ᢏ㜖暭 ⛉⅓⏟, [China National Biotec Group Company], (Baidu Encyclopedia ⓒᗘⓒ⛉), Accessed 2018. https://baike.baidu.com/item/%E4%B8%AD%E5%9B%BD%E7%94%9F%E7%8 9%A9%E6%8A%80%E6%9C%AF%E9%9B%86%E5%9B%A2%E5%85%AC% E5%8F%B8 9 Liu, Xueshang, 259. 7

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The Blood Stations As now has become obvious, the mounting evidence in the Henan AIDS epidemic all seemed to point toward one site of origination: plasma collection at government-sanctioned blood stations. These stations drew on the recent techniques of plasma collection, which had been developed initially for the treatment of burn patients. In the 1970s, plasma collection was made a conventional practice in Japan, the US, and Europe. In 1979, plasma collection was piloted at the Tianjin Central Blood Station and was instituted across China shortly thereafter. Four years later, in 1983, the first Chinese citizen to be infected with HIV was a hemophilia patient, who had been injected with a “coagulation factor,” imported from the US. At that time, China was just beginning to establish and expand its relevant medical practices, and had to rely almost entirely on imported blood products. Following the aftermath of this first HIV case, China’s Health Department expressed growing concerns over the safety of blood products imported from Europe and the US. By 1984, a ban had been placed on foreign plasma and human albumin in a concerted effort to keep AIDS out of China. The consequences of this ban, however, were equally concerning, as most domestic clinics now faced severe shortages of blood products. Unwilling to return to risky imports, China’s need to produce its own domestic blood products became apparent. To ensure safe practices, the scientist, Junxiang Liuࡈ䳭⒈, and his colleague compiled a Plasmapheresis manual in hopes of successfully regulating the extraction procedures to protect patients.10 However, several years later, plasma stations mushroomed, and the focus now shifted to the lucrative potential of plasma extraction. As a result, in 1992, the Health Department of Henan Province and the Provincial Red Cross Blood Center signed an ambitious contract that would lead to an extraction quota twice the number of any previous year. Because these goals were not feasible under the existing Red Cross infrastructure, additional government-run blood stations were rapidly introduced. Thus, by 1993, thirty-three blood stations in Zhumadian, and hundreds in Xinyang District had already appeared. In the midst of these ambitious projects, however, few stations paid due attention to safety procedures.11

10

Liang Shen ỿு, Qi Fei⁽⳼, and Li Junjie ᮤಇᮽ, “Sanshi nian caixue shi” ୕ ༑ᖺ㔗⾑ྐ [30-year history of blood collection], Southern Weekly ༡᪉࿘ᮎ, October 23, 2008, http://www.infzm.com/content/18896/0. 11 Ibid.

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In 1994, just one year after the institution of these blood stations, the first HIV-infected plasma donors were diagnosed. The Health Departments of Henan, Anhui, and Hebei Provinces all ordered the shutdown of their plasma apheresis stations in April 1995. However, such orders were only partially followed, as many stations were only recently built and had yet to recoup their construction costs. Although some of the government's blood stations did in fact close, the incentive to continue collecting huge profits led to a large number of underground plasma collection stations. Even more scandalous than these underground operations, though, was the systematic omission of information that prevented villagers from knowing the true cause of the other stations’ closures. They were left in the dark about the growing epidemic and were not informed of the continued risks of selling plasma to the stations still in operation. In Guomei Xia’s 2002 book, The Report on AIDS Problems in China, a former donor diagnosed with HIV disclosed, In 1992, I sold blood to Jiaozuo in Henan Province. After selling it for 12 times, I was found carrying hepatitis C, so I was not allowed to sell it anymore ... But, in 1995, I heard that anyone could sell blood in Henan, so I went to Nanyang City ... At that time, there were dozens of underground blood stations in Nanyang. Each of them had hundreds of people selling blood. In addition to the Sichuanese, I also met people from Hubei, Hunan, and Anhui. Some people’s blood did not come out smoothly, so they hanged themselves upside down on the beam to make it flow better.12

At that time, worrying they would lose the opportunity to sell their blood, some donors rushed their brothers, sisters, and even children to the remaining blood stations. As a result, the year prior to the provincial government’s termination of these operative blood stations produced the highest percentage of infected donors. Ke Zhang, an infectious disease doctor from Beijing, who treated patients in Henan, collected data that indicated a staggering “89.3% of patients were infected with HIV/AIDS in 1995.”13 Thus, despite the technique arising in the Era of Global Health and serving as a vital course of treatment for burn patients, plasma collection carries with it a much darker history of abuse in China. By moving from the 12 Yaojie Gao 㧗⪀㳨, “Wode Maodie Shiguang” ᡃⓗ⪄⪊㗝ℰ [My Elderly Life], (BBC.com Chinese website, October 23, 2013), https://www.bbc.com/zhongwen/simp/china/2013/10/131023_100women_gaoyaojie. 13 Ke Zhang, ⼇⏖, “Henan aizibing wunian diaocha baogao” Ἑ༡Ⱅ⁠⑓஬ᖺ寪 㟌㊌␱ [Five year investigation report on Henan AIDS], (Beijing Spring, 2005), beijingspring.com/c7/pic/ad.doc.

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historical development of AIDS in Henan to the present continuation of this regional epidemic, the following sections seek to show just how deep this abuse has been.

The Paid Blood Donors To be sure, various other stories about the Henan AIDS disaster have begun to emerge in field reports, research papers, and novels. Some are extremely sad, others almost unbelievable. I have deliberately avoided the more dramatic accounts and instead opted for a more quantified and descriptive overview in order to emphasize the magnitude of the disaster. At the outset, it should be noted that Southeast Henan is one of the least developed areas in China. It had a population of 100 million in 2008 and suffered from limited resources and predominantly barren land. People had not had enough to fill their stomachs for a long time. Their biggest dreams revolved around one day producing enough food to feed themselves and their families. Although they were paid relatively little by selling blood, it still exceeded what they could earn working in the fields. To earn enough money even to dine at a local restaurant and bring home leftovers was already sufficient to incentivize blood extraction. Government propaganda unsurprisingly emphasized the reciprocal financial gains the plasma economy would produce for both individuals and society in this resourcestrapped region. Yet, as tempting as selling blood became, its deadly effects quickly grew apparent. In Zhu Lao’er’s family, for instance, six members were infected with HIV through plasma donations. Zhu (1955-2007) was a poor peasant from Silver Village. He had never attended a school and did not even know the characters of his name. He started to sell his blood when he was eighteen years old to pay for his father’s medical bills. He invited his wife and his friends to sell blood in the 1980s when the government’s message was “Donating blood is honorable.” They used the money to pay for medical bills, kids’ tuitions, and family planning violation fines. In the late 1980s, they started to sell plasma. His records showed donations of 5000cc a day in five different stations. Around 1990, selling blood was like a snowball effect that involved more and more people, including his two sons and two daughters-in-law. His three brothers and their wives were also infected with HIV. In his extended family, twelve people were infected, and six had died by the time when Zhu was interviewed by Liu in 2006. Zhu and other donors expressed unbearable regret over the decision to sell their plasma during their interviews. They repeatedly told Liu, “If only they knew that selling blood would lead to catching AIDS, then they would have never done it, no

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matter how much money the buyer offered. They would never have sold their blood even if they had to beg for food or starve to death!” Zhu and his family were never informed of the risks involved, and some continued to sell their blood until 1998, after which point all the collection stations had been closed.14 Zhu Lao’er himself died of AIDS in 2007.15 In another instance, in 2001, Yaojie Gao visited a village devastated by AIDS and spoke with four widowers in the course of just one morning. Each of the men had two to four children, and none had adequate food, clothing, or parental support. When Gao was curious as to why more women died of AIDS than men, she learned that villagers generally held the belief that women had more blood in their bodies because of their menstrual cycles, and thus were better candidates for blood donations. Families were consequently quick to ask their female members to sell blood, and the ensuing gender gap in mortality rates left behind many fathers to raise their young children alone.16 By 2004, scholars were warning that “China’s AIDS orphans problem is unfolding on a massive scale in central China as a result of tainted plasma donation practices during the mid-1990s.”17 Many children lost both parents due to AIDS. In family after family, mothers and fathers are dying, leaving as many as 200,000 children either parentless or in the care of aging grandparents in Henan alone.18 Numbers related to HIV/AIDS are considered state secrets and not available to researchers and journalists. Therefore, whoever undertakes research on the epidemic has to construct their own database. In a rare case, the Minister of Health, Zhang Wenkang, released some alarming figures in 2002. The number of HIV-infected and AIDS patients in China had reached one million. The spread of AIDS caused by irregular and illegal blood collection activities around 1995 involved twenty-three provinces, autonomous regions, and municipalities. The infection rate of plasma donors was generally 10%–20%, and even reached 60% in key villages.19

14

Ibid., 49–50. Liu, Xueshang, 41–42. 16 Gao, Wode Maodie Shiguang, 64–65. 17 Kaufman et al., AIDS and Social Policy in China, 10. This book followed a conference at Harvard in 2004. 18 Alice Park, “China’s Secret Plague,” Time Magazine, December 10, 2003, http://content.time.com/time/magazine/article/0,9171,557056,00.html. 19 Health News ೺ᗣ㊌, December 27, 2002, “Maixue Chuanbo Aizibing he Guojia Jimi” ⌽堧ἇ㒔剥㺲䖬⑳⛤⮝㜡⮭ [Selling Blood Spreading AIDS and the National Secret], (quoted in Boxun.com, ༤宖㖗既伸December 29, 2002), https://www.peacehall.com/news/gb/pubvp/2002/12/200212290253.shtml. 15

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Despite the growing awareness of the AIDS epidemic, the government deliberately took action to deny the link between plasma donations and sharply increased mortality rates. As a result, the overall number of fatalities due to AIDS is difficult to estimate. However, the numbers Liu gathered through door-to-door surveys in Silver Village can be compared with the numbers reported by cadres in Houyang Village. The former had a population of 2,600 people composed of 600 households. More than 1,000 had donated blood by 2006, and of these individuals, 400 were infected with HIV, while 245 had died of AIDS by December 31, 2011. Houyang, on the other hand, had a population of 4,000 residing in 1,200 households, and Liu reports that 1,800 donated blood, while 300 died.20 With almost one in ten persons falling victim to the AIDS epidemic in Silver and Houyang Villages, it is also important to discuss the responses that doctors and researchers offered in light of the growing disaster.

Doctors and Researchers Of the hundreds of thousands of Chinese doctors, only four explicitly stood up in protest about what was taking place in Henan.21 All four of them have suffered ongoing harassment, threats, obstructions, and rejections from the Chinese government. Each has shown incredible bravery and leaves behind a touching story. Here, I will elect to introduce one. It is impossible not to talk about Yaojie Gao when we talk about fighting HIV/AIDS in China, and she is often considered “the first person of nonofficial AIDS prevention in China.” A gynecologist by profession, her career as an activist began in 1996, when she was attending a patient diagnosed with AIDS after receiving a postpartum blood transfusion. Once Dr. Gao discovered the cause of this patient’s illness, she began to trace the outbreak of HIV infections in several rural villages to poorly sanitized blood stations. Even though she had retired from her profession at that time, Gao began her long and difficult journey of speaking out against the AIDS epidemic. In 1996, she began an education campaign in Henan Province that extended

20

Liu, “Henan aizi shijian” https://www.hrichina.org/chs/zhong-guo-ren-quanshuang-zhou-kan/liu-qian-he-nan-ai-zi-bing-shi-jian-zhen-xiang-bi-xu-da-bai-xie 21 Xueqin Zhu ᮒᏛ໅, “Zhongguo chule ge Gao Yaojie” ୰ᅜฟ஢୭㧗⪀㳨[China has a Yaojie Gao], (China Citizen Movement ୰ᅜබẸ㏅⊏, October 5, 2016), https://cmcn.org/archives/27325.

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throughout China, advocating for prevention and treatment.22 Gao, who is in her nineties now, is still persistently fighting for the same cause while in exile in New York City. Before she escaped China in 2009, Gao visited about 1,000 families with AIDS patients in more than one hundred villages across sixteen provinces and municipalities. She received 15,000 letters from patients with AIDS and other sexually transmitted diseases and replied to each one of them. While in China, she personally assisted 164 AIDS orphans, while AIDS patients and family members visited her home almost every day. Once, she received fifty-eight visitors within a month. She authored, compiled, printed, and mailed 1.3 million volumes of AIDS prevention materials, all at her own expense. In total, she has spent over one million RMB of her own savings, award money, lectures, and book contribution fees in order to educate and treat people suffering from the Henan blood disaster. Although Gao was rated as the “Touched China Character of the Year” in 2004, and was awarded numerous international awards, she was constantly blocked, harassed, threatened, and watched over by the local government officials. In 2007, Dr. Gao was awarded the “Global Leadership Award, Women Changing Our World” by the Vital Voices Global Partnership. However, such public recognition was overshadowed by government censorship, as Henan provincial authorities held her under house arrest to prevent her from attending the ceremony. Furthermore, she was also pressured by local officials to sign a statement saying that she was “unable to travel due to poor health.”23 She eventually succeeded in going to the ceremony. Nevertheless, her initial trip to the US only further provoked the government’s curtailment of Dr. Gao’s personal freedom. After returning to China, her phone was monitored, and officers followed her whenever she left the house. While at home, police surrounded her residence, especially when she was invited to attend yet another awards ceremony. She finally decided to leave China after growing increasingly worried that the data she collected on AIDS in China would fall into the hands of government officials. When she eventually arrived in the United States, she was eightythree years old, unable to speak English, and all alone. In an interview

22

U. S. Congress, Senate (USCS), Gao Yaojie: Physician, Grandmother and Whistleblower in China’s Fight against HIV/AIDS, Washington: Government Publishing House, 2010, 2. 23 Jim Yardley, “China Covers up Detention of AIDS Doctor,” New York Times, February 16, 2007, https://www.nytimes.com/2007/02/16/world/asia/16china.html.

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before the World AIDS Day in 2016, she announced the completion of eight books, all aimed at exposing the true source of AIDS in China.24 In addition to the activism of the few health practitioners like Yaojie Gao, a small number of researchers have also endeavored to expose the Henan AIDS epidemic. Again, I will focus on one such figure, Qian Liu, who was a sociologist in the Henan Academy of Social Sciences. She had spent six years conducting research in a local AIDS-affected village and completed a 350-page book documenting the progression of the blood disaster. She met Yaojie Gao five years after Gao had been fearlessly fighting AIDS on the front line. Liu was shocked, inspired, and ultimately convinced by Gao to join the struggle. Liu was able to carry out her research on HIV/AIDS in Henan Province with the support of the National Social Science Fund. In this respect, she was more fortunate than Gao to have begun her work at a time when the Chinese government started admitting their cover-up of the early HIV outbreaks. China’s recent handling of SARS had drawn global criticism, and it now wanted to show the world they were capable of dealing with these epidemics. As a result, China started to invest resources toward this end. However, as Liu soon realized, her situation was no better than Gao’s when it came to collecting true data and reporting the facts. Moreover, her heartfelt suggestions concerning the government’s approach to managing the disaster went largely unheeded. This shift in government support arose after Liu started to extend her research beyond the objectives of the provincial party committee, who were largely concerned with promoting the surface-level achievements they had made to support AIDS victims. Under their directive, Liu was approved to visit a model AIDS village that featured the “Infrastructure boosting project,”25 designed for villages ravaged by the epidemic. Though she later 24

Siling Luo, 伾⛂渗, “Fang ai doushi Gao Yaojie 90 sui le, weihe reng nu?” 㜵Ⱅ ᩯኈ㧗⪀㳨90ⱨṭ㸪ḡἼẴ⿹Ƣ[Why is the 90 years old AIDS fighter Yaojie Gao still angry?], (New York Times Chinese Website, November 30, 2016), https://cn.nytimes.com/china/20161130/gao-yaojie-aids/. 25 The so-called “Infrastructure boosting project” is the most noticeable action that Henan provincial and local governments took in helping AIDS villages to recover. They selected thirty-eight key villages from the epidemic area as “model villages of AIDS prevention and treatment” and built a new road, a deep well, a school, a health center, a nursing home for AIDS orphans and elders, and an activity room for CCP members: six facilities were constructed per model village. These facilities, designed primarily to serve as physical spectacles, drew a substantial amount of money from the funds allotted to AIDS victims. In reality, however, such projects offered minimal benefits to patients and their families. What they did achieve, was a positive improvement in the image of provincial and local governments in Henan. See Liu,

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came to realize that the project served primarily as a showcase to improve the images of provincial and local governments. Local officials immediately antagonized her when they discovered her plan to live in an AIDS village for a significant amount of time. Her research investigations were severely obstructed thereafter, and several prearranged interviews with the Civil Affairs Department and the Epidemic Prevention Department were suddenly canceled. Even the documents she had been previously promised were withheld. After being virtually cut off from all government support, an assistant from the County Party Committee even admitted that “people avoided her after hearing she had stayed in the village for a long time.” The implied rationale behind her ostracization hinged primarily on the fact that her close connection to the victims made it too difficult for the government to mislead her with their usual tricks. She had already learned too much to be fooled. As a result, she did not obtain any information from them.26 Still, despite the lack of government support, Liu spent six years in an AIDS village and continued to collect data, conduct interviews, and keep a written record of what was happening “on the ground.” Her field report, Death in Blood War, is a factual account of the miserable tragedies in Henan’s rural areas. It also includes the testimonies and historical accounts of the local epidemic, which she intended to share with the AIDS-affected population in Henan. The reception of her work on the mainland, however, has been limited. She was not able to find a willing domestic publisher and was instead forced to publish in Taiwan. Whenever she attempted to bring copies to the mainland, they were confiscated by Chinese Customs inspection, effectively preventing those for whom this book was written from ever reading it. In short, censorship has plagued Liu’s research at every turn. She was warned many times not to speak about AIDS and even told that AIDS issues were not allowed to be publicized, reported, investigated, and researched.27 However, just as with Yaojie Gao, Qian Liu has doggedly continued her efforts to publicize the truth of the Henan AIDS disaster. She was invited to give talks during the World AIDS Day, as well as on other occasions around Henan aizi shijian. For further detailed descriptions of these projects, please see the following section on “Government officials.” 26 Qian Liu, ี೒Xueshang—Zhongguo Henan HIV/AIDS baogao ⾑㭮—୰ᅜἙ༡ HIV/AIDS ㊌␱ [Death in Blood War: Field Report on HIV/AIDS in Henan China]. Taipei: Tonsan Pub. 2012. 293-94. 27 Qian Liu, ี೒, “Buxiang chenmo”୙᝿ἀ㯱 [Do not want to be silent], Democratic China Ẹ୺୰ᅜ, March 6, 2017), http://www.minzhuzhongguo.org/MainArtShow.aspx?AID=80763.

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China and abroad. Although her speeches have left lasting impressions on their respective audiences, most Chinese people remain unaware of this humanitarian disaster. As may be surmised, Liu’s strong stance and provocative message made it difficult for her to publish her articles in China. While she has tried to post them on social media, they were often blocked and deleted. Given her ongoing challenges, her academic superiors tried to convince her many times to keep quiet but her answer is always the same, “I can’t.”28

Government Officials In contrast to the activism of researchers and health practitioners, such as Liu and Gao, government officials also comprise another important class of actors involved in the Henan disaster, albeit for entirely different reasons. Without their enthusiastic encouragement, peasants arguably would not have so quickly participated in the proposed “plasma economy.” Their aggressive promotion of the program —when combined with the region’s financial desperation—played a significant role in the rising trend of blood extraction in rural Henan. Moreover, once the epidemic had been identified, these same enthusiasts were decidedly reticent in their responses to the problem. Although they received the report confirming the existence of HIV infected blood donors, they neither reported such information to higher authorities nor took cautious action to improve the quality control at blood collection stations. Nevertheless, government officials’ involvement in the disaster was not merely limited to passive indifference and negligence. Their meager responses were also buttressed by intentional efforts to suppress evidence and research, as in the aforementioned case of Qian Liu. When local individuals became frustrated with the provincial and local governments’ attempts to cover up the problem at hand, some took their reports and grievances to the central government. Yet, rather than taking action to rectify matters, the provincial government chose to penalize this group of whistleblowers through either demoting or dismissing them from their positions. In 1994, for example, Shuping Wang, a blood analyst, discovered HIV-infected persons among blood donors and began reporting her findings to the provincial government. The provincial government flatly rejected her report and abstained from introducing any remedial measures. Wang was so worried that she took the blood sample to Beijing for testing and confirmation. When the news reached the Central Government, the national 28

Ibid.

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leaders were shocked by the seriousness of the problem. They ordered Henan policymakers to ban all blood donations and close all blood stations immediately. However, the local government not only failed to take measures to ban the blood stations but also proceeded to relieve Wang from her post. Two years after the Central Government’s initial orders were sent to Henan, all blood stations were finally closed. Within this final period of operation, however, more than 300,000 additional persons were infected with HIV in Henan and the surrounding areas. In other words, the delayed termination of the plasma economy had left a full-fledged humanitarian disaster in its wake.29 In the particularly odious example of Silver Village, a health worker sent reports of “suspected AIDS” victims to the epidemic prevention departments in the township and the county when the death toll began to climb sharply in 1998. The county department tested blood samples of this village and confirmed AIDS as the cause of recent deaths. Nevertheless, this information was suppressed. At a village health workers' conference, they were directed by their superior institutions to inform the public that the increased death toll was due to an “unknown fever.” This systematic suppression of information continued until October of 2000.30 Local government obstructed any activities of investigation, assistance, education, treatment, and research on AIDS issues and patients. Besides Gao and Liu, Ke Zhang, an infectious disease doctor based in Beijing, also witnessed the rising death toll and urged officials to intervene. The response he received clearly showed they did not care about the patients and justified their inaction by pointing to the fact that the disease had no cure. In their view, patients could only wait for death, and “When they all died after a few years, it would be all right.”31 These government officials cared more about economic development than the mortality rate of AIDS patients, because the former determined their promotion while the latter did not. Zhang went to Henan to treat AIDS patients on the weekends. When he advised patients to test for HIV at the Epidemic Prevention Station, the Henan Provincial Department of Health wrote a letter of complaint to the Ministry of Health. It stated that Zhang interfered with the department’s HIV/AIDS prevention work and requested his hospital prevent him from going to Henan.32 This letter came at a time of “ambitious scale-up treatment,” and they could have used Zhang’s help. The local officials were quick to learn how to deal with the higher authorities. The central government learned their lessons in the experience 29

Zhang, Henan, 7. Liu, Xueshang, 43. 31 Ibid. 15. 32 Zhang, Henan, 3. 30

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of dealing with SARS in 2002–2003, and they were immediately applying the measures that were successful in AIDS management, most importantly making local officials accountable. The Health Minister and the Beijing Mayor were ousted for their mismanagement of the SARS crisis. More than 120 officials were fired or penalized. It was estimated that nearly 1,000 government officials had been disciplined for the same reason. These actions shook the complacency of local government officials, who then abandoned their initial hesitation and jumped onto the anti-SARS bandwagon.33 The provincial and health officials in Henan Province also quickly learned the lesson. It seemed they abandoned the strategy of inaction and put on a great show of “taking aggressive actions to change the passive image they had before.” Fujie Zhang, the Director of the Division of Treatment and Care at the National Center for STD/AIDS Prevention and Control, praised Henan in their fight against AIDS in 2004: The Henan provincial government, the prefectural government, and the county government have devoted substantial resources to improve basic infrastructure and medical resources. In high-prevalence areas of Henan, new roads, water towers, schools, and clinics have been built. Thousands of physicians, nurses, and health workers have participated in provincial training courses on HIV/AIDS. An extensive list of free medications for HIV-related conditions has been made widely available to supplement ARV drugs. HIV/AIDS has clearly been a top priority for the Henan government and Henan health authorities.34

This relates to the “Infrastructure boosting project,” which Qian Liu calls “The biggest fraud in the AIDS disaster in Henan.”35 According to her, in March 2004, the Ministry of Health again ordered Henan to “investigate the epidemic.” In June, Henan authorities launched a large-scale AIDS prevention and treatment operation under pressure from the upcoming 15th World AIDS Conference (Bangkok, Thailand, July 12–15, 2004). The most noticeable action of the operation was to select thirty-eight key villages in 33

Yanzhong Huang, “The SARS Epidemic and Its Aftermath in China: A Political Perspective,” in Learning from SARS: Preparing for the Next Disease Outbreak: Workshop Summary, ed. Stacey Knobler et al. (Washington DC: National Academies Press, 2004), https://www.ncbi.nlm.nih.gov/books/NBK92479/. 34 Fujie Zhang, Michael Hsu, Lan Yu, Yi Wen, and Jennifer Pan, “Initiation of the National Free Antiretroviral Therapy Program in Raral China,” in AIDS and Social Policy in China. Edited by Joan Kaufman, Arthur Kleinman, and Tony Saich, (Cambridge, MA: Harvard University Asia Center, 2006), 115. 35 Liu, Henan aizi shijian, https://www.hrichina.org/chs/zhong-guo-ren-quanshuang-zhou-kan/liu-qian-he-nan-ai-zi-bing-shi-jian-zhen-xiang-bi-xu-da-bai-xie.

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the epidemic areas as “Model Villages for AIDS Prevention and Control” and implement the “Infrastructure boosting project.” It was an emergency construction to be completed in one month. In late August 2004, a Hong Kong Phoenix TV Chief Executive was invited to Henan. The Deputy Secretary of the Henan Provincial Party Committee accompanied him to an AIDS village where the “Infrastructure boosting project” was implemented. He was so impressed that Phoenix Satellite TV reported the visit that same night, which changed the image of the Henan authorities on the AIDS issue. As mentioned previously, Qian Liu had a chance to visit such projects with her colleagues two months after the TV broadcast. They were just as impressed as the head of Phoenix TV. In addition to several events, they met twenty-four orphans who stayed in a beautiful “Sunshine Home,” where they appeared to enjoy their lives. However, a year later, during her fieldwork, Liu passed by another “Sunshine Home” and found the gate locked and then learned that almost all of the “Sunshine Homes” were set aside for show only. The twenty-four orphans she met on her first visit were actually borrowed from several other villages. Similarly, on the occasion of higher authorities’ visits or reporters’ interviews, those who represented AIDS patients and health workers were all assigned ahead of time. Because the visits could directly affect their posts, local officials made sure visitors and (especially) their superiors would only see what they arranged for them.36 These projects were both deceiving and misleading because resources and attention were focused on the thirty-eight key villages, which made people outside of the province think that only these villages were infected with AIDS. In fact, these key villages only made up a small portion of all the AIDS locations. Countless other villages impacted by the epidemic remained without doctors and medicine; and no one cared.37 Even in the key villages, medicines and financial support were often too little, too late, or existed only on paper.38

Conclusion Epidemics are not merely public health issues, but also thoroughly political in nature. The prevention, monitoring, and management of these issues require organized and committed political leadership. Treating the epidemic, publicizing scientific knowledge, organizing medical treatment, 36

Ibid. Zhang, Henan, 17. 38 Liu, “Henan aizi shijian,” https://www.hrichina.org/chs/zhong-guo-ren-quanshuang-zhou-kan/liu-qian-he-nan-ai-zi-bing-shi-jian-zhen-xiang-bi-xu-da-bai-xie. 37

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requesting international assistance, and rebuilding inadequate rural health care systems, are all activities carried out by government officials. Looking back at what happened, and continues to happen in Henan, the provincial and local government officials have chronically failed to understand this. They did not view the disaster as an effect of their own involvement, or a problem relevant to their own political responsibilities. But why? As this discussion shows, the chain of responsibility in China tends to flow one way. In Huang’s terms, the corruption and lack of genuine public servility in the CCP is because “government officials ultimately remain responsible not to the public but to the higher authorities. Hence, the government will always be more sensitive to pressure that comes top down, rather than bottom up.”39 It is, therefore, more important for the officials to please and impress their superiors and easier to deceive the public than to show initiative in resolving actual problems. As a result, their implementation of “damage control” measures had little to do with achieving genuine solutions. This kind of structure fosters a culture of bureaucratic obedience that appears indifferent to the sufferings of ordinary people. Even when the central government intended to implement policies that benefited the people and the nation, corruption at local levels hindered such attempts. Since official acknowledgment of the disaster took place, international health care professionals, policy-makers, and activists have held numerous conferences to discuss the situation in China and offered their recommendations and support. For instance, in 2006, the medical anthropologist Paul Farmer expressed his optimism over China’s future, stating that “The early years of an AIDS epidemic are the time to ensure that sensible and informed policies are adopted and explosive epidemics averted. China still exerts some centralized control over the nation’s health policy, [which gives us] another reason for hope.”40 Others, however, point to the more bleak realizations concerning the “shortage of social, economic, and behavioral research in planning the China AIDS response.”41 To date, the Chinese government still seems unwilling to invest resources in these types of public safety research and epidemic prevention plans. As to the limited number of research projects domestically produced on such topics, they have continually been censored and denied publication (as the cases of Qian Liu, Yaojie Gao, and Ke Zhang clearly suggest). International and domestic attention should not obscure the greater and more direct influence of the local government and its officials. In the CCP 39

Huang, SARS Epidemic, https://www.ncbi.nlm.nih.gov/books/NBK92479/. Paul Farmer, A Biosocial Understanding of AIDS in China, (Cambridge, MA: Harvard University Asia Center, 2006), xxi. 41 Kaufman et al., AIDS and Social Policy in China, 7. 40

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and government bureaucratic system, officials at every level are compelled to remain obedient to the government, but not to the people they were meant to serve. Even though the officials do not intentionally harm people, when it comes to implementing programs and policies, the security of their careers is held as the highest priority. In sum, it is not difficult to understand why officials endeavored to cover up the Henan AIDS disaster, both insofar as they were negligent in treating the epidemic and to the extent that they actively intervened in research and activist movements. We can no longer explain the scope of the disaster and its present persistence exclusively in terms of global inequities and unequal world economic systems. China must also begin to face its own political shortcomings. Looking ahead, Yanzhong Huang’s analysis of the SARS epidemic in China remains highly relevant here. He writes, “A political analysis of the crisis not only demonstrates crucial linkages between China’s political system and its pattern of crisis management but also sheds light on the government’s ability to handle the next disease outbreak.”42 The party-state in China does not lack the resources to handle, treat, and prevent such an epidemic. Its political system allows for the mobilization of officials and the public from the top to the very bottom of society. With such immense power, however, comes an increased likelihood of deception. As Huang argues, in China, “if indeed an outbreak is imminent, a local government official concerned about his post may well choose to lie.”43 Therefore, In the absence of fundamental changes in the political system and a comprehensive epidemic control plan, not only is the same pattern of coverup and inaction likely to be repeated, but the government will find it increasingly difficult to control the multiple public health challenges it is now facing.44

This emphatic warning has been further proven through the ensuing AIDS disaster in Henan. The question of what would happen when the next humanitarian disaster hits China has since been partially and tragically answered. The Covid-19 pandemic began as an outbreak in Wuhan province, where fear of political repercussions prevented and delayed essential communications between the local and central governments. It has become clear that, if we are to have any hope in the effectiveness of China’s response to future disasters, its political system will need to change.

42

Huang, SARS Epidemic, https://www.ncbi.nlm.nih.gov/books/NBK92479/. Ibid. 44 Ibid. 43

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Bibliography Baike Baidu ⓒᗘⓒ⛉, “Zhongguo Shengwu Jishu Jituan Gongsi” ୰ᅜ⏕ ≀ᢏ㜖㞟⛉බྖ [China National Biotec Group Company]. Baidu Encyclopedia ⓒᗘⓒ⛉㸦accessed 2018㸧 https://baike.baidu.com/item/%E4%B8%AD%E5%9B%BD%E7%94 %9F%E7%89%A9%E6%8A%80%E6%9C%AF%E9%9B%86%E5% 9B%A2%E5%85%AC%E5%8F%B8 Bush, George W. “State of the Union Address.” Washington Post, January 28, 2003. http://www.washingtonpost.com/wp-srv/onpolitics/transcripts/ bushtext_012803.html. Farmer, Paul. “Preface: A Biosocial Understanding of AIDS in China.” In AIDS and Social Policy in China. Edited by Joan Kaufman, Arthur Kleinman, and Tony Saich. xix-xxii. Cambridge, MA: Harvard University Asia Center, 2006. Gao㸪 Yaojie 㧗⪀㳨. “Wode Maodie Shiguang” ᡃⓗ⪄⪊㗝ග [My Elderly Life]. BBC.com Chinese website. October 23, 2013. https://www.bbc.com/zhongwen/simp/china/2013/10/131023_100wom en_gaoyaojie. Kaufman, Joan, Arthur Kleinman, and Tony Saich. eds. AIDS and Social Policy in China. Cambridge, MA: Harvard University Asia Center, 2006. Health News ೺ᗣ㊌, December 27, 2002, “Maixue Chuanbo Aizibing he Guojia Jimi” ⌽⾑ἇ᧛Ⱅ⁠⑓࿴ᅜᐙᮘᐦ [Selling Blood Spreading AIDS and the National Secret]. (quoted in Boxun.com, ༤宖᪂既⨒ December 29, 2002), https://www.peacehall.com/news/gb/pubvp/2002/12/200212290253.sht ml. Huang, Yanzhong. “The SARS Epidemic and Its Aftermath in China: A Political Perspective.” In Learning from SARS: Preparing for the Next Disease Outbreak: Workshop Summary. Edited by Stacey Knobler et al. Washington DC: National Academies Press. 2004. https://www.ncbi.nlm.nih.gov/books/NBK92479/. Liu, Qianี೒, “Buxiang chenmo” ୙᝿ἀ㯱 [Do not want to be silent]. Democratic China Ẹ୺୰ᅜ, March 6, 2017. http://www.minzhuzhongguo.org/MainArtShow.aspx?AID=80763. Liu, Qianี೒. “Henan aizi shijian, zhenxiang bixu dabai—xiezai 2016 nian shijie aizibing ri qianxi” Ἑ༡Ⱅ⁠஦௳㸪┿┦ᚲ桢኱ⓑ̾෗ᅾ 2016ᖺୡ⏺Ⱅ⁠⑓᪥๓ኤ [Henan AIDS incident, the truth must be

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revealed—Written on the eve of 2016 World AIDS Day]. Human Rights in China ୰ᅜே㜪. (accessed November 10, 2016), https://www.hrichina.org/chs/zhong-guo-ren-quan-shuang-zhoukan/liu-qian-he-nan-ai-zi-bing-shi-jian-zhen-xiang-bi-xu-da-bai-xie. Liu, Qian ี೒. Xueshang—Zhongguo Henan HIV/AIDS Baogao ⾑㭮̾୰ ᅜἙ༡HIV/AIDS㊌࿌ [Death in Blood War: Field Report on HIV/AIDS in Henan China]. Taipei: Tonsan Pub., 2012. Luo, Siling伾ᅄ渗. “Fang ai doushi Gao Yaojie 90 sui le, weihe reng nu?” 㜵Ⱅᩯኈ㧗⪀㳨90ⱨ஢㸪ḡఱ௔ᛣ㸽[Why is the 90-years old AIDS fighter Yaojie Gao still angry?]. New York Times Chinese Website. November 30, 2016. https://cn.nytimes.com/china/20161130/gaoyaojie-aids/. Messac, Luke, and Prabhu Krishna. “Redefining the Possible: The Global AIDS Response.” In Reimagining Global Health: An Introduction. Edited by Paul Farmer et al. Berkeley and Los Angeles: University of California Press. 2013. Park, Alice. “China’s Secret Plague.” Time Magazine. December 10, 2003. http://content.time.com/time/magazine/article/0,9171,557056,00.html. Shen, Liang ỿு Qi Fei⁽⳼ and Li Junjie ᮤಇᮽ. “Sanshi nian caixue shi” ୕༑ᖺ㔗⾑ྐ [30-year history of blood collection]. Southern Weekly ༡᪉࿘ᮎ. October 23, 2008. http://www.infzm.com/content/18896/0. U. S. Congress, Senate (USCS). Gao Yaojie: Physician, Grandmother and Whistleblower in China’s Fight against HIV/AIDS. Washington: Government Publishing House. 2010, 2. Yardley, Jim. “China Covers up Detention of AIDS Doctor.” New York Times. February 16, 2007. https://www.nytimes.com/2007/02/16/world/asia/16china.html. Zhang, Fujie, Michael Hsu, Lan Yu, Yi Wen, and Jennifer Pan. “Initiation of the National Free Antiretroviral Therapy Program in Raral China.” In AIDS and Social Policy in China. Edited by Joan Kaufman, Arthur Kleinman, and Tony Saich. 96-124. Cambridge, MA: Harvard University Asia Center, 2006. Zhang, Ke⼇ྍ. “Henan aizibing wunian diaocha baogao” Ἑ༡Ⱅ⁠⑓஬ ᖺ寪㟌㊌࿌ [Five-year investigation report on Henan AIDS]. Beijing Spring, 2005. beijingspring.com/c7/pic/ad.doc. Zhu, Xueqin ᮒᏛ໅. “Zhongguo chule ge Gao Yaojie” ୰ᅜฟ஢୭㧗⪀ 㳨 [China has a Yaojie Gao]. China Citizen Movement ୰ᅜබẸ㏅⊏. October 5, 2016. https://cmcn.org/archives/27325.

CHAPTER NINE NON-COMMUNICABLE DISEASE EPIDEMIC: IDEOLOGIES AND INSTITUTIONS OF MODERNITY JOSHUA S. YANG

Communicable diseases have accounted for a vast proportion of disease and mortality experiences over the course of human history, and disease epidemics have been an entrenched element of human societies. Classical Greek literature provides one of the first clear accounts of a communicable disease epidemic in Athens during the Peloponnesian War, with references to diphtheria and malaria evident in Greek writings. From the Roman Empire until the Middle Ages, epidemic outbreaks included smallpox, measles, typhoid fever, influenza, leprosy, and plague.1 Advances in scientific discovery and medical practice, expansion of sound public health measures, and economic development over the past 150 years have resulted in an epidemiologic transition; that is, a shift in disease burden from communicable to non-communicable diseases (NCDs).2 Among the fifty-six million deaths worldwide in 2014, thirty-eight million were due to NCDs, with nearly three quarters occurring in low and middleincome countries. For example, cardiovascular diseases made up nearly half of all NCD deaths (46.2%) followed by cancers (21.7%), respiratory diseases (10.7%), and diabetes (4%).3 Often considered old-age conditions, NCDs exact a significant toll on premature death.4 Among individuals ages 1

George Rosen, A History of Public Health, Revised Expanded Edition (Baltimore, MD: Johns Hopkins University Press, 2015), 5–36. 2 Abdel R. Omran, “The Epidemiologic Transition: A Theory of the Epidemiology of Population Change,” The Millbank Memorial Fund Quarterly 49, no. 49 (October 1971): 509–38. 3 World Health Organization, Global Status Report on Noncommunicable Diseases 2014 (Geneva: WHO Press, 2014), 9. 4 United Nations, “Progress on the Prevention and Control of Non-Communicable Diseases, A/72/662.”

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thirty to seventy, in 2015, fifteen million deaths were a result of NCDs, more than preventable deaths from communicable diseases and perinatal conditions (twelve million) and injuries and violence (five million). By 2030, NCDs are projected to kill an additional fifty-two million. In describing the global burden of disease from NCDs, the World Health Organization (WHO) and United Nations (UN) have both described the global burden of disease from NCDs as an epidemic.5 Concerted global action on NCDs began with the WHO’s World Health Report 1997 which focused on chronic conditions.6 The report set off a series of events over a decade, which culminated in the UN High-Level Meeting on Non-Communicable Diseases held in 2011, the Political Declaration of the High-Level Meeting of the General Assembly on the Prevention and Control of Non-Communicable Diseases (2011), and the incorporation of an NCD-related target in the UN Sustainable Development Goals. Since 2011, three foundational consensus documents under the auspices of the WHO were established: Ɣ A global monitoring framework which created nine voluntary targets and twenty-five indicators to measure progress toward NCD reduction. Ɣ A global action plan that outlines a set of consensus interventions for the Member States to consider implementing at the national level. Ɣ A global coordinating mechanism created to advance the implementation of interventions. While these changes mark a significant global effort, they may be insufficient considering the entrenched and structural nature of the causes of NCDs.

Corporate Role in NCDs Policy actions are especially unclear when it comes to the role of corporate actors and unhealthy commodities industries, which have been identified as major drivers of the NCD epidemic.7 These include the tobacco, 5 World Health Organization, Global Status Report, 9; and United Nations, “Progress on the Prevention.” 6 World Health Organization, The World Health Report 1997: Conquering Suffering, Enriching Humanity (Geneva: WHO Press, 1997). 7 Rob Moodie, David Stuckler, Carlos Monteiro, Nick Sheron, Bruce Neal, Thaksaphon Thamarangsi, Paul Lincoln, et al., on behalf of The Lancet NCD Action Group, “Profits and Pandemics: Prevention of Harmful Effects of Tobacco, Alcohol,

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alcohol, and ultra-processed food and drink industries. Unlike traditional notions of infectious disease epidemics caused by microbiological agents transmitted by vectors or through other natural channels, transnational corporations are social, political, and economic actors, which produce disease through active and intentional efforts to maximize consumption of their products. As markets for their products in high-income countries become saturated, they spread the NCD epidemic through expansion into new markets in low- and middle-income countries, which often have fewer resources than high-income countries to control NCDs. The corporate and economic environment in which NCDs thrive is a historically contingent, uniquely modern entity. Modernity refers to the specific period, which emerges from the European Enlightenment and is linked to concepts such as secularism, rationality, science, progress, and the individual. More important for the present analysis are the institutions of modernity, such as the nation-state, political liberalism, and capitalism.8 In their earliest form, corporations were created as an instrument of government to increase their wealth and power, and depended on government bodies to function.9 They played instrumental roles in the colonial interests of Western European nations, operating as quasi-states in colonial territories. Corporations helped finance the continental conflicts, which led to the Treaty of Westphalia and the birth of nation-states and were instrumental in the efforts of nation-states to increase their power in the mercantilist period.10 Adam Smith’s critique of the monopolistic activity of the dominant British corporation, the British East India Company, in The Wealth of Nations, coupled with John Locke’s political writings, marked a turn away from mercantilism to capitalist economies and political liberalism, two essential institutions of modernity. Far from a decline into irrelevance with the fall of mercantilism, however, the corporation persisted to become economically and politically dominant. A series of legal decisions in the latter half of the 19th century constructed the corporation as a free and independent being analogous to

and Ultra-Processed Food and Drink Industries,” The Lancet 381, no. 9867 (2012): 670–79. 8 Thomas E. Kaiser, “Enlightenment,” in Oxford Encyclopedia of the Modern World, ed. Peter N. Stearns (Oxford: Oxford University Press, 2008); and John Scott and Gordon Marshall, A Dictionary of Sociology, (Oxford: Oxford University Press, 2009). 9 Joel Bakan, The Corporation (New York: Free Press, 2004), 16. 10 David Rothkopf, Power, Inc. (New York: Farrar, Straus, Giroux, 2012), 74–100.

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human beings.11 Treated this way, corporations were given the rights and protections of free individuals and the modern corporate era began. Yet, corporations are not like individuals: they are better able to draw on the aggregate financial capital of an unlimited number of people, have far greater resources to influence political decision-making and social trends, may exist in perpetuity, and usually abide by an obligation to put the interests of shareholders above any other interests. By their nature, the goals of transnational corporations in unhealthy commodities industries are in opposition to NCD prevention and control. For NCDs, the fundamental logic of the corporation suggests that transnational tobacco, alcohol, and ultra-processed food and drink corporations will continue to make every effort to promote consumption of their products—in spite of calls to partner in efforts to reduce NCD burdens—because their profits depend on it. The challenge to NCD prevention and control posed by commercial interests is not merely from transnational corporations as singular entities that promote the consumption of unhealthy commodities, but the broader economic system within which corporations are the dominant institutional form and the governments that create and maintain it. Much as corporations have come to be defined as natural, independent entities, proponents of laissez-faire capitalism convey an ideal of market-based economies as natural and self-guiding through price mechanisms and Adam Smith’s “invisible hand.” Yet, the historical record suggests that the emergence of corporate capitalism has been anything but natural, brought into being through the efforts of vested business interests and legitimized by the work of free-market intellectuals. The early 20th century was the high-water mark for corporate dominance, and the American business class was venerated for leading the economy to great heights as a result. The stock market was a source of easy wealth, and there was little political challenge to capitalism. The period of business expansion, however, was accompanied by progressivism, which viewed government as a way to expand freedom for more people through social programs. Thus, the growth in government during the interwar years sparked an intellectual resistance that espoused a free-market ideology based on individual liberty and limited government. The emerging ideology suggested human freedom was rooted in rational, self-interested actors governed by market forces, laying the roots of what is now known as neoliberalism.12 The Great Depression, however, represented a crisis in confidence in the unregulated market, ushering in Keynesianism as the 11

Bakan, Corporation, 16. Daniel Stedman Jones, Masters of the Universe: Hayek, Friedman, and the Birth of Neoliberal Politics (Princeton, NJ: Princeton University Press, 2012), 2–3.

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dominant economic doctrine and relegating neoliberal thinkers into a discredited, minority position. Roosevelt’s New Deal and the rise of Nazi Germany and communism in Russia, however, fueled neoliberal intellectuals’ drive to continue developing their ideas. Neoliberal intellectuals were not alone in their resistance to the New Deal program. The government protected unionization efforts, established a national minimum wage and maximum workweek, distributed monetary relief, employed people through public works programs, created unemployment insurance, enacted Social Security, regulated financial markets, and built the national infrastructure. For these efforts, the business class viewed the Roosevelt administration (1933–45) as a threat to the laissez-faire policies of the early 20th century by which they had accumulated their wealth and power.13 Business leaders organized the American Liberty League to amplify the voice of business in government and promote its interests. The National Association of Manufacturers also organized against the New Deal policies.14 The short-term impact on government policy was limited, and organizing efforts by the business community begun in the early 1930s would wax and wane through the post-war years. Nevertheless, the development of a network of like-minded individuals and political infrastructure to advocate for free-market principles was essential to future success. One essential relationship was that of Jasper Crane, former vice president of DuPont Chemical, board member of the Foundation for Economic Education, ardent opponent of the New Deal, and Friedrich von Hayek, an Austrian economist and leading free-market intellectual.15 In his crusade to roll back government intrusion in business, Crane felt that freemarket ideas needed to be clarified and sharpened, that a “bible” of free enterprise was needed. He found his ideological foundation in Hayek’s The Road to Serfdom, and the two men became partners in a political project to reassert free-market ideals. Crane would become the most active American businessperson in helping Hayek establish the Mont Pelerin Society—a group of intellectuals and later businesspersons devoted to developing and promoting free-market ideas. Business leaders had found the ideological foundation for their political goals, and free-market intellectualism a source of patronage for their work. The postwar prosperity experienced under Keynesian economic principles and New Deal liberalism kept the political aspirations of the 13

Kim Phillips-Fein, Invisible Hands: The Businessmen’s Crusade against the New Deal (New York: W. W. Norton, 2009), 9. 14 Ibid., 10–15. 15 Ibid., 41–43.

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business community at bay and prevented neoliberal intellectual ideals from penetrating the mainstream. In the 1970s, however, increasing public protest and government regulation, a “call to arms” in the business community, and the recessions of the 1970s marked an opportunity for the business community’s political infrastructure to mobilize the intellectual achievements of the Mont Pelerin Society to reorient macroeconomic policy. Beginning with the Kennedy Administration (1961–63) and running through the Carter Administration (1977–81), labor, environmental, and consumer protection groups made significant progress in remaking the government and federal policy to protect workers, consumers, and the public.16 The business community, however, viewed these victories as existential threats, and in the summer of 1971, a memo prepared for the Chamber of Commerce by Lewis Powell prompted a re-energized business response. The memo, titled “The Attack on the Free Enterprise System,” suggested that the American economic system was under broad attack on multiple public fronts. American businesspersons needed to acknowledge the new reality and mobilize their resources to engage in public debate and the political system to protect free enterprise and individual freedom.17 The memorandum sparked public comments by corporate leaders, re-energized organizations such as the Chamber of Commerce and American Enterprise Institute, and led to the founding of the Heritage Foundation, the Business Roundtable, and others that advocated pro-market policies. When inflation, unemployment, and economic stagnation marked the recessions of the 1970s, new popular doubt was cast on the ability of Keynesian policies to improve the economy, opening the door to new economic ideas. The newly active and well-organized proponents of free markets filled the policy gap with solutions and ideologies that had been developed and refined since the Great Depression. Though conventional history ties neoliberal takeover of government to the conservative governments of President Reagan in the United States and Prime Minister Thatcher in the UK, early adoption of neoliberal policies was evident in the policies of a Democratic President and a Democraticcontrolled Congress that passed legislation to cut the capital gains tax while raising payroll taxes.18 Thus, the persistent efforts of pro-market intellectual and business actors since the Great Depression finally saw the fruits of their

16 Nicholas Freudenberg, Lethal but Legal: Corporations, Consumption, and Protecting Public Health (Oxford: Oxford University Press, 2016), 72–75. 17 Phillip-Fein, Invisible Hands, 158–60. 18 Jacob S. Hacker and Paul Pierson, Winner-Take-All Politics (New York: Simon and Schuster, 2010), 98–100.

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labor in a radical transformation from New Deal liberalism to the neoliberal political economy in the 1970s. The changing economic environment, which had once limited the impact of corporations on public life, led to changes in corporate norms, would expand their economic impact and political influence, and magnify their influence on public health. First, corporations adopted a shorter time horizon in which to maximize returns to investors from decades to quarters or years, prioritizing short-term profitability over long-term safety of new products and sustainability of production patterns. Second, financial investment tools such as derivatives and commodities futures yielded higher margins of return on investments than corporations producing goods and services. This placed pressure on non-financial industries to overlook the potential harms posed by their products in order to maintain profitability vis-à-vis the financial sector. Third, a central goal of the business community’s political engagement was deregulation—the removal of efforts to regulate corporate activity or to weaken enforcement—that led to less protection from potentially harmful effects of consumer goods. Fourth, corporations advocated for a lower tax burden as a means of spurring economic growth. Less tax revenue for governments, however, leads to diminished public health and safety net services that can exacerbate health disparities while creating more capital for corporations to encourage consumption of goods that lead to NCDs. Fifth, corporate advocacy of privatization of public services such as education, healthcare, and law enforcement led to increased costs, allocation of services based on ability to pay, and decreased the stability of services due to market volatility. Finally, industries moved towards market concentration—a reduction in the number of companies—as a means of achieving greater scale and reducing competition. Market concentration can lead to lower prices, increasing exposure to and risk from unhealthy commodities, and consolidate political power among the largest global corporations.19 The modern multinational corporations barely resemble the first legally incorporated and state-protected entities, and their normative environment has led corporations to use specific tactics to gain competitive advantage and profits. Tactics include engaging in misleading scientific activity; shaping public opinion through public relations campaigns, advertising and marketing of harmful products; manipulating products to maximize

19

Freudenberg, Lethal but Legal, 78–85.

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consumption; becoming entrenched in political lobbying and influence; and taking legal action to protect their interests.20

The Individuation of Public Health As free-market ideology became more dominant in the 1970s and unleashed the power of corporations, public health was retreating from its ancient roots in social activism and turning toward lifestyle and behavioral interventions. Modern public health was built on Greek ideas of environmental causes of disease. The Hippocratic idea that disease originated in man and his environment gained renewed interest in the Enlightenment period in the work of William Petty. He pioneered the concept of political arithmetic, a quantitative expression of an emerging philosophy of health in the 18th century, which began to focus on the environmental causes of disease.21 Political arithmetic gave credence to environmental causes of disease and symbolized a belief that the rules which governed the relationship between disease and environmental variables could be discovered through quantification. Petty’s work, however, had limited immediate policy impact, and the environmentalist view of health was not turned into action until almost the middle of the 19th century. Petty’s political arithmetic and an environmentalist view of disease became actionable ideas within the social consequences and public health problems created by industrialization. Edwin Chadwick was instrumental in shaping the English Poor Law of 1834, which led to the public health challenges faced in industrial areas. As a member of the Royal Commission of Enquiry into the Poor Laws, he focused on the health of the poor and held “a concept of preventive social action applicable to the problems of poverty and disease.”22 His investigation into the relationship between health and poverty incorporated a desire to use data to calculate measures of health for populations and to examine the environmental conditions as causes of disease. In the Report… on an Inquiry into the Sanitary Conditions of the Labouring Population of Great Britain released in 1842, Chadwick helped to establish that disease was related to environmental conditions. The report 20 William Wiist, “The Corporation: An Overview of What It Is, Its Tactics, and What Public Health Can Do,” in The Bottom Line or Public Health, ed. William Wiist (Oxford: Oxford University Press, 2010), 3–72. 21 James C. Riley, The Eighteenth Century Campaign to Avoid Disease (London: Palgrave MacMillan, 1987), 1–30. 22 George Rosen, “Economic and Social Policy in the Development of Public Health,” Journal of the History of Medicine vol. 8, no. 4 (1953): 423.

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redirected the focus of public health away from medicine to engineering and social reform, creating institutions into which later, more accurate medical knowledge from the germ theory of disease could be inserted. It promoted governmental administrative interventions for health and established the model for modern public health.23 As the 19th century came to a close, public health efforts significantly improved health status, while the impact of medicine remained limited. The advent of biomedicine stemming from germ theory discoveries, however, would be a decisive turn in the values and focus of public health. The germ theory of disease set off a biomedical revolution, which was part of a broader emergence of the role of science and technology that shaped public health and medicine in the early 20th century.24 The tenets of public health sanitarians aligned well with early discoveries in microbiology and bacteriology. New urban centers were seen as breeding grounds for disease, and control of infectious diseases viewed the individual within his or her environment. Microorganisms which caused disease could be destroyed through improved sanitation or in the body. The joint efforts of public health and medicine had a dramatic effect on the health burden in the first half of the 20th century, with infectious diseases declining significantly. Greater acceptance of the germ theory and innovations in medical technologies, however, ultimately shifted attention not only to microorganisms, but also the individual bodies in which they were housed. Diseases became dissociated from the environment and less and less attention was paid to social, economic, environmental, and political determinants.25 Modern medicine, dispensed by physicians and in increasingly sophisticated hospitals, improved the legitimacy and authority of the discipline and physicians vis-à-vis public health practitioners. Though public health did not give up its environmental orientation entirely, it ceded authority to biomedicine and adopted the particular scientific orientation of biomedicine and laboratory science in lieu of political engagement and social reform.26 23

Ibid. Allan M. Brandt, “Behavior, Disease, and Health in the Twentieth-Century United States,” in Morality and Health, ed. Allan M. Brandt and Paul Rozin (New York: Routledge, 1997); and Amy L. Fairchild, David Rosner, James Colgrove, Ronald Bayer, and Linda P. Fried, “The Exodus of Public Health: What History Can Tell Us About The Future,” American Journal of Public Health 100, no. 1 (2010): 54– 63. 25 Brandt, “Behavior, Disease, and Health,” 63. 26 Allan M. Brandt and Martha Gardner, “Antagonism and Accommodation: Interpreting the Relationship between Public Health and Medicine in the United 24

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By mid-century, life expectancy had increased, and risks shifted to chronic or non-communicable diseases. The single-entity causal model popularized by the germ theory, however, was insufficient to address the complexity of chronic disease, giving rise to the concept of risk and modern epidemiological practice. Major epidemiological studies such as the Framingham Study (which beganin 1948 and is on-going) and the Human Population Laboratory of Alameda County, California, identified a host of behavioral risk factors, which could reduce the likelihood of acquiring chronic diseases.27 Data on chronic disease risk factors were accompanied by a radical change in health discourse in the 1970s, which reconfigured the meaning of and responsibility for health. Control over health was placed on individuals, as opposed to the environment or microorganisms, and behaviors such as physical inactivity, poor diet, and cigarette smoking came to be associated with moral failing. Corporate and business interests manufactured unhealthy products, shaped preferences for them, and created disease-inducing environments that were absolved of any responsibility.

Neoliberal Political Rationality The rise of corporate power and retreat from social and political activism in public health toward changing behaviors can be understood within the Mont Pelerin Society’s broader hegemonic neoliberal project. Neoliberalism should be seen as part of circuitous discursive processes that make commonsensical the order and interaction of specific policies, programs, and governmentality.28 Foucault defined government as “the conduct of conduct”29 and governmentality as a general term referring to the ways in which governing is thought about and systematically rationalized to organize human conduct.30 Neoliberal governmentality is a specific mentality of governing which shifts the locus of governing from the government to individual self-regulation. It is a rationality, which invents States during the 20th Century,” American Journal of Public Health 90, no. 5 (2000): 707–15; and Fairchild et al., “Exodus of Public Health.” 27 Brandt, “Behavior, Disease, and Health,” 63. 28 Simon Springer, “Neoliberalism as Discourse: Between Foucauldian Political Economy and Marxian Poststructuralism,” Critical Discourse Studies 9, no. 2 (2012): 133–47. 29 Colin Gordon, “Governmental Rationality: An Introduction,” in The Foucault Effect: Studies in Governmentality, ed. Graham Burchell, Colin Gordon, and Peter Miller (Chicago: University of Chicago Press, 1991), 48. 30 Mitchell Dean, Governmentality: Power and Rule in Modern Society (London: Sage Publications, Ltd., 2010), 16–51.

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“new quasi-entrepreneurial and market models of action”31 for the conduct of individuals, groups, and institutions. Neoliberalism specifies an ideal role of the state vis-à-vis the economy to ensure economic competitiveness through market mechanisms. It does not reject government action but views the role of government as constructing the conditions for markets and competitive entrepreneurialism to govern conduct. Neoliberal policies and programs are often equated with the Washington Consensus. Coined by John Williamson, the Washington Consensus is a series of macroeconomic recommendations and stipulations for foreign lending that emphasizes a market economy, trade, foreign direct investment, and interest rate liberalization. It includes specific macroeconomic policies such as fiscal discipline, privatization of state assets, deregulation, and property rights. Many of these recommendations became codified in structural adjustment programs of the 1970s, and promoted by international financial institutions such as the International Monetary Fund and World Bank.32 Criticisms of neoliberal effects on health are not new.33 Rushton and Williams suggest that it constitutes a “deep core” of global health, an “overarching logic and a background set of assumptions and values that has influence across policy areas and social spaces.”34 They view neoliberalism as affecting global health policy in three ways. First, it urges a diminished role of the state in society, diffusing power and authority across a wider range of social and political actors. Second, neoliberalism ties to a specific set of policy recommendations such as trade liberalization and privatization. Third, neoliberalism interacts with other paradigms of global health in ways 31 Gordon Burchell, “Liberal Government and Techniques of the Self,” in Foucault and Political Reason, ed. Andrew Barry, Thomas Osborne, and Nikolas Rose (Chicago: University of Chicago Press, 1996), 27. 32 James Pfeiffer and Rachel Chapman, “Anthropological Perspectives on Structural Adjustment and Public Health,” Annual Review of Anthropology 39, (2010): 149– 65; and Ronald Labonte and David Stuckler, “The Rise of Neoliberalism: How Bad Economics Imperils Health and What To Do About It,” Journal of Epidemiology and Community Health 70, no. 3 (2016): 312–18. 33 Sara Glasgow and Thomas Schrecker, “The Double Burden of Neoliberalism? Noncommunicable Disease Policies and the Global Political Economy of Risk,” Health Place 34 (2015): 279–86; Gavin Mooney, “Neoliberalism Is Bad For Our Health,” International Journal of Health Services 42, no. 3 (2012): 383–401; and Vicente Navarro, "Neoliberalism, ‘Globalization,’ Unemployment, and the Welfare State,” International Journal of Health Services 28, no. 4 (1998): 607–82. 34 Simon Rushton and Owain David Williams, “Frames, Paradigms and Power: Global Health Policy-Making under Neoliberalism,” Global Society 26, no. 2 (2012): 147–67.

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that promote individualization of global health problems. With respect to NCDs, Glasgow and Schrecker suggest neoliberal influences lead to individualization of health and disease and construction of individuals as entrepreneurs, self-governing subjects who bear responsibility for the management of their health.35 The prevailing view of neoliberalism in the NCD domain is of a shrinking state and shifting responsibility to individuals. Foucault’s analysis of the evolution and implications of neoliberal ideology is instructive for understanding the parallel phenomena of the rise of corporate capitalism and the individuation of public health.36 He suggests that the German neoliberal project was an effort to define state legitimacy and self-limitation on the basis of economic freedom.37 It grew in opposition to illiberal policies of national socialism: a protected economy, state socialism, planned economy, and Keynesian-style interventionism that came together during Nazism. As an alternative, German neoliberalism promoted a system of governmentality which promoted the free market as the organizing principle of government, not just the economy. It asserted that the central activity of markets was competition. This created the political space for the emergence of the corporation as a naturalized entity with personhood and the dominant actor in a laissez-faire, free-market capitalist economy. From competitive markets arises inequality, viewed as inherent in properly functioning markets. Thus, disproportionate corporate power is not anomalous or particularly problematic, and inequality is not a condition to be ameliorated through social policy attempting to counter market-derived inequalities; any such action undermines the natural competitive character of markets. Instead, markets should be allowed to function and protect against “the risk of life, the inevitability of old age and death”38 through the accumulation of an individual’s private reserve of income created through a competitive marketplace. Social policy, in this view, should move away from state provision of social protection against risks and focus on creating conditions in which competition can occur, and economic actors undertake and confront risks that enable capital accumulation. The result, as Foucault suggests, is an “individualization of social policy and individualization through social policy, instead of collectivization and socialization by and in social policy.”39 35

Glasgow and Schrecker, “The Double Burden of Neoliberalism?” 279–86. Michel Foucault, The Birth of Biopolitics (New York: Palgrave Macmillan, 2008). 37 Burchell, “Liberal Government,” 22. 38 Foucault, Birth of Biopolitics, 144. 39 Ibid. 36

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In contrast, Foucault suggests that American neoliberal scholars reconfigured Adam Smith’s view of the factors of production, leading to the idea of human capital. Individuals were transformed into enterprise units leveraging their human capital stocks to produce an earnings stream. Individuals are entrepreneurs, using their capital to consume for the ultimate goal of their own personal satisfaction, not through exchange but production. Society, then, is a collection of individuals as enterprise-units. The generalization of the “enterprise form” to all forms of conduct is the essential character of American neoliberal thought.40 Economic interpretation of domains previously considered non-economic established market rationality as a form of governmentality referred to as neoliberal political rationality. Though the individual enterprise may occupy and operate within non-economic domains, it continues to employ market rationality. The model of the market economy becomes a principle through which nonmarket social relationships, social phenomenon, and individual behavior are analyzed, assessed, and understood. Thus, not only do health care and public health become reframed as modes to “improve human capital,”41 but interventions are structured to support individuals as entrepreneurs of themselves, achieving health through individual decision-making within the principles of a market economy.

Neoliberal Political Rationality in Reducing NCDs In the neoliberal formulation, the dominant source of NCDs—corporate activity and power—and a lifestyle-focused approach adopted in conventional public health practice are misaligned. In the 1990s, some public health experts responded by reintroducing the ethos of social medicine in response to the individuation of disease.42 Focusing on neoliberal economic ideology and corporate capitalism, conflict over occupational diseases and with “Big Tobacco,” “Big Food,” and “Big Pharma” has introduced modified environmentalism in public health, focused not on sanitation and the physical environment, but the political and economic determinants of disease. Though widely acknowledged as major sources of NCDs, the political capacity and expertise to confront vested corporate and political interests in NCDs and the hegemonic capitalist economic system are lacking within the public health community. Within this historical and intellectual context, the emphasis on lifestyle interventions to reduce the NCD burden 40

Burchell, “Liberal Government,” 29. Foucault, Birth of Biopolitics, 230. 42 Dorothy Porter, “How Did Social Medicine Evolve, and Where is it Heading?” PLOS Medicine 3, no. 10 (2006): 399, doi.org/10.1371/journal.pmed.0030399. 41

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in consensus documents from the WHO and UN reflects the dominant frame of the present period of public health, seemingly far removed from the political and social activism of an earlier era. The Global Action Plan for the Prevention and Control of Noncommunicable Diseases 2013–2020 (GAP)43 falls short of the kind of social medicine that is probably needed to confront NCDs. This plan acknowledges broad economic and political forces dominated by transnational corporations, but orients its specific policy recommendations around individualized and market-based interventions. The prevalence of neoliberal political rationality in the 2013 GAP is evident in its justification for state action on NCDs as economic investment. Recommended interventions are “affordable for all countries” that “give a good return on investment.” Furthermore, “continuing ‘business as usual’ will result in loss of productivity and an escalation of health care costs in all countries. The cumulative output loss … is estimated to be US 47 trillion.”44 Thus, the “action plan should be seen as an investment prospect” because it provides direction for countries to: Ɣ Safeguard health and productivity of populations and economies. Ɣ Create win-win situations that influence the choice of purchasing decisions related to food, media, information and communication, technology, sports and health insurance. Ɣ Identify potential for new, replicable and scalable innovations that can be applied globally to reduce burgeoning health care costs in all countries.”45 Objective 3 of the GAP 2013 is to “reduce modifiable risk factors for noncommunicable diseases and underlying social determinants through the creation of health-promoting environments” (emphasis added).46 Prior to introducing specific policy options for Member States, the 2013 GAP locates the causes of NCDs in the “societal conditions in which people are born, grow, live and work …Upstream policy and multisectoral actions to address these social determinants of health will be critical for achieving sustained progress in the prevention and control of noncommunicable

43 World Health Organization, Global Action Plan for the Prevention and Control of Noncommunicable Diseases 2013–2020 (Geneva: WHO Document Production Services, 2013). 44 World Health Organization, Global Action Plan, 10. 45 Ibid. 46 World Health Organization, Global Action Plan, 29.

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diseases.”47 The plan identifies industry as both a domain in which multisectoral action must take place and as a potential partner, but excludes specific recommendations for broader regulation of corporate entities, aside from the tobacco industry.  Policy options for Member States to reduce NCD burdens revolve around four behaviors: tobacco use, physical inactivity, unhealthy diet, and harmful use of alcohol. An examination of policy options shows different approaches based on the behavioral goals of abstention (tobacco use), moderation (harmful alcohol use), or modification (diet and physical inactivity). For tobacco use, policy options trend to structural interventions, which do not rely on individual choice for their impact. These include 100% smoke-free environments; mass media campaigns and product warning labels to warn people about the dangers of tobacco use; bans on tobacco advertising, promotion, and sponsorship; regulation of product contents and emissions; and taxes on tobacco products. Recommendations to reduce the harmful use of alcohol in the 2013 GAP are not well-developed, and though they involve a combination of structural (e.g., limiting availability and marketing of alcohol, and use of pricing policies) and behavioral policies (e.g., drunk-driving measures), and efforts to reduce the impact of harmful use of alcohol, they are weak and unspecific. Policy options for promoting a healthy diet are in stark contrast to those for tobacco. These include: x Promoting exclusive breastfeeding.  x Developing guidelines and measures to increase availability, affordability, and consumption of fruits and vegetables.  x Engaging food retailer to improve availability, affordability, and acceptability of healthier food products.  x Promoting provision and availability of food in all public institutions.  x Creating tax incentives for behaviors associated with healthier food consumption.  x Providing greater opportunities for utilization of healthy agricultural products.  x Informing and encouraging customers about healthy diet. x Create health and nutrition promoting environments. x Promoting nutrition labeling. 

47

World Health Organization, Global Action Plan, 21.

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Altogether, these recommendations attempt to expand and make more accessible and appealing a healthy food market and incentivize healthy dietary choices. Aside from suggestions to reformulate the contents of food products and regulate marketing to children, the recommendations do nothing to alter the ultra-processed food and beverage market, relying on market competition among products, and steering individual choices to healthier diets through education. Transnational food and beverage corporations are left to continue their market dominance and drive the increase in NCDs. Recommendations to increase physical activity reflect the market orientation observed in policy options to improve diets. These include urban planning and transportation policies for active transport; provision of physical education; creating built and natural environments which support active transport and recreation; and mass and social media campaigns to motivate exercise. By focusing on increasing opportunities for physical activity, recommendations do not address industrial factors that inhibit physical activity. These factors include occupational characteristics such as the inability to secure a living wage, irregular and inconsistent work hours, and non-unionization restrictions; labor market factors such as reliance on temporary contract work, gender discrimination, the informal work sector, and downsizing, subcontracting, and outsourcing; the contracting welfare state; and income inequality, all of which have posed structural barriers to active transport and recreation. In addition to the goal of abstaining from tobacco use, the pariah status of the tobacco industry, and the absence of any need for, or health benefit from smoking, may make it easier to recommend policy interventions that regulate industrial activity related to smoking. Three other industries— alcohol, food, and beverage—come out of the 2013 GAP relatively unscathed. Though the industry is identified as a domain in need of intervention, it is rendered invisible within repeated calls for “multi-sectoral action” and policy options that are either vague and weak or oriented toward creating options that support healthier decisions. Neoliberal political rationality in the 2013 GAP preserves corporate power and the economic system within which corporations thrive while individuating social policy and shifting responsibility to entrepreneurial decisions individuals make about their health.

New Approaches for NCD Prevention and Control Despite the rapid progress in the global NCD policy domain, actions taken to reduce NCDs have been insufficient and uneven. For example, the

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UN Secretary-General remarked in 2017 that “138 Member States demonstrated very poor or no progress” towards global goals set three years earlier. He cited political choices, health systems, national capacities, international finance, and industry interference as key obstacles.48 The analysis of the neoliberal political rationality in the 2013 GAP above suggests that individuation of disease is insufficient to deal with the current NCD epidemic. This finding reinforces previous arguments that specific recommendations from WHO and other public health organizations tend to undergo “lifestyle drift.” As a result of this individuation of disease, few policy recommendations significantly address the root causes of NCDs—a uniquely modern political economy of the individual, economy, and state. In order to more fully address the increasing burden of NCDs, public health policies and programs must go beyond the individual behavior/lifestyle approach and address the structural underpinnings of NCDs, or the enduring social relations and systems that determine risk for and distribution of NCDs.49 Recommendations for action on NCDs, which focus on change within social, political, and economic systems remain underdeveloped. A structural approach conceives of the NCD epidemic as the byproduct of changes to domestic and international systems that have dramatically altered modes of living and created environments that encourage consumption patterns, which lead to NCDs. These structural changes have been facilitated by several factors, including industrialization, urbanization, globalization, expansion of capitalism, and rapidly changing technology. All these factors are leveraged by transnational corporations to expand the NCDs epidemic. Fundamentally, power relationships between transnational corporations, governments, and the public will need to change in order to elevate the position of traditionally excluded or marginalized groups in the governance of NCDs. The World Health Organization and other UN agencies play a central role in this with their ability to use their global position to legitimize and establish governance alternatives among Member States. Power structures that focus on increasing government and private sector accountability to the public and obligating them to enact remedies are an initial step to shift power from government and industry to the public. The relative political power of corporations compared to advocates of the public good must be more equitable, with limits placed on the financial and political influence on decision-making. Specific policy changes include

48

United Nations, “Progress and Prevention,” 6-9. Joshua S. Yang, Hadii M. Mamudu, and Rijo John, “Incorporating a Structural Approach to Reducing the Burden of Non-Communicable Diseases,” Globalization and Health 14 (2018): 66. 49

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ensuring fair employment and decent work in employment;50 a global trade regime which makes all trade negotiations transparent and prevents trade agreements from interfering, undermining, or preempting governments’ ability to regulate and protect against products related to NCDs; and macroeconomic policies that can minimize inequalities at the root of NCDs. These policy options are only an initial effort to develop structural interventions targeting NCDs. Newly conceived and innovative policies are needed to expand the menu of structural policy alternatives to address NCDs. More importantly, political pressure and courage will be needed to implement and refine them in order to maximize action on NCDs.

Conclusion The spread of NCDs worldwide defies traditional models of disease epidemics, which have dominated human history. No longer is the focus of inquiry on microbiological agents of disease and vectors that transmit them. Instead, the causal agents of NCDs are the transnational corporations which develop products and marketing campaigns visible and ubiquitous in our everyday lives. They promote the unending consumption of their products because the inherent logic of the modern corporate form pursues profit from its consumers rather than their long-term well-being. Corporations, however, do not exist in a vacuum. They are upheld and sustained through the specific ideologies developed by the Mont Pelerin Society, laissez-faire economics that reject government meddling in markets—and places its trust in markets—to produce prosperity and ensure individual liberty. The expansion of ideologies of individual liberty and market optimization has spread into non-economic domains, neoliberal political rationality that has seized on and crystallized the movement toward the individuation of public health. The influence of neoliberal political rationality on public health has been so complete, it is considered a “deep core” of global health, and is evident in the guiding NCD policy documents for WHO Member States such as the 2013 GAP. Ending the epidemic of NCDs will require dislodging entrenched political, economic, and social relationships at the national and international levels. Such a process would begin with a fundamental rethinking of power relationships, decision-making, the nature of economic production, and the relationships between power and wealth. These changes and efforts to 50 Joan Benach, Carles Muntaner, Orielle Solar, Vilma Santana, and Michael Quinlan, “Conclusions and Recommendations for the Study of Employment Relations and Health Inequalities,” International Journal of Health Services 40, no. 2 (2010): 315–22.

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implement them, however, will face powerful opposition from entrenched vested interests that benefit from existing political and economic arrangements. Ideas alone do not result in social change; they materialize only through sustained social mobilization and collective action. Daunting as such a task may seem, the history of public health provides instructive examples of successful social reform for improved health and equity. First, however, the field of public health and its practitioners will have to rediscover its original ethos of political engagement and environmental change, updated to the challenges of the uniquely modern circumstances of political liberalism and neoliberal capitalism.

Bibliography Bakan, Joel. The Corporation. New York: Free Press, 2004. Benach, Joan, Carles Muntaner, Orielle Solar, Vilma Santana, and Michael Quinlan. “Conclusions and Recommendations for the Study of Employment Relations and Health Inequalities.” International Journal of Health Services 40, no. 2 (2010): 315–22. Brandt, Allan M., and Martha Gardner. “Antagonism and Accommodation: Interpreting the Relationship between Public Health and Medicine in the United States during the 20th Century.” American Journal of Public Health 90, no. 5 (2000): 707–15. Brandt, Allan M. “Behavior, Disease, and Health in the Twentieth-Century United States.” In Morality and Health, edited by Allan M. Brandt and Paul Rozin, 53–77. New York: Routledge, 1997. Burchell, Gordon. “Liberal Government and Techniques of the Self.” In Foucault and Political Reason, edited by Andrew Barry, Thomas Osborne, and Nikolas Rose, 19–36. Chicago: University of Chicago Press, 1996. Dean, Mitchell. Governmentality: Power and Rule in Modern Society. London: Sage Publications, 2010. Fairchild, Amy L., David Rosner, James Colgrove, Ronald Bayer, and Linda P. Fried. “The Exodus of Public Health: What History Can Tell Us About the Future.” American Journal of Public Health 100, no. 1 (2010): 54–63. Foucault, Michel. The Birth of Biopolitics. New York: Palgrave Macmillan, 2008. Freudenberg, Nicholas. Lethal but Legal: Corporations, Consumption, and Protecting Public Health. Oxford: Oxford University Press, 2016.

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Glasgow, Sara, and Thomas Schrecker. “The Double Burden of Neoliberalism? Noncommunicable Disease Policies and the Global Political Economy of Risk.” Health Place 34 (2015): 279–86. Gordon, Colin. “Governmental Rationality: An Introduction.” In The Foucault Effect: Studies in Governmentality, edited by Graham Burchell, Colin Gordon, and Peter Miller, 1–51. Chicago: University of Chicago Press, 1991. Hacker, Jacob S., and Paul Pierson. Winner-Take-All Politics. New York: Simon and Schuster, 2010. Kaiser, Thomas E. “Enlightenment.” In Oxford Encyclopedia of the Modern World. Edited by Peter N. Stearns. Oxford: Oxford University Press, 2008. Labonte, Ronald, and David Stuckler. “The Rise of Neoliberalism: How Bad Economics Imperils Health and What To Do About It.” Journal of Epidemiology and Community Health 70, no. 3 (2016): 312–18. Moodie, Rob, David Stuckler, Carlos Monteiro, Nick Sheron, Bruce Neal, Thaksaphon Thamarangsi, Paul Lincoln, Sally Casswell, on behalf of The Lancet NCD Action Group. “Profits and Pandemics: Prevention of Harmful Effects of Tobacco, Alcohol, and Ultra-Processed Food and Drink Industries.” The Lancet 381, no. 9867 (2012): 670–79. Mooney, Gavin. “Neoliberalism is Bad for Our Health.” International Journal of Health Services 42, no. 3 (2012): 383–401. Navarro, Vicente. “Neoliberalism, ‘Globalization,’ Unemployment, Inequalities, and the Welfare State.” International Journal of Health Services 28, no. 4 (1996): 607–82. Omran, Abdel R. “The Epidemiologic Transition: A Theory of the Epidemiology of Population Change.” The Millbank Memorial Fund Quarterly 49, no. 4 (October 1971): 509–38. Pfeiffer, James, and Rachel Chapman. “Anthropological Perspectives on Structural Adjustment and Public Health.” Annual Review of Anthropology 39 (2010): 149–65. Phillips-Fein, Kim. Invisible Hands: The Businessmen’s Crusade against the New Deal. New York: W. W. Norton, 2009. Porter, Dorothy. “How Did Social Medicine Evolve, and Where Is It Heading?” PLOS Medicine 3, no. 10 (2006): 399. Accessed May 18, 2018. doi.org/10.1371/journal.pmed.0030399. Riley, James C. The Eighteenth Century Campaign to Avoid Disease. London: Palgrave MacMillan, 1987. Rosen, George. “Economic and Social Policy in the Development of Public Health.” Journal of the History of Medicine 8 (1953): 406–30.

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Rosen, George. A History of Public Health, rev. ed. Baltimore, MD: Johns Hopkins University Press, 2015. Rothkopf, David. Power, Inc. New York: Farrar, Straus, Giroux, 2012. Rushton, Rushton, and Owain David Williams. “Frames, Paradigms and Power: Global Health Policy-Making under Neoliberalism.” Global Society 26, no. 2 (2012): 147–67. Scott, John, and Gordon Marshall. A Dictionary of Sociology. Oxford: Oxford University Press, 2009. Springer, Simon. “Neoliberalism As Discourse: Between Foucauldian Political Economy and Marxian Poststructuralism.” Critical Discourse Studies 9, no. 2 (2012): 133–47. Stedman Jones, Daniel. Masters of the Universe: Hayek, Frieman, and the Birth of Neoliberal Politics. Princeton, NJ: Princeton University Press, 2012. United Nations. “Progress on the Prevention and Control of NonCommunicable Diseases, A/72/662.” Accessed May 5, 2018. https://digitallibrary.un.org/record/1474584?ln=en. Wiist, William. The Bottom Line or Public Health. Oxford: Oxford University Press, 2010. World Health Organization. Global Action Plan for the Prevention and Control of Noncommunicable Diseases 2013–2020. Geneva: WHO Document Production Services, 2013. World Health Organization, Global Status Report on Noncommunicable Diseases 2014. Geneva: WHO Press, 2014. Accessed May 15, 2018. https://digitallibrary.un.org/record/1474584?ln=en. World Health Organization. The World Health Report 1997: Conquering Suffering, Enriching Humanity. Geneva: WHO Press, 1997. Yang, Joshua S., Hadii M. Mamudu, and Rijo John. “Incorporating a Structural Approach to Reducing the Burden of Non-communicable Diseases.” Globalization and Health 14 (2018): 66.

CHAPTER TEN INDUSTRY’S ROLE IN THE METABOLIC DISEASE PANDEMIC LISA CRUMMETT

Chronic diseases are non-communicable diseases of long duration that generally have a slow progression. Unlike infectious diseases that are caused by some sort of pathogen (often a virus or bacterium), chronic diseases are often associated with an unhealthy lifestyle or behavior and are thus, highly preventable. Chronic diseases have long surpassed infectious diseases in mortality rate and disease burden. They are responsible for 71% of deaths globally, ranging from 37% in low-income countries to 88% in high-income countries.1 Chronic diseases that top the scales of global mortality include cardiovascular diseases (heart attacks and stroke), chronic obstructive pulmonary disease (COPD), dementia-associated diseases, cancer of the lungs, bronchus, and trachea, and diabetes (Fig. 1).2 In addition to being the leading cause of death and disability worldwide, chronic diseases represent an enormous economic burden. In the United States, chronic conditions account for 81% of hospital admissions, 91% of prescriptions filled, and 75% of all physician visits.3 Further, 86% of the $2.7 trillion in annual healthcare expenditures is from treating those with chronic and mental health conditions.4 Comparing global mortality data

1

World Health Organization, WHO, “Global Health Estimates: Deaths by Cause, Age, Sex, by Country and by Region, 2000–2016” (Geneva: World Health Organization, 2018). 2 Ibid. 3 Gerald Anderson, Partnership for Solutions. Chronic Conditions: Making the Case for Ongoing Care (Princeton NJ: Robert Wood Johnson Foundation, 2002). 4 Jessie Gerteis, David Izrael, Deborah Deitz, Lisa LeRoy, Richard Riccardi, Therese Miller, and Jayasree Basur, Multiple Chronic Conditions Chartbook. (Rockville, MD: Agency for Healthcare Research and Quality, 2014).

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from 2016 (Fig. 1) to data collected in 2010 (Fig. 2), there has been a stark increase in chronic disease and a subsequent decline in infectious disease.

Figure 1. Top ten global causes of death, 2016. Source: Global Health Estimates 2016, Deaths by Cause, Age, Sex, by Country and by Region, 2000-2016, (Geneva: World Health Organization, 2018), available at https://www.who.int/healthinfo/global_burden_disease/estimates/en/.

Figure 2. Top ten global causes of death, 2000. Source: Ibid.

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The global shift from infectious disease to chronic disease has been attributed to several prevalent risk factors including tobacco use, poor diet, physical inactivity, and alcohol consumption.5 High blood pressure and hyperlipidemia are also included as prevalent risk factors for chronic disease,6 but these risk factors are actually components of metabolic syndrome. Metabolic syndrome (MetS) is a cluster of metabolic disorders (excess fat around the waist, dyslipidemia, hypertension, and insulin resistance) that significantly increases one’s risk of two major chronic diseases, type two diabetes, and cardiovascular disease.7 The International Diabetes Federation (IDF) has stated that one-quarter of the world’s population has MetS. In the United States, MetS has skyrocketed in prevalence over the past 30 years,8 as have metabolic diseases in general, which are chronic diseases that stem from metabolic dysfunction (cardiovascular disease, fatty liver disease, type 2 diabetes). The total cost of the global metabolic disease pandemic, including the cost of health care and loss of potential economic activity, is in the trillions.9 Insulin resistance, or impaired insulin-mediated glucose uptake, is the core abnormality that ties together all of the abnormalities associated with MetS.10 This is why MetS has been referred to as insulin resistance syndrome. Therefore, understanding the causes and preventions of insulin resistance, the doorway 5 Ursula E. Bauer, Peter A. Briss, Richard A. Goodman, and Barbara A. Bowman, “Prevention of Chronic Disease in the 21st Century: Elimination of the Leading Preventable Causes of Premature Death and Disability in the USA,” The Lancet 384 (2014): 45–52. 6 Ibid. 7 James B. Meigs, Peter W. F. Wilson, Caroline S. Fox, et al., “Body Mass Index, Metabolic Syndrome, and Risk of Type 2 Diabetes or Cardiovascular Disease,” Journal of Clinical Endocrinology and Metabolism 91 (2006): 2906–12. 8 Sadhbh O'Neill, and Lorraine L. O'Driscoll. “Metabolic Syndrome: A Closer Look at the Growing Epidemic and Its Associated Pathologies,” Obesity Reviews 16 (2015): 1–12; and Arupendra Mozumdar, and Gary Liguori, “Persistent Increase of Prevalence of Metabolic Syndrome among US Adults: NHANES III to NHANES 1999–2006,” Diabetes Care 34, (2011): 216–19. 9 Mohammad G. Saklayen, “The Global Epidemic of the Metabolic Syndrome,” Current Hypertension Reports 20 (2018): 12. 10 Ralph A. DeFronzo, and Ele Ferrannini, “Insulin Resistance: A Multifaceted Syndrome Responsible for NIDDM, Obesity, Hypertension, Dyslipidemia, and Atherosclerotic Cardiovascular Disease,” Diabetes Care 14 (1991): 173–94; Enzo Bonora, “Insulin Resistance as an Independent Risk Factor for Cardiovascular Disease: Clinical Assessment and Therapy Approaches.” Avances en diabetología,” 20 (2005): 255–61; and Gerald M. Reaven, “Role of Insulin Resistance in Human Disease,” Diabetes 37 (1988): 1595–1607.

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to metabolic syndrome and various chronic diseases, is of utmost importance if we hope to improve our chronic disease trajectory.

The Insulin Resistance and Diabetes Pandemic Insulin resistance is the first step on the pathway to type 2 diabetes (T2D). People who are diagnosed with prediabetes typically already exhibit insulin resistance (their fasting plasma glucose is between 100–125 mg/dL, or hemoglobin A1C is between 5.5 and 6.4%). The function of insulin is to signal our cells to take up glucose from the blood. Cells metabolize glucose into adenosine triphosphate (ATP), which is cellular energy required to carry out a variety of cellular functions. Insulin also signals the liver to store excess glucose as glycogen (liver starch) or to convert excess glucose to fat if the glycogen quota is filled. If cells lose their sensitivity to insulin, termed insulin resistance or prediabetes, then the pancreas produces more insulin to compensate. Over time, the pancreas can eventually become overworked causing insulin production to decline. This condition is T2D, a disease characterized by excessive levels of glucose in the blood because our cells are not able to take in glucose without the insulin signal present (fasting plasma glucose is greater than 126 mg/dL or hemoglobin A1C is greater than 6.5%). Conversely, Type 1 diabetes (T1D) occurs when the immune system attacks the pancreatic cells that produce insulin. Only 5% of people with diabetes have T1D, while 95% have T2D.11 For this reason, I will focus on T2D. Based on data from the 2017 National Diabetes Statistics Report, in 2015, 33.9% of the US adult population had prediabetes and 12.2% had diabetes, of which 23.8% were undiagnosed.12 It was also reported that nearly half of US adults over the age of 65 had prediabetes, and one-quarter of them had diabetes in 2015.13 T2D used to be referred to as adult-onset diabetes because it was only observed in adults, but from 2011 to 2012, there were 5300 newly diagnosed cases of T2D in children and adolescents age 10 to 19 years.14 From 2002 to 2012, the rate of newly diagnosed T2D cases among youth increased by 4.8% per year adjusted for age, sex, and

11 Centers for Disease Control and Prevention, CDC, National Diabetes Statistics Report, 2017. Atlanta, Ga: Centers for Disease Control and Prevention, US Department of Health and Human Services, 2017. 12 Ibid. 13 Ibid. 14 Ibid.

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ethnicity.15 The increasing economic costs associated with treating T2D (after adjusting for inflation) is staggering; the cost has increased by 26% in only five years, from 2012 to 2017.16 The CDC ranked diabetes mellitus as the 7th leading cause of death in the US, in 2016, based on data from death certificates, which can list various complications from diabetes as the cause of death rather than diabetes itself.17 A recent analysis of the National Health Interview Survey (NHIS) from 1997–2009 and the National Health and Nutrition Examination Survey (NHANES) from 1999–2010, showed that diabetes is the third leading cause of death in the United States and the authors call for robust population-level interventions aimed at diabetes prevention and care.18 Possibly the most alarming statistic regarding T2D is the projected rate of increase in the coming years; a staggering 54% of Americans are projected to have diabetes (more than 54.9 million Americans) between 2015 and 2030.19 In addition to diabetes ranking high in associated causes of death in the United States (#3 based on national health surveys),20 other chronic diseases stemming from metabolic dysfunction also rank high in causes of death for men and women21 with “diseases of the heart” ranked first, “cerebrovascular disease” (stroke) ranked fifth, and “chronic liver disease and cirrhosis” ranked ninth (only in males). Alzeimer’s disease, ranked sixth, has been linked to vascular problems associated with MetS.22 Given that the 15 Elizabeth J. Mayer-Davis, Jean M. Lawrence, Dana Dabelea, Jasmin Divers, et al., “Incidence Trends of Type 1 and Type 2 Diabetes among Youths, 2002–2012,” New England Journal of Medicine 376 (2017): 1419–29. 16 American Diabetes Association, “Economic Costs of Diabetes in the U.S. in 2017,” Diabetes Care 41, no. 5 (2018): 917–28. 17 National Center for Health Statistics, “Health, United States with Chartbook on Long-term Trends in Health.” Hyattsville, MD: National Center for Health Statistics, 2017. 18 Andrew Stokes and S. H. Preston, “Deaths Attributable to Diabetes in the United States: Comparison of Data Sources and Estimation Approaches,” PLOS ONE 12 (2017): e0170219. 19 William R. Rowley, Clement Bezold, Yaseman Arikan, Erin Byrne, and Shannon Krohe, “Diabetes 2030: Insights from Yesterday, Today, and Future Trends,” Population Health Management 20 (2017): 6–12. 20 Stokes and Preston, “Deaths Attributable to Diabetes,” e0170219. 21 CDC,”National Diabetes.” 22 Francesco Panza, Vincenza Frisardi, Cristiano, Capurso, Bruno P. Imbimbo, Gianluigi Vendemiale, Andrea Santamato, Grazia D' Onofrio, et al. “Metabolic Syndrome and Cognitive Impairment: Current Epidemiology and Possible Underlying Mechanisms.” Journal of Alzheimer's Disease 21 (2010): 691–724; and Blazej Misiak, Jerzy Leszek, and Andrzej Kiejna. “Metabolic Syndrome, Mild

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prevalence of metabolic syndrome has ballooned over the past 30 years,23 and research has shown that insulin resistance lies at the root of MetS and various chronic diseases,24 it is critical that we investigate what specific environmental exposure(s) could be responsible for this recent and pronounced upturn in prevalence.

Sugar is a Major Provocateur of Metabolic Syndrome and Many Chronic Diseases Although there are multiple causes and risk factors that can be implicated in the development of MetS, there is clear scientific evidence that a high intake of added sugars is likely the biggest contributor to metabolic dysfunction and MetS.25 Table sugar (sucrose) is a disaccharide composed of glucose and fructose bonded together. It has been given many names (caramel, agave nectar, evaporated cane juice, and many others). I refer to all of these as added sugars because they are added to foods and are functionally the same in terms of how they are metabolized. Intrinsic sugar (contained within whole fruits and vegetables) is not equivalent to extrinsic or added sugar metabolically,26 and throughout I will focus on added

Cognitive Impairment and Alzheimer’s Disease—The Emerging Role of Systemic Low-grade Inflammation and Adiposity.” Brain Research Bulletin 89 (2012): 144–49. 23 Saklayen, “Global Epidemic,” 12. 24 O’Neill, and O’Driscoll, “Metabolic Syndrome,” 1–12; DeFronzo, and Ferrannini, “Insulin Resistance,” 173–94; and Reaven, “Role of Insulin Resistance,” 1595– 1607. 25 Mark J. Dekker, Qiaozhu Su, Chris Baker, Angela Rutledge, and Khosrow Adeli, “Fructose: A Highly Lipogenic Nutrient Implicated in Insulin Resistance, Hepatic Steatosis, and the Metabolic Syndrome,” American Journal of Physiology and Metabolism 299 (2010): E685–E694; Roya Kelishadi, Marjan Mansourian, and Motahar Heidari-Beni, “Association of Fructose Consumption and Components of Metabolic Syndrome in Human Studies: A Systematic Review and Meta-analysis,” Nutrition 30 (2014): 503–10; Jung S. Lim, Michele Mietus-Snyder, Annie Valente, Jean-Marc Schwarz, and Robert H. Lustig, “The Role of Fructose in the Pathogenesis of NAFLD and the Metabolic Syndrome,” Nature Reviews Gastroenterology and Hepatology 7 (2010): 251; and Angela C. Rutledge, and Khosrow Adeli, “Fructose and the Metabolic Syndrome: Pathophysiology and Molecular Mechanisms,” supplement, Nutrition Reviews 65 (2007): S13–S23. 26 Natasha Tasevska, S. Runswick, A. Welch et al., “Urinary Sugars Biomarker Relates Better to Extrinsic Than to Intrinsic Sugars Intake in a Metabolic Study with Volunteers Consuming Their Normal Diet,” European Journal of Clinical Nutrition 63, (2009): 653.

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sugars.27 Now, let us compare the two simple sugars found in sucrose, glucose and fructose. Glucose is prevalent in complex carbohydrates that we recognize as starchy foods such as bread, rice, pasta, and potatoes, but it is also found in simple carbohydrates such as cookies, cake, and soda because it comprises half of every sucrose molecule. Glucose is easily metabolized into cellular energy by every cell in our body because every cell has glucose transporters. Unlike glucose, fructose is never found alone in nature, as it is bound to glucose to form the disaccharide sucrose. Fructose is the sweeter half of sucrose, and this is why corn syrup (pure glucose) is chemically altered to yield the ubiquitous sweetener known as high fructose corn syrup, which is 53-55% fructose and 42-45% glucose. Fructose has been scientifically shown to be a major provocateur of insulin resistance and T2D both in epidemiological studies and experimental (physiological) studies.28 The main reason that fructose, whether it be in the form of high-fructose corn syrup or table sugar, is a far greater provocateur of metabolic dysfunction and disease compared to glucose is that only the liver metabolizes the vast majority (~ 95%) of fructose that enters our bloodstream.29 Its cellular uptake is unregulated, whereas 20% of the glucose that enters our bloodstream is metabolized by the liver, and its cellular uptake is regulated by insulin. This means that after consuming a meal that is rich in added sugars, which is very common in the western industrial diet, fructose bombards the liver and leads to excess substrate in our liver cells, ultimately leading to excess uric acid and fat production (Fig. 3).30 Excess uric acid production is a consequence

27

Ibid. Dekker, et al., “Fructose: A Highly Lipogenic Nutrient,” E685–E694; Kelishadi, et al., “Association of Fructose Consumption,” 503–10; Lim, et al., “Role of Fructose,” 251; and Rutledge and Adeli, “Fructose and Metabolic Syndrome,” S13S23. 29 Sam Z. Sun, and Mark W. Empie, “Fructose Metabolism in Humans—What Isotopic Tracer Studies Tell Us,” Nutrition & Metabolism 9 (2012): 89; and Karen. L. Teff, Sharon S. Elliott, Matthias Tschöp, et al., “Dietary Fructose Reduces Circulating Insulin and Leptin, Attenuates Postprandial Suppression of Ghrelin, and Increases Triglycerides in Women,” Journal of Clinical Endocrinology & Metabolism 89 (2004): 2963–72. 30 Miguel A. Lanaspa, Laura G. Sanchez-Lozada, Yea-Jin Choi, et al., “Uric Acid Induces Hepatic Steatosis by Generation of Mitochondrial Oxidative Stress: Potential Role in Fructose-Dependent and Independent Fatty Liver,” Journal of Biological Chemistry 287 (2012): 40732–744; Peter A. Mayes, “Intermediary Metabolism of Fructose,” supplement, American Journal of Clinical Nutrition 58 (1993): S754–S65; and Richard J. Johnson, Takahiko Nakagawa, Laura. G. 28

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of fructose metabolism using up large quantities of adenosine triphosphate (ATP) and leaving behind excess adenosine monophosphate (AMP), which is used to produce uric acid (Fig. 3).31 To make matters worse, humans lack a functional gene for uricase, the enzyme that breaks down uric acid, and this magnifies our uric acid load, which causes oxidative stress in the liver.32 Oxidative stress leads to de novo lipogenesis (fat synthesis) and inflammation in the liver.33 In addition to the elevated fat production associated with excess uric acid, the excess carbon load in liver cells (from a high fructose diet) leads to increased synthesis of various lipid metabolites including diacylglycerol (DAG), low-density lipoprotein (LDL), very lowdensity lipoprotein (VLDL), and triglycerides,34 all of which can foment insulin resistance or pre-diabetes (Fig. 3).35 Furthermore, high levels of LDL, VLDL, and triglycerides are well-known markers for cardiovascular disease.36 Excess uric acid also increases one’s risk for cardiovascular Sanchez-Lozada et al., “Sugar, Uric Acid, and the Etiology of Diabetes and Obesity,” Diabetes 62 (2013): 3307–15. 31Lanaspa, et al., “Uric Acid,” 40732–744. 32 James T. Kratzer, Miguel A. Lanaspa, Michael N. Murphy, et al., “Evolutionary History and Metabolic Insights of Ancient Mammalian Uricases,” Proceedings of the National Academy of Sciences, (2014): 201320393. 33 Ibid.; and Carmelinda Ruggiero, Antonio Cherubini, Alesandro Ble, et al., “Uric Acid and Inflammatory Markers,” European Heart Journal 27 (2006): 1174–81. 34 Kelishadi et al., “Association of Fructose,” 503–10; David Faeh, Kaori Minehira, Jean-Marc Schwarz et al., “Effect of Fructose Overfeeding and Fish Oil Administration on Hepatic De Novo Lipogenesis and Insulin Sensitivity in Healthy Men,” Diabetes 54 (2005): 1907–13; Elizabeth J. Parks, Lauren E., Skokan, Maureen T. Timlin, and Carlus S. Dingfelder, et al., “Dietary Sugars Stimulate Fatty Acid Synthesis in Adults,” Journal of Nutrition 138 (2008): 1039–46; and Yu-Hui Zhang, Tao An, Rong Cheng Zhang et al., “Very High Fructose Intake Increases Serum LDL-Cholesterol and Total Cholesterol: A Meta-Analysis of Controlled Feeding Trials,” Journal of Nutrition 143 (2013) 1391–98. 35 Kelishadi et al., “Association of Fructose,” 503–10; Faeh, et al., “Effect of Fructose Overfeeding,” 1907–13; G. Boden, X. Chen, J. Ruiz et al., “Mechanism of Fatty Acid Induced Inhibition of Glucose Uptake,” Journal of Clinical Investigation 93, (1994): 2438–46; M. K. Krssak, K. Falk Petersen, A. Dresner, et. al., “Intramyocellular Lipid Concentrations Are Correlated with Insulin Sensitivity in Humans: A 1H NMR Spectroscopy Study,” Diabetologia 42 (1999): 113-6; and Gerald I. Shulman, “Cellular Mechanisms of Insulin Resistance,” Journal of Clinical Investigation 106 (2000): 171–76. 36 Sandeep Bansal, Julie E. Buring, Nader Rifai, et al., “Fasting Compared with Nonfasting Triglycerides and Risk of Cardiovascular Events in Women,” JAMA 298 (2007): 309–16; J. E. Hokanson, and M. A. Austin, “Plasma Triglyceride Level Is a Risk Factor for Cardiovascular Disease Independent of High-Density Lipoprotein

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disease by causing dysfunction in the cells that line blood vessels.37 This impairs nitric oxide (a blood vessel relaxer) and causes hypertension.38 Thus, the take-home message from all of this biochemistry is that high intake of added sugars (and associated fructose) leads to metabolic dysfunction that begins with the liver but ultimately leads to systemic insulin resistance and T2D (Fig. 3).39 Also, fructose is associated with other metabolic diseases such as non-alcoholic fatty liver disease40 and cardiovascular disease.41 In a recent study of obese children with metabolic Cholesterol Level: A Meta-analysis of Population-Based Prospective Studies,” Journal of Cardiovascular Risk 3 (1996): 213–19; Rishi K. Wadhera, D. L. Steen, I. Khan, et al., “A Review of Low-density Lipoprotein Cholesterol, Treatment Strategies, and Its Impact on Cardiovascular Disease Morbidity and Mortality,” Journal of Clinical Lipidology 10 (2016): 472–89; and Raimond Pechlaner, Sotirios Tsimikas, Xiaoke Yin, et al., “Very-Low-Density Lipoprotein–Associated Apolipoproteins Predict Cardiovascular Events and Are Lowered by Inhibition of APOC-III,” Journal of the American College of Cardiology 69 (2017): 789–800. 37 Wan-Jing Ho, Wen-Pin Tsai, Kuang-Hui Yu et al., “Association between Endothelial Dysfunction and Hyperuricaemia,” Rheumatology 49 (2010): 1929–34. 38 Christine Gersch, Sergiu P. Palii, Kyung Mee Kim et al., “Inactivation of Nitric Oxide by Uric Acid,” Nucleosides, Nucleotides & Nucleic Acids 27 (2008): 967–78; and Jing Fang, and Michael H. Alderman, “Serum Uric Acid and Cardiovascular Mortality: The Nhanes I Epidemiologic Follow-up Study, 1971–1992,” JAMA 283 (2000): 2404–10. 39 Fumiaki Imamura, Laura O’Connor, Zheng Ye, et al., “Consumption of Sugar Sweetened Beverages, Artificially Sweetened Beverages, and Fruit Juice and Incidence of Type 2 Diabetes: Systematic Review, Meta-analysis, and Estimation of Population Attributable Fraction.” BMJ 351 (2015): h3576; Vasanti S. Malik, Barry M. Popkin, George A. Bray et al., “Sugar-sweetened Beverages and Risk of Metabolic Syndrome and Type 2 Diabetes.” Diabetes Care 33 (2010): 2477–83; and Kimber L. Stanhope, “Sugar Consumption, Metabolic Disease and Obesity: The State of the Controversy,” Critical Reviews in Clinical Laboratory Sciences 53 (2016): 52–67; Reaven, “Role of Insulin Resistance,” 1595–1607; National Diabetes Statistics Report, “Economic Costs of Diabetes”; and Mayer-Davis, et al., “Incidence Trends of Type 1 and Type 2,” 1419–29. 40 Xiaosen Ouyang, Pietro Cirillo, Yuri Sautin et al., “Fructose Consumption as a Risk Factor for Non-alcoholic Fatty Liver Disease.” Journal of Hepatology 48 (2008) 993–99; Maria Maersk, Anita. Belza, Hans Stødkilde-Jørgensen, et al.,”Sucrose-sweetened Beverages Increase Fat Storage in the Liver, Muscle, and Visceral Fat Depot: A 6-mo Randomized Intervention Study,” American Journal of Clinical Nutrition 95 (2012): 283–89: and Nimer Assy, Gattas Nasser, Iad. Kamayse et al., “Soft Drink Consumption Linked with Fatty Liver in the Absence of Traditional Risk Factors.” Canadian Journal of Gastroenterology 22 (2008): 811–16. 41 Bauer, et al., “Prevention of Chronic Disease,” 45–52; Mozumdar, et al., “Persistent Increase,” 216–19; and CDC, “National Diabetes Statistics Report”;

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syndrome, when dietary sugar was reduced and replaced with starch while keeping caloric intake constant, there was a significant improvement in metabolic health for the participants within nine days, including reduced diastolic blood pressure, reduced triglyceride and LDL cholesterol levels, improved hyperinsulinemia and glucose tolerance, and weight loss.42 With a focus on the United States, how much sugar do Americans consume, and could that explain the rising metabolic disease epidemic?

Figure 3. Fructose metabolism in hepatocytes (liver cells). An excessive fructose load is first phosphorylated into fructose-1-phosphate by fructose kinase. This first step is consumptive of adenosine triphosphate (ATP) and leads to significant uric

James B. Meigs, et al., “Body Mass Index,” 2906–12; and O'Neill and O’Driscoll, “Metabolic Syndrome,” 216–19. 41 Dekker, et al., “Fructose: A Highly Lipogenic Nutrient,” E685–E694; Kelishadi, et al., “Association of Fructose Consumption,” 503–10; and Rutledge and Adeli, “Fructose and Metabolic Syndrome,” S13–S23. 42 Robert H. Lustig, Kathleen Mulligan, Susan M. Noworolski, Viva W. Tai, Michael J. Wen, Ayca ErkinဨCakmak, Alejandro Gugliucci, and JeanဨMarc Schwarz. “Isocaloric fructose restriction and metabolic improvement in children with obesity and metabolic syndrome.” Obesity 24 (2016): 453-460.

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acid production43, which leads to oxidative stress in the cell. Most of the fructose eventually enters mitochondria for the Krebs Cycle (thick black arrow). Some fructose-1, 6-bisphosphate is converted to xylolose-5-phosphate, which, through a cascade, activates carbohydrate responsive element binding protein (ChREBP), which activates the fat synthesis cascade.44 Combined with the effects of uric acid, this ensures a large amount of citrate is available for excess fat production45 from fructose carbon. The resulting excess very low-density lipoprotein (VLDL) concentration in the blood leads to dyslipidemia and insulin resistance (IR) in muscle tissue.46 Excess lipid in the liver leads to non-alcoholic fatty liver disease (NAFLD)47, and the associated inflammation (plus oxidative stress and endoplasmic reticulum stress) leads to IR in the liver.48 With IR in many tissues, the pancreas over-produces insulin, leading to hyperinsulinemia,49 which blocks leptin signaling 43 Lanaspa, et. al., “Uric Acid Induces Hepatic Steatosis,” 40732-40744; R.J. Johnson, Y.Y. Sautin, and W.J. Oliver, et. al. “Lessons from comparative physiology: could uric acid represent a physiologic alarm signal gone awry in western society?” Journal of Comparative Physiology B 179 (2009): 67-76. 44 T. Kabashima, T. Kawaguchi, BE Wadzinski, et. al., “Xylulose 5-phosphate mediates glucose-induced lipogenesis by xylulose 5-phosphate-activated protein phosphatase in rat liver,” Proceedings of the National Academy of Sciences 100 (2003): 5107-5112. 45 Faeh, et. al., “Effect of Fructose Overfeeding,” 1907-1913; Parks, et. al., “Dietary Sugars Stimulate Fatty Acid Synthesis,” 1039-1046; Zhang, et. al., “Very High Fructose Intake,” 1391-1398. 46 Dekker, et al., “Fructose: A Highly Lipogenic Nutrient,” E685–E694; H. Basciano, L. Federico, K. Adeli, “Fructose, insulin resistance, and metabolic dyslipidemia,” Nutrition & Metabolism 2 (2005): 5; Krssak, et. al., “Intramyocellular lipid concentrations,” 113-116; E. Montell, M. Turini, and M. Marotta, et. al. “DAG accumulation from saturated fatty acids desensitizes insulin stimulation of glucose uptake in muscle cells,” American Journal of Physiology-Endocrinology and Metabolism 280 (2001): E229-E237. 47 Dekker, et al., “Fructose: A Highly Lipogenic Nutrient,” E685–E694; P. Jegatheesan and J.P. de Bandt, “Fructose and NAFLD: The multifaceted aspects of fructose metabolism,” Nutrients 9 (2017): 230; T. Jensen, M.F. Abdelmalek, S. Sullivan, et. al., “Fructose and sugar: a major mediator of nonalcoholic fatty liver disease,” Journal of hepatology 68 (2018): 1063-1075; Ouyang, et. al., “Fructose consumption,” 993-999; V. Zámbó, L. Simon-Szabó, P. Szelényi, et. al. “Lipotoxicity in the liver,” World Journal of Hepatology 5 (2013): 550. 48 Dekker, et al., “Fructose: A Highly Lipogenic Nutrient,” E685–E694; Lim et. al. “The role of fructose,” 251; and Rutledge and Adeli, “Fructose and Metabolic Syndrome,” S13–S23. 49 Michael H. Shanik, Yuping Xu, Jan. Škrha et al., “Insulin Resistance and Hyperinsulinaemia: Is Hyperinsulinaemia the Cart or the Horse?” supplement, Diabetes Care 31 (2008): S262–S68; Robert H. Lustig, “Childhood Obesity: Behavioral Aberration or Biochemical Drive? Reinterpreting the First Law of Thermodynamics,” Nature Reviews Endocrinology 2 (2006): 447.

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(leptin resistance).50 Without the leptin signal, the hunger center is activated,51 which leads to the overeating of energy-dense foods. This repeating loop leads to type 2 diabetes (T2D).52 Thick arrows indicate large carbon loads. Black arrows and text indicate metabolic abnormalities caused by excess fructose consumption. Dashed lines indicate multiple steps represented by a single line.

Over the past three decades, the average daily intake from added sugars (kcal/day) in the United States has increased by 35% for adults53 with the average American consuming 82 grams per day.54 This far exceeds the World Health Organization recommendation of no more than ~25 grams per day per 2000 calorie diet.55 The biggest source of fructose, via added sugars, in the American diet comes from sweetened beverages, contributing 34.4% of added sugars.56 Several robust meta-analyses have reported significant correlations between sweetened beverage consumption and the risk of developing T2D,57 independent of body weight gain or total energy intake.58

50 M. Kellerer, R. Lammers, Fritsche et al., “Insulin Inhibits Leptin Receptor Signalling in HEK293 Cells at the Level of Janus Kinase-2: A Potential Mechanism for Hyperinsulinaemia-associated Leptin Resistance,” Diabetologia 44, no. 9 (2001): 1125–32; Alexandra Shapiro, Nihal Tümer,Yongxin Gao et al., “Prevention and Reversal of Diet-induced Leptin Resistance with a Sugar-free Diet despite High Fat Content.” British Journal of Nutrition 106 (2011): 390–97. 51 R.S. Ahima and J.S. Flier “Leptin,” Annual review of physiology 62 (2000): 413437; Jeffrey M. Friedman, and Jeffrey L. Halaas, “Leptin and the Regulation of Body Weight in Mammals,” Nature 395 (1998): 763; E. Isganaitis and R.H. Lustig, “Fast food, central nervous system insulin resistance, and obesity,” Arteriosclerosis, thrombosis, and vascular biology 25 (2005): 2451-2462. 52 Isganaitis and Lustig, “Fast food,” 2451-2462. 53 Elyse S. Powell, Lindsey P. Smith-Taillie, and Barry M. Popkin, “Added Sugars Intake across the Distribution of US Children and Adult Consumers: 1977–2012,” Journal of the Academy of Nutrition and Dietetics 116 (2016): 1543–50, e1541. 54 R. Belthene Ervin, and Cynthia L. Ogden, “Consumption of Added Sugars Among U.S. Adults, 2005–2010,” U.S. Department of Health and Human Services: National Center for Health Statistics, (2013). 55World Health Organization, “WHO Calls on Countries to Reduce Sugar Intake among Adults and Children,” http://www.who.int/mediacentre/news/releases/2015/sugar-guideline/en/ 56 Adam Drewnowski, and Colin D. Rehm, “Consumption of Added Sugars among US Children and Adults by Food Purchase Location and Food Source,” American Journal of Clinical Nutrition 100 (2014): 901–07. 57 Imamura, et al., “Consumption of Sugar Sweetened Beverages,” h3576; Vasanti S. Malik, et al., “Sugar-Sweetened Beverages,” 2477–83; and Stanhope et al., “Sugar Consumption, Metabolic Disease,” 52–67. 58 Ibid.

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As with all chronic diseases, metabolic dysfunction, via high intake of added sugars, would typically take many years to develop. But given the constant bombardment of the liver by fructose from the global industrial diet (rich in processed foods that are devoid of fiber and high in added sugars), the outcome of metabolic disease is highly likely.59 The extremely addictive nature of sugar makes this outcome even more probable for many people.60

Private Money Has Muddied the Role of Sugar in the Development of Chronic Disease In a recent review of sugar consumption, metabolic disease, and obesity, the author concluded that consumption of added sugars is associated with the development of fatty liver, dyslipidemia, insulin resistance, hyperuricemia, cardiovascular disease, and type 2 diabetes. Many of these associations are independent of body weight gain or total energy intake.61 Four studies claimed no association between sugar consumption and metabolic dysfunction but they were industry-funded or conducted by investigators who received consulting fees from industries with strongfinancial interests in maintaining high levels of sugar consumption.62 Later that same year, another review claimed that singling out added sugars as unique culprits for metabolic diseases such as obesity, diabetes, and cardiovascular disease appears inconsistent with modern, high-quality evidence and is very unlikely to yield health benefits.63 However, the authors of that second review admitted conflicts of interest in that they had received unrestricted grants and consulting fees from ConAgra Foods, Kraft 59

Robert H. Lustig, Fat Chance: Beating the Odds against Sugar, Processed Food, Obesity, and Disease (Hammondsworth, UK: Penguin Books, 2013). 60 Serge H. Ahmed, Karine Guillem, and Youna Vandaele, “Sugar Addiction: Pushing the Drug-sugar Analogy to the Limit,” Current Opinion in Clinical Nutrition and Metabolic Care 16 (2013): 434–39; and Nicole M. Avena, Pedro Rada; and Bartley G. Hoebel, “Evidence for Sugar Addiction: Behavioral and Neurochemical Effects of Intermittent, Excessive Sugar Intake,” Neuroscience & Biobehavioral Reviews 32, no. 1 (2008): 20-–39. 59. Rudolph Spangler, Knut M. Wittkowski, Noel L. Goddard et al., “Opiate-like Effects of Sugar on Gene Expression in Reward Areas of the Rat Brain.” Molecular Brain Research 124 (2004): 134–42. 61 Stanhope, “Sugar Consumption, Metabolic Disease,” 52–67. 62 Ibid. 63 James M. Rippe, and Theodore J. Angelopoulos, “Relationship between Added Sugars Consumption and Chronic Disease Risk Factors: Current Understanding,” Nutrients 8 (2016): 697.

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Foods, the Florida Department of Citrus, PepsiCo International, the Coca Cola Company, the Corn Refiners Association, Weight Watchers International, and various publishers.64 In fact, review articles with a financial conflict of interest with the food industry are significantly more likely to provide a conclusion of no or lesser association between sugarsweetened beverages and obesity or weight gain than those without them.65 A meta-analysis from 2016 highlights the strong influence of one particular industry, the sugar-sweetened beverage (SSB) industry. The authors looked at two groups of studies. One group reported no association between SSB and obesity, and a second group found evidence of association. Among the first group of 26 studies, all had funding ties to the SSB industry. Among the second group of 34 studies, only one had financial ties to the SSB industry. This second group found evidence that greater consumption of SSB yielded higher levels of obesity and diabetes-related outcomes.66 The Center for Science and Democracy at the Union of Concerned Scientists published a document in 2014, entitled “Added Sugar, Subtracted Science: How Industry Obscures Science and Undermines Public Health.” It provides five tactics that industries use to obscure scientific evidence of the dangers of sugar consumption, which include: (1) attacking the science, (2) spreading misinformation, (3) deploying industry scientists, (4) influencing academia, and (5) undermining policy.67 The New York Times published an article in 2015 that provided a recent example of how the industry has obscured science using tactics 1–4 described above.68 The exposé revealed that Coca-Cola provided financial and logistic support to a 64

Ibid. Maria Bes-Rastrollo, Matthias B. Schulze, Miguel Ruiz-Canela, and Miguel A. Martinez-Gonzalez, “Financial Conflicts of Interest and Reporting Bias Regarding the Association between Sugar-sweetened Beverages and Weight Gain: A Systematic Review of Systematic Reviews,” PLoS Medicine 10 (2013): e1001578; and José Massougbodji, Yann Le Bodo, Ramona Fratu et al., “Reviews Examining Sugar-sweetened Beverages and Body Weight: Correlates of Their Quality and Conclusions,” American Journal of Clinical Nutrition 99 (2014): 1096–1104. 66 Dean Schillinger, Jessica Tran, Christina Mangurian et al., “Do Sugar-sweetened Beverages Cause Obesity and Diabetes? Industry and the Manufacture of Scientific Controversy,” Annals of Internal Medicine 165 (2016): 895–97. 67 Gretchen Goldman, Christina. Carlson, Deborah Bailin et al., Added Sugar, Subtracted Science: How Industry Obscures Science and Undermines Public Health Policy on Sugar (Cambridge: MA: Union of Concerned Scientists, 2014). 68 Anahad O’Connor, “Coca-Cola Funds Scientists Who Shift Blame for Obesity Away From Bad Diets,” accessed October 19, 2018, https://well.blogs.nytimes.com/2015/08/09/coca-cola-funds-scientists-who-shiftblame-for-obesity-away-from-bad-diets/. 65

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nonprofit organization called Global Energy Balance Network (GEBN). It was comprised of several academic scientists, whose main message was that weight-conscious Americans are overly fixated on how much they eat and drink and do not pay enough attention to exercise, and that message was perpetuated via journal articles, scientific conferences, and social media.69 The aim of GEBN was to shift the blame for obesity and metabolic disease from America’s diet to America’s lack of exercise. Coca-Cola provided $1.5 million to start GEBN, and in 2008, they gave nearly $4 million to fund the research of two of GEBN’s founders. These founders were Dr. Steven N. Blair, a professor in the Arnold School of Public Health at the University of South Carolina and Gregory A. Hand, a professor in the School of Public Health at West Virginia University.70 One year after the New York Times exposé was published, Gregory A. Hand was asked to step down as Dean of the School of Public Health at West Virginia University but he is still employed there as a professor.71 Industries can also undermine public policy (tactic 5 mentioned previously). For instance, lobbyists from food industries help block legislation that would limit the consumption of sweetened beverages or junk food by lobbying Congress. They may make political contributions to lawmakers, or even influence the deliberation process that takes place at federal agencies.72 Such efforts have been made at the state and federal levels as well as the international level. In 2003, “Diet, Nutrition, and Prevention of Chronic Disease Technical Report Series (TRS) 916”73 was created by the WHO and the UN Food and Agriculture Organization (FAO) and it called for limiting the population’s mean intake of added sugars to 10 percent or less of total energy.74 After this report was released to the public, there was aggressive lobbying from sugar producers and sugar exporting countries. 69

Ibid. Ibid. 71 Corporate Crime Reporter, “Gregory Hand Forced Out As Dean of West Virginia School of Public Health amid Controversy over Coca-Cola Funding,” accessed October 19, 2018, https://www.corporatecrimereporter.com/news/200/gregoryhand-forced-out-as-dean-of-west-virginia-school-of-public-health-amidcontroversy-over-coca-cola-funding/. 72 Goldman, et al., “Added Sugar, Subtracted Science.” 73 World Health Organization, WHO, “WHO/FAO Joint Expert Consultation on Diet, Nutrition and the Prevention of Chronic Diseases,” accessed February 29, 2012. https://who.int/dietphysicalactivity/publications/trs916/en/. 74 Chizuru Nishida, Ricardo Uauy, Shiriki Kumanyika et al., “The Joint WHO/FAO Expert Consultation on Diet, Nutrition and the Prevention of Chronic Diseases: Process, Product, and Policy Implications,” Public Health Nutrition 7 (2004): 245– 50. 70

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The Sugar Association demanded that Congress withdraw its contribution of $406 million dollars to the WHO unless the WHO withdrew their guidelines.75 The Sugar Association, along with six other big food industries, pressured Tommy Thompson, the U.S. Secretary of Health and Human Services (George W. Bush Administration), to use his influence to withdraw the WHO report.76 These lobbying efforts successfully blocked the WHO’s immediate adoption of their proposed strategy.77 A similar situation transpired in 2010 when New York City mayor, Michael Bloomberg, asked the USDA’s permission to add sugary drinks to the list of prohibited food-stamp purchases for New York City residents in hopes of improving the health of low-income households. The USDA declined this request after heavy lobbying from the soda industry. Unfortunately, industry-funded scientific research, whose findings oppose the vast majority of non-industry funded scientific research, has provided mixed signals to the scientific community and the public. These mixed signals can be co-opted by lobbyists of food and beverage industries to block legislation that could reduce profits of said industries. A specific example of mixed signals from the scientific community appearing in the public arena is the extent to which added sugars have been implicated as a cause or risk factor for T2D in public diabetes websites. I have observed that a high intake of added sugars has been excluded as a cause or risk factor for T2D from the majority of diabetes websites. In fact, Diabetes.org, which is the most frequently visited and cited diabetes website, does not include any sugar-associated vocabulary under causes and preventions for T2D. The most highly cited causes or risk factors of T2D on diabetes websites are overweight/obesity and being sedentary (Crummett et al. in preparation). Ironically, both of these conditions have been implicated as a direct result of high sugar consumption interfering with hormonal signaling. To be more specific, fructose overload in the liver causes our biochemistry to shift toward the orexigenic (appetite-stimulating) side of metabolism. This engenders excessive hunger, insulin release, lipogenesis, and fat storage,78 75 Sarah Boseley, and Jean McMahon, “Political Context of the World Health Organization: Sugar Industry Threatens to Scupper the WHO,” International Journal of Health Services 33 (2003): 831–33; and Kaare. R Norum, “World Health Organization’s Global Strategy on Diet, Physical Activity, and Health: The Process behind the Scenes,” Scandinavian Journal of Nutrition 49 (2005): 83–88. 76 Boseley, and McMahon, “Political Context WHO,” 831–33. 77 Ibid. 78 Kelishadi, et al., “Association of Fructose Consumption,” 503–10; Kimber L. Stanhope, Jean Marc Schwarz, Nancy L. Keim et al., “Consuming Fructose-

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especially visceral fat, leading to higher body weight.79 As previously discussed, fat production is further enhanced by fructose-mediated uric acid production.80 Sedentary behavior can also be a product of high sugar intake, as it leads to insulin resistance, which then leads to high circulating levels of insulin81 and triglycerides,82 both of which lead to weight gain and leptin resistance.83 Leptin is the hormone that makes us feel productive rather than sluggish.84 Thus, by focusing on overweight/obesity and being sedentary as the major causes/risk factors for T2D, we are putting the cart before the horse. These are the downstream consequences of high sugar intake. Rather than blaming the outcome, sluggishness and weight gain, we should focus on high sugar intake itself, which scientific research has shown to be a major cause of insulin resistance and metabolic disease, including T2D.

sweetened, not Glucose-sweetened, Beverages Increases Visceral Adiposity and Lipids and Decreases Insulin Sensitivity in Overweight/Obese Humans,” Journal of Clinical Investigation 119 (2009): 1322–34; Kim A. Lê, Michael Ith, Roland Kreis, et al., “Fructose Overconsumption Causes Dyslipidemia and Ectopic Lipid Deposition in Healthy Subjects with and without a Family History of Type 2 Diabetes,” American Journal of Clinical Nutrition 89 (2009): 1760–65; Norman K. Pollock, Vanessa Bundy, William Kanto et al., “Greater Fructose Consumption Is Associated with Cardiometabolic Risk Markers and Visceral Adiposity in Adolescents,” Journal of Nutrition 142 (2012): 251–57; Andreas Lindqvist, Annemie Baelemans, Charlotte Erlanson-Albertsson, “Effects of Sucrose, Glucose and Fructose on Peripheral and Central Appetite Signals,” Regulatory Peptides 150 (2008): 26–32; and Lustig, “Childhood Obesity,” 447. 79 Lenny R. Vartanian, Marlene B. Schwartz, Kelly D. Brownell, “Effects of Soft Drink Consumption on Nutrition and Health: A Systematic Review and MetaAnalysis,” American Journal of Public Health 97 (2007): 667–75. 80 Lanaspa, et al., “Uric Acid,” 40732–744; Richard J. Johnson, Yuri Y. Sautin, William J. Oliver et al., “Lessons from Comparative Physiology: Could Uric Acid Represent a Physiologic Alarm Signal Gone Awry in Western Society?” Journal of Comparative Physiology 179 (2009): 67–76. 81 Lustig, “Childhood Obesity,” 447; and Shanik et. al., “Insulin Resistance,” S262– S68. 82 Kelishadi et al., “Association of Fructose,” 503–10; Faeh, et al., “Effect of Fructose,” 1907–13; and E. J. Parks, et al., “Dietary Sugars,” 1039–46. 83 Lustig, “Childhood Obesity,” 447; William Alan Banks, A. B. Coon, Sandra M. Robinson et al., “Triglycerides Induce Leptin Resistance at the Blood-brain Barrier.” Diabetes 53 (2004): 1253–60; Kellerer, et. al. “Insulin Inhibits Leptin Receptor Signalling,” 1125–32; and Shapiro, et. al., “Prevention and Reversal,” 390–97. 84 Rexford S. Ahima, and Jeffrey S. Flier, “Leptin,” Annual Review of Physiology 62 (2000): 413–37: Friedman and Halaas, “Leptin and the Regulation,” 763.

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Conclusion: Where Do We Go From Here? We need broad public consensus that high intake of added sugars is a major contributor to MetS and many chronic diseases that have high death and disability tolls. Only then will there be a greater effort by governments around the world to draft public policies that reduce the accessibility to unhealthy foods high in added sugars and increase the accessibility to nutritious foods with no added sugars. Such public policies are especially important for protecting the health of the most vulnerable segments of the world’s populations, including children and adolescents. Youth are developing food habits that will stick with them for life as they lack the knowledge and maturity to avoid sodas and sugar-laden sweets. Another vulnerable segment of the population includes people who fall into a lower socioeconomic bracket. In the United States, the government subsidizes the production of commodity crops (corn, soy, wheat), keeping the price of these products very low. Since these commodity crops are the main ingredients in cheap processed foods, they attract families on tight budgets. In addition, these foods are convenient and often addictive. The poor are more likely to have unhealthy diets and reside in food deserts, or residential areas that only have convenience stores or gas stations instead of grocery stores. Subsequently, their access to nutritious whole foods is severely restricted, and they are more likely to develop chronic diseases. For these reasons, we need governments around the world to enact legislation that will protect the most vulnerable segments of the population from chronic diseases through various forms of prevention. In 2016, the World Health Organization called for governments around the world to introduce a tax on sugary drinks. They made this recommendation based on evidence and facts, such as people who consume at least one sugar-sweetened beverage (SSB) per day have an 83–98% higher incidence of diabetes compared with those who consumed fewer than one SSB per month.85 Some countries that currently have excise taxes on sugary drinks include France, Estonia, Finland, Hungary, India, Brazil, Mexico, and the United States. A comprehensive literature review of sugarsweetened beverage (SSB) taxes and/or price increases and their impact on consumption levels, overweight, obesity, and BMI from the United States, Brazil, and Mexico reported that an increase in the price of SSBs is associated with a decrease in consumption. The higher the price increase,

85

Matthias B. Schulze, J. E. Manson, David S. Ludwig et al., “Sugar-sweetened Beverages, Weight Gain, and Incidence of Type 2 Diabetes in Young and Middleaged Women,” JAMA 292 (2004): 927–34.

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the greater the reduction in consumption.86 Furthermore, six studies from the United States showed that a higher price could also lead to a decrease in BMI and the prevalence of overweight and obesity,87 which are markers for metabolic disease. An economic-epidemiological modeling study reported that a higher SSB tax could mitigate rising T2D and obesity rates in both rural and urban populations in India.88 A similar study done in the United States projected that increasing current SSB taxes to one penny per ounce, over a period of ten years, would prevent 2.4 million diabetes person-years (2.6% reduction in T2D incidents), 95,000 coronary heart events, 8,000 strokes, and 26,000 premature deaths while avoiding more than $17 billion in medical costs.89 Other non-tax restrictions on products with added sugars could also be enacted, such as banning SSBs from schools or workplaces. In Wales, they have banned fizzy soft drinks, including diet or sugar-free versions, from primary and secondary schools. In Australia and Brazil, officials have banned beverages with sweeteners from schools. In the United States, 70% of all interventions associated with reducing SSB consumption in schools, regardless of whether they targeted individuals, their environment, or both, were effective in decreasing SSB consumption. A study conducted in the U.S., in 2019, showed that banning the sales of SSBs in the workplace resulted in a significant reduction in SSB intake, which was associated with a significant reduction in waist circumference and insulin resistance.90 If we want to see government legislation that restricts access to food and beverage products that are high in added sugars, there must first be a broad public consensus that high intake of added sugars leads to various metabolic diseases such as type 2 diabetes and cardiovascular disease. The biggest obstacle to this broad public consensus is the tremendous influence that food and beverage industries have on government and even academia to protect 86

Maris A. Cabrera Escobar, J. Lennert Veerman, Stephen M. Tollman et al., “Evidence That a Tax on Sugar-sweetened Beverages Reduces the Obesity Rate: A Meta-analysis.” BMC Public Health 13 (2013): 1072. 87 Ibid. 88 Sanja Basu, Sukumar Vellakkal, Sutapa Agrawal et al., “Averting Obesity and Type 2 Diabetes in India through Sugar-sweetened Beverage Taxation: An Economic-Epidemiologic Modeling Study,” PLoS Medicine 11 (2014): e1001582. 89 Y. Claire Wang, Pamela Coxson, Yu-Ming Shen, Lee Goldman, and Kirsten Robbins-Domingo. “A Penny-per-ounce Tax on Sugar-sweetened Beverages Would Cut Health and Cost Burdens of Diabetes.” Health Affairs 31 (2012) 199–207. 90 Elissa S. Epel, Alison Hartman, Laurie M. Jacobs, Cindy Leung, Michael A. Cohn, Leeane Jensen, Laura Ishkanian et al. “Association of a workplace sales ban on sugar-sweetened beverages with employee consumption of sugar-sweetened beverages and health.” JAMA Internal Medicine 180 (2020): 9-16.

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the sales of their products. This scenario is very similar to Big Tobacco’s efforts to thwart scientific research that showed a direct relationship between smoking tobacco and lung cancer, which dates back to the first Surgeon General’s report in 1964. The good news is that Big Tobacco eventually lost the fight and laws were passed that required warning labels be put on cigarette packages that linked smoking tobacco to cancer. There were also laws passed that reduced the accessibility and advertising of cigarettes. There are lessons to be learned from this history. Even though years of mounting scientific evidence showed an association between smoking tobacco and lung cancer, it was not until documents were brought forward that demonstrated corporate corruption (hiding scientific findings and fabricating or modifying data) that there was finally broad public consensus that smoking tobacco caused lung cancer. In the case of sugar and metabolic disease, food and beverage industries (Coca Cola, Pepsi, Kraft, General Foods, Nestle, Nabisco, etc.) are the equivalent to Big Tobacco. As was done with Big Tobacco, we must shine a spotlight on corporate corruption that has infiltrated scientific research on the role of sugar in metabolic disease, making it clear that the controversy about sugar and metabolic disease is fabricated. This generation is expected to be the first to live longer lives than our children who are suffering from obesity and type 2 diabetes earlier in life than ever before.91 We have ended up in this health crisis largely from private interests being placed above public health. Therefore, it is my hope that we can avert this health crisis if we start taking the opposite approach. We must vote for policies and politicians that make public health a top priority by passing laws that (1) restrict access to unhealthy foods and increase access to healthy foods, (2) ensure that schools have enough government funding to serve healthy lunches rather than rely on private money from food and beverage companies, (3) prevent food and beverage companies from marketing unhealthy products to children, (4) ensure that federal nutrition guidelines are developed within government agencies that do not have an inherent conflict of interest (i.e. the USDA), (5) work toward introducing grocery stores into regions that are considered food deserts, and (6) reallocate government subsidies to support the growth of whole 91 David S Ludwig, “Lifespan Weighed Down by Diet.” JAMA 315, no. 21 (2016): 2269–70; and S. Jay Olshansky, Douglas J. Passaro, Ronald C. Hershow, Jennifer Layden, Bruce A. Carnes, Jacob Brody, Leonard Hayflick, Robert N. Butler, and David B. Allison, “A Potential Decline in Life Expectancy in the United States in the 21st Century.” New England Journal of Medicine 352 (2005): 1138–45.

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nutritious foods (fruits, vegetables, legumes), making them more affordable for everyone.

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Malik, Vasanti S., Barry M. Popkin, George A. Bray, Jean-Pierre Després, Walter C. Willett, and Frank B. Hu. “Sugar-sweetened Beverages and Risk of Metabolic Syndrome and Type 2 Diabetes.” Diabetes Care 33 (2010): 2477–83. Massougbodji José, Yann Le Bodo, Ramona Fratu, and Phillippe De Wals. “Reviews Examining Sugar-sweetened Beverages and Body Weight: Correlates of Their Quality and Conclusions.” American Journal of Clinical Nutrition 99 (2014): 1096–1104. Mayer-Davis, Elizabeth J., Jean M. Lawrence, Dana Dabelea, and Jasmin Divers. “Incidence Trends of Type 1 and Type 2 Diabetes among Youths, 2002–2012.” New England Journal of Medicine 376 (2017): 1419–29. Mayes Peter A. “Intermediary Metabolism of Fructose.” supplement, American Journal of Clinical Nutrition 58, S5 (1993): 754S–S765. Meigs, James B., Peter W. F. Wilson, Caroline S. Fox, Ramachandran S. Vasan, David M. Nathan, Lisa M. Sullivan, and Ralph B. D'Agostino. “Body Mass Index, Metabolic Syndrome, and Risk of Type 2 Diabetes or Cardiovascular Disease.” Journal of Clinical Endocrinology and Metabolism 91 (2006): 2906–12. Misiak, Blazej, Jerzy Leszek, and Andrzej Kiejna. “Metabolic Syndrome, Mild Cognitive Impairment and Alzheimer's Disease—The Emerging Role of Systemic Low-grade Inflammation and Adiposity.” Brain Research Bulletin 89 (2012): 144–49. Montell, E., M. Turini, and M. Marotta, et. al. “DAG accumulation from saturated fatty acids desensitizes insulin stimulation of glucose uptake in muscle cells.” American Journal of Physiology-Endocrinology And Metabolism 280, no. 2 (2001): E229-E237 Mozumdar, Arupendra, and Gary Liguori. “Persistent Increase of Prevalence of Metabolic Syndrome among US Adults: NHANES III to NHANES 1999–2006.” Diabetes Care 34 (2011): 216–19. National Center for Health Statistics. Health, United States with Chartbook on Long-term Trends in Health. Hyattsville, MD: National Center for Health Statistics, 2017. Nishida, Chizuru, Ricardo Uauy, Shiriki Kumanyika, and Prakash Shetty. “The Joint WHO/FAO Expert Consultation on Diet, Nutrition and the Prevention of Chronic Diseases: Process, Product and Policy Implications.” Public Health Nutrition 7 (2004): 245–50. Norum, Kaare R. “World Health Organization's Global Strategy on Diet, Physical Activity and Health: The Process behind the Scenes.” Scandinavian Journal of Nutrition 49 (2005): 83–88.

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O'Connor, Anahad.”Coca-Cola Funds Scientists Who Shift Blame for Obesity Away From Bad Diets.” New York Times, 2015. https://well.blogs.nytimes.com/2015/08/09/coca-cola-funds-scientistswho-shift-blame-for-obesity-away-from-bad-diets/ Olshansky, S. Jay, Douglas J. Passaro, Ronald C. Hershow, Jennifer Layden, Bruce A. Carnes, Jacob Brody, Leonard Hayflick, Robert N. Butler, David B. Allison, and David S. Ludwig. “A Potential Decline in Life Expectancy in the United States in the 21st Century.” New England Journal of Medicine 352 (2005): 1138–45. O'Neill, Sadhbh, and Lorraine O'Driscoll. “Metabolic Syndrome: A Closer Look at the Growing Epidemic and Its Associated Pathologies.” Obesity Reviews 16 (2015): 1–12. Ouyang, Xiaosen, Pietro Cirillo, Yuri Sautin, Shannon McCall, James L. Bruchette, Anna Mae Diehl, Richard J. Johnson, and Manal F. Abdelmalek. “Fructose Consumption as a Risk Factor for Non-alcoholic Fatty Liver Disease.” Journal of Hepatology 48 (2008): 993–99. Panza, Francesco, Vincenza Frisardi, Cristiano, Capurso, Bruno P. Imbimbo, Gianluigi Vendemiale, Andrea Santamato, Grazia D' Onofrio, Davide Seripa, Daniele Sancarlo, Alberto Priotto, et al. “Metabolic Syndrome and Cognitive Impairment: Current Epidemiology and Possible Underlying Mechanisms.” Journal of Alzheimer's Disease 21 (2010): 691–724. Parks, Elizabeth J., Lauren E. Skokan, Maureen T. Timlin, and Carlus S. Dingfelder. “Dietary Sugars Stimulate Fatty Acid Synthesis in Adults.” Journal of Nutrition 138 (2008): 1039–46. Pechlaner, Raimund, Sotirios Tsimikas, Xiaoke Yin, Peter Willeit, Ferheen Baig, Peter Santer, Friedrich Oberhollenzer, George Egger, Joseph L. Witztum, Veronica J. Alexander, et al. “Very-Low-Density Lipoprotein– Associated Apolipoproteins Predict Cardiovascular Events and Are Lowered by Inhibition of APOC-III.” Journal of the American College of Cardiology 69 (2017): 789–800. Pollock, Norman K., Vanessa Bundy, William Kanto, Catjerine L. Davis, Paul J. Bernard, Haidong Zhu, Bernard Gutin, and Tanbin Dong. “Greater Fructose Consumption Is Associated with Cardiometabolic Risk Markers and Visceral Adiposity in Adolescents.” Journal of Nutrition 142 (2012): 251–57. Powell, Elyse S., Lindsey P. Smith-Taillie, and Barry M. Popkin. “Added Sugars Intake across the Distribution of US Children and Adult Consumers: 1977–2012.” Journal of the Academy of Nutrition and Dietetics 116 (2016): 1543–50.e1541.

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CHAPTER ELEVEN EVOLUTION OF INFECTION RESISTANCE IN LARGE POPULATIONS PARVIN SHAHRESTANI

How We Came to Understand Pathogens Our experiences with recent outbreaks of Ebola Viral Disease and the current Covid-19 pandemic remind us of the continued challenges infectious diseases pose to the global community. At the same time, these recent experiences shine a light on our expectations and abilities to manage infectious diseases today compared to the past. It is easy to forget how recently we discovered that infections are caused by living organisms. Before the nineteenth century, plagues spread quickly, devastating human populations. In those days, physicians did not understand the causes of infection, and epidemics were commonly thought to result from poisonous (miasmatic) gasses.1 Despite the existence of microscopes and knowledge about microorganisms, which date back to Antonie van Leeuwenhoek (1632–1723), physicians did not connect microbes and infectious diseases until the mid-1800s. Germ theory emerged from the collective work of researchers, and some remain renowned figures. In 1850, John Snow traced the cholera epidemic to a water pump in London. Not long after, Joseph Lister introduced antiseptic surgery, and Louis Pasteur’s careful experiments provided more support for the idea that microorganisms can cause infection. In 1876, Robert Koch demonstrated that the bacterium Bacillus anthracis caused anthrax. These efforts laid the foundation for the development of vaccines and antibiotics in the twentieth century. Even before we understood germ theory, public health measures in many countries sought to clean the air, water, and soil, and thereby reduced the prevalence of infection. When doctors and public health officials understood that microorganisms could cause disease, they fought for the 1

William Hardy McNeill, Plagues and Peoples (New York: Anchor, 1998).

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chlorination and boiling of water, mosquito and rodent control, pasteurization of milk, and sterilization of surgical instruments. Similar campaigns led to vaccination, hand washing by health care providers, wearing masks to prevent the spread of infection, proper disposal of human wastes, inspection of food for contaminants, effective burial practices, and the use of antibiotics. These measures were collectively so effective at reducing infectious disease that by the 1960s, infectious disease was no longer the primary cause of mortality in developed countries. In the United States, mortality from infectious diseases declined by over 90% between 1900 and 1996.2 The effective control of infectious disease started before we even understood the molecular biology of viruses, bacteria, and fungi, and then further improved with a molecular understanding of pathogenesis. By 1981, we knew quite a bit about infectious disease. But when AIDS cases began to spread in the USA, all of our knowledge about infectious disease did not prevent an epidemic. Since then, in the age of “–omics,” we have gathered genomic, transcriptomic, and proteomic data for many of the pathogens that infect humans, as well as for host organisms, including humans. Understanding that infectious diseases are caused by microbes was necessary for the level of control we have today over the spread and treatment of infections. However, with all of our information now, we are still unlikely to prevent the next epidemic of infectious disease. I argue that it is insufficient to learn only about the microbes that infect us, and that we must also study how our bodies defend against those microbes, and that such studies can benefit from model organisms. I further argue that pathogen and host, and their interactions, can only be sufficiently understood in the context of their evolutionary histories. Thus, further improvements in the prevention and treatment of infectious disease will require a solid understanding of and appreciation for evolutionary biology.

Human Immune Defense and the Need for Models We live in mutualism with many bacteria and fungi that reside in our bodies and never cause an infection.3 In many cases, these microbes are beneficial for us. Even the mitochondria of our cells, the so-called powerhouses of cells, are thought to have originated as free-living 2

Gregory L. Armstrong, Laura A. Conn, and Robert W. Pinner, “Trends in Infectious Disease Mortality in the United States during the 20th Century,” JAMA 281, no. 1 (1999): 61–66. 3 Ron Sender, Shai Fuchs, and Ron Milo, “Revised Estimates for the Number of Human and Bacteria Cells in the Body,” PLoS Biology 14, no. 8 (2016): e1002533.

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microbes.4 A minuscule proportion of microorganisms are pathogens. What determines the pathogenic nature of a microbe depends in part on its relationship with the host immune defenses. Our first line of defense upon pathogen exposure is the physical and chemical barriers that work to keep the pathogen out of our bodies, such as our skin, mucus, and stomach acids. When pathogens move past these barriers and into the body, our immune systems usually react. The human immune response can be sub-divided into innate immunity and adaptive (or acquired) immunity, but the two parts of the immune response work collaboratively. Innate immunity is present from birth and is nonspecific, targeting many types of pathogens. It also includes our inflammatory response to infection and tissue damage. Adaptive immunity, on the other hand, targets specific pathogens. Simpler organisms, such as insects, have an innate immune response, but not an adaptive immune response. The adaptive immune response allows humans and other mammals to learn about and store information about pathogens so that when the body is reintroduced to the pathogen for a second time, the body can activate an immune response faster and more effectively than the first time. This activation is especially relevant when the pathogen in question has evolved mechanisms to evade the innate immune response. Indeed, this is the principle on which vaccination operates. A vaccine may introduce a dead or weakened pathogen into our body, giving our immune defense a chance to learn and store information about the pathogen. When we encounter the pathogen’s active form in the future, our body is prepared to fight. But some pathogens evolve very fast and become so different in a short amount of time that they can evade our immune response even if we have been vaccinated. Sometimes the immunity that is developed through vaccination wears off over time, and we become susceptible to infection even if we have been vaccinated and the pathogen has remained the same. Nevertheless, the benefit of vaccination for preventing infectious disease is undeniable, especially when we follow the research-based medical guidelines for each vaccine. In the human body, it is difficult to identify which parts of our anatomy belong to the immune system. The system integrates with the tissues of many organs, including the gastrointestinal tract and skin. Lymphoid tissues are also part of the immune system, and these are everywhere in the body. Two primary lymphoid tissues are the thymus gland and bone marrow, where immune response cells form and mature. Secondary lymphoid tissues include the spleen, lymph nodes, and tonsils. 4 Michael W. Gray, Gertraud Burger, and B. Franz Lang, “Mitochondrial Evolution,” Science 283, no. 5407 (1999): 1476–81.

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When microbes enter the fluid between cells (interstitial fluid), they may be pulled into the lymphoid tissues, where they may be contained and destroyed by immune cells. The primary immune cells of the immune response are white blood cells, also known as leukocytes. These cells are larger than red blood cells but are much fewer in numbers. White blood cells are sometimes categorized based on their functions. For example, neutrophils, macrophages, and monocytes are white blood cells that are categorized as phagocytes, based on their ability to engulf and ingest pathogens through a process called phagocytosis. Other functional categories of white blood cells include the cytotoxic cells that kill the cells they attack (eosinophils and some lymphocytes are leukocytes that fall into this functional category) and the antigen-presenting cells that display parts of foreign proteins on their cell surface (such as macrophages, monocytes, dendritic cells, and some lymphocytes). The commonly talked about “B cells,” “T cells,” and “natural killer cells” are types of lymphocytes. Some cells, such as B cells that differentiate into plasma cells, can make and release many antibodies very quickly into the body, making up the “humoral immunity,” which relies on soluble antibodies of the plasma. While we know many of the molecules, cells, and mechanisms involved in human immune defense, we do not yet know all of them. Nor do we have an exhaustive list of immune defense genes. Researchers around the world are still actively working on identifying genes in the human genome that contribute to immune defense. A thorough understanding of immune defense is complicated by the fact that the environment affects this trait. For example, long-term stress is associated with a lower ability to fight infection.5 While some experts believe the hormones involved in stress are responsible for this effect, it is not exactly clear how this happens. The immune defense may also be affected by diet. For example, a diet high in agricultural foods such as dairy and grains can result in systemic inflammation in a large majority of the world’s population, diminishing the immune defense’s ability to fight infection. Other environmental influences on our immune defense include temperature, smoking, sleep deprivation, alcohol consumption, and likely many other unknown factors. In other words, we do not know enough about all of the factors that contribute to our ability to withstand or fight infections. Moreover, immune defense researchers distinguish between “tolerance of” and “resistance to” infection. Imagine that two individuals, persons A and B, receive the same infection dose of a bacterial pathogen. Person A may clear the infection or prevent the pathogen from multiplying, while the pathogen reaches high 5

Firdaus S. Dhabhar, “Effects of Stress on Immune Function: The Good, the Bad, and the Beautiful,” Immunologic Research 58, no. 2–3 (2014): 193–210.

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numbers within the body of person B. In this case, we would say that the two individuals differ in their resistance to infection, or in their ability to resist or prevent the infection from multiplying. It is also possible for people to differ in their tolerance to infection. For example, if persons A and B received the same infection and the pathogen grew to the same high numbers in both of them, but person A barely exhibited any symptoms of illness while person B was very sick, then it may be that person A can tolerate the infection much better. A complete understanding of immune defense will need to differentiate among variables that make some individuals more tolerant of or resistant to the same infection dose, including overall health, age, sex, and reproductive status. Another complication in studying immune defense is that different pathogens may elicit different immune responses. Thus, understanding immune defense against one pathogen in detail does not necessarily closely translate to how the body fights other pathogens. Moreover, even if we reach a better understanding of immune defense against every known pathogen, we will still face the complication that immune defense is a quantitative character, not a qualitative one. In any human population, individuals will vary on a spectrum on how effectively their immune defense functions against a particular pathogen. It is not clear what factors contribute to the trait variation among individuals of a population. Experts do not know how much variation can be explained by genes or the environment, interactions among genes, and interactions between genes and the environment. A better understanding of immune defense can help future medical practitioners to personalize treatments for infection based on the traits of the individual that they are treating. But how can we elucidate all of the unknowns about immune defense given the complexity of this trait? One promising approach is to use model organisms to study immune defense. Model organisms, such as mice and fruit flies, are commonly used in biology and medical research laboratories. When using model organisms, experimenters can control or vary many of the factors that cannot be directly studied in humans and can perform careful hypothesis testing with rigorous experimental designs. Our ability to leap forward in our understanding of immunity rests in large part on model organisms.

Fruit Flies as a Model for Human Immune Defense The laboratory fruit fly, scientifically known as Drosophila melanogaster, was historically used to lay the foundations for most of what we now know about genetics. This species shares genetic similarities with humans, with estimates of 70% shared disease genes between fruit flies and humans.

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Embryonic development is similar, as are the genes involved in heart function, glucose-intolerance, and other health-relevant traits. When it comes to immune defense, fruit flies have an innate immune response, but not an adaptive one. Yet the innate immune response of fruit flies is very similar to that of humans; therefore, fruit fly immune defense has become a model for understanding human innate immunity.6 Studies of fruit flies have made such substantial contributions to our understanding of immune defense that, in 2011, biologist Jules A. Hoffmann was awarded the Nobel Prize in Physiology and Medicine based on his laboratory’s experimentation. When flies encounter pathogens, the cuticle (the outer covering of an insect) provides an initial epithelial barrier defense, similar to our skin. Behavioral responses also help reduce infections in flies. For example, when fungi or bacteria touch the fly cuticle, the fly begins to groom itself thoroughly, similar to hand washing or showering in humans. Once a pathogen has penetrated the body cavity, a systemic immune response is activated. Activation occurs through the expression of genes in immune defense pathways. In these pathways, much like in other biological pathways, a series of genes are expressed into proteins. The proteins interact with each other to cause a specific outcome. In the case of the immune defense pathways, Toll and Imd, it is the production of antimicrobial peptides, which are proteins that attack microorganisms. The Toll pathway is used in defense against fungi and some types of bacteria (Gram-positive bacteria).7 The human pathway that is similar to the fruit fly Toll pathway has a much more complex name: myeloid differentiation primary response protein 88 (MYD88)-dependent Toll-like receptor (TLR) pathway. The Imd pathway, which fruit flies use to defend against Gram-negative bacteria,8 is similar to the human tumor necrosis factor (TNF) pathway and TIR domaincontaining adaptor protein inducing INFȕ (TRIF)-dependent TLR pathways. The names of these pathways are much simpler for fruit flies than for humans, as are the pathways themselves. This allows experimenters to study the effects of genes and gene interactions in detail. Genes of the Toll and Imd pathways are predominantly expressed in the fruit fly fat body, which is similar to the human liver.

6

Nicolas Buchon, Neal Silverman, and Sara Cherry, “Immunity in Drosophila melanogaster—from Microbial Recognition to Whole-organism Physiology,” Nature Reviews Immunology 14, no. 12 (2014): 796. 7 Susanna Valanne, Jing-Huan Wang, and Mika Rämet, “The Drosophila Toll Signaling Pathway,” Journal of Immunology 186, no. 2 (2011): 649–56. 8 Henna Myllymäki, Susanna Valanne, and Mika Rämet, “The Drosophila Imd Signaling Pathway,” The Journal of Immunology 192, no. 8 (2014): 3455–62.

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Most immune defense research, in humans and fruit flies, has focused on defenses against bacteria and viruses. In comparison, we know little about how the body fights fungal infections. Immune defense against fungal pathogens is the focus of my research laboratory. There are two important reasons to study fungal infections in fruit flies. First, given the genetic similarities between humans and fruit flies, understanding the fruit fly immune defense against fungal infection will give us insight into human biology. Second, fungal pathogens have great potential for use in biological control of insect crop pests and insect vectors of human disease, such as the mosquitos that vector malaria. Therefore, understanding insect immune defense against fungi can help us toward more effective biological control efforts, thus impacting global health and agriculture. The main fungal pathogen used in my laboratory is the entomopathogenic Beauveria bassiana. Some strains of this fungus can be used in controlling insect crop pests that threaten food security.9 Currently, researchers are optimizing the effectiveness of this fungus for use in biological control of mosquito vectors of human disease.10 Yet others have shown this pathogen’s effectiveness in controlling bed bugs. Susceptibility to infection with B. bassiana is variable among individuals of insect populations. In trying to identify which factors make some fruit flies more susceptible to infection than others, we stumbled upon a sexual dimorphism in susceptibility to infection, with females dying faster of fungal infection compared to males at the same infection dose.11 Across many animal species, females and males differ in anatomy and physiology. So perhaps it is not surprising that they also differ in immune defense as a result of the different evolutionary pressures that act on the sexes. Our experiments revealed that this sex difference was in part due to cuticular differences between the sexes, but that most of the difference relied on an expression of the genes of the Toll pathway. Surprisingly, a 9

Óscar Dembilio, Enrique Quesada-Moraga, Cándido Santiago-Álvarez, and Josep A. Jacas, “Potential of an Indigenous Strain of the Entomopathogenic Fungus Beauveria bassiana as a Biological Control Agent against the Red Palm Weevil, Rhynchophorus ferrugineus,” Journal of Invertebrate Pathology 104, no. 3 (2010): 214–21. 10 Minehiro Ishii, Hirotaka Kanuka, Athanase Badolo, Wamdaogo M. Guelbeogo, Masanori Koike, and Daigo Aiuchi, “Proboscis Infection Route of Beauveria bassiana Triggers Early Death of Anopheles Mosquito,” Scientific Reports 7, no. 3476 (2017): 3476. 11 Parvin Shahrestani, Moria Chambers, John Vandenberg, Kelly Garcia, Glen Malaret, Pratik Chowdhury, Yonathan Estrella, et al., “Sexual Dimorphism in Drosophila melanogaster Survival of Beauveria bassiana Infection Depends on Core Immune Signaling,” Scientific Reports 8, no. 12501 (2018): 12501.

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gene in the Imd pathway, known as relish, also affected the sex difference, even though the Imd pathway was traditionally not thought to be involved in defense against fungal infection. This result suggests that the pathways of immune defense are more complex than had been previously thought. Further investigation revealed that the direction of the sex difference in response to infection could be reversed in some cases. Specifically, we compared fly lines, a group of individuals that are almost entirely genetically identical to each other. When we compared ~300 fly lines for sexual dimorphism in response to infection with a fungus, we found males were more susceptible than females in some fly lines. This result suggested that sex differences in immune defense depend on many factors, not just the known genes of known immune pathways. We mapped the immune defense information for these ~300 fly lines to genetic information for these fly lines and identified several novel candidate genes for immune defense. Interestingly, our list of candidate genes included genes from the Imd pathway, once again suggesting that immune defense pathways are complex, and casting doubt on previously accepted canonical immune pathways. Moreover, the direction of sex difference in immune defense was also affected by diet and mating. Whether males or females survived infection better changed when flies from the same fly line were tested under dietary conditions that varied in ratios of sugar to proteins, and under different mating conditions (virgin, mated once, or mated multiple times). To further investigate immune defense genes and identify novel genes that were not previously known, we set out to do an experimental evolution project. With experimental evolution, laboratory populations can be selected (through laboratory natural selection) for different characteristics. In this case, we selected some fly populations for decreased susceptibility to fungal infection and compared them to control populations on a genomic level. First, we needed a genetically diverse population that had high levels of variation in immune defense. Such a diverse population was created by mixing flies from five geographic locations around the world (New York, Netherlands, Zimbabwe, Beijing, and Tasmania).12 The lab-created population was highly genetically diverse, representing global genetic diversity for immune defense. We then divided this population into eight subpopulations, each with 10,000 individuals. Four of these populations were selected for decreased susceptibility to infection (in other words, increased survival of 12 Jennifer K. Grenier, J. Roman Arguello, Margarida Cardoso Moreira, Srikanth Gottipati, Jaaved Mohammed, Sean R. Hackett, Rachel Boughton, Anthony J. Greenberg, and Andrew G. Clark, “Global Diversity Lines–A Five–Continent Reference Panel of Sequenced Drosophila Melanogaster Strains,” G3: Genes, Genomes, Genetics 5, no. 4 (2015): 593–603.

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infection). We accomplished lower susceptibility by infecting all 10,000 members of each population with the fungus B. bassiana and waiting for 80% of the population to die of infection. Only the surviving 20% of individuals reproduced and contributed genes to the next generation. We also set up four control populations, in which none of the flies were infected, and a random 20% of the population got to pass on genes. After just five generations of selection, the four selected populations had already become significantly differentiated from the four control populations in their susceptibility to infection. It was clear that differences in immune defense could evolve very quickly. After nineteen generations of selection, the difference in immune defense between the selected and control populations was large, allowing the selected populations to survive for several days longer in the presence of infection compared to flies from the control populations. However, the evolution of better immune defense came at a cost to the selected flies, resulting in them living significantly shorter lives in the absence of infection. In other words, populations that had better immune defense survived better in the presence of infection but worse in the absence of infection, compared to populations that were not selected for improvements in immune defense. This result shows that immune defense is costly and trades off with other traits. We next extracted genetic material (DNA) from the two types of populations: those with improved immune defense and their controls. We compared the genetic material of these populations in order to identify which parts of the DNA have changed as a result of selection for better immune defense. In these comparisons, we found that several locations along the DNA had changed because of selection for better immune defense. However, none of these changes resulted from new mutations. Instead, at every altered location in the DNA, the change was only in the frequencies of the variants. For example, imagine that at some location on the DNA, the ancestral population had 20% adenine (one of the four nucleotide types of DNA; the other three are guanine, cytosine, and thymine) and that this frequency had increased to 70% after being selected for improved immune defense. In this case, we would compare these percentages (20% and 70%) to each other with a statistical test to determine if the difference is statistically significant. If it is indeed significant, then that location on the DNA might be important for conferring immune defense differences. In this way, we identified potential candidate genes that may be involved in immune defense. We also analyzed the locations on the DNA where the frequency of a variant increased to 100% in one type of population but not the other, leading to a few additional candidate genes.

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While our research has identified novel candidate genes for immune defense, much more research is needed. Nevertheless, our work supports the idea that model organism research is a promising approach for illuminating genetic and environmental factors that affect immune defense. The information we are collecting is useful for controlling dangerous insect vectors and better understanding immune responses in organisms that act in surprisingly similar ways to humans, despite their different appearances.

Population-Level Immune Defense in the Context of Evolution For as long as humans have existed, they have co-existed with pathogens. Why then have we not evolved to no longer get infected? In 1994, Randy Nesse and George Williams described a six-part answer to this question.13 First, we are locked in a co-evolutionary arms race with pathogens. As we evolve to evade the pathogen, the pathogen evolves to evade our defenses. Since most human pathogens evolve faster than we do (because they have shorter lifespans and larger population sizes), we continue to be susceptible to infection. Second, in some cases, natural selection may not be fast enough to keep up with rapid environmental changes. One example is that most humans today eat grains and dairy, but we are not adapted to digest these foods because we did not eat them until recently in our evolutionary histories.14 This is especially true for older adults because the forces of natural selection are weakest at this stage, leading to elderly individuals being more maladapted to their environments.15 Third, evolution is limited even if there is unlimited time, by the laws of physics, and by trade-offs between traits. For example, in our fruit fly populations that were selected for improved immune defense, longevity without infection was reduced. If a few generations pass without exposure to pathogens, we would expect susceptibility to infection to return due to the trade-offs, or costs, of maintaining strong immune defense. Fourth, natural selection cannot predict the future. Evolving to fight a 13

Randolph M. Nesse, and George C. Williams, Why We Get Sick: The New Science of Darwinian Medicine (New York: Vintage, 1994). 14 M. R. Rose, G. A. Rutledge, L. G. Cabral, L. F. Greer, A. L. Canfield, and B. G. Cervantes, “Evolution and the Future of Medicine,” in On Human Nature, ed. Michel Tibayrenc and Francisco J. Ayala (San Diego: Academic Press, 2017), 695– 705. 15 Michael Rose, Thomas Flatt, Joseph L. Graves Jr., Lee F. Greer, Daniel E. Martinez, Margarida Matos, Laurence Mueller, Robert Joseph Shmookler Reis, and Parvin Shahrestani. “What is Aging?” Frontiers in Genetics 3 (2012): 134.

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particular pathogen today will not necessarily prepare us to fight an unknown pathogen that we may encounter several generations in the future. Fifth, natural selection will favor reproductive success even at the cost of vulnerability to infection. For example, in fruit flies, females that mate and reproduce are more susceptible to infection than females that remain virgins,16 but they pass on their genes to the next generation despite their increased susceptibility to infection. Similarly, the sixth point is that natural selection does not necessarily favor health and well-being, it favors reproductive success, and as such, our defenses to infection, such as nausea and fever, may actually be adaptive. Despite the limitations of evolution by natural selection, model organism research has shown that improved immune defense can evolve in large genetically diverse populations and that this evolution can be very fast. Experts have also witnessed rapid evolutionary change in fruit fly experimental evolution studies of other traits, including longevity, starvation resistance, and body size. What these traits have in common is that they are all quantitative. On the genetic level, these traits are all highly multigenic, meaning that many genes affect the traits. The genes, in turn, may interact with each other and with the environment. One point that geneticists debate is whether traditional molecular genetic approaches are insufficient and even misleading for identifying genes that are involved in complex traits. Only a small subset of genes and processes that can be mutated in the lab to cause a change in a trait is expected to be responsible for trait variation in nature. When mutated genes produce a large effect on a trait, they are likely to have negative consequences on other traits. Thus, they are also likely to be selected against by natural selection in real populations. Consider, for example, two of the best-known genes for lifespan extension in fruit flies: methuselah and Indy (I’m not dead yet). When these genes are mutated intentionally, they result in changes in lifespan. However, when we experimentally evolved large fruit fly populations for differences in lifespan and compared the genomes of these populations, the genes methuselah and Indy did not appear in our analysis.17 This finding suggests that considerable lifespan differences evolved without these known genes, which can influence lifespan in the laboratory. The approach of experimental evolution and whole-genome sequencing with model organisms has the potential to identify genes that affect a trait 16 Robin A. Schwenke, Brian P. Lazzaro, and Mariana F. Wolfner, “Reproduction– immunity Trade-offs in Insects,” Annual Review of Entomology 61 (2016): 239–56. 17 Molly K. Burke, Joseph P. Dunham, Parvin Shahrestani, Kevin R. Thornton, Michael R. Rose, and Anthony D. Long, “Genome-wide Analysis of a Long-term Evolution Experiment with Drosophila,” Nature 467, no. 7315 (2010): 587.

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that also exists and varies in natural populations, making this approach preferable to traditional molecular genetics for studying complex traits such as immune defense. This approach will implicate genes that are present in natural populations at frequencies that are not near zero. To give a human example, consider a gene that causes Progeria. Individuals who have Progeria live short lives and exhibit many symptoms that resemble aging, such as wrinkles, hair loss, and cardiovascular disease. While Progeria undoubtedly affects lifespan, this syndrome occurs in about one in every four million births worldwide. Given the rarity of Progeria, the genes involved in Progeria are not responsible for all of the lifespan variation that exists among individuals of any human population. Traditional molecular genetics can identify genes similar to the one that causes Progeria. But genes that can be mutated in the lab to create a drastic decrease or increase in lifespan may be non-existent or rare in real populations, and therefore cannot be responsible for the variation in lifespan that exists in large natural populations. Just because a gene can affect lifespan, it doesn’t mean that the gene exists in nature at frequencies that matter. We can extend the same argument to immune defense. When studying genes that contribute to immune defense variation in large populations, we need to consider evolutionary forces acting on those genes. Model organism research rooted in evolutionary biology has made substantial contributions to our understanding of many complex traits already, and more recently, biologists have extended this approach to immune defense. But in the USA, much of our public is uncomfortable, both with evolution-based research and with animal-based research. The media is prone to misunderstanding and misrepresenting this science, increasing the challenges for gaining research grants and funding. Will we be prepared for the next epidemic of infectious disease? I think we have come a very long way in just a short time in controlling infectious disease. We have identified that living organisms cause infections, we have taken various public health measures, and we have eliminated many of the most severe diseases, one disease at a time, with vaccination. We are also improving our approach to antibiotics. Nevertheless, our continued susceptibility to infection reflects Theodosius Dobzhansky’s excellent insight that “Nothing in biology makes sense except in the light of evolution.” To make better sense of host-pathogen interactions, and to be prepared for the next epidemic, we must invest in evolutionary approaches to infectious disease research.

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Bibliography Armstrong, Gregory L., Laura A. Conn, and Robert W. Pinner. “Trends in Infectious Disease Mortality in the United States during the 20th Century.” JAMA 281, no. 1 (1999): 61–66. Buchon, Nicolas, Neal Silverman, and Sara Cherry. “Immunity in Drosophila melanogaster—from Microbial Recognition to Wholeorganism Physiology.” Nature Reviews Immunology 14, no. 12 (2014): 796. Burke, Molly K., Joseph P. Dunham, Parvin Shahrestani, Kevin R. Thornton, Michael R. Rose, and Anthony D. Long. “Genome-wide Analysis of a Long-term Evolution Experiment with Drosophila.” Nature 467, no. 7315 (2010): 587. Dembilio, Óscar, Enrique Quesada-Moraga, Cándido Santiago-Álvarez, and Josep A. Jacas. “Potential of an Indigenous Strain of the Entomopathogenic Fungus Beauveria bassiana as a Biological Control Agent against the Red Palm Weevil, Rhynchophorus ferrugineus.” Journal of Invertebrate Pathology 104, no. 3 (2010): 214–21. Dhabhar, Firdaus S. “Effects of Stress on Immune Function: The Good, the Bad, and the Beautiful.” Immunologic Research 58, no. 2–3 (2014): 193–210. Gray, Michael W., Gertraud Burger, and B. Franz Lang. “Mitochondrial Evolution.” Science 283, no. 5407 (1999): 1476–81. Grenier, Jennifer K., J. Roman Arguello, Margarida Cardoso Moreira, Srikanth Gottipati, Jaaved Mohammed, Sean R. Hackett, Rachel Boughton, Anthony J. Greenberg, and Andrew G. Clark. “Global Diversity Lines–A Five–Continent Reference Panel of Sequenced Drosophila Melanogaster Strains,” G3: Genes, Genomes, Genetics 5, no. 4 (2015): 593–603. Ishii, Minehiro, Hirotaka Kanuka, Athanase Badolo, Wamdaogo M. Guelbeogo, Masanori Koike, and Daigo Aiuchi. “Proboscis Infection Route of Beauveria bassiana Triggers Early Death of Anopheles Mosquito.” Scientific Reports 7, no. 3476 (2017):3476. McNeill, William Hardy. Plagues and Peoples. New York: Anchor, 1998. Myllymäki, Henna, Susanna Valanne, and Mika Rämet. “The Drosophila Imd Signaling Pathway.” Journal of Immunology 192, no. 8 (2014): 3455–62. Nesse, Randolph, M., and George C. Williams. Why We Get Sick: The New Science of Darwinian Medicine. New York: Vintage, 1994. Rose, Michael, R., G. A. Rutledge, L. G. Cabral, L. F. Greer, A. L. Canfield, and B. G. Cervantes. “Evolution and the Future of Medicine,” In On

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Human Nature, 695–705. Edited by Michel Tibayrenc and Francisco J. Ayala. San Diego: Academic Press, 2017. Rose, Michael, Thomas Flatt, Joseph L. Graves Jr., Lee F. Greer, Daniel E. Martinez, Margarida Matos, Laurence Mueller, Robert Joseph Shmookler Reis, and Parvin Shahrestani. “What is Aging?” Frontiers in Genetics 3 (2012): 134. Schwenke, Robin A., Brian P. Lazzaro, and Mariana F. Wolfner. “Reproduction–immunity Trade-offs in Insects.” Annual Review of Entomology 61 (2016): 239–56. Sender, Ron, Shai Fuchs, and Ron Milo. “Revised Estimates for the Number of Human and Bacteria Cells in the Body.” PLoS Biology 14, no. 8 (2016): e1002533. Shahrestani, Parvin, Moria Chambers, John Vandenberg, Kelly Garcia, Glen Malaret, Pratik Chowdhury, Yonathan Estrella, Ming Zhu, and Brian P. Lazzaro. “Sexual Dimorphism in Drosophila melanogaster Survival of Beauveria bassiana Infection Depends on Core Immune Signaling.” Scientific Reports 8, no. 1 (2018): 12501. Valanne, Susanna, Jing-Huan Wang, and Mika Rämet. “The Drosophila Toll Signaling Pathway.” Journal of Immunology 186, no. 2 (2011): 649–56.

CHAPTER TWELVE TRAGEDY AT THE TROPIC OF CAPRICORN: NINETEENTH CENTURY GLOBALIZATION AND EPIDEMIOLOGICAL CHANGE ON TWO SIDES OF SOUTH AMERICA IAN READ

In August 1850, the son of one of Chile’s most famous independence fighters stepped up to a podium to deliver a prestigious address at his national university. The speaker, Doctor Juan Mackenna, shared an idea with most doctor-scholars in Chile and other parts of the western world that the general health and race of a people and character of their nation were pieced together by wind, rain, and heat.1 In the Hippocratic tradition, Mackenna began with a eulogy of Chile that had inspired his father to battle the Spanish for independence. A “mildness of climate” prevailed rather than “foci of miasmatic emanations so common among other countries.” However, from here, he veered sharply, most likely to the discomfort of the frocked men in their somber auditorium. “The temperament of the Chilean race was not what it is today,” he said. His father’s generation “had a type of robustness, but without the inflexible and barbarous character of the inhabitants of the icy zones; and was of a gentle nature, but without touching on the humiliating timidity of those who inhabit the ardent climates.”2 Using modern statistical techniques and the powers of state surveillance, MacKenna argued that hospital and parish death records demonstrated a trend in mortality that put the nation and its 1

Genevieve Miller, “Airs, Waters, and Places” in History,” Journal of the History of Medicine and Allied Sciences 17, no.1 (January 1962):129–140; David Cantor, ed., introduction, “The Uses and Meanings of Hippocrates” in Reinventing Hippocrates, (Aldershot UK: Ashgate Publishing, (2002). 1–16. 2 Juan Mackenna, “De las causas de la mortalidad en Chile fundadas en la desproporcion entre el temperamento de los hijos del país i su clima,” Anales de la Universidad de Chile: memorias científicas y literarias 38, (1850): 134.

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people at no lesser risk than “extermination.”3 This mortal diagnosis was owed to the diseased temperament and habits increasingly disconnected from the nation’s healthy climate. Speaking as the son of a man widely considered to have helped birth the nation, MacKenna helped usher in a new era of increased pessimism that became what the Chilean elite eventually and commonly called “the social question.” By the late nineteenth century, views of Chile’s climate transformed from a sunny optimism to stormy pessimism. This transformation also included the nation and a semi-national race of people by extension. Furthermore, this zeitgeist went well beyond Chile, as moods soured about health, climate, and national health on both sides of the American Tropic of Capricorn. The American Tropic of Capricorn is a vast area traversed by an imaginary boundary. Today the line is mostly a curiosity, but for European mariners and settlers during the 15th to 19th centuries it marked an atmospheric barrier that held the torrid back from the temperate. Looking toward this barrier, Chileans, Brazilians, and Argentines wove reactions to a more fertile and dangerous disease environment, perceptions of local climates, and the character and race of their people into the fabric of young nations. Furthermore, they did so in ways that were relative to the wealthy and socalled civilized nations of the North Atlantic, which were also undergoing shifts in disease environments, but in ways that boosted confidence in national health. This chapter makes two broad and interconnected arguments, one historical and the other methodological. I present evidence that the elite in many parts of South America experienced a grand loss of confidence that stemmed from a worsening of the physical disease environment and the easy extension of very old stereotypes about the tropics. Even as some aspects of health improved, several fearsome infectious diseases, including cholera, yellow fever, bubonic plague, and smallpox, either arrived or worsened. By the second half of the 1800s, these diseases not only killed more people in Brazil, Argentina, and Chile but also severely damaged confidence in the identities of nations whose problems were increasingly seen as regional or national rather than “American.” Throughout most of the nineteenth century, most diseases were rooted in place and inseparable from the local climate. Local environments could condition even “contagious” diseases such as smallpox and measles and influence conceptions of the race or races of the nation and the habits of its ordinary people. Prominent doctors of the American hemisphere distinguished or measured civilization by the presence or absence of particular types of infections, particularly those that disfigured and defaced, such as leprosy or the buboes of plague. For this 3

Ibid., 138.

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reason, the arrival of new plagues in South America, together with very old stereotypes, infected not just the bodies of national citizens but also the body politic itself. Brazil experienced the greatest fall from grace, with opinions almost uniformly positive during the colonial and early national periods, but almost consistently negative by the second half of the nineteenth century. Historians have sometimes accepted that the European critics of the New World’s tropical climate applied to Brazil, but this modern idea needs revision. To do so, I draw from a diverse collection of famous and lessknown publications, ranging from general encyclopedias and school primers on geography to traveler reports and accounts by Portuguese and Brazilian residents written in English, Spanish, Portuguese, French, and German. These show that even the fiercest critics of the Americas usually viewed Brazil as an exception to the “torrid zone” before 1850. Take Cornelius de Pauw and William Robertson, two men most credited with developing the thesis that the animals and peoples demonstrated natural inferiority in the Americas.4 Both claimed Atlantic winds “refreshed” Brazil. Robertson traced this to the sixteenth-century research of Jose de Acosta. 5 For de Pauw, it was not so much “an East wind that thus refreshes the atmosphere between the tropics and of the new continent,” but the eternal snows, rising mists, and the shadows projected by the Cordilleras (Andes). He added: “If this wind took so much cold by passing the sea-track which separates Guinea [Africa] and Brazil, it would have to take five times more crossing the South [Pacific] Ocean, and the Indian Ocean, and consequently render the eastern coast of Africa more temperate than Chile: which is obviously contradicted by experience.”6 The idea that Brazil had an exceptionally beautiful and healthy climate may have reached its zenith in the early nineteenth century. José Caetano Gomes wrote in 1800, “Since the Province of Brazil is considered the best Colony in the World, it does not feel any of the scourges of nature, for there are no earthquakes,

4

Georges-Louis Leclerc, Comte de Buffon, Natural History, General and Particular, trans. William Smellie, vol. 5 (Edinburgh: William Creech, [1749] 1780) had already argued this idea for the animals of the Americas. 5 William Robertson, Works of William Robertson 9, no. 11 (London: W. Sharp & Son, [1777] 1820), 352–53. 6 Cornelius de Pauw and Antoine-Joseph Pernety, Recherches philosophiques sur les Américain, ou, Mémoires intéressantes pour servir à l'histoire de l'espece humaine, (London, 1771), 193–94.

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hurricanes, volcanoes, famines, or pests; enjoying a benevolent climate and with the exception of some thunderstorms, which serve to purify its air.”7 Travelers and observers compared Brazil to other regions, often pointing out that Brazil was healthy despite the ancient Greek and European beliefs that any wet, hot, and verdant place was dangerous and unsupportive of civilization. Charles Van Lede wrote in 1813, “In Bahia, which is about the same parallel as Sierra Leone, the land, constantly refreshed by the strong sea breezes, has no pestilential germ.”8 Alexander Caldcleugh, a Scotsman who had previously visited North Carolina, said, “It can be no longer doubtful, which is the healthier climate, Brazil or the United States.” The U.S., “in spite of the cleared state of the country, and the frosts of winter, which might be supposed to destroy the seeds as well as arrest the progress of contagion, is annually visited by a fever of the most destructive and cruel nature.”9 When Charles Darwin visited Peru in 1839, he claimed “[diseasecausing] miasma is not always produced by a luxuriant vegetation with an ardent climate: for many parts of Brazil, even where there are marshes and a rank vegetation, are much more healthy than this sterile coast of Peru.”10 Throughout the colonial and early national periods, many saw Brazil’s avoidance of common infectious diseases as the best evidence for Brazil’s blessed climate.11 Within Brazil, the country’s intellectual and political elite proudly concurred with their foreign observers and visitors, including liberals and conservatives, who agreed with little else. Brazilian statesmen believed its verdant and abundant nature nearly ensured the prospects of the nation. In the 1820s and 1830s, senators and congressmen often used the words “pleasant,” “sweet,” and “favorable” to describe Brazil’s climate and drew direct connections between it and the fertility of the soil and good 7

Joze Caetano Gomes, Memoria sobre a cultura, e productos da cana de assucar. (Lisbon, 1800), 10. 8 Charles Maximilien Louis van Lede, De la colonisation au Brésil Mémoire historique, descriptif, statistique et commercial sur la province de Sainte-Catherine; formant le deuxième rapport à la Société belge-brésilienne de colonisation; contenant la constitution du Brésil, sa situation financière, etc. (Brussels: A. Decq, 1845). 9 Caldcleugh, Alexander, Travels in South America during the Years 1819–21: Containing an Account of the Present State of Brazil, Buenos Ayres and Chile (London: John Murray, 1825), 20. 10 Charles Darwin, Journal of Researches into the Geology and Natural History of the Various Countries Visited by H. M. S. Beagle: under the Command of Captain Fitz Roy, R. N. from 1832 to 1836 (London: H. Colburn, 1839). 11 Ian Read, “Yellow Fever in Brazil’s Era of Epidemics (1849–1909),” (Paper presented at the 27th Annual World History Association Conference, Milwaukee, June 2018).

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health of Brazilians. Among thousands of pages of minutes from the General Assembly, I found no one who depicted Brazil’s climate negatively until the late 1840s, although a few complained of Rio de Janeiro and specific locations that were either too swampy or prone to drought. Senators claimed their nation’s climate was superior to Mexico and the United States, and the world would observe this difference in future population growth and wealth.12 Officials recognized that Brazil was at the same latitude as Africa and could be just as hot and humid, but to use the words of Senator Costa Ferreira, “It was tempered by the winds, by rains and by the rivers that face the seas.” He added an “eternal spring covers its plains with cheerful green, trees that offer flowers and succulent fruit nearly all year.”13 Likewise, in 1827, Deputy Bernardo Pereira de Vasconcelos argued that Brazil’s climate was similar to that of Africa, but was cooled by breezes, traversed by rivers, and refreshed by rains. Tens of thousands of slaves arrived in Brazil each year and found a familiar but improved climate. Vasconcelos, who was one of the most powerful politicians in the early empire and an influential figure on slavery, told his colleagues in the Assembly that “blacks” (prêtos, enslaved and free) were the most “prolific,” or reproductive, as a result of the climate.14 Brazil’s doctors also demonstrated a very positive attitude toward Brazil’s climate. Numerous articles published in medical journals described the importance of climate on health. In 1841, the Annaes da Medicina Pernambucana, the medical journal of a newly created Society of Medicine, exclaimed that one of their important goals was to investigate any new epidemics, but “there is no doubt that such scourges will almost never have their cradle within the happy climate which we inhabit.”15 Two thousand miles to the south, the medical community in Rio de Janeiro published two professional journals in the 1840s. In these, they were more focused on local concerns, but when Brazil’s climate was discussed in general, it was described in the same salubrious terms. For instance, J. J. Rodrigues wrote in “Naval Medicine” that the doctors and nurses of Brazil’s navy had to treat cases of smallpox, scabies, measles, and scurvy, but from his view in the 12

Brazil, Annaes do Parlamento Brasileiro [hereafter APB], vol. 1 (Rio de Janeiro: Typographia do Imeperial Instituto Artistico, [1826] 1874), 7; APB, vol. 2 (Rio de Janeiro: Typographia de H. J. Pinto [1832] 1879), 186. 13 APB, vol. 3 (Rio de Janeiro: Typographia da Viuva Pinto & Filho [1839] 1885), 98. 14 APB, vol. 3 (Rio de Janeiro: Typographia de H. J. Pinto [1827] 1875), 28. 15 Antonio Peregrino Maciel Monteiro, “Discurso,” Annaes da Medicina Pernambucana, no. 1 (1842):14.

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mid-1840s, Brazil was “healthy, with our climate, and free of the epidemics that devastate Europe and Asia,” such as cholera and yellow fever.16 Although doctors had begun to debate whether Rio de Janeiro presented more health risks than other cities, some expressed outrage in 1845, when a Portuguese newspaper printed the claim that the province of Rio de Janeiro’s climate was as unhealthy as the central-west coast of Africa (“Benguela and Angola”). This “calumny” was motivated by the “malevolent purpose of banishing European immigration” according to the Archivo Medico Brasileiro. Evidence for Brazil’s good health came in the extraordinarily long life of some Brazilians. The Revista Medica Fluminense listed 35 men and women who lived past 100, including a “negro slave” who worked at the Acupe sugar mill in Bahia and lived to the age of 130. Although parts of the nation had a hot climate, “Brazilian longevity” was hardly impaired because its people had adapted to their climate.17 Brazil’s heat worried some doctors, but risks could be eliminated with a proper lifestyle and disciplined habits. According to one member of Pernambuco’s Society of Medicine, the “excessive” heat of our “latitude” ensures that “our bodies almost continuously and copiously sweat,” placing a burden on the lymphatic system. “Whites” (brancos), as strangers to the climate, suffer the most, becoming weak and as pale as wax.18 Another doctor of the same society explained that there was much “sympathy” between the skin and digestive tract. “In the torrid zone, where the skin is in permanent excitement, [one must] conserve the intestinal tube from irritation.”19 He recommended against the “abuse” of salty and spicy foods, alcoholic drinks, coffee, and tea.20 Others suggested cold or tepid baths and light exercise at cooler points of the day. With these habits, one might live as long as the slave of the Bahia sugar mill. Three centuries of positive opinions about Brazil’s climate and health ended abruptly. In fact, after 1850, foreign and visiting writers were more likely to view Brazil’s climate as unhealthy. With the easier movement of people and goods came the knowledge of Brazil’s immense diversity, including its variety of climates. In an essay titled the “Influence of Climate, in a Commercial, Social and Humanizing Point of View,” John Disturnell 16

J. J. Rodrigues, “Medicina Naval,” Archivo Medico Brasileiro 2, no. 12 (1845): 282. 17 “Longevidade Brasileira” Revista Medica Fluminens no.4 (July 1839): 145. 18 Manoel Pereira Teixeira, “Causas do Hydrocele,” Annaes da Medicina Pernambucana no. 2 (1842): 68 19 Ibid. 20 José Joaquim de Moraes Sarmento, “Relatorio,” Annaes da Medicina Pernambucana no. 5 (1843): 233.

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writes, “In the vicinity of the Amazon, and in the northern parts, great tropical heats prevail; but these are tempered by the excessive humidity of the atmosphere, and the copious dews. The great alluvial plains in the Northwest and West, being inundated for several months in the year, are exceedingly unhealthy.”21 Seventeen years later, Louis Agassiz, professor of zoology and geology at Harvard, thought the Amazon was as salubrious and “genial to the white race as any part of the world having a similar temperature.” However, he admitted that his opinion was “contrary to generally received notions and that the valley of the Amazon, in particular, has a very bad reputation.”22 The Brazilian elite began to see their climate as a serious problem for attracting European laborers after importation of African slaves ended under British pressure in 1850. While nearly everyone agreed that the southern highlands, including São Paulo, remained healthy, others pointed to new pestilence. Three new diseases, yellow fever, cholera and smallpox, either arrived or worsened. Rui Barbosa, one of the founders of the Republican regime and coauthor of the Brazilian Constitution of 1891, wrote the “destruction caused by plagues, defamation by our climate, disastrous reputation of poor health, and incalculable influence exerted by this phantasm for the settlement of this territory, has marked it to the foreigner as the habitat of death.”23 Eight years later, the bubonic plague appeared for the first time, and this biblical scourge confirmed the worst. Around the same time, Chile’s reputation was also tainted, though somewhat differently. During the late colonial and early national period, it had consistently been described as having one of the best climates. William Robertson’s account from 1777 is typical: “[Chile’s] climate is the most delicious in the New World, and is hardly equaled by that of any region on the face of the earth. While bordering the Torrid Zone, it never feels the extremity of heat, being screened on the east by the Andes, and refreshed from the west by cooling sea breezes.”24 An English traveler, Maria Graham, lost her husband to fevers when they rounded Cape Horn on their journey from England, but she remained in Chile, living independently for 21 John Disturnell, Influence of Climate, in a Commercial, Social, Sanitary, and Humanizing Point of View: Being a Paper Read before the American Geographical and Statistical Society (New York: C. Scribner, 1860), 22. 22 Louis Agassiz, “The Amazon River, Climate, Etc.” New York Association for the Advancement of Science and Art, lecture, Feb. 11, 1867, reprinted in Disturnell, Influence of Climate, 297. 23 This quote appears in “Pretexto Inepto,” the leading editorial article of A Imprensa, 6 February 1899. Barbosa was Editor-in-Chief and if he did not write it, he certainly believed and approved it. 24 William Robertson, The History of the Discovery and Settlement of America (New York: Harper & Brothers [1777] 1837), 342.

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a year. She said, “I cannot conceive a finer climate than that of Chile, or one more delightful to inhabit; and, now I am accustomed to the trembling of the earth, even that seems a less evil than I could have imagined.”25 Many other Chileans besides Doctor Juan MacKenna accepted these exaltations as truth.26 As in Brazil, the most powerful politicians in Chile held the same views of climate and health as its foreign visitors, at least until the disease environment and reputations began to change. Various Ministers of Finance (Hacienda) and the Interior who served in the 1830s and 1840s commented on Chile’s luck in their annual reports. In 1835, Joaquin Tocornal, the Minister of the Interior, argued that Chile’s population was generally healthy and expanding rapidly. “In this respect, Chile is similar to few European nations, which because of the lack of comforts in which the [Chilean] poor (clase ínfima) live, must be due to the beneficent influence of the climate on the vigorous constitution of the inhabitants of our lands.”27 The “benign” climate of Chile “neutralized” epidemic diseases, according to Ramón Luis Irarrázaval, who served as Minister of Finance and Minister of the Interior between 1837 and 1844. He wrote in 1839, “It is a great fortune that in Chile we do not see those epidemics of a malignant nature that reign with such consternation in other countries, which among us would be doubly deplorable because of the lack of aid we have to deal with such calamities.”28 After 1850, more of Chile’s hospital and parish records were collected, mortality tables constructed, and health and longevity compared to Europe. In a sharp turn from the optimism of the 1830s and 1840s, statistics of the second half of the century painted an alarming picture. Like Juan MacKenna, many others sought ways to explain how infants and adults died 25

Maria Graham, Journal of a Residence in Chile, during the Year 1822, and a Voyage From Chile to Brazil in 1823 (London: Longman, Hurst, Rees, Orme, Brown, and Green, 1824), 331. 26 Pedro Lautaro Ferrer Rodríguez, Historia general de la medicina en Chile: (documentos inéditos, biografías y bibliografías): desde el descubrimiento y conquista de Chile, en 1535, hasta nuestros días (Santiago: Imprenta Talca de J. Martin Garrudo, 1904), 42–43. 27 Joaquin Tocornal, “Memoria que el Ministro de Estado en el Departamento del Interior presenta al Congreso Nacional. Año de 1835” Discursos de apertura en las sesiones del congreso, i memorias ministeriales correspondientes a la administración Prieto, vol.1 (Santiago: Imprenta del Ferrocarril, 1858), 81. 28 Ramon Luis Irarrazaval, “Memoria que el Ministro de Estado en el Departamento del Interior presenta al Congreso Nacional. Año de 1839,” Discursos de apertura en las sesiones del congreso, i memorias ministeriales correspondientes a la administración Prieto, vol. 1 (Santiago: Imprenta del Ferrocarril, 1858), 125.

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more rapidly with climatic endowment long considered generative. Blame often landed on the growing numbers of urban poor, whose “ignorance” and “antipathy to hygiene” mattered much more than the lack of public health services provided by the state.29 Others, such as Adolfo Murillo and Eduardo Lira Errázuriz, argued Chile’s climate aggravated “the lymphatic, the nervous, and the bilio-nervous” temperaments, especially within its dirty and miasmatic cities.30 Doctor-scholars came to view Chile as afflicted, whether its sun resplendent or its fogs miasmatic and choking. In a fascinating graphic illustration (Fig. 1), Gabriel Carrasco, an Argentine lawyer who at the time directed his country’s census office, drew attention to Chile’s widely recognized health problems by comparing the birth and death statistics of Chile to Argentina. He found that from 1899 to 1900, Chile’s rates of infant mortality were “truly alarming” and placed “that country among those with the worst conditions in the world.” He could not offer a good explanation, for “its climate was good, its physical conditions excellent, so that the cause of this excessive mortality should be sought in the lack of public and private hygiene.” In illustrating these differences, Carrasco vividly symbolized Chilean and Argentine birth rates as a set of blond children wrapped in cloth diapers, while infant mortality was depicted as dark skeletons. For Argentina, the infant, with its face confidently turned away, towers over the skeleton. Chile’s symbolic child is much shorter and, somewhat apprehensively, looks death in the eye. Its “height” reaches only 111,000 births, barely taller than the “grinning” skeleton. By the early nineteenth century, Chile’s problems with new or worsening infectious disease and extraordinarily high infant mortality were increasingly attributed to causes that individuals could control through hygiene, with the state mostly designated to play an instructional role.31 The older idea, proposed by Murillo and Errázuriz that disease was caused by a mismatch of constitutions and the climates was giving way to an emphasis on hygiene.

29

Óscar Mac-Clure Hortal, En los orígenes de las políticas sociales en Chile, 1850– 1879 (Santiago: Universidad Alberto, 2012), 146–159. 30 Adolfo Murillo, “Breves apuntes para servir a la estadística médica i a la nosolojía chilenas,” Anales de la Universidad de Chile 47 (1875): 37; and Eduardo Lira Errázuriz, Apuntes sobre hijiene chilena (Santiago: Imprenta Gutenberg, 1884), 31. 31 Gabriel Carrasco, Argentina y Chile al comenzar el siglo XX: comparaciones gráficas y estadísticas (Buenos Aires: Compañía Sud-Americana de Billetes de Banco, 1902), 41–44.

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Figure 1: Infant mortality in Chile and Argentina. Source: Carrasco, Gabriel. Argentina y Chile al comenzar el siglo XX: comparaciones gráficas y estadísticas. Buenos Aires: Compañía Sud-Americana de Billetes de Banco, 1902, p. 43.

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In Argentina, even though not everyone shared Carrasco’s selfcongratulatory tone in respect to its neighbors, a durable pride meant the nation’s climate was never seen as abetting disease, as was common in Brazil after 1850. Nor did doctors and politicians criticize the health of its citizens as much as their counterparts in Chile in the late 1800. During the three centuries as a colony and first century as a nation, Argentina was viewed as having a blessed, healthy climate (Tables 7 and 8), as good or better than the United States and Europe.32 The capital, Buenos Aires (“good air”) was true to its name except maybe for a few days when the pomperos, or cold southern winds of winter, were not blowing too sharply.33 When Commodore George Anson visited La Plata (Colonial Argentina) in 1741, he wrote that “a milder climate, yield them a better protection.”34 Raynal (Guillaume-Thomas-François), who engaged in rhetorical duels with Voltaire and Thomas Paine, wrote that the country was “healthy and pleasant, and the air temperate.”35 In 1828, twelve years after independence, J. A. Beaumont visited and wrote a book about the prospects of emigration and investment. He observed, The country, which is traversed by the Rio de la Plata and its tributary rivers, unquestionably presents the most extensive regions of fertility and healthfulness united, which is to be found on earth; almost the whole of it 32 Alexander Caldcleugh, Travels in South America, 20. “At any rate it can be no longer doubtful which is the healthier climate, Brazil or the United States. The latter, in spite of the cleared state of the country, and the frosts of winter, which might be supposed to destroy the seeds as well as arrest the progress of contagion, are annually visited by a fever of the most destructive and cruel nature—one that physicians are not decided whether it is imported or indigenous.”; “The climate [of the Argentine Republic] is as healthy and as favorable to vigour and longevity as that of England, or any other country of Europe.”; William Hadfield, Brazil and the River Plate in 1868 (London: Bates, Hendy and Company,1869), 294. 33 For example, “The fact that the climate of Buenos Ayres must be very beneficial to health is evident from the proportion of births to death; the city has therefore not received its name without merit. Nevertheless, in June, July, August, and September are infrequently a thick fog rises from the river, which is very hostile to the lungs. Also the violent winds coming from the Pampas, which is called the Pamperos, are very troublesome to the inhabitants.” (Allgemeine geographische Ephemeriden, 1802, Vol. 10, 298). 34 Anson, George. A Voyage Round the World, in the Years 1740, 1741, 1742, 1743, 1744. London: F. C. & J. Rivington, [1748] 1821, 74. 35Guillaume Thomas François Raynal. A Philosophical and Political History of The Settlements and Trade of the Europeans in East and West Indies, vol. 2 (Dublin: John Exshaw, 1779 ), 367–68.

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During the second half of the nineteenth century, as Brazil’s healthy reputation collapsed and serious fears arose among Chileans, most writers of Argentina continued the tradition of encomium, but a few doubts appeared. Visitors warned that the drastic changes in temperature and winds could invite misery.37 The Argentine Commission on Agriculture was skeptical about whether its people were capable of basic hygiene. A census commission wrote in 1891: It is of the utmost urgency for the future welfare of the country that the causes of the great mortality amongst infants should be sought for and checked. The rigorous application of the principles of hygiene would undoubtedly diminish the present high rate of mortality for it cannot be denied that the main factors in the production of such rates are the antihygienic surroundings amidst which children are for the most part compelled to live, the violent and sudden changes of temperature to which the climate of Buenos Ayres, more perhaps than any other climate in the world, is so peculiarly liable, the cold and humid atmosphere, and the lack of proper care. (92).38

36 J. A. B. Beaumont, Travels in Buenos Ayres, and the Adjacent Provinces of the Rio de la Plata, (London: James Ridgway, 1828), 15. 37 Argentina. Comision sobre la Agricultura, Ganaderia, Organización y Economica Rural. Viajes y estudios de la Comisión Argentina sobre la Agricultura, Ganadería, Organización y Economia Rural en Inglaterra, Estados-Unidos y Australia por Ricardo Newton y Juan Llerena, comisionados por el Exmo. gobierno de Buenos Aires, vol 7-8 (Buenos Aires: Imprenta y Fundicion de Tipos "La República," 1882), 289; Thomas A. Turner who lived in Argentina from 1885 and 1890 wrote “No part of the country is so subject to violent alternations of temperature, or has such an uncertain rainfall, as Buenos Ayres. Its climate is, indeed, one of the most variable in the world. In the hottest days of summer, the thermometer may register in two or three hours a fall of ¿fteen to thirty degrees Fahrenheit; so that if one has left home in the morning in summer attire, in order to return without catching a severe cold, one has to send for over coat, flannels, and winter clothing.” Argentina and the Argentines: Notes and Impressions of a Five Years' Sojourn in the Argentine Republic, 1885–90 (London: Swan Sonnenschein, 1892), 221. 38 Thomas A Turner, Argentina and the Argentines - Notes and Impressions of a Five Years' Sojourn in the Argentine Republic, 1885-90 (London: Swan Sonnenschein, 1892), 92.

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Ten years later, however, Carrasco would boast of Argentina’s superior infant mortality rate. Despite a few pessimistic voices among Argentina’s elite, most agreed that the nation did better than its neighbors did. In sum, for three immense nations composing a landmass much larger than either Europe or the United States, we see attitudes about climates and national health turn from panegyric and confident to deprecating and disquieting. Why? The answer must integrate, or mesh, the physical and cultural. In other words, when seeking answers to these changes, we cannot only consider the categories, language, or beliefs projected onto the world, or confine ourselves to “natural” processes that condition people. As this essay shows, the epidemiological environment for Chile, Argentina, and Brazil became more fertile when increased movements of goods and peoples expanded networks of disease. Unlike the northern and eastern shores of the Atlantic, these three countries had been spared from epidemics of cholera, urban yellow fever, and malaria.39 Yet, after the California and Australian gold booms in 1849 and 1851, hundreds of thousands of North American travelers and European immigrants traversed the southern Atlantic, and ships often returned filled with Brazilian coffee, Argentine wheat, and Chilean nitrates. The old barrier against the pandemics of Asia, Europe, and North America, created by the long diagonal passage across the Atlantic Ocean, was breached by multitudes of people harboring pathogens, some who arrived in record speeds by trim clipper ships and steam engines. With people and goods travel germs.40 Figure 2 shows the epidemics and pandemics of influenza, cholera, yellow fever, and bubonic plague that struck Europe, North America, and South America between 1780 and 1910. Before 1849, Europeans and North Americans repeatedly suffered from these diseases, while Brazil, Argentina, and Chile were spared. After 1849, the pattern reversed. Most of these diseases disappeared from large parts of the North Atlantic but became serious problems elsewhere in the Americas. In addition to the fast-moving and fatal diseases, often portrayed by the scythe of the reaper, epidemics of smallpox and tuberculosis worsened.

39 Donald B. Cooper, “The New ‘Black Death’: Cholera in Brazil, 1855–1856,” Social Science History 1, no. 4 (1986 ): 467–88; Ian Read, “Do Diseases Talk? Writing the Cultural and Epidemiological History of Disease in Latin America,” Latin American Perspective 44, no.4 (2016):192–200. 40 Mark Harrison, Contagion: How Commerce Has Spread Disease (New Haven: Yale University Press, 2013); Ian Read, “Do Diseases Talk?” 192–200.

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Figure 2: Pandemics and epidemics, 1780 – 1910.

Smallpox may have been the biggest killer of the set, and public health officials recorded more frequent and more virulent epidemics by the second half of the nineteenth century.41 The populations of many cities grew 41

Hortal Mac-Clure, En los orígenes, 53–116; Ian Read, “Environmental and Cultural Frames in Histories of Disease: The Case of Smallpox in Brazil,” American Association for the History of Medicine (May 2015),

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exponentially, creating environments that packed people together, denying them safe drinking water, adequate nutrition, and few incentives or opportunities for smallpox vaccination. Improved statistics reflected physical trends in sickness and death, and they also permitted these trends to be recognized and given a name. With recognition came a realization. For example, Chilean officials began measuring infant mortality in the 1840s, prompting Juan MacKenna to believe his father’s nation faced an existential threat. Disease often occurs by a physical change in the relationship between microbes and humans. When the relationship changes rapidly across a community, and with much pain, the event is called an epidemic. These periods of fear and grief are always understood using pre-existing categories and norms and thus culture. Stereotypes matter, especially for colonized peoples. Europeans and their colonial offshoots had more than a millennium of ideas that equated the tropics with ill health. When Brazil’s environment changed for the worse, it was much easier to place the entire country into this pre-existing category. Before, Brazil’s landscape was most likely to be seen as a place blessed by nature, and an exception within the tropics to require explanation; but when new epidemics arrived, Brazil fit the old pattern with little more said.42 It may be for this reason that some historians forget that Brazil was widely believed to be a very healthy place for more than three centuries.43 Finally, we may speculate on another semantic and cultural shift occurring in the nineteenth century that may have helped tarnish the reputation of these regions. During the colonial and early national periods, Brazil, Chile and Argentina were often seen as independent of one another, grouped as “Spanish America” and “Portuguese America,” or united with the rest of the hemisphere as “America” and the “New World.” The perception that these places were part of something called “South America” grew in the 1800s, while the term “Latin America” did not catch on until the end of the century. Although this chapter does not elaborate on http://empireofbrazil.org/journal/2015/5/1/american-association-of-the-history-ofmedicine-2015.html. 42 James Johnson, The Influence of Tropical Climates, More Especially the Climate of India, on European Constitutions; the Principal Effects and Diseases Thereby Induced, Their Prevention or Removal, and the Means of Preserving Health in Hot Climates, Rendered Obvious to Europeans of Every Capacity: An Essay. (London: J. J. Stockdale, (1813); and James Ranald Martin, Influence of Tropical Climates on European Constitutions Including Practical Observations on the Nature and Treatment of the Diseases The of Europeans on Their Return from Tropical Climates (London: J. Churchill, 1861). 43 David Arnold, Warm Climates and Western Medicine: The Emergence of Tropical Medicine, 1500–1900 (Amsterdam: Rodopi, 2003).

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this idea, it could be argued that a shift that involved the environment as much as semantics helped divorce these nations from Europe, the United States, and Canada.44 Did these new regional labels fit with dichotomies of north/south, rich/poor, and healthy/diseased in ways that remain powerful today? Historians may find answers in Atlantic and hemispheric health and cultural histories. I am not suggesting that a changing physical epidemiological environment was presupposed by cultural beliefs and categories at this part of the Tropic of Capricorn. I believe these case studies show how diseases are manifestations of broadly shifting relations of 1) microbes that often mutate and evolve rapidly, 2) animal and insect vectors that can shift their habitats, and 3) humans who transform their physical environments and intentionally or unintentionally configure these relations. Interdependent relations of living things, micro- or macroscopic, matter as much as the way that these things are culturally understood, but neither comes first. I believe that over the last four decades, historians of medicine have become much more interested in the cultural construction or operation of diseases than the changing physicality of living relationships of microbial forms that clearly affect pain and mortality at the societal level. In a popularly quoted passage, Charles Rosenberg and Janet Golden assert, “In some ways disease does not exist until we have agreed that it does, by perceiving, naming, and responding to it.” I wonder if historians may sometimes take this idea too far, by suggesting that the perceptions of diseases in the world are more dynamic than the world itself. There is, of course, great dynamism in both. For example, rather than only “framing” disease by culture, the tragedy at the Tropic of Capricorn shows culture and beliefs can just as easily be “framed” by the changing physicality and relations that give rise to new diseases among or beyond humans.

44

Michel Gobat “The Invention of Latin America: A Transnational History of AntiImperialism, Democracy, and Race,” The American Historical Review 118, no. 5 (2013), 1345–75. That “Latin Americans” used these terms more readily during the nineteenth century can be seen using Google Book’s Ngram Viewer tool. This tool looks at word frequency across billions of pages of books. In English books published between 1800 and 1940, “South America” grows in the 1830s and 1910s, while “Latin America” appears more commonly only after 1900. A similar pattern emerges with “America del Sur,” “Sudamerica,” “America Latina” in Spanish and “SudAmerika” and “Lateinamerika” in German.

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Bibliography A Imprensa (Rio de Janeiro), February 6, 1899, 1. Agassiz, Louis. “The Amazon River, Climate, Etc.” Lecture, New York Association for the Advancement of Science and Art, February 11, 1867. Anson, George. A Voyage Round the World, in the Years 1740, 1741, 1742, 1743, 1744. London: F. C. & J. Rivington, [1748] 1821. Arnold, David. Warm Climates and Western Medicine: The Emergence of Tropical Medicine, 1500–1900. Amsterdam: Rodopi, 2003. Beaumont, J. A. Travels in Buenos Ayres, and the Adjacent Provinces of the Rio de la Plata: With Observations, Intended for the Use of Persons who Contemplate Emigrating to that Country; Or, Embarking Capital in Its Affairs. London: James Ridgway, 1828. Buffon, Georges Louis Leclerc. Natural History, General and Particular, vol. 5. Translated by William Smellie. Edinburgh: William Creech, 1780. Caldcleugh, Alexander. Travels in South America vol.1. London: John Murray, 1825. Caldcleugh, Alexander. Travels in South America, During the Years 181920-21: Containing an Account of the Present State of Brazil, Buenos Ayres, and Chile. London: John Murray, 1825. Cantor, David. “The Uses and Meanings of Hippocrates.” In Reinventing Hippocrates, 1-16. London: Ashgate Publishing, 2002. Carrasco, Gabriel. Argentina y Chile al comenzar el siglo XX: comparaciones gráficas y estadísticas. Buenos Aires: Compañía Sud-Americana de Billetes de Banco, 1902. Carrasco, Gabriel. Argentina y Chile al comenzar el siglo XX: comparaciones gráficas y estadísticas. Buenos Aires: Compañía SudAmericana de Billetes de Banco, 1902. Comisión sobre la Agricultura, Ganaderia, Organización y Economica Rural of Argentina Government. Viajes y estudios de la Comisión Argentina sobre la Agricultura, Ganadería, Organización y Economia Rural en Inglaterra, Estados-Unidos y Australia por Ricardo Newton y Juan Llerena, comisionados por el Exmo. gobierno de Buenos Aires. Buenos Aires: Imprenta y Fundicion de Tipos “La República”, 1882. Cooper, Donald B. “The New “Black Death”: Cholera in Brazil, 1855– 1856.” Social Science History 10, no. 4 (Winter 1986), 467–88. doi:10.2307/1171027. Darwin, Charles. Journal of Researches into the Geology and Natural History of the Various Countries Visited by H. M. S. Beagle: under the

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Command of Captain Fitz Roy, R. N. from 1832 to 1836. London: H. Colburn, 1839. De Pauw, Cornelius, and Antoine-Joseph Pernety. Recherches philosophiques sur les Américain, ou, Mémoires intéressantes pour servir à l'histoire de l'espece humaine. London 1771. Disturnell, John. Influence of Climate, in a Commercial, Social, Sanitary, and Humanizing Point of View: Being a Paper Read Before the American Geographical and Statistical Society. New York: C. Scribner, 1860. Errázuriz, Eduardo L. Apuntes sobre hijiene chilena. Santiago: Imprenta Gutenberg, 1884. Gobat, Michel. “The Invention of Latin America: A Transnational History of Anti-Imperialism, Democracy, and Race.” The American Historical Review 118, no. 5 (December 2013), 1345–75. doi:10.1093/ahr/118.5.1345. Gomes, Joze C. Memoria sobre a cultura, e productos da cana de assucar. Lisbon: Off. da Casa Litteraria do Arco do Cego,1800. Graham, Maria. Journal of a residence in Chile, during the year 1822, and a voyage from Chile to Brazil in 1823. London: Longman, Hurst, Rees, Orme, Brown, and Green, 1824. Hadfield, William. Brazil and the River Plate in 1868. London: Bates, Hendy and Company, 1869. Harrison, Mark. Contagion: How Commerce Has Spread Disease. New Haven: Yale University Press, 2013. Irarrazaval, Ramon L. “Memoria que el Ministro de Estado en el Departamento del Interior presenta al Congreso Nacional. Año de 1839.” In Discursos de apertura en las sesiones del congreso, i memorias ministeriales correspondientes a la administración Prieto, 125. Santiago: Imprenta del Ferrocarril, 1858. Johnson, James. The influence of tropical climates, more especially the climate of India on European constitutions. London: J. J. Stockdale, 1813. Lede, Charles V. De la colonisation au Brésil: mémoire historique, descriptif, statistique et commercial sur la province de SainteCatherine, formant le deuxième rapport à la Société belge-brésilienne de colonisation, contenant la constitution du Brésil, sa situation financière, etc. Brussels: A. Decq, 1845. “Longevidade Brasileira.” In Revista Medica Fluminens, 4th ed., 145. 1839. Mac-Clure Hortal, Oscar. En los orígenes de las políticas sociales en Chile: (1850-1879). Santiago: Ediciones Universidad Alberto Hurtado, 2012.

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Mackenna, Juan. “De las causas de la mortalidad en Chile fundadas en la desproporcion entre el temperamento de los hijos del país i su clima.” In Anales de la Universidad de Chile, 133–44. Santiago: University of Chile, 1850. Martin, James R. The influence of tropical climates on European constitutions. London: J. Churchill, 1861. Miller, Genevieve. “‘Airs, Waters, and Places’ in History.” Journal of the History of Medicine and Allied Sciences XVII, no. 1 (January 1962), 129–40. doi:10.1093/jhmas/xvii.1.129. Monteiro, Antonio M. “Discurso.” In Annaes da Medicina Pernambucana 1, no.14 (1842). Murillo, Adolfo. “Jeografía Médica: Breves apuntes para servir a la estadística médica i a la nosolojía chilena. Trabajo destinado al Congreso jeográfico internacional frances.” In Anales de la Universidad de Chile 47, no. 37. Santiago: University of Chile, (1875). National Congress of Brazil. Annaes do Parlamento Brasileiro Tomo I. Rio de Janeiro: Typographia do Imeperial Instituto Artistico, 1874. http://bd.camara.gov.br/bd/handle/bdcamara/30460. National Congress of Brazil. Annaes do Parlamento Brasileiro Tomo II. Rio de Janeiro: Typographia de H. J. Pinto, 1879. http://bd.camara.leg.br/bd/handle/bdcamara/28921. National Congress of Brazil. Annaes do Parlamento Brasileiro Tomo III. Rio de Janeiro: Typographia de H. J. Pinto, 1875. http://bd.camara.gov.br/bd/handle/bdcamara/30959. National Congress of Brazil. Annaes do Parlamento Brasileiro Tomo III. Rio de Janeiro: Typographia da Viuva Pinto & Filho, 1885. Raynal, Abbé. A Philosophical and Political History of the Settlements and Trade of the Europeans in the East and West Indies vol.2. Translated by J. J. Justamond. Dublin: John Exshaw, 1779. Read, Ian. “Yellow Fever in Brazil’s Era of Epidemics (1849–1909).” Paper presented at the 27th Annual World History Association Conference, Milwaukee, June 2018. Read, Ian. “Do Diseases Talk? Writing the Cultural and Epidemiological History of Disease in Latin America.” Latin American Perspectives 44, no. 4 (March 2016): 192–200. doi:10.1177/0094582x16635294. Read, Ian. “Environmental and Cultural Frames in Histories of Disease: The Case of Smallpox in Brazil.” Paper presented at American Association for the History of Medicine, Yale University, May 2015. Robertson, William. The History of the Discovery and Settlement of America. New York: Harper & Brothers, 1837.

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PART III: CO-EMERGENCE AND CO-RESOLUTION OF EPIDEMICS

CHAPTER THIRTEEN WHAT PLACES EBOLA IN THE REALM OF THE “GLOBAL”? A VIEW FROM HISTORY MONICA H. GREEN

In an essay on the question of whether “the world changed” because of September 11, 2001, terrorist attacks on the United States, Nicholas B. King challenged the notion that the attacks were sui generis, outside of anything that could have been known or predicted. “We must also [challenge the sui generis narrative],” he says, “because the axiom of historical exceptionalism threatens to hijack our understanding of related issues.”1 King, who trained both in the history of science and in medical anthropology, brings a historian’s need to see larger patterns and trajectories in the responses to the terrorist attacks on the United States in 2001, and the subsequent build-up of anxiety about bioterrorism. In a different vein, medical anthropologist Christos Lynteris, talking about natural epidemics, has argued that “while it is widely accepted today that infectious disease epidemics are the result of long-term and complex social, ecological, economic and political processes, outbreaks are, more often than not, experienced on the ground as unexpected eruptions.” Epidemics, he argues, are both “process” and “event” processes, for those who study them at a distance, but emphatically events (with distinct chronological specificity), for those immediately affected by them.2 “What is the relation,” he asks, “between the epidemiological reality of outbreaks as conditioned by longterm social, political, economic, demographic and ecological factors, and

1 Nicholas B. King, “The Scale Politics of Emerging Diseases,” Osiris 19 (2004): 62–76. 2 Christos Lynteris, “Epidemics as Events and as Crises: Comparing Two Plague Outbreaks in Manchuria (1910–11 and 1920–21),” Cambridge Anthropology 32, no. 1 (Spring 2014): 62–76.

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the empirical reality of outbreaks as ruptures of the social, political and economic continuum?”3 As a historian myself, in no way do I wish to occlude the construction of “evental” histories of what transpired during the 2013–15 Ebola crisis in Guinea, Sierra Leone, and Liberia, and the many other places that were pulled in, in whatever ways. There will be many histories that need to be told, of the afflicted, their families and communities, of the healthcare workers who tended them and, in some cases, perished with them, and the manifold political and economic disruptions that rippled throughout much of the rest of the world. The present essay, however, is intended to open a space for the “process” history of the Ebola crisis that sets it into a larger history of global diseases. In one important respect, the 2013–2015 West African Ebola outbreak ranks as an event without precedent, in that Ebola had never (so far as we know) presented before in fully urbanized contexts and therefore had never manifested in such an epidemiologically complex way. It was, in effect, a “new disease”—new not simply for the peoples of a wide area of Africa, but also for the global health community, whose learned responses to the disease (which has been known to biomedical science since 1976) were clearly inadequate for the way it was presenting in 2014. But diseases have always been “emerging,” and the field of global health history, a new area within the history of medicine, not only examines those diseases that are (or have been) globally distributed, but it addresses the critical ways in which human uses of biophysical and cultural environments have exacerbated, limited, or ameliorated the effects of pathogens on human communities. Applying such an analysis to Ebola, as I will explain below, shows that it is likely not true, that Ebola had never been present in West Africa before, nor was it unimaginable that Ebola could have broken out as the sustained, urbanized epidemic that it in fact became. Thus, for all the reasons we validly need to insist on the specifics of the 2013–2015 West African Ebola crisis, the particular histories of colonial and post-colonial development and exploitation, the particular effects of civil war in undermining and impoverishing the public health infrastructure, the particular dynamics of the local ethnic groups and their own long legacies with their land and their environment, and, of course, the particular characteristics of the Ebola Virus Disease as a biological phenomenon. We also need to be careful not to treat this episode as sui generis, a situation so unique that it sits outside our ability to interpret it, and to learn from it. 3

Christos Lynteris, “Introduction: The Time of Epidemics,” Cambridge Anthropology 32, no. 1 (Spring 2014): 24–31.

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Historical analysis can be many things, and analyses that reach into pasts of varying depths and trajectories to explain the West African Ebola outbreak have been offered by a variety of observers who have looked at the failures of global health funding or the larger effects of colonial and post-colonial economic pressures in West Africa by journalists, anthropologists, and public health analysts, both inside and outside the affected countries. One should add, too, a new cohort of “historians,” geneticists, who have been contributing to historicizing this outbreak with close-to-real-time analyses of the viral strains. The latter group’s work has contributed most to the account I offer here, which treats the disease organism itself as a historical “actor.”

On the Relevance of History in an Emerging Epidemic As Lynteris observes, “What matters to those experiencing [an epidemic] outbreak is not the past but the brutal present and how to survive it.”4 When I first began to consider Ebola as a “global disease” with its own process, I certainly had no illusion that any intervention I could make as a historian would offer immediate aid to sufferers, their loved ones, or their caretakers. However, I did believe that I might help educate the broader public about the severity of the outbreak and the need for more concerted intervention. In reading the first news reports of the Ebola outbreak in April and May 2014, I had not paid attention to where the outbreak was happening. This is ironic, of course, since one of the truisms I teach my students is that every “global” disease that exists in the world today started out as a local outbreak. Epidemiological mapper Tom Koch describes the process in a simple but recognizably logical fashion: a disease moves from being a local outbreak to a regional epidemic, and then a global pandemic.5 But there is actually little to suggest that the globalization of any disease is merely a matter of simple geometric spread in an ever-expanding radius.6 Further evidence of my own inability to conceive of the unfolding Ebola outbreak outside of a “local” framework comes from the fact that, on June 4

Lynteris, “Epidemics as Events,” 26.

5 Tom Koch, “Ebola: Epidemics, Pandemics and the Mapping of their Containment,”

Remedia [blog], (September 22, 2014), accessed July 13, 2015, http://remedianetwork.net/2014/09/22/ebola-epidemics-pandemics-and-themapping-of-their-containment/. 6 Monica H. Green, “The Globalisations of Disease,” in Human Dispersal and Species Movement: From Prehistory to the Present, ed. Nicole Boivin, Rémy Crassard, and Michael D. Petraglia (Cambridge: Cambridge University Press, 2017): 494–520.

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20, 2014, I had downloaded Melissa Leach’s April 3, 2014 entry on The Lancet Global Health Blog. A month later, I realized how prescient her observations had been, and how little I had initially heeded them. Leach raised the important points that (a) the inherent poverty of the region also needed to be factored in, and (b) “the narrative of rapid, sudden emergence of a disease like Ebola can overlook longer histories of interaction, which can offer valuable clues as to how to deal with it” (emphasis added). She suggested that Ebola might not, in fact, be “une maladie étrange” from the perspective of rural (as opposed to urban) informants in Guinea (had they been asked). “[T]he current epidemic [might be] an epidemic of diagnosis rather than of disease.”7 None of this made an impression on me at the time. I was drawn into the unfolding Ebola outbreak in the midst of a crosscountry move in July 2014. That was when I read Lisa Schnirring’s piece in CIDRAP News: “West Africa Ebola Outbreak Total Tops 1,000.”8 According to the July 19 report from the WHO, there had been 632 deaths by that point, for a total of 1048 cases. “Over 1000” is no magical number for the historian. For me, it set off an alarm bell for reasons related to a different epidemic. The HIV/AIDS pandemic came into medical and cultural awareness in the U.S. starting in 1981. In 1983, Larry Kramer published his “scream heard round the world,” the essay “1,112, and Counting.”9 Kramer’s essay was the cri de coeur that made the severity of the spreading disease in the U.S. gay community no longer deniable: “When we first became worried, there were only 41. In only twenty-eight days, from January 13 to February 9 [1983], there were 164 new cases—and 73 more dead. The total death tally is now 418.” Kramer, of course, was seeing HIV/AIDS as a “local” disease from the perspective of New York City. He certainly knew then of outbreaks in Los Angeles and San Francisco and may have known something of reports from Western Europe. However, he was almost certainly blind at the time to the immensity of suffering that was

7

Melissa Leach,. “Ebola in Guinea—People, Patterns, and Puzzles,” The Lancet Global Health Blog. April 3, 2014, accessed June 20, 2014, and March 24, 2019, archived at https://www.thelancet.com/journals/langlo/blog, 474–75. 8 Lisa Schnirring, “West Africa Ebola Outbreak Total Tops 1,000,” CIDRAP News, July, 21 2014, accessed July 21, 2014, http://www.cidrap.umn.edu/news-perspective/ 2014/07/west-africa-ebola-outbreak-total-tops-1000. 9 Larry Kramer, “1,112, and Counting,” originally published in New York Native, 59 (March 1983): 14–27. Republished on The Bilerico Project, with introduction by Karen Ocamb, June 14, 2011, accessed July 17, 2015, http:// www.bilerico.com/2011/06/larry_kramers_historic_essay_aids_at 30.php.

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already occurring in Africa and other parts of the world.10 The metaphor of the iceberg—only part of a massive danger being visible to the viewer—is often used in epidemiology, and it is one, historians should be more alert to.11 Schnirring’s report of over 1,000 cases of Ebola on July 2, 2014, thus sounded a similar alarm: this disease was moving fast, it was likely bigger than anyone knew, and it was out of control. When I started collecting materials on Ebola in mid-summer 2014, I had no expertise in its history other than the normal “talking points” that most historians of medicine probably knew. I, of course, knew that Ebola had first been recognized in two outbreaks in Central Africa in 1976, that it had periodically reared its head in subsequent decades, most famously in the outbreak in Kikwit in 1995. Followed in close succession by the first clinical descriptions of HIV/AIDS in 1981, Ebola had become the poster child for “emerging diseases” when discourse around that concept gelled in a famous Institute of Medicine study published by the United States Academy of Medicine in 1992.12 I knew, from my work in the development of the field of Global Health, that Ebola had propelled the careers of several in the postsmallpox generation of global health workers. In the Anglophone press, there has been considerable reportage of Ebola outbreaks, with book-length studies appearing from global health reporter Laurie Garrett and others.13 Among historians, however, the disease has been invisible. As of 2015, when I assessed the state of the field, there had been zero studies about Ebola in the top English-language, French, German, Spanish, and Italian medical history journals in the forty years since the disease’s discovery.14 10

The first clinical reports of Africans who presented with symptoms of the disease were published in Europe in 1983; The first published clinical reports directly from Africa didn’t appear until 1984. 11 Monica H. Green, “The Value of Historical Perspective,” in Ashgate Research Companion to the Globalization of Health, ed. Ted Schrecker (Aldershot, UK: Ashgate, 2012): 17–37. 12 Frank M. Snowden, “Emerging and Reemerging Diseases: A Historical Perspective,” Immunological Reviews 225 (2008): 9–26. 13 Garrett’s first book recounted the 1976 outbreak in Yambuku, see Laurie Garrett, The Coming Plague: Newly Emerging Diseases in a World Out of Balance (New York: Farrar, Straus & Giroux, 1994); while her second book recounted the 1995 outbreak in Kikwit, Zaire, see Garrett, Betrayal of Trust: The Collapse of Global Public Health (New York: Hyperion, 2000): and Richard Preston, The Hot Zone (New York: Random House, 1994), similarly recounted the recent history of what were then called hemorrhagic fevers. 14 On July 13, 2015, I surveyed the following journals, in their online formats, for the word “Ebola,” looking for any discussions beyond just a passing reference as an analogy: Bulletin of the History of Medicine (0), Journal of the History of Medicine

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In four decades, History, as a discipline proved itself virtually worthless in creating any kind of narrative for this disease. The only even moderately extended account of Ebola I found in a history of medicine book were two pages devoted to the disease in a survey, Disease and the Modern World.15 Ironically, then, for all the mileage Ebola has received in “emerging diseases” discourse, it has been poorly integrated into disease history. By August 13, 2014, I had posted my first “Ebola Teaching Notes” online in the hopes that other teachers who were about to return to the classroom would have some ready-made notes for leading their own students into an informed awareness of this unfolding epidemic.16 This had followed an awful sequence of news coming out of West Africa and beyond: schools were being closed, flights canceled, Nigeria was on the alert for an imported case. I decided to prepare to “teach the crisis” in my “History of Global Health” course. I gathered scientific reports on the disease, not only so I would better understand its nature (mode of transmission, incubation period, clinical course, fatality rates, etc.), but also—crucially for me—so that I could begin to piece together its history as a human disease. Of what relevance were past studies of Ebola when the disease was ripping exponentially through new, completely vulnerable populations? Did the “process” of Ebola matter when the “event” was completely out of control? As a historian, I always believe process—the long story—matters. In this circumstance, it was the only thing I had to offer. My approach to the global history of health—the global histories of infectious diseases—is not grounded on compiling lists of outbreaks, but rather on reconstructing the evolutionary histories of the pathogenic organisms and how those histories intersect and intertwine with human history. I had a formula for “learning” about a new disease: see what the genetics has to say about how old the organism is and where it came from (in looking at infectious diseases, one always treats the organism as a separate actor). Learn all the basics of the disease (the entry and manifestation of the pathogen in the human body, characteristics of the causative organism, zoonotic reservoir [if any], mode and Allied Sciences (0), Canadian Bulletin of Medical History (0), Social History of Medicine (0), Medical History (0), Dynamis: Acta Hispanica ad Medicinae Scientiarumque Historiam Illustrandam (0), Sudhoffs Archiv, Gesnerus: Swiss Journal of the History of Medicine and Sciences (0), Medizinhistorisches Journal (0), Medicina nei Secoli (0). 15 Mark Harrison, Disease and the Modern World: 1500 to the Present Day (Cambridge UK: Polity Press, 2004). 16 Monica H. Green, “Global History of Health–Teaching Notes on Ebola” (as of 08-13-2014), posted on Academia.edu, 08/13/2014, https://www.academia.edu/ 7965438/Global_History_of_Health, Teaching_Notes_on_Ebola_August 13, 2014._

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and rates of transmission, incubation period, serial interval, clinical effects, lethality, and other sequelae). Assess what other kinds of evidence there might be (osteological, documentary) for the disease’s effects in the past, and finally, construct a “narrative” for the disease that moves from origin to global distribution to (if relevant) biomedical identification and control. Getting a timeframe for the history of Ebola was essential, so I started with genetics. I already knew that the “biological clocks” used in phylogenetic dating were suspect, and, barring the discovery of any aDNA (“ancient DNA”) of the Ebola virus, we would have no good idea of the organism’s age until better consensus formed in that discipline. However, the geneticists had already been active in the 2014 outbreak. The first study published ahead of print on April 16 (the finalized version would appear in September) was Baize et al.’s claim that the West African strain was a new clade in the Ebola Virus Disease lineage.17 These claims were challenged by subsequent studies by Dudas and Rambaut and Calvignac-Spencer,18 who argued that it was rooted squarely within the Zaire strain. Reports in the Recombinomics newsletter on July 29, 2014, and August 11, 2014, argued that all 101 samples studied to that point were clonal, confirming that only human-to-human transmission (and not independent transmissions from animals) seemed to be responsible for the continuing West African outbreak. In August 2014, working with samples from 99 sequenced Ebola virus genomes from 78 patients in Sierra Leone, Gire et al. reported, “[T]his West African variant likely diverged from Middle African lineages (2004), crossed from Guinea to Sierra Leone in May 2014, and exhibited sustained human-to-human transmission subsequently, with no evidence of additional zoonotic sources” (See Fig. 1).19

17

Sylvain Baize, et al. 2014. “Emergence of Zaire Ebola Virus Disease in Guinea— Preliminary Report,” New England Journal of Medicine 371 (September 19, 2014): 1418–25, first published online April 16, 2014. 18 Gytis Dudas and Andrew Rambaut, “Phylogenetic Analysis of Guinea 2014 EBOV Ebolavirus Outbreak,” PLoS Currents: Outbreaks 1, no. 6 (May 2, 2014): 1– 11; and Sébastien Calvignac-Spencer, Jakob M. Schulze, Franziska Zickmann, and Bernhard Y. Renard. “Clock Rooting Further Demonstrates that Guinea 2014 EBOV is a Member of the Zaïre Lineage,” PLOS Currents Outbreaks 6 (June 16, 2014), http://currents.plos.org/outbreaks/article/clock-rooting-further-demonstrates-thatguinea-2014-ebov-is-a-member-of-the-zaire-lineage/. 19 “BEAST’ stands for “Bayesian Evolutionary Analysis by Sampling Trees.” It is a software used to assess molecular sequence variation, as part of probabilistic models for phylogenetic inference. Stephen K Gire, Augustine Goba, Kristian G. Andersen, Rachel S. G. Sealton, Daniel J. Park, Lansanna Kenneh, Simbirie Jalloh, et al. “Genomic Surveillance Elucidates Ebola Virus Origin and Transmission during the

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Figure 1: Molecular dating of the 2014 outbreak. “BEAST dating of the separation of the 2014 lineage from central African lineages [SL, Sierra Leone; GN, Guinea; DRC, Democratic Republic of Congo; time of most recent common ancestor (tMRCA), September 2004; 95% highest posterior density (HPD), October 2002 to May 2006].” (Gire et al. 2014, Fig. 3a).

I knew, of course, that as a zoonotic disease residing in animal reservoirs, it was certainly possible that Ebola had reached West Africa ten or more years earlier without causing any human cases. However, I was unprepared for what I actually found. Already in my first “Ebola Teaching Notes,” August 13, I had captured such studies as Heymann et al., 1980, documenting the presence of Ebola cases in 1972 in northwestern Zaire. It was four years before the first presumed outbreak, showing evidence that 7% of the residents tested appeared to show antibodies to the virus in their blood.20 This was not surprising to me (even though I had quite forgotten that Melissa Leach had already predicted that such “pre-histories” of the

2014 Outbreak.” Science 345, no. 6202 (September 12, 2014): 1369–72. First published online August 28, 2014 (see Fig. 1). 20 D. L. Heymann, J. S. Weisfeld, P. A. Webb, K. M. Johnson, T. Cairns, H. Berquist, “Ebola Hemorrhagic Fever: Tandala, Zaire, 1977–1978,” Journal of Infectious Diseases 142, no. 3 (1980): 372–376.

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disease would be found),21 as I had already become familiar with the “silent” phase of emerging diseases, the stage before which an epidemiological pattern is noticed or systematic clinical diagnoses made.22 I had also begun to survey the literature on the presence of Ebola in non-human primate populations, which was also a signal that it might threaten human populations because of our genetic similarities. In addition, I had located the Changula and colleagues July 17, 2014 study suggesting that filoviral hemorrhagic fevers like Ebola were likely found in more areas than current epidemiological indicators had documented.23 I also located Thomas Geisbert and Peter Jarhling’s “Exotic Emerging Viral Diseases: Progress and Challenges,” published in 2004,24 where I first encountered the name of Jürgen Knobloch, a researcher at the BernhardNocht-Institut für Tropenmedizin at the University of Hamburg. Geisbert and Jahrling cited a 1980 study by Knobloch and colleagues on Lassa fever. I never followed up on that citation, but I must have googled Knobloch’s name in the following weeks and found a reference to another work he had published in 1982—“A Serological Survey on Viral Haemorrhagic Fevers in Liberia.” It was published in the Annales de l’Institut Pasteur/Virologie, a journal that was discontinued in 1988 and, significantly not regularly indexed in the old print IndexMedicus published by the National Library of Medicine, but later became the foundation for the online PubMed bibliography. Indeed, a search for the Knobloch et al. 1982 study on Google Scholar indicated the research had been cited only five times, and only twice in contexts that related to Ebola.25 21

Leach, “Ebola in Guinea,” 474–75. Monica H. Green, “The Black Death and Ebola: On the Value of Comparison,” in Pandemic Disease in the Medieval World: Rethinking the Black Death, ed. Monica H. Green. ix–xx. (Amsterdam: Arc Medieval Press, 2015). 23 Katendi Changula, Masahiro Kajihara, Aaron S. Mweene, Ayata Takada, “Ebola and Marburg Virus Diseases in Africa: Increased Risk of Outbreaks in Previously Unaffected Areas?” Microbiology and Immunology 58, no. 9 (2014): 483–91. 24 Thomas W. Geisbert and Peter B. Jahrling, “Exotic Emerging Viral Diseases: Progress and Challenges,” supplement, Nature Medicine 10, (2004): S110–S121. 25 J. Knobloch, E. J. Albiez, H. Schmitz, “A Serological Survey on Viral Haemorrhagic Fevers in Liberia,” Annales de l’Institut Pasteur/Virologie 133, no. 2 (1982): 125–28. One of the few citations of Knobloch’s research that I found, in fact, was in a 2008 study whose lead author was Sheik Humarr Khan, the Sierra Leonean researcher who succumbed to Ebola on July 29, 2014. See, Khan, et al., “New Opportunities for Field Research on the Pathogenesis and Treatment of Lassa Fever,” Antiviral Research 78 (2008):103–115; the study did not, however, explicitly mention Knobloch’s findings about Ebola. The Knobloch et al. 1982 study was also cited by B. Le Guenno “Le virus Ebola: données écologiques,” Virologie 22

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Upon receiving a copy of Knobloch and colleagues’ 1982 study via Interlibrary Loan in the early hours of September 3, 2014, it became immediately obvious to me what the significance of the oversight was. In line with the mounting evidence, I had assembled information from the genetic studies that the strain of Ebola currently circulating in West Africa had likely branched off from the main strain in West Central Africa, perhaps in the mid-2000s (cited above). Knobloch and colleagues had reported in 1982 that they were finding Ebola antibodies in 6% of the serological samples that had been collected from 488 patients in Liberia in 1978 and 1979. Similar findings of Ebola antibodies in West African populations had been reported earlier in 2014 (see samples collected in 2006–2008).26 In other words, these findings suggested that Ebola was not a “new” disease in West Africa at all. Although the reliability of the testing mechanisms used in the 1970s has since been questioned, Knobloch and his colleagues’ warning was stark and clear: Considering that active cases of Ebola or Marburg virus disease have never been reported from Liberia, the occurrence of these specific antibodies was surprising. The results seem to indicate that Liberia has to be included in the Ebola and Marburg virus endemic zone. Therefore, the medical personnel in Liberian health centres should be aware of the possibility that they may come across active cases and thus be prepared to avoid nosocomial epidemics.27

I included Knobloch et al.’s warning in my September 3, 2014 “Ebola Teaching Notes,” as well as other data on the question of Ebola’s pre-history in West Africa. The following week, I also notified the authors of a new 1, hors-série 1, Hors série no. 1 (Janvier–Février 1997): 23–30, which likewise does not appear in the PubMed index. 26 Randal J. Schoepp, et al., “Undiagnosed Acute Viral Febrile Illnesses, Sierra Leone,” Emerging Infectious Diseases 20, no. 7 (July 2014): 1176–82. The research, published in July 2014 (I first accessed it on August 27), presented a study of serological samples primarily from Sierra Leone from 2006–2008, with the finding that Ebola antibodies showed up in 8% of samples. About a week later, medical anthropologist Adia Benton informed me via e-mail of another study that had produced similar findings: Fransje W. Van der Waals, et al., “Hemorrhagic Fever Virus Infections, in an Isolated Rainforest Area of Central Liberia: Limitations of the Indirect Immunofluorescence Slide Test for Antibody Screening in Africa,” Tropical and Geographic Medicine 38 (1986), 209–14. (She had previously announced this on her Twitter feed, @Ethnography911, on August 31, 2014, but I only discovered it on September 8). The R. Schoepp et al. research cited neither of the 1980s studies reporting Ebola antibodies in Liberia. 27 Knobloch et al., “A Serological Survey,” 128.

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mapping study on Ebola, which was published online on September 8, 2014, (as explained to me in a personal note from the lead author). I deliberately focused on recognized human outbreaks and animal infections, both to ensure the reliability of the geographic data and because the techniques testing for seropositivity were in use in the 1970s and ‘80s had since been superseded by more reliable PCR (polymerase chain reaction) methods.28 Knobloch and colleagues had, importantly, included just such a qualification as a coda to their study: “Recent investigations doubt the specificity of the indirect immunofluorescence antibody test concerning Ebola and Marburg viruses. Thus the significance of the antibodies to Ebola and Marburg viruses identified in Liberia requires further evaluation.”29 Was it solely because of the ensuing civil wars in Liberia and Sierra Leone that “further evaluation” never seemed to have happened in West Africa? How much further any awareness spread of my discovery that Ebola might have had a “pre-history” in West Africa is unclear. My September 3, 2014 “Ebola Teaching Notes” were accessed only 61 times in the subsequent month, although I did include the information on the apparent pre-history of Ebola in West Africa in all my subsequent notes and lectures. It may have been a separate process of “discovery” that led to the announcement in April 2015 in the New York Times by three public health researchers (two of them Liberian) that they had “stumbled” upon Knobloch’s 1982 study.30 “Yes, We Were Warned About Ebola,” ran the headline. The New York Times ran a follow-up piece on the question two weeks later. They reported this discovery of the earlier serological studies and pointed out (again) that the serological tests available in the 1970s had been superseded by more reliable tests suggesting new research should be conducted on archived samples to confirm Ebola’s earlier presence in West Africa. “Medical Detectives in West Africa,” the Times reported, “are now seeking to establish whether the virus had previously infected people there. The research is part of a broader push to better understand where Ebola might

28

David Pigott, personal communication, September 8, 2014; see Pigott study: Nick Golding, Adrian Myline, Zhi Huang, Andrew J. Henry, Daniel J. Weiss, Oliver J. Brady, Moritz U. G. Kraemer, David L. Smith, Catherine L. Moyes, et al. “Mapping the Zoonotic Niche of Ebola Virus Disease in Africa.” eLIFE Sciences 3 (September 8, 2014): e04395. DOI: http://dx.doi.org/10.7554/eLife.04395. 29 Knobloch et al., personal communication to K. M. Johnson. 30 Bernice Dahn, Vera Mussah, and Cameron Nutt, “Yes, We Were Warned About Ebola,” New York Times, April 2015, 7, http://www.nytimes.com/2015/04/08/ opinion/yes-we-were-warned-about-ebola.html.

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strike next, and to strengthen surveillance and health systems in hopes of preventing future outbreaks.”31 As Dahn and colleagues noted, the early serological studies should have been enough to raise the alarm and prompt further assessment of the question of Ebola’s presence in West Africa. At the very least, as Knobloch and colleagues noted in 1982, local health workers should have been warned. Bernice Dahn and her colleagues pointed the finger at this particular failure in knowledge production, in essence, a colonialist practice of scientific research done by, and published for, non-Africans. The European researchers came, did their work, and then returned home to create knowledge that furthered their own careers in a European context, but left the vulnerable populations of Liberia unaware of their findings. Importantly, Dahn and colleagues omit noting information that was included in the 1982 study itself: “Travail présenté a la 2e Conférence Internationale sur L’impact des maladies à virus sur le développement des pays africains et du Moyen-Orient, 1-6 décembre 1980, Nairobi.” (“The Impact of Viral Diseases on the Development of African Countries and the Middle East,” December 1–6, 1980, Nairobi). A Google search for the conference name produced a number of published studies that emerged from this 1980 Nairobi meeting, including a study on Rift Valley Fever that appeared in the same issue of the Annales de l’Institut Pasteur/Virologie and which was likewise not indexed by Index Medicus.32 Dahn and colleagues perhaps overestimated how effectively knowledge circulates even within the “metropoles” of western science production. While it is possible that Ebola research was eclipsed by its younger rival, HIV/AIDS, in emerging disease research (as already noted), Ebola stayed alive in “emerging diseases” discourse, which was developing in global health circles between 1992 and 2014. It is likely that this “forgetting” of the findings from the 1980s reflects both the poverty of the science infrastructure within the affected countries themselves, and the mundane accidents of oversight that are in fact quite common in the production of academic knowledge. Knobloch and colleagues’ work had been discoverable to a French epidemiological geographer, Clélia Gasquet when she was preparing her PhD thesis in 2010, but that study focused on Ebola in Gabon and the Democratic Republic of Congo, again occluding the West African area from view.33 31 Pam Belluck and William J. Broad, “Ebola Lying in Wait,” New York Times, April 20, 2015, http://www.nytimes.com/2015/04/21/health/ebola-lying-in-wait.html. 32 K. S. E. Abdel-Wahab, “Follow-up Studies in Human Infections by Rift Valley Fever Virus,” Annales de l’Institut Pasteur/Virologie 133, no. 2, (1982): 145–150. 33 I only discovered Gasquet’s 2010 thesis in September 2015, while researching the present essay. Gasquet cites Knobloch et al., “A Serological Survey,” 125–28; and

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Dahn and colleagues’ rediscovery of the “lost” Ebola findings of the 1980s occurred as the “event” of the Ebola crisis was ending. (Liberia’s incidence numbers had been dropping in April 2015 when Dahn and colleagues were writing, and it would soon reach the first of at least two “countdowns” to being declared Ebola-free.) The transition to the analyzing “process” had begun. Historicizing the outbreak was now a healthcare priority. In terms of my own “knowledge production,” my approach to the Ebola crisis from the perspective of a historian eight months earlier in the fall of 2014 had already proved valuable. I had been able to make sense of the genetic data, the epidemiological mapping data, and the hints coming from the serological studies that Ebola likely was not a new disease in West Africa. The threat may have been present for some time. Together, in fact, the serological and the genetics information suggested that Ebola might have come to West Africa in more than one wave. The Ebola outbreak in West Africa was thus becoming familiar to me in its outlines, its trajectory as a process, and as an emerging zoonotic disease that was beginning to establish it in the realm of the knowable.

On the Value of Analogy Nevertheless, none of that knowledge lessened the fact that Ebola was still a new epidemic disease, with mounting weekly incidence rates throughout the weeks in August and September 2014 when I was initially assembling a historical background. “Event” continued to be more pressing than “process.” Because I seemed to be one of the few medical historians trying to disseminate information on the outbreak, consequently I became something of a clearinghouse for information within a small circle of people with global health interests.34 In October, I received phone calls from Van derWaals, et al., “Hemorrhagic Fever Virus Infections,” 209–214, but offers no further analysis on the implications of their findings for West Africa. 34 Other historians who would contribute opinion pieces on the outbreak included Americanist Janet Golden, “Historical Antecedents to Experimental Ebola Treatments” [interview with historian of therapeutics, Scott Podolsky], The Public’s Health. Philly.com, August 19, 2014, http://www.philly.com/philly/blogs/public_ health/Historical-antecedents-to-experimental-Ebola-treatments.html;Janet Golden, “Yellow Fever and Ebola: Similar Scourges, Centuries Apart” [interview with disease historian, Margaret Humphreys], The Public’s Health. Philly.com, 28 October 2014; and David Oshinsky “Ebola and the Epidemics of the Past” Wall Street Journal, October 17, 2007, both drawing parallels from American history; and environmental historian Gregg Mitman, “Ebola in a Stew of Fear,” New England Journal of Medicine 371 (November 6, 2014): 1763–65, first published online September 17, 2014.

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reporters from the BBC News and the New York Times.35 Neither phone interview was published, but both reflected the level of hysteria that was now mounting. I, a medievalist with developing research focus on the “Black Death,” the largest pandemic in human history, was now a relevant authority. In fact, my expertise with the Black Death was relevant, but not for the reasons with which I was apparently approached. Among the major infectious diseases of human history, Ebola is comparable only to plague (caused by the bacterium Yersinia pestis) in its swiftness and case fatality rates in the absence of biomedical interventions.36 But the Black Death (and subsequent plague epidemics) took place in a world without airplanes or high-tech telecommunications, without the World Health Organization (WHO) or International Health Regulations (IHR), without cell phones or Twitter. In fact, I have already written about some ways in which Ebola and the plague pandemics can be compared usefully, rather than speciously, as “silent” local epidemics that suddenly break into international catastrophes, as zoonoses that challenge our sense of how diseases exploit human chains of connectivity.37 Similarly, Liu and colleagues have suggested parallels between the current Ebola outbreak and the 1910–1911 pneumonic plague outbreak in Manchuria.38 However, neither of those studies had been published at the time, and I do not think that either reporter had called me wanting to hear about zoonotics or the relations between disease and the environment. Precipitating the calls from two major news organizations, I believe, was a mounting sense of terror. Despite Ebola’s identification as a filovirus in 1976, no effective therapy or vaccine had been developed in the subsequent 40 years.39 Healthcare workers were using the same methods of basic physical barriers (rubber gloves, boots, and masks) and sterilization (chlorine) or destruction of used equipment that had been adopted in the first outbreak in 1976. In terms of the historical importance of the 2013– 35

Contact with the BBC was on October 13, 2014; with the New York Times on October 17, 2014. 36 Cholera usually has a faster period from infection to symptomatic phase and can kill in some cases in less than 24 hours. However, case fatality rates are significantly lower than those reported for either Ebola or plague. 37 Green, “Black Death,” ix–xx. 38 He Liu, Mingli Jiao, Siqi Zhao, Kai Xing, Ye Li, Ning Ning, Libo Liang, et al., “Controlling Ebola: What We Can Learn from China’s 1911 Battle against the Pneumonic Plague in Manchuria,” International Journal of Infectious Diseases 33 (2015): 222–26. 39 There were several drugs and vaccines in various stages of trials, some of which would be utilized in clinical use in the coming months.

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2015 Ebola outbreak, Tyvek®, the key material used for personal protective equipment (PPE), and chlorine solutions played a far greater role than any drug. The continuing terror that Ebola elicited throughout much of 2014 was that despite the provision of protective gear, so many healthcare workers were succumbing to the disease, whose case fatality rates remained as high as any we have estimated for historical epidemics of plague.40 Although something equivalent to PPE was developed for plague doctors (the wellknown beak-faced mask and body-covering coat and gloves), that would not happen until the seventeenth century, 300 years after Europe had been wrestling almost continuously with that fearsome disease.41 We were seemingly as helpless in the face of Ebola as people in late medieval and early modern times against the plague. Underlying both calls were questions about quarantine and cordons sanitaires, whose origins as public health inventions are rightly connected to plague.42 The documented cases in Guinea, Sierra Leone, and Liberia had been rising almost every week since August 2014, and, ever since late July, the predictions of exponential growth

40As

of the September 23, 2015 weekly report, the WHO reported 881 confirmed health worker infections in Guinea, Liberia, and Sierra Leone and 513 reported deaths. World Health Organization, WHO, “Ebola Situation Report–September 2, 2015,” accessed Sept 23, 2015, http://apps.who.int/ebola/current-situation/ebolasituation-report-september-2015; see also David K. Evans, Markus Goldstein, and Anna Popova, “Health-care Worker Mortality and the Legacy of the Ebola Epidemic,” Lancet Global Health (July 8, 2015), DOI: http://dx.doi.org/10.1016/S2214-109X(15)00065-0. 41 See Ann G. Carmichael, “SARS and Plagues Past”, in SARS in Context: Memory, History, Policy, ed. by Jacalyn Duffin and Arthur Sweetman (Montreal: McGillQueen’s University Press, 2006), pp. 43-68, on the development of the “plague doctor” outfit in the 17th century and its parallels to other barrier methods used by practitioners in outbreaks in the 20th and 21st centuries. 42 On the history of quarantine, see Mirko Dražen Grmek, “Le concept d’infection dans l’antiquité et au moyen âge, les anciennes measures sociales contra les maladies contagieuses et la foundation de la première quarantine à Dubrovnik (1377),” in Radovi sa Meÿunarodnog simpozija u povodu šestote obljetnice dubrovaþke karantene: Dubrovnik, 29. i 30. rujna 1977, Rad Jugoslavenske akademije znanosti i umjetnosti, 384: Razred za medicinske znanosti, 16 (Zagreb: Jugoslavenska akademija znanosti i umjetnosti, 1980), 9–55; Zlata Blazina-Tomic and Vesna Blazina, Expelling the Plague: The Health Office and the Implementation of Quarantine in Dubrovnik, 1377–1533 (Montreal: McGill-Queen’s University Press, 2015); and Nükhet VarlÕk, Plague and Empire in the Early Modern Mediterranean World: The Ottoman Experience, 1347–1600 (Cambridge: Cambridge University Press, 2015).

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coming from the mathematical modelers were becoming increasingly dire.43 With Ebola striking outside of Africa (Thomas Eric Duncan was diagnosed in Dallas in late September along with two nurses who cared for him; and a nurse’s assistant in Madrid who had participated in the care of a priest evacuated out of Sierra Leone was diagnosed with the disease on October 6), the fears of a pandemic were seemingly being realized. Ebola did not become a pandemic in 2014, but in October, I was not in a position to assure reporters that it would not. By late summer in 2014, I disagreed with the narratives being told about the outbreak. The West African Ebola outbreak was widely accepted as a “perfect storm,” and an unprecedented (and unpredictable) coincidence of circumstance and bad luck: (1) a viral disease that had never struck urban populations before, suddenly afflicting (2) societies still only beginning to recover from years of civil war, who (3) and weak, underfunded, and understaffed health infrastructures.44 It is certainly true that no known outbreak of Ebola Virus 43

The mood was captured by a piece that appeared in October: Joel Achenbach, Lena H. Sun, and Brady Dennie, “The Ominous Math of the Ebola Epidemic,” Washington Post, October 9, 2014. http://www.washingtonpost.com/national/healthscience/the-ominous-math-of-the-ebolaepidemic/2014/10/09/3cad9e76-4fb2-11e48c24-487e92bc997b_story. html. 44 The first use I found of the “perfect storm” metaphor with respect to the 2013– 2015 West African Ebola outbreak is credited to Robert Garry, a virologist at Tulane University, who cited the factors of West Africa’s greater connectivity and what he believed at the time was a reduced lethality of the West African strain of EVD, “A Perfect Storm,” The Economist (July 8, 2014). Some other examples of the “perfect storm” metaphor include Brenda Goodman, “Fighting Fear, Fatigue on the Front Lines of Ebola,” WebMD (August 7, 2014), http://www.webmd.com/news/20140807/fear-fatigue-ebola (citing Joseph Fair, PhD, a molecular virologist working with the Department of Defense); Peter Piot, “Ebola’s Perfect Storm,” Science 345, no. 6202 (September 12, 2014): 1221; Mitya Underwood, “The Perfect Storm: How Ebola has Taken Hold of West Africa,” The National, Last modified September 28, 2014, The National, accessed 24 September 2015, http://www.thenational.ae/arts-lifestyle/the-review/the-perfect-storm-howebola-has-taken-hold-of-west-africa; Jennifer Yang, “What Went Wrong in Response to the Ebola Crisis?” Toronto Star, Oct. 17, 2014, https://www.thestar.com/news/world/2014/10/17/what_went_wrong_in_response_t o_the_ebola_crisis.html. Yang reported use of the “perfect storm” metaphor in an internal WHO document. Médecins Sans Frontières contested the “perfect storm” narrative as diverting attention away from the very obvious deterioration in public health infrastructures, and continued that critique in their one-year anniversary report of March 23, 2015: Médecins Sans Frontières, Pushed to the Limit and Beyond: A Year into the Largest Ever Ebola Outbreak (March 23, 2015), https://www.msf.org/ebola-pushed-limit-and-beyond.

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Disease had ever reached this scale, but little else was unusual about the outbreak from a long historical perspective. Poverty and the after-effects of war are situations many societies throughout history have dealt with as exacerbating factors in epidemic disease.45 The impact of “rural” diseases once they break into urban areas from a certain perspective can be seen as the very definition of an epidemic, and the definition of a pandemic lies in its tapping into networks of urban congregations.46 This reliance on human networks is, in fact, a more important consideration than geographical distance or proximity per se. Every disease that is now globally distributed was once “local” in origin. Moreover, I have already questioned above the notion that global diseases necessarily become so simply through a geometric process of expansion in ever-widening radiuses. In calling diseases “global,” I mean something more than just geography. We may consider three precepts I developed for global health history.47 First, while disease knows no borders and political boundaries or jurisdictions are irrelevant, many aspects of human knowledge production do know such borders. We know now that Ebola had already crossed the political borders between Guinea, Sierra Leone, and Liberia by at least April 2014, and that this historical circumstance was of enormous importance in the fractured political and public health response to the disease in those early months.48 But, political borders also impact knowledge production. The German researchers Knobloch and colleagues published (in English) in the French Institut Pasteur Annales/Virologie in 1982, while the Dutch researchers 45

The arrival of cholera in Haiti in October 2010, following the devastating earthquake of January of that year, is one such example. 46 In my work on plague, Monica H. Green, “Editor’s Introduction” to Pandemic Disease in the Medieval World: Rethinking the Black Death, inaugural issue of The Medieval Globe 1, no. 1–2 (Fall 2014): 9–26, I adopted the definition of “pandemic” used by D. M. Morens, G. K. Folkers, and A. S. Fauci, “What Is a Pandemic?,” Journal of Infectious Diseases 200, no. 7 (2009): 1018–21. They identify wide geographic extension, disease movement, high attack rates and explosiveness, minimal population immunity, novelty, infectiousness, contagiousness, and severity as the most commonly used features in describing disease outbreaks as “pandemic”. 47 Green, “Value of Historical Perspective.” 48 Guillaume Lachenal, “Outbreak of Unknown Origin in the Tripoint Zone,” Limn, 5 (2015), accessed September 25, 2015, https://limn.it/articles/outbreak-ofunknown-origin-in-the-tripoint-zone/. Importantly, Lachenal also shows some ways in which cross-border exchanges can be productive of greater health control, suggesting that “several elements of the very infrastructure used in the current response are inherited from the years of trypanosomiasis control” from the 1930s and ’40s.

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Van der Waals and colleagues published (again in English) in the Dutch journal, Tropical and Geographical Medicine in 1986. Although the Van der Waals piece was indexed in Index Medicus/PubMed, unlike the study by Knobloch and colleagues, we should remember that, in the context of print production of scientific knowledge, those physical parameters of knowledge production were significant in the age before the Internet and electronically transmissible documents. Similarly, historians, working with written documents, usually work in regional or national archives, and often have linguistic skills limited to particular national traditions. If the disease crosses the border, can its researcher always effectively follow it? Second, a “global” disease calls for analysis with depth in time, more than the past decade or even half-century. In pushing time depth, I wish to challenge any assumption that we already know in advance the point of origin. Clearly, the current West African Ebola outbreak seems to have a much longer history than anyone knew, and if the history of filoviruses is, in fact, centuries-old, this may have implications for inherited immune profiles that would need researching. The third element of an adequate “global” analysis asks that we be simultaneously expansive in both chronology and geography in laying out the distinctive features of “global” diseases—or those that have “global” potential. What has allowed the eight diseases I study to be paradigmatically global is that they have the ability to use behaviors unique to the human species as a means of propagation.49 Some global diseases have become obligate human pathogens, organisms obligated to stay with their human host. Into this category fall smallpox, syphilis, and HIV/AIDS.50 They have no known animal or environmental reservoirs, even if they originally emerged as zoonotics. They travel when our bodies travel. Others (malaria, plague, and cholera) “travel” with us because we create microenvironments in which the pathogen or, in the case of malaria and plague, the vector thrives.51 We do not yet know what has caused the massive die-offs in certain non-human primate populations that have been attributed to Ebola, and so we cannot yet know if those are sustained primate-to-primate infections or multiple cases of zoonotic transfer.52 In the context of the 49

Green, “Globalisations of Disease,” 494–520. Although both leprosy and tuberculosis are also often discussed as human obligate diseases, in fact anthroponotic (human-to-animal) and zoonotic (animal-to-human) transmission seems likely to have been a factor in both diseases’ histories. 51 Malaria and its causative plasmodia species actually constitute “semi-obligate” diseases, but I will not belabor that point here. 52 B. Le Guenno, “Le virus Ebola: données écologiques,” Virologie 1, Hors série no. 1 (Janvier –Février 1997): 23–30; Bas Huijbregts, Pauwel De Wachter, Louis 50

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2013–2015 West African outbreak, however, it is clear that Ebola became an obligate human pathogen. Genetics research confirms that this was all the same strain of the Ebola virus moving without ceasing through thousands of human bodies. But, unlike leprosy, TB, and smallpox, which long ago developed mechanisms for respiratory transfer, Ebola effectively harnessed distinctively human behaviors besides sexual intercourse as its chief mode of transmission: caretaking of the ill, and burial practices for loved ones. It did this in the context of the uniquely human environment of urban areas. Human infectious diseases can often become quite different entities when they present in urban situations rather than rural ones. That, of course, was one of the “perfect storm” elements of the Ebola narrative— that it had never been seen in an urban context. However, it was hardly an unforeseeable development, as it would come into an urban context, either in terms of West Africa’s changing economies or in terms of what we know about EVD itself. And, as I have said, that is the essence of what “global” diseases do—they tap into the most essential elements of human connections and exploit them. To consider what we have witnessed, we might think comparatively through other emerging disease histories. There are diseases that spread quickly and develop into epidemic outbreaks. The vector-borne diseases, including plague, make a less than ideal comparison since the addition of the vector (and all the environmental parameters that go with its reproduction) adds a complication. Of the eight diseases I study, smallpox—another obligate viral disease with a similar disease interval to Ebola (about one month from infection to death or resolution of the acute phase of illness)— offers a better comparison. Smallpox also offers a useful historical model because its symptoms are often distinctive enough that we can show Sosthène Ndong Obiang and Marc Ella Akou, “Ebola and the Decline of Gorilla Gorilla gorilla and Chimpanzee Pan troglodytes Populations in Minkebe Forest, North-eastern Gabon,” Oryx 37, no. 4 (October 2003): 437–43; Sally A. Lahm, Maryvonne Kombila, Robert Swanepoel, Richard F. W. Barnes, “Morbidity and Mortality of Wild Animals in Relation to Outbreaks of Ebola Haemorrhagic Fever in Gabon, 1994–2003,” Transactions Medicine and Hygiene of the Royal Society of Tropical 101 (2007): 64–78; P. D. Walsh, T. Breuer, C. Sanz, D. Morgan, D. DoranSheehy, “Potential for Ebola Transmission between Gorilla and Chimpanzee Social Groups,” American Naturalist 169, no. 5 (2007): 684-689; Céline Devos, Peter D. Walsh, Eric Arnhem and Marie-Claude Huynen, “Monitoring Population Decline: Can Transect Surveys Detect the Impact of the Ebola Virus on Apes?” Oryx 42, no. 3 (June 2008): 367–374; and J. J. Muyembe-Tamfum, S. Mulangu, J. Masumu, J. M. Kayembe, A. Kemp, and J. T. Paweska. “Ebola Virus Outbreaks in Africa: Past and Present.” Onderstepoort Journal of Veterinary Research 79 no. 2 (2012): Art. #451, http://dx.doi.org/10.4102/ojvr.v79i2.451.

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confidence in identifying the disease when it is being recounted in different historical scenarios.53 According to the latest genetic reconstruction, smallpox arose as an obligate human pathogen just about 2000–2500 years ago, likely emerging from an ancestor that could infect a variety of hosts (and likely retaining that “generalist” capacity for some time thereafter).54 If, in fact, what we now understand as the variola virus is indeed the descendant of a generalist zoonotic virus that developed “specialist” capacities, then we would need to posit a chain of human-to-human transmissions continuously from that day until 1977 when the last naturally acquired human case of the disease occurred. The complication with smallpox is that survivors acquire lifelong immunity: they cannot be reinfected nor (aside from their scabs) pass the disease on to new hosts once they have passed the active phase of the disease, which lasts about one month. In other words, smallpox needed villages and towns and eventually cities to sustain its chain of infection for 2000–2500 years. By the tenth century CE, the physician Abu Bakr Muhammad ibn Zakariya al-Razi (c. 865–925/35) described smallpox as an endemic disease of children.55 Al-Razi was working in the city of Baghdad, which may have been one of the largest cities in the world at the time, with a population of about one million. For most of smallpox’s history, we should think of endemic reservoirs of the disease (like medieval Baghdad), where the immunological naïves would be mostly children and adult immigrants, and epidemic corridors that linked them, where smallpox would be imported occasionally in flare-ups and would be an equal opportunity killer of immunologically naïve adults as well as children. In North America, for example, it seems there were no endemic reservoirs for the disease prior to

53

On debates among historians of medicine about retrospective diagnosis, see Monica H. Green, “Taking ‘Pandemic’ Seriously: Making the Black Death Global,” in Pandemic Disease in the Medieval World: Rethinking the Black Death, inaugural issue of The Medieval Globe 1, no. 1–2 (Fall 2014): 27–61. Ancient DNA (“aDNA”) for variola has not yet been identified that predates the mid-17th century though there are now established paleopathological methods for documenting potential smallpox infection from earlier skeletal remains. See Anna T. Duggan, Maria F. Perdomo, Dario Piombino-Mascali, Stephanie Marciniak, Debi Poinar, Matthew V. Emery, Jan P. Buchmann, et al., “17th Century Variola Virus Reveals the Recent History of Smallpox,” Current Biology 26, no. 24 (December 19, 2016): 3407–12. 54 Chad Smithson, Jacob Imbery, and Chris Upton, “Re-Assembly and Analysis of an Ancient Variola Virus Genome,” Viruses 9, no. 9 (2017): 253. 55 Rhazes (Muhammad ibn Zakariya al-Razi), A Treatise on the Smallpox and Measles, trans. William Alexander Greenhill (London: Sydenham Society, 1848).

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the late 18th century when population centers large enough to sustain endemic disease finally developed.56 Smallpox may seem far in the rear-view mirror of humanity now, but that is simply a function of our having lost from active practice over the past forty years most of the healthcare workers—and academic researchers— who worked with it firsthand prior to its eradication in 1977. Even as recently as the early 1970s, smallpox vaccination teams were engaged in a “getting to zero” campaign much like what was happening in West Africa in 2015. The difference is that they began their project with an effective vaccine in hand, which gave them the knowledge that, for any new victim of the disease that was found, they could protect most of the surrounding contacts. The lack either of an effective drug or, until summer 2015, a proven vaccine against Ebola is what makes a comparison with disease spread in pre-modern cities a reasonable exercise. When thinking of smallpox, therefore, we should think of that two thousand yearlong unbroken chain of human-to-human contact that began, perhaps, with some innocent interaction between a camel herder and an agriculturalist; that sustained the virus through millions of other bodies; and that used humans’ networks of cities and towns to keep that chain of infection going. Millions of people throughout the world were affected by smallpox throughout its long reign. The potential for growth—for the transition of an organism from a rare, rural killer to an urban terror—should not be assumed to lie in the genetic mutation of the organism itself, but rather in the pathways we humans create for it. A chart published in mid-August 2014 (Figure 2) showed the “deaths per day” in the three affected West African countries from Ebola (4) compared to the major killers currently in the region: Lassa fever (14 per day), tuberculosis (110), diarrhea (404), malaria (552), and HIV/AIDS (685). Similar comparison charts were published in other venues, in some cases with the implicit message: Ebola is nothing to worry about. The problem with such charts was that they had no time-depth—no historicity.57 Three of the six diseases listed are among my eight “paradigmatic diseases” that I use to encapsulate humankind’s history with infectious diseases. Yes, 56

Green, “The Globalisations of Disease,” 494–520. I was greatly aided in making this realization by the useful analysis of Greg Laden’s blog post of September 11, 2014. See Greg. Laden, “Has #Ebola Death Toll Surpassed Malaria in West Africa?,” Greg Laden’s Blog, ScienceBlogs, posted 09/11/2014, http://scienceblogs.com/gregladen/2014/09/11/has-ebola-death-tollsurpassed-malaria-in-west-africa/, which broke down the Ebola numbers in comparison to malaria, showing that, already by that point, Ebola was likely outranking malaria in terms of weekly mortality rates. 57

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there was a time when the numbers infected with any one of those diseases would have been so small to be “nothing to worry about.” However, once those diseases began to establish a bigger footprint, affecting more populations, their impact became significant.

Figure 2: “The Killers: Deaths Per Day, Ebola Affected Countries,” from The Economist, “Fever Rising: The Spread of Ebola in West Africa is Deeply Troubling for the Region and the World,” August 14, 2014. https://amp.economist.com/international/2014/08/15fever-rising.

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Where was that tipping point for each disease? Vivax malaria (now dominant in Asia as well as the Americas) and falciparum malaria (the type most dominant in sub-Saharan Africa) are thought to be many thousands of years old, far too long ago for us to describe the exact context of their birth as human diseases closely, even if certain minimal demographic conditions would have been necessary.58 Other major infectious diseases, however, can now be more closely tracked in terms of the circumstances of their emergence as pathogens of major epidemiological importance; for many of these, the connections with major climate shifts or demographic upheavals is becoming clear.59 The exponential growth of HIV/AIDS from the time of its emergence ca. 1920 to 1981, when it was first clinically described, and to the present day, has been plausibly reconstructed by combined genetic and historical analysis.60 I asked my students, if they could have stopped HIV/AIDS when there were only 4 (or 8 or 1000) people infected in the 58 On the malaria pathogen Plasmodium falciparum, see Guillaume Laval, Stéphane Peyrégne, Nora Zidane, Christine Harmant, François Renaud, et al., “Recent Adaptive Acquisition by African Rainforest Hunter-Gatherers of the Late Pleistocene Sickle-Cell Mutation Suggests Past Differences in Malaria Exposure,” American Journal of Human Genetics 104 (2019), 553–56; and James L. Webb, Jr. “Early Malarial Infections and the First Epidemiological Transition,” in Human Dispersal and Species Movement from Prehistory to the Present, ed. Nicole Boivin, Rémy Cressard, and Michael Petraglia (Cambridge: Cambridge University Press, 2017), 477–93. 59 This work has advanced significantly since 2014. For example, on plague, see Nicolás Rascovan, Karl-Göran Sjögren, Kristian Kristiansen, Rasmus Nielsen, Eske Willerslev, et al., “Emergence and Spread of Basal Lineages of Yersinia Pestis during the Neolithic Decline,” Cell 176, no. 1 (January 10, 2019), 295–305. e10; and Gérard Chouin, “Reflections on Plague in African History (14th–19th c.),” Afriques (September 2018), mis en ligne le 24 décembre 2018, consulté le 25 mars 2019.http://journals.openedition.org/afriques/2228; Bernice Dahn, Vera Mussah, and Cameron Nutt, “Yes, We Were Warned About Ebola,” New York Times, 7 April 2015, http://www.nytimes.com/2015/04/08/opinion/yes-we-were-warned-aboutebola.html. The ages of the several lineages of tuberculosis that affect humans are currently being contested; see, among others, Kristen I Bos, Kelly M. Harkins, Alexander Herbig, Mireia Coscolla, Nico Weber, Iોaki Comas, Stephen A. Forrest, et al., “Pre-Columbian Mycobacterial Genomes Reveal Seals as a Source of New World Human Tuberculosis,” Nature 514 (October 23, 2014): 494–97, published online August 20, 2014; and Sebastien Gagneux, “Ecology and Evolution of Mycobacterium tuberculosis.” Nature Reviews: Microbiology 16, no. 4 (2018): 202– 13. 60 Ibid.; Michael Worobey, Thomas D. Watts, Richard A. McKay, Marc A. Suchard, Timothy Granade, et al., “1970s and 'Patient 0' HIV-1 Genomes Illuminate Early HIV/AIDS History in North America,” Nature 539, no.7627 (2016): 98–101.

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world, wouldn’t they try? If we could have stopped the 2013–2015 West African Ebola outbreak at 11 deaths, instead of 11,000, shouldn’t we have?

Witnesses at the Creation: The West African Ebola Crisis and Its Implications for Global Health In September 2014, a colleague and historian of medicine, Stephen Casper, and I submitted a proposal for a panel for the American Association for the History of Medicine (AAHM) scheduled to meet the following year. We had hoped that we could talk in the past tense about the West African Ebola outbreak, but by the time the AAHM meeting came around in May 2015, the pessimism of our title proved warranted. “Witnesses at the Creation: The West African Ebola Crisis and Its Implications for Global Health” was meant to flag the sobering fact that we—the world—had just watched the creation of a new human disease, still (at that time) being passed on in an unbroken chain from human body to human body. The outcome had been predicted by the World Health Organization (WHO) Ebola Response Team in the September 23, 2014 report, which made a startling, historic statement: “For the medium term, at least, we must therefore face the possibility that EVD [Ebola Virus Disease] will become endemic among the human population of West Africa, a prospect that has never previously been contemplated.”61 The WHO’s prediction came true: at the time I first drafted this paper in May 2015, Ebola was still endemic in Guinea, Sierra Leone, and Liberia, with about 30 cases being found each week. In other words, there were more new cases found each week in May 2015 than the highest number of total infections in half of the 23 previously known Ebola outbreaks.62 New insights were being realized about the virus’s persistence in immunologically protected areas of the body (testes, eyes, perhaps the 61 WHO, World Health Organization Ebola Response Team, “Ebola Virus Disease in West Africa — The First 9 Months of the Epidemic and Forward Projections,” New England Journal of Medicine 371, no. 16 (October 16, 2014): 1481–95, advanced online publication, September 23, 2014. 62 As of the September 23, 2015 weekly report, the WHO reported 881 confirmed health worker infections in Guinea and 513 reported deaths, WHO (World Health Organization), “Ebola Situation Report–September 2, 2015,” accessed Sept 23, 2015, http://apps.who.int/ebola/current-situation/ebola-situation-report-september2015. See also David K. Evans, Markus Goldstein, and Anna Popova, “Health-care Worker Mortality and the Legacy of the Ebola Epidemic,” The Lancet Global Health, Published online: July 8, 2015, DOI: http://dx.doi.org/10.1016/S2214109X(15)00065-0.

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brain) that could make an individual infectious long after the virus had cleared from the blood. Moreover, whether survivors remained infectious to others or not, it was clear that the list of physical sequelae to the disease (not to mention the emotional and social ones) was growing ever longer, with joint pains, weakness, and blindness possibly leading to life-long disability.63 For all the reasons the birth of HIV/AIDS as a human disease around 1920 was not witnessed—the supposed isolation of the hunter or other individual first infected, the slow and (largely) invisible incubation of the disease in rural populations, the initially low reproduction rates of transmission, the focus of colonial health systems in Kinshasa (once the disease reached its first major urban hub) on other health conditions—we could not claim, in the 2013–2015 West African outbreak, that we had not borne witness to the birth of a new human-adapted disease.64 It unfolded in full view of the world, down to the last tweet. Our panel “Witnesses at the Creation” was also meant to implicate historians of medicine and health specifically in the shared task of recognizing this moment of birth and acknowledging our duty to be involved in its containment. Ebola has been called “a virus that strives toward pandemic status.”65 Ebola did not reach pandemic status in 2014, but it very easily could have. Ebola’s power to tap into human modes of connection is now proven and it has already taken its place with the great global diseases of human history. Because of the virus’s possibly widespread distribution enzootically throughout wide stretches of Central and West Africa, like plague, it should be considered a permanent threat to humankind, demanding vigilant monitoring in whatever its persistent animal reservoirs turn out to be and possibly, like smallpox until the 1970s demand comprehensive prophylactic vaccination programs.66 I have provided this reconstruction of my own involvement in the historical analysis of the 2013–2015 West African Ebola outbreak not simply as an example of “knowledge construction,” but also as a call to 63 Ian Mackay, “Post-Ebola Syndrome or Just Chronic Ebola Virus Disease...?” Virology Down Under 8 (August 2015), http://virologydownunder.blogspot.com.au/2015/08/post-ebola-syndrome-or-justchrnic.html. 64 My description here presents the reconstructed history of Group M, the cause of the worldwide pandemic. See Nuno R. Faria, Andrew Rambaut, Marc A. Suchard, Guy Baele, Trevor Bedford, Melissa J. Ward, Andrew J. Tatem, “Early Spread and Epidemic Ignition,” Science 3 (October 2014): 56–61. 65 Koch, “Ebola: Epidemics, Pandemics.” 66 Siv Aina J. Leendertz, Jan F. Gogarten, Ariane Düx, Sebastien Calvignac-Spencer, Fabian H. Leendertz, “Assessing the Evidence Supporting Fruit Bats as the Primary Reservoirs for Ebola Viruses,” EcoHealth 13, no. 1 (2016): 18–25.

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other historians to join me. My colleague Stephen Casper noted a silence surrounding Ebola at the 2015 historians of medicine meeting, despite the engaged discussion at our well-attended panel.67 If I could press his observations further, my sense of (American) historians’ reticence to engage was not simply unfamiliarity with West Africa and its recent history or specific knowledge about Ebola Virus Disease as a biological organism. As I have explained, I shared those incapacities. What I think we generally lack, as a field, is competence to envisage a world beyond the narratives of “identification and control” that have served as the trajectory for biomedicine’s rise in the past century, which has coincided with the rise of our historical field. What I have tried to do in this essay is to lay out an interpretive framework into the West African Ebola outbreak that can be placed—at least as a way of beginning to frame it— as “process” and not simply as “event.” Historical analysis is critical now and not at some distant point in the future. Beyond the obvious fact that the addition of time-depth to any socially, culturally, politically, and biologically complex situation is always vital, there is no longer any need for historians to wait for an “archival record” to be created by the slow accumulation of doctors’ case histories, investigative commissions’ reports, least of all the slow arrival of print newspapers. As I have said recently, because of chronological and evidentiary overlap, histories of infectious disease should “move toward a consilient historiography, one that takes both physical (in this case, biological) continuities and perceived experiences of disease into account.”68 The limit of history in the comparative mode is that every analogy can only be stretched so far: every historical event is contingent, a unique mix of the moment, the actors (including the pathogen), and the circumstances that create it. Rightly, most criticisms of the delayed and clumsy reaction to the Ebola outbreak have focused on the failures of public health infrastructure in West Africa and those of the international response: there was too little infrastructure already in place to handle a quickly moving, highly lethal epidemic, and too rigid an international health bureaucracy to mount an effective response. But I think we should not underestimate the fact that even had there been a stronger healthcare infrastructure, the power 67

Stephen T. Casper, “Afterthought. Witnesses at the Creation: The West African Ebola Crisis and Its Implications for Global Health,” accessed September 23, 2015, https://www.academia.edu12261100/Afterthoughts_Witnesses_at_the_Creation_T he_West_African_Ebola_Crisis_and_Its_Implications. 68 Monica H Green, “Climate and Disease in Medieval Eurasia,” Oxford Research Encyclopedia of Asian History, ed. David Ludden (New York: Oxford University Press, 2018), DOI: 10.1093/acrefore/9780190277727.013.6.

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of Ebola as a killer was fierce. Although its reproduction rate generally remained low, because of the severity of the disease it caused and the lack (at the time) of any test for infection prior to the manifestation of symptoms, its power to terrify remained. It was transmitted as effectively in an urban hospital in Dallas as it was in Guinea. The character of this particular disease, and the fact that, until the end of July 2015, when the success of the Canadian vaccine was announced, there were only barrier and sanitation measures to prevent its spread, which further reinforces parallels with epidemic outbreaks of the 19th century and before. There is no question that the 2013–2015 West African Ebola outbreak will be seen as a turning point in history for the three West African countries most immediately affected, but also for the WHO, for its global health governance, for the role of medical science in Africa, and possibly also for the roles of both “emerging disease” discourse and public health infrastructure in shaping global health policy and investments. This, then, is the reason why I believe that Ebola is best categorized now as a “global” disease. In 2015, Peter J. Hotez published an analysis of the distribution of what have been called “Neglected Tropical Diseases” for some years. These had been assumed to be concentrated in the world’s poorest countries (particularly in Africa). Nevertheless, once actual prevalence data were closely examined, it was clear that up to 60% of cases were found in the socalled G20 countries. The same was found to be true of what are still the world’s top killers among infectious diseases: HIV/AIDS, tuberculosis, and malaria.69 Hotez’s study thus challenges the very notion of the category “Neglected Tropical Disease” as it has been used in global health discourse. I would argue against any such limiting designation concerning Ebola, too. Nicholas King, with whose work on bioterrorism I began this essay, makes the sound observation that historians “understand both the positive and negative power of analogical reasoning.”70 And like King, “I counsel caution, but I urge engagement.” “[W]e [historians] can learn from the distant and immediate past, and we can understand the subterranean contours of contemporary discussions.”71 Having been a historian-intraining myself in the early ’80s, I remember the slow pace of scholarly communication, the inequities between rich universities with vast libraries and institutions with lesser endowments, and perhaps most important, the 69 Peter J. Hotez, “Blue Marble Health and ‘The Big Three Diseases’: HIV/AIDS, Tuberculosis, and Malaria,” Microbes and Infection 17, no. 8 (2018): 539–41. 70 Nicholas B. King, “The Influence of Anxiety: September 11, Bioterrorism, and American Public Health” Journal of the History of Medicine 58, no. 4 (October 2003): 440. 71 Ibid., 441.

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bibliographical firewalls between disciplines. Whatever the reasons for historians’ slowness as a discipline in helping to understand the HIV/AIDS pandemic, those no longer apply. We, who have at our fingertips longer and deeper histories of what infectious epidemic diseases have done to human societies, should be leading the way in showing the comparative utility of that knowledge, and fusing it with new forms of knowledge production being created by our sister disciplines, evolutionary genetics, bioarchaeology, and so forth. Moreover, we should be using new technology platforms and new economic models of scholarly publication to make the results of our work as widely available as possible.

Bibliography Abdel-Wahab, K. S. E. “Follow-up Studies in Human Infections by Rift Valley Fever Virus.” Annales de l’Institut Pasteur/ Virologie 133, no. 2 (1982): 145–50. Achenbach, Joel, Lena H. Sun, and Brady Dennie. “The Ominous Math of the Ebola Epidemic.” Washington Post, October 9, 2014. http://www.washingtonpost.com/national/healthscience/the-ominousmath-of-theebolaepidemic/2014/10/09/3cad9e76-4fb2-11e4-8c24487e92bc997b_story.html. Baize, Sylvain, Delphine Pannetier, D. Pharm, Lisa Oestereich Toni Rieger, Lamine Koivogui, N’Faly Magassouba, Barrè Soropogui, Mamadou Saliou Sow, Sakoba Keïta, et al. “Emergence of Zaire Ebola Virus Disease in Guinea—Preliminary Report.” New England Journal of Medicine 371 (September 19, 2014): 1418–25. First published online April 16, 2014. Belluck, Pam and William J. Broad. “Ebola Lying in Wait.” New York Times, April 20 2015, http://www.nytimes.com/2015/04/21/health/ebola-lying-in-wait.html. Blazina-Tomic, Zlata and Vesna Blazina. Expelling the Plague: The Health Office and the Implementation of Quarantine in Dubrovnik, 1377–1533. Montreal: McGill-Queen’s University Press, 2015. Bos, Kristen I., Kelly M. Harkins, Alexander Herbig, Mireia Coscolla, Nico Weber, Iોaki Comas, Stephen A. Forrest, Josephine M. Bryant, Simon R. Harris, and Verena Schuenemann, et al. “Pre-Columbian Mycobacterial Genomes Reveal Seals as a Source of New World Human Tuberculosis.” Nature 514 (October 23, 2014): 494–97. Published online August 20, 2014. Calvignac-Spencer, Sébastien, Jakob M. Schulze, Franziska Zickmann, and Bernhard Y. Renard. “Clock Rooting Further Demonstrates that Guinea

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Goodman, Brenda. “Fighting Fear, Fatigue on the Front Lines of Ebola.” WebMD. August 7, 2014. http://www.webmd.com/news/20140807/fear-fatigue-ebola. Green, Monica H. “The Black Death and Ebola: On the Value of Comparison.” In Pandemic Disease in the Medieval World: Rethinking the Black Death, ed. Monica H. Green. ix–xx. Amsterdam: Arc Medieval Press, 2015. Green, Monica H. “Climate and Disease in Medieval Eurasia.” In Oxford Research Encyclopedia of Asian History, edited by David Ludden. New York: Oxford University Press, 2018. DOI: 10.1093/acrefore/9780190277727.013.6 Green, Monica H. “Global History of Health: Teaching Notes on Ebola” (as of 08132014). Posted on Academia.edu, 08/13/2014, https://www.academia.edu/7965438/Global_History_of_Health__Teaching_Notes_on_Ebola_08_13_2014_ . Green, Monica H. “The Globalisations of Disease.” In Human Dispersal and Species Movement: From Prehistory to the Present, ed. Nicole Boivin, Rémy Crassard, and Michael D. Petraglia. 494–520. Cambridge: Cambridge University Press, 2017. Green, Monica H. “Taking ‘Pandemic’ Seriously: Making the Black Death Global.” In Pandemic Disease in the Medieval World: Rethinking the Black Death. Inaugural issue of The Medieval Globe 1 no. 1–2 (Fall 2014): 27–61. Green, Monica H. “The Value of Historical Perspective.” In The Ashgate Research Companion to the Globalization of Health, ed. Ted Schrecker. 17–37. Aldershot, UK: Ashgate, 2012. Grmek, Mirko Dražen. “Le concept d’infection dans l’antiquité et au moyen âge, les anciennes measures sociales contra les maladies contagieuses et la foundation de la première quarantine à Dubrovnik (1377).” In Radovi sa Meÿunarodnog simpozija u povodu šestote obljetnice dubrovaþke karantene: Dubrovnik, 29. i 30. rujna 1977, Rad Jugoslavenske akademije znanosti i umjetnosti, 384: Razred za medicinske znanosti, 16 (Zagreb: Jugoslavenska akademija znanosti i umjetnosti, 1980): 9-55. Harrison, Mark. Disease and the Modern World: 1500 to the Present Day. Cambridge, UK: Polity Press, 2004. Heymann, D. L., J. S. Weisfeld, P. A Webb, K. M Johnson, T. Cairns, H. Berquist. “Ebola Hemorrhagic Fever: Tandala, Zaire, 1977–1978.” Journal of Infectious Diseases 142, no. 3 (1980): 372–76. Hotez, Peter J. “Blue Marble Health and ‘The Big Three Diseases’: HIV/AIDS, Tuberculosis, and Malaria.” Microbes and Infection 17, no. 8 (2015): 539–41.

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CHAPTER FOURTEEN IMMEMORIAL: THE POETICS OF AIDS— A CONVERSATION WITH RUDY LEMCKE TINA TAKEMOTO

I first encountered Rudy Lemcke’s work at Picturing AIDS, 1986–1996, a retrospective of his AIDS artwork at the San Francisco LGBT Community Center in 2007. I was particularly moved by his video Where the Buffalo Roam in which Lemcke uses John Cage’s musical composition The Perilous Night as an editing framework for juxtaposing documentation of ACT-UP protests with evocative images of slain buffalo (Fig. 1).1 In December 2014, Rudy and I sat down for a conversation about his work at his studio in San Francisco, California. We discussed the poetics and politics of AIDS in light of his work in the traveling exhibition Art AIDS America, co-curated by Jonathan D. Katz and Rock Hushka. The interview was published in 2015 in The College Art Association’s Art Journal Open. In 2018, we sat down again to expand this conversation and reflect on the exhibition’s tour and its impact. The following conversation is the product of those two conversations. The exhibition venues include West Hollywood Library and One Archive Gallery and Museum, CA (June 1–September 6, 2015); Tacoma Art Museum, WA (October 3, 2015–January 10, 2016); Zuckerman Museum of Art, GA (February 20–May 22, 2016); The Bronx Museum of the Arts, NY (June 23–September 11, 2016); Alphawood Gallery, IL, (December 1, 2016–April 2, 2017). TAKEMOTO: We should start by talking about your early work, your influences and how your work about AIDS relates to this work. You have been making art since the late 70s, can you describe your early work and influences? 1

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LEMCKE: I was influenced by what was going on around me in art and philosophy. The seventies were a time of Conceptual Art, Earthworks, Minimalism. Philosophy, in general, was dominated by post-structuralism. So that is where I entered the scene. I guess I can trace a line from the work of Michel Foucault and his important book The Order of Things, to the work of John Cage, to my early performance installations, my artwork about AIDS, political and cultural activism, experimental video, and most recently, video games and curatorial projects. All of these activities fold back upon themselves in many ways over the years. Life has a way of making more sense when looking back, doesn’t it? I can navigate a certain narrative course through the work that shows the path to my current interest in video game design and curatorial work, and how the epidemic changed that course and shaped the direction of my work. There are probably other narrative paths through my work, but this one makes the most sense to me now. TAKEMOTO: Why Michel Foucault? LEMCKE: I studied philosophy in school and not art, but making the leap from philosophy to conceptual art wasn’t that big of a leap. Philosophy is a form of conceptual art. Michel Foucault was part of a movement called poststructuralism. This was a movement that took hold in the late 60s and 70s and has resonance even now. The key takeaway for this movement was that it decentered the idea of human subjectivity—that “MAN” in the cultural sense is not an essential being with preconditioned structures of knowledge. Post-structuralists theorized that we are the product of our cultural conditioning, genetic make-up, and familial and social status; that our identity is constructed. It’s not to say it is arbitrary but not essentially fixed. Foucault’s theories primarily address the relationship between power and knowledge, and how they are used as a form of social control through societal institutions. The focus on Foucault and the post-structuralists was an interest in how language, culture, and politics form the conditions in which we as humans are known. TAKEMOTO: How did this philosophy influence your art? LEMCKE: The work that interested me most in the mid-70s was the work of John Cage—composer and artist. It’s actually hard to categorize his work because it was really a hybrid of conceptual art, life art, performance art, and music. He was a student of Zen and was interested in the idea of chance, and of the random, ephemeral qualities of experience. In his most famous

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piece called 4’33, he gave a concert where he sat silently at the piano for four and one-half minutes, putting the focus of the work on the audience and the experience of listening rather than on the playing of a piece by a master pianist. The sounds in the audience – the audience’s restless movement, breathing, and occasional coughs – became the music. His musical notations (his scores) were brilliant. They were works of art. They included opportunities for chance and free play to operate in the course of performing his music. It was his performance notations that most interested me as an artist. So, from Foucault, comes this idea of exploring the fields of knowledge and power – the frames, the rules of the game within which we can know the world through language. My early work and actually the work I’m doing today, foreground the “un-fixed,” referential frames where the conditions of meaning are made possible. From Cage, I saw his musical scores as a way of mapping performance as a set of rules—the conditions within which we can experience a work of art through the performance and our interaction with it. My early work centered around creating performance scores and realizing these scores as installations that the viewer could move through and perform— conceptually. I didn’t intend for the viewer to actually perform the movements or actions described in the notations. It was always the idea of moving through a set of predetermined rules for performance that I was getting at in the artwork. This influenced my early drawings, and even now with my work in video games, I’m still exploring these conditions for making an experience possible (Fig. 2). TAKEMOTO: One of your drawings was in the Art AIDS America exhibition. Can you talk a little about this piece in relation to John Cage? LEMCKE: In 1985, I met John Cage at the alternative art space La Mamelle in San Francisco at his reception for The First Meeting of the Satie Society. For this piece, Cage worked with two computer programmers who input texts from Henry David Thoreau, Marcel Duchamp, Marshall McLuhan, and James Joyce. They wrote an algorithm that generated mesostic poems from random configurations of words that were “performed” live on a computer screen. A mesostic poem has a word or phrase written vertically and a series of horizontal words or phrases intersecting the vertical phrase. I was working with ideas of language and temporality and creating performance notations and installations that were deeply indebted to Cage, so this was an important moment for me as an artist.

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The mid-1980s was also a time when AIDS entered our world. I was particularly struck by how AIDS as an idea was manifesting in different ways for various people and elicited a broad range of representations and responses. In my work, I wanted to reflect on AIDS not only as a biological event but also as a complex cultural phenomenon that had complicated meanings. I was reading Finnegans Wake and loved how Joyce invented beautiful words that could subtly shift the meaning of a sentence. The words made sense but also appeared as nonsense. I started writing down Joycean words that had a certain feeling tone and resonance. Cage’s mesostic poems came to mind, and I thought of making AIDS poems from the words I had collected. I called this series of drawings Fin Again(s) Wake. I think of them as drawings but also as a type of writing or notation that came out of my earlier work in which I used scores as the conceptual structure for generating installations. For instance, in my 1979 untitled performance installation for breathing, I marked the ground with chalk. The Xs indicated where the viewer should inhale, exhale, and hold the breath (Fig. 3). The installation was less about formal spatial relationships than the temporal aspects of the performance notations. TAKEMOTO: Were all the words that you used in your mesostic poems taken from Finnegans Wake? LEMCKE: No. I started by picking the name of a drug that was currently being used to treat HIV/AIDS. I used this word as the vertical spine of the poem. Then I would generate a poem that could be read horizontally using Joyce’s words from my notebook (Fig. 4). I didn’t use a computer and it wasn’t really a chance operation, but there was a randomness and improvisational aspect to my process. Just as a performer of a Cage score is often free to create variations within a set of parameters set by the composer, I produced numerous configurations of words based on a given framework. I wasn’t trying to recreate Cage’s piece but rather a new series of work influenced by Cage’s process. Foscarnet is the title of the piece from this Fin Again(s) Wake series included in the Art AIDS America exhibition (Fig. 5). Foscarnet was used to help treat a form of blindness that affected people with HIV. TAKEMOTO: Can you read the Foscarnet poem and then talk about your choice of Joyce’s words?

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LEMCKE: I’ve actually never read the poem out loud for someone or performed it this way. It is more of a thought piece. But I will try. “Fuggus soddenly lostchance facts rassembling certainly in parfect sight.” TAKEMOTO: How would you “translate” this poem? What thoughts come to mind for you as you read it? LEMCKE: I guess it would read something like: “Focus suddenly, see suddenly, a last chance, possibly a lost chance, these facts, these drugs, resembling certainty, having the promise of a certain cure, uncertainty about this all, my imperfect sight, seen clearly, not clearly at all, imperfect, not certain, in perfect sight.” The words are meant to be seen or felt as conceptual clusters, floating in and out of meaningfulness. I made this drawing using alphabet stencils in very faint graphite on paper. Initially, it just looks like a plain piece of paper on the wall. You can barely see the text. First, you see a faint cluster of words on the page that may or may not seem to relate to dying or loss. Then slowly as the name of the drug becomes legible along the vertical axis, only to retreat back into the cluster of words that provisionally holds its meaning. I was very aware of all of the new HIV/AIDS “wonder drugs” that were coming out in the press and on the market at the time. I wanted to make this series of works to gesture toward the range of emotions attached to these drugs: the evasiveness, uncertainty, and precarity of hope for possible “cures” that were coming into sight and then becoming unfocused, lost. These mesostic AIDS poems, which are composed of words about being in the wake of death, also contain within them a way of “living” with AIDS. TAKEMOTO: Jacques Derrida writes about the double valence of “pharmakon” as both a poison and a cure. Didn’t many of the early HIV/AIDS drugs also have devastating side effects? LEMCKE: Absolutely. At the beginning of the crisis, many of the drugs and the dosages were completely experimental and so harsh on the system that people wondered which was worse, the disease or the cure. TAKEMOTO: I am struck by your choice of Foscarnet as a drug that attempts to cure blindness but also as a metaphor for the ability or willingness to see or not see the HIV/AIDS pandemic. LEMCKE: Yes, the idea of blindness and recognition resonates in a whole other register in relation to art and politics. In this regard, Fin Again(s) Wake

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wasn’t just a variation on Cage’s work but also marked my departure from it. While there is a beauty to Cage’s language play and the undecidability of meanings within abstraction, AIDS changed the playing field of queer art for me and for a lot of queer artists. Making art could no longer simply be a linguistic or theoretical experiment. We were now working within social and political systems of power that were literally killing people. I felt the ethical imperative to foreground the reality of the AIDS crisis, to respond to this political moment, and to make art that spoke to its urgency without reducing the message. I wasn’t interested in making agitprop. I was seeking more complicated multivalent ways of seeing the disease. TAKEMOTO: How do you think artworks about AIDS were able to shape the way we think about the pandemic? LEMCKE: In the 1980s, there was a culture war going on that was led by conservative Republican politicians and religious right leaders. One battlefield was about how we, as a society, would define AIDS—not as a disease but as a “thing” or “event” in the world. The political Right’s tactic was to demonize homosexuality and anything they considered outside of their own belief system. Their goal was to dominate the political landscape with the help of bigoted religious beliefs anchored in homophobia, sexism, and racism. When AIDS arrived, conservatives were able to crystallize their prejudices into a shadow image of people, whom they would label as unworthy of legal protection or dignity for that matter. People who contracted the disease were thought of as social and religious pariahs who brought about their own deaths. This was the insidious and conscious political climate that dominated the politics of the late 80s in America. What I think art and AIDS activism did on a fundamental level was to take back our identity and empower ourselves to make choices about living with this disease and to demand our rights as citizens to proper health care and legal protection. Over the course of a few years, the term “AIDS victim” (used in the early days of the epidemic) morphed into the term “person living with HIV/AIDS.” This is an important rhetorical move. It was something that happened in “ordinary” language that shifted because of an active counter-movement on the part of AIDS activists to reclaim how we addressed people living with the disease. To cite an example of how this shift occurred, there was an exhibition of photography in the late 80s by an artist named Nicholas Nixon (part of a retrospective of his works of portraiture). One of the sections of this exhibition showed portraits of people dying of AIDS. I’m certain that the intention was to provoke understanding and compassion by showing these portraits. But the exhibition was very

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publicly criticized by the LGBT community for reproducing a stereotype of people with AIDS as victims who were suffering from a condition that warranted our pity. An important AIDS activist Michael Callen stated at a protest rally, and I am paraphrasing, but the heart of his statement was, “I am not an AIDS victim. I am a person with AIDS.” The term PWA (Person with AIDS) came into use during this period of the late 80s – the emphasis was on “living” with a condition and away from “victim” status. This shift in perception came from within the gay movement and bubbled up as a protest against a visual stereotype. It marked an important moment because it changed the way we spoke about AIDS and spoke about ourselves. It was claiming the right to visibility and self-determination, and was a turning point and an extension of the greater LGBT rights movement and liberation movements in general. It fundamentally impacted the way politicians, medical professionals, and social service organizations began to speak about people affected by the disease. It changed how we thought about ourselves as a community. In many ways, AIDS art and AIDS activism are the same thing. TAKEMOTO: How do you see the relationship between AIDS art and activism? LEMCKE: Art and activism are part of a spectrum of visual and linguistic practices that shape the way we think and talk and see ourselves; they give voice to how we see and speak about ourselves and that this process can change culture. I talked earlier about Foucault’s ideas about systems of power and knowledge—how we are thrown into a readymade world. This is not a one-way street with fixed rules. Power is maintained by the repetition and reproduction of these systems—and when this reproduction is interrupted by the actions of individuals like artists and activists, their mechanisms of change begin to open. TAKEMOTO: You first exhibited this work in 1989. How was it received in light of other artwork about AIDS? Could you talk a little bit about your own involvement in art and activism? LEMCKE: There was a certain moment in the art world during the late 1980s and early 1990s when art about AIDS was very visible and my work was a part of that moment. My model for an AIDS memorial for Harvey Milk Plaza in San Francisco was included in Media to Metaphor, curated by Robert Atkins and Tom Sokolowiski in 1987, and several of my paintings based on The Wizard of Oz were included in Group Material’s

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AIDS Timeline presented at the Berkeley Art Museum in 1989 and the 1991 Whitney Biennial (Fig. 6-7). Ironically, The Wizard of Oz, which was the most private and personal work that I made as a gift for a friend who had recently been diagnosed with HIV, became my most public work. There was a timeliness about AIDS artwork that grew out of a sense of urgency as well as feelings of anger, fear, and confusion that cut deeply into the heart of our lives. It was within this framework that much of the iconic work about HIV/AIDS was created. Today, people are looking at the work of that period again, or maybe even discovering it for the first time. It is a painful part of American history that I think a lot of Americans would like to forget. But it’s also a significant part of our queer history and identity, which is exactly why Art, AIDS, America was such an important exhibition. TAKEMOTO: Can you talk a little about your own experiences in the early days of the epidemic and how it influenced your art? LEMCKE: In the early 1980s, when people didn’t even know HIV/AIDS was a virus, it was reported in the news as a gay cancer. In 1982, I remember being in the Castro and seeing an image, taken by local photographer Rink, in the window of Star Pharmacy. It showed a close up of a Kaposi’s sarcoma lesion with a caption about a mysterious cancer that seemed to be affecting gay men (Fig. 8). I can’t express to you the sense of panic that was in the air. I distinctly remember that moment, looking at that photo with a group of people on the street. It was pretty terrifying. The mainstream media did its best to keep the general panic directed at gay men, so we had to turn to alternative news sources. In San Francisco, The Bay Area Reporter (B.A.R.) was a local source of news, treatment information, and personals. The obituary section in the back of the paper sometimes went on for several pages. I vividly recall going through this section and cutting out pictures of people I knew or even recognized. I’d say to myself, “Oh, I knew him,” or “That’s the guy from the video store.” I kept these pictures in a box. Years later, in 1995, I was invited to be in a 20-year retrospective of Southern Exposure Gallery in San Francisco. I was reading Derrida’s book Cinders and thinking about embers, cinders, and ashes. I decided that I wanted to recreate the idea of an obituary section within the exhibition itself to commemorate the losses that occurred during the lifespan of the gallery. Using the pictures I had cut from the B.A.R. obituaries, I lit each one with a match and as it burned I laid the burning ember on the canvas. I put out the flame with dripping beeswax and titanium white oil paint until the ashes were encased and partially erased or obscured (Fig. 9-10). I repeated this process until I used all of the obituaries.

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TAKEMOTO: Derrida suggests that “no cinder exists without fire” and that the cinder is both a bodily trace and a reminder of the flame that can never be restored. LEMCKE: That’s exactly what I was getting at. Even now, the materials in the painting are still changing with age. As the wax becomes darker, the faces are harder to recognize. I think the fact that the piece is still transforming itself over time makes it more poignant and meaningful. TAKEMOTO: Your work slows down the grieving process by encasing the portraits in beeswax. We can still see some of the fragments of faces but we are also bearing witness to the loss of lives that can never be restored. Are you also engaging with the unrepresentability of loss? LEMCKE: Yes. I was inspired by Jean-Francios Lyotard’s idea of the “immemorial” which he describes as “that which can never be remembered (represented to consciousness) nor forgotten (consigned to oblivion). It is that which returns uncannily.” TAKEMOTO: Immemorial is also the title of a performance piece that you did at the de Young Museum in San Francisco. LEMCKE: In 1992, I was invited to do a performance at the de Young for Day Without Art, a day of action and mourning responding to the AIDS crisis. There were two parts to Immemorial. The center of the installation was a 17 x 17 foot steel garden that I unceremoniously assembled in the museum courtyard. Then I enacted a die-in with de Young staff and visitors (Fig. 11-12). During AIDS protests, people would perform die-ins by falling down on the ground as others drew their outlines in chalk. The trope was taken from police crime scenes and was meant to represent the place where a dead body was found. In the context of an AIDS demonstration, it was a political action that symbolized the lives lost in the epidemic. TAKEMOTO: Unlike being in the midst of a protest that is moving down the street, your performance enabled people to experience a die-in within a quiet, intimate space where participants and viewers had the opportunity to literally slow down and contemplate their actions. Can you describe the experience? LEMCKE: I remember being completely absorbed in the performance. Most of the time I was just interacting with one other person while viewers

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watched from the edges. For the people who let me draw the outlines of their bodies, it felt like they were making a personal, sincere statement by collaborating with me--politically and emotionally. The performance went on for several hours until we formed a huge chalk circle of body outlines. The die-in became more symbolic than the ones that I had participated in on the street because it was happening as a memorial within this privileged institutional space rather than in front of the FDA building or a political target. But the action felt just as significant. Ten years after the performance, I made a short experimental documentary in which I juxtaposed footage from Immemorial with my documentation of the ACT-UP die-ins taking place on Market Street and Castro in the early 1990s (Fig. 13). The video now serves as both a record of activist history and an art event observed from a distance. Seeing this footage side-by-side reminds us that the missing lives, the absence circumscribed by these bodily traces cannot be restored or resolved—the immemorial. TAKEMOTO: In your video installation The Uninvited, which is also in Art AIDS America, the shadow puppets seem to echo this idea of the missing or absent body, too. How did you develop this piece? LEMCKE: I was reading Julia Kristeva’s The Powers of Horror and I wanted to do a piece about abjection – the experience of being cast out or the experience of an irreconcilable state that one can’t come to terms with. On the surface, the narrative is about a Vietnam veteran suffering a mental collapse or PTSD. He is homeless and possibly has HIV/AIDS. The specifics of the character’s life and places he describes are purposefully left ambiguous. The piece tries to bring the viewer into his state of irreconcilable dissonance of body, place, and memory. It visually references the Balinese shadow puppet theater. For my version, I created anthropomorphic figures from found materials and showed their shadows performing a type of ceremonial dance while the lines of a poem slowly reveal themselves on the screen (Fig. 14-15). The poem is about the collapse of meaning that comes with the loss of connection to the body and to one’s sense of home. Lines such as “What foreign place is this?” or “My America - Maybe it was something I saw on T.V.” appear and disappear from the screen. The “sweet, poisonous” music referred to in the poem is echoed in the soundtrack evoking the nightmare of cultural and physical invasion and the untranslatable voices and shadows that haunt him. I originally made The Uninvited as an interactive computer-based artwork in 2003. But the technology that I used to develop the piece as a CD-ROM using Adobe Flash fell out of fashion and the format for showing

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it became technologically obsolete. In 2006, I remade The Uninvited as a single channel video installation that interacts with the audience in a different way. The projector for the installation is placed on the floor so that the viewers have to walk in front of the projector. In order to see the piece, the viewers also momentarily become one of the shadows on the screen. The Uninvited has had three iterations since I first created it, including a standalone single channel video. TAKEMOTO: Can you describe this shift toward experimental video and new media? How did it affect your work? LEMCKE: I saw new media as an extension of the way I had been making art – about presenting fluid presentational systems that the viewer interacts with to bring about a unique aesthetic experience. It’s always been more about foregrounding systems than it has been about producing a final form and object. Software applications and creative coding have replaced the performance scores and installations. TAKEMOTO: How do you see the relationship between the work you did about AIDS and the work you have done since? LEMCKE: To put it very simply, my work about AIDS returns “uncannily” in everything I do. In 2015, I worked on a short film called (Orpheus) The Poetics of Finitude. This experimental video weaves together my anime-style fairytale version of the Orpheus myth with excerpts from Jean Cocteau’s surrealist film Orpheus (1950). In my version of Orpheus, I am foregrounding the idea of human finitude and understanding one’s mortality as the moment of individuation and coming into our unique awareness of the self and identity. This is a slightly different reading than Cocteau’s in which he is trying to grasp the source or meaning of the poetic. For him, the poetic is understood in the context of transgression in terms of desire and death. I don’t think that either of these interpretations elides the other. But by placing these perspectives side-by-side, my video puts both readings of Orpheus into play. Together they offer a reckoning with death— with finitude—that brings with it a type of forgetfulness; and it is this hidden/revealed relation to death that is the source of the poetic and one’s authentic self. Getting back to your question, what I now understand about my postAIDS work is that I am still dealing with and will probably continue dealing with issues of political and personal rupture, memory, loss, and, to be honest, a certain melancholy that comes from living so “close to the knife”

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for so many years. The ghosts of the friends who have passed away still haunt me—not in a paralyzing way—but I feel their absence. Sometimes when I walk down Castro Street or see men in line for prescriptions at Walgreens or see someone that I knew from back in the day, it triggers a memory and the circumstances surrounding that moment in time. I think as individuals and as a community, we can move on after trauma, even after a crisis that has had a defining impact on our identity. But it’s not by forgetting or turning away that makes this movement possible, quite the opposite. It is precisely in that looking back, in the joyful preservation of what we have come to value from the past and a willingness to consider new ways of thinking and seeing that make the horizon of future worlds visible. TAKEMOTO: What is that horizon for you? LEMCKE: I guess I am still trying to see what can’t be clearly seen – some future “turning” within the present. In fall 2017, I was awarded an artist residency at the de Young Museum. I called the installation The New World. The work was centered on a video game called Pansy Farm where a determined fairy navigates the scene of a collapsed museum by blowing up icons of Modern Art. The game level repeats itself over and over until the player quits the scene. The fairy character is the same character that appears in the Orpheus video from 2015. It’s part of a new queer myth narrative structure that I’m working through in my recent work with game development (Fig. 17). In The New World installation, I wanted to think about the role of the museum as the archive of material culture and open the possibility of creating a new way of thinking about our relationship to it. It’s about rethinking how we write histories and our relationship to the past. The video game was projected on one of the walls of the gallery and on the opposite wall was a projection of the website of the Fine Arts Museum of San Francisco’s permanent collection. Over the course of the residence, I worked with the gallery visitors on new game level designs and on characters and how they interacted in these levels. The point wasn’t to reinvent the museum. It was more about breaking down fixed ways of thinking about history and memory. On the floor of the space was an array of 100 purple velvet pansies that were hand sewn for the installation. It took me months to sew the pansies. They represented the field of loss and absence upon which a new structure could be built. The pansy field is a conscious reference to the installation Immemorial that I created at the de Young for the Day Without Art in 1992,

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almost 25 years earlier. It was with a certain joyful irony that I was able to readdress the past and future. TAKEMOTO: Do you have any closing thoughts about contextualizing your work here or about being in this anthology? LEMCKE: The thesis of this anthology, as I understand it, is to discuss how the signification of epidemics and particularly AIDS are formed in and by our political and cultural discourses. It demonstrates how disease does not simply present itself as a biological process, but that it is the result of a complex system of knowledge that we actively shape in a process of something like co-emergence. The philosophical underpinning of this thesis about language and cultural production has always been at the core of my work and grew more focused because of the AIDS epidemic. I’m happy to have the opportunity to share my work in this way. The center of cultural gravity shifted during this period and would rewrite the history of American art and most certainly the history of my own life and art.

Bibliography Ault, Julie. Show and Tell: A Chronicle of Group Material (London: Four Corners Books, 2010). Blanchot, Maurice. The Gaze of Orpheus, and Other Literary Essays, trans. P. Adams Sitney (Barrytown, N.Y.: Station Hill Press, 1981). Cage, John. Silence: Lectures and Writings (Middletown, Conn.: Wesleyan University Press, 1961). Derrida, Jacques Cinders, trans. Ned Lukacher (Lincoln & London: University of Nebraska Press, 1991). Derrida, Jacques. Of Grammatology, trans. Gayatri Chakravorty Spivak (Baltimore, MD and London, UK: Johns Hopkins University Press, 1976). Foucault, Michel. The Archaeology of Knowledge: and the Discourse on Language, trans. Alan Sheridan (New York: Vintage Books, 1982). Foucault, Michel. The Order of Things: An Archaeology of the Human Science, trans. Alan Sheridan (New York: Vintage Books, 1994). Joyce, James. Finnegans Wake (United Kingdom: Faber and Faber, 1939). Katz, Jonathan David, and Rock Hushka. Art AIDS America (Seattle: University of Washington Press, 2015). Kristeva, Julia. Powers of Horror. An Essay on Abjection, trans. Léon S. Roudiez (New York: Columbia University Press, 1982).

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Readings, Bill. Introducing Lyotard: Art and Politics (London: Routledge, 1991). Shilts, Randy. And the Band Played On: Politics, People, and the AIDS Epidemic (New York: St. Martin’s Press, 1987).

EPILOGUE ANDREA PATTERSON AND IAN READ

As we send this book to typesetting, the coronavirus gains a deadly foothold worldwide. It reveals that we have entered a new era of epidemics. Before any of us had heard of COVID-19 or realized the world would change (or revert) so suddenly, Jonathan Katz wrote the foreword of this book. In many ways, it is an eerily prescient choice of epitaph evoking the now all too apparent issues with testing and quarantine. Katz describes epidemics as virulently splintering and cleaving. This virulence may be biological, like the transfer of a virus through sex, the invisible film of a touched surface, or a breath of air. Yet epidemic diseases are experienced mostly through their social virulence and exposure of pre-established hierarchies. Indeed, outbreaks are never egalitarian in their impact, and never cleave in the same way. People assumed to be “infected” or possessing the insidious power to “infect” can evoke violent fears that clutch to old prejudice. As Katz wrote, “beneath that lies an all too human desire to locate, name, enumerate and then excise the unknowable threats that haunt all existence.” With anxious eyes we look ahead, but we should also look back. Our current age of infectious diseases, including HIV/AIDS, Ebola, Zika, and those caused by the coronaviruses (SARS, MERS, COVID-19), can be blamed on greater and faster movements of people. Since the early modern era, history recorded two previous periods that were characterized by an increase in terrifying plagues. They have marked a significant stage of human migration and globalization. When the first Europeans and enslaved Africans crossed the Atlantic Ocean in the late fifteenth and sixteenth centuries, they unknowingly carried with them a set of destructive diseases that depopulated the Americas. The specific diseases that killed millions of indigenous peoples are uncertain; most probably they are smallpox, measles, and influenza. Europeans took advantage of the devastation to win wars, enslave, occupy, and settle. Beginning in the 19th century, revolutions in industry and transportation set into motion another wave of mass migration. Rapidly evolving urban

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centers became harbors for infectious diseases, among them cholera, typhoid, dysentery, tuberculosis, and influenza, that depended on a steady stream of mostly poor and desperate migrants for dispersal. This second period of epidemics helped create more activist governments and a wave of public health measures. Such changes were facilitated by an increased understanding of disease-causing microorganisms and revolutionary drug discoveries. Modern medicine and public health have vastly improved control over infectious diseases, reduced mortality rates, and extended life spans, especially among the wealthier countries. The third and current era of new epidemics began with the AIDS pandemic in the 1980s. Environmental degradation, poaching, wildlife trades, and hyper-globalization increasingly provide fertile grounds for outbreaks that are less likely constrained to nations or regions. The viruses causing HIV/AIDS, Ebola, Zika, SARS, MERS, and COVID-19 have “spilled over” from animals to humans, threatening global populations. As more vectors carrying pathogens invade new hosts, older and more familiar scourges such as yellow fever, malaria, and dengue fever dramatically extend their regional threat, in part, as a result of climate change. Additionally, a multitude of infectious diseases is becoming increasingly difficult to combat with our miracle drugs as microorganisms rapidly evolve resistant strains. We confront alarming questions: What may curb the dramatic rise of infectious diseases? How are we to address and mitigate the devastation they may bring? COVID-19 painfully brings these questions into the public awareness, and many aspects of this unfolding pandemic reiterate the central message and findings of this book. Although SARS-CoV-2, the virus responsible for this disease, seems new and alien, it has a long evolutionary history. Coronaviruses are a large family of zoonotic pathogens (transmission from animals to humans) that are widely present in diverse bat and bird species. They have been a part of human and other animal life for millennia. Some research suggests an even more ancient viral lineage with a common ancestor for coronaviruses dating back millions of years.1 These viruses likely sparked epidemics in the past, some that historians might have “retrospectively diagnosed” as something else, like influenza.

1

Joel O. Wertheim, Daniel K.W. Chu, Joseph S. M. Peiris, Sergei L. Kosakovsky Pond, and Leo L. M. Poon, “A Case for the Ancient Origin of Coronaviruses,” Journal of Virology 87, no. 12 (June 2013): 7039–7045. https://doi.org/10.1128/JVI.03273-12.

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As the current coronavirus pandemic so terrifyingly demonstrates, a virus is much more than a phylogenetic “curiosity.” The discussion of Ebola (chapter 13) vividly illustrates that the terror of an epidemic “should not be assumed to lie in the genetic mutation of the organism itself, but rather in the pathways we humans create for it.” COVID-19 is undeniably the result of biological and ecological processes, yet as is true in this pandemic and the other plagues described in this volume, social, economic, and political forces can facilitate or curb pathogenic development. While we may be far from understanding the biochemical and physical processes leading to this coronavirus infection, we experienced, early on, the tremendous impact cultural, economic, and political climates can have on its containment and treatment. For example, fear of political repercussions prevented and delayed essential communications about the initial COVID-19 outbreak between the local and central governments in China, and subsequently between China and the international community. Similarly, in the early 1990s, AIDS killed hundreds of thousands in Henan Province, China (chapter 8). Corruption, deception, and inefficiency characterized government responses to the epidemic that were aimed to please Beijing’s political leadership rather than secure the health of citizens in the province. Thus, plasma collection stations were not closed, despite the known risks involved. A suicide epidemic of mostly young people in Oceana (chapter 2) presents another case where local health and healthcare were structured to serve larger, distant bureaucratic interests. In the 1980s, academics and state officials, blinded to the root causes of the deaths in unequal world systems and colonialism, used the tragedy to reinforce those systems. We witnessed the rapid global spread of COVID-19 with fear of economic repercussions dictating inadequate policies for its containment in the early stages of the disease. As a result of not following the advice for containment and social distancing from governments that dealt with the first wave of deaths from this pandemic, western societies have thus far experienced a higher fatality rate and will face far-reaching social, economic, and political consequences. Considerations that place economic profits over community health are often (if not generally) at the core of epidemic diseases. The pursuit of profit may give opportunities to pathogenic disease, and it can slow reaction when the trade-off is its containment over revenue. When afflictions are born from consumer habits and mass marketing that make multinational corporations or governments trillions in profits or tax revenues, the trade-off is almost impossible. By way of illustration,

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COVID-19 is taking many of its victims from people who suffer preexisting conditions, including complications from smoking, poor diets, and sedentary lifestyles. If the coronavirus is a killer, then “Big Tobacco,” “Big Food” and “Big Pharma” that mass-produce and manipulate people into habitually consuming their products are accomplices to the crime (chapter 9). Major corporations have used obfuscation to deny the science that exposes their role in driving epidemic disease (chapter 10). Similarly, opioids and guns claim millions of lives worldwide every year, because they have been so accessible and promoted by special interest groups vested with medical and political authority. Social repercussions and stigmatization of individuals (regardless of their infection status) began well before the World Health Organization declared COVID-19 a pandemic in March 2020. Politicians and pundits implied entire regions as “diseased” through labels such as “Chinese virus” or “Wuhan virus.” We have since seen a rise in hate crimes against Asian Americans, attacks on foreigners in India, increased antagonism between rural and urban populations, and younger and older generations. Hate and blame are familiar features of epidemics, as evidenced in the discussion of incarceration and sterilization policies directed at leprosy patients in Japan (chapter 3). Behavior protocols are also less successful when patients are subject to bias, judgment, and discrimination, factors directly linked to increased HIV transmission rates in Latino gay communities (chapter 5) and African-American women experiencing addiction, violence, or homelessness (chapter 6). Nevertheless, stigmatization already complicates the tracing of those infected with the coronavirus disease. COVID-19 equally reveals how poverty and race expose vulnerabilities in disproportionately contracting the disease, in the unequal access to healthcare and treatment, and the drastically disparate survival rates. This volume provides useful and relevant analyses of how epidemics impact marginalized groups (due to culture, race, gender, class, sexuality, and region) and discusses alternative and promising treatment strategies to counter these effects, as exemplified in community-based participatory research. It is too early into the COVID-19 pandemic to comment on “best” practices for prevention, diagnosis and containment, nor do we want to speculate on the trajectory for treatment and drug development. The discussions in this volume illustrate the complex web of knowledge production, socioeconomic conditions, and power relations that control the fight against epidemic diseases, particularly in the initial response and early phases of

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drug development (chapter 7). What has become abundantly clear, however, is that an acute international shortage and the lack of foresight to create sufficient national emergency stockpiles of basic protective gear are now killing front-line health workers. This is rather incomprehensible given our recent experiences and unpreparedness with Ebola in Western Africa (chapter 13) or pandemic influenza. In fact, some of the wealthiest nations appear as helpless in protecting this crucial first line of defense in the case of COVID-19 as we were with SARS in 2003 and Ebola in 2014. COVID-19 provides another instance of how the physical and ideological worlds are invariably linked. In this pandemic, like others, nature and society interact to create, sustain, transform, or contain the disease. As we live (or partly re-live) this pandemic, few would argue that one discipline alone can or should make sense of it. It certainly commands the broadest of approaches, an openness to ideas, and far-reaching collaboration of experts from across vastly different fields. In this volume, we have called this approach radical interdisciplinarity. We contend that identifying, surviving, or controlling epidemics requires more than a collection of diverse (autonomous) disciplinary insights. Instead, we should create conceptual connections and integrate knowledge. For example, a collaboration of research in microbiology, immunopathology, clinical epidemiology, genetics, and mathematical modeling to provide both the knowledge and technology for a vaccine. We also depend on political scientists and experienced diplomats to guide us at a moment that, in the words of United Nations Secretary-General António Guterres, “has no parallel in the recent past.” Policy decisions to address this crisis need to be informed by the critical insights historians can provide beyond the recent past. What can we expect to see in an increasingly interdependent and hyper-national world? At a time when we move more rapidly towards an ever more virtual world in which the existing inequalities of the real world may be amplified? Such questions matter for sociologists. They are equally relevant for psychologists who study human reaction in the face of shared external threats. Additionally, artists, linguists, and behaviorists collectively contribute to our understanding of the many diverse impacts social distancing may have: through the creation of images that give shape to a shared meaning and by analyzing actions that are expressed within norms. A global phenomenon requires a global response. If we embrace open borders, affordable travel, and global supply chains, then societies will have to make tough choices by somehow balancing security with liberty. This

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book draws attention to just how precarious and devastating these decisions can be. COVID-19 already evokes a climate of fear in which everyone can be seen as a potentially infectious body. Reminiscent of other epidemics, it can turn people and countries against each other, intensify ideological divides, deepen racial and class tensions, and reverse social, economic, and political progress around the world. Still, we are witnessing extraordinary acts of heroism in the COVID-19 pandemic, in particular doctors and nurses struggling to save lives when a lack of simple protective gear endangers their own. As in other crises, there is potential for unity as grassroots volunteers, billionaire philanthropists, and nations are coming together to provide services and goods. Pandemics eventually end. Today, this may occur within globally interconnected scientific and laboratory systems that share scientific knowledge. Nonetheless, its implementation requires international norms and efforts, as is the case with vaccination and therapeutic protocols. We have learned from the recent past that success is rarely the result of a teleological march of scientific progress, but rather depends on multiple institutional forces interacting. “Success” may be fully containing pathogens (e.g., smallpox), transforming them with therapeutics into far less deadly diseases (e.g., HIV), and mitigating and monitoring seasonal or endemic threats to which we have no cure (e.g., influenza). To find appropriate resolutions, we need an interdisciplinary approach that focuses on innovative ways to address collective human suffering and encourages inclusive participation to identify and combat these formidable biosocial forces. This approach is not secondary to pathology nor independent from epidemiology. When we challenge established power relationships, redefine the hierarchical flow of knowledge production, and bridge the gap between the biophysical and cultural environments, we will affect some control over how epidemics shape us and we shape them. —Orange County, California, May 2020

INDEX

A abolitionism, 44, 56 abstention, 256 action at a distance, 65 Aids Coalition to Unleash Power (ACT UP), 173-174 acute infectious diseases bubonic plague, 21, 29, 308, 313, 319, 341 cholera, 29, 92, 112, 125, 126, 293, 308, 312, 313, 319, 345, 378 diphtheria, 92, 119, 242 dysentery, 50, 92, 112, 125, 126, 207, 378 scarlet fever, xv, 92, 126 smallpox, 7-8, 21, 29, 31, 50, 92, 119, 123, 242, 308, 311, 313, 319-321, 332, 345-348, 352, 377, 382 typhoid, xv, 50, 92, 112, 116, 117, 121-126, 242, 378 typhus, 92 see also Black Death; black plague adaptive immunity, 295 adenosine monophosphate (AMP), 270, 349 adenosine triphosphate (ATP), 266, 270, 272 Aedes aegypti, 29 Agassiz, Louis, 313 AIDS grapevine, 202 AIDS-associated retrovirus (ARV), 201, 236 Al-Razi, Muhammad ibn Zakariya (Rhazes), 21, 347 alcoholic fatty liver disease, 271, 273

alcoholism, 67 alpha interferon, 199–200, 205–206 American Association for the History of Medicine (AAHM), 320, 351 analogy on the value of, 177, 340, 353 pharmacological, 156 Annaes da Medicina Pernambucana, 311–312 anthropology, 14, 69, 83, 110, 112, 115, 134, 154, 252, 328–329 Anti-Tuberculosis League, 125 antimetabolite concept, 207–208, 216 antiretroviral therapy (ART), 133134, 168 archaeogenetics, 21, 355 Archivo Medico Brasileiro, 312 Athens, 242 Atlanta, 114-115,121-122 Atlanta Constitution, 118–124 Atlantic slave trade, 49–53, 56 azidothymidine (AZT), 22, 197– 198, 206–209, 214–215 B Bacillus anthracis, 293 bad genes, 128 Baghdad, 347 Ball, Charles, 53 Barbot, Jean, 46 Beaumont, J. A., 317 Beauveria bassiana, 299 behavior protocol, 380 Bicknell, John, 43–44 Big Food, 24, 254, 278, 380 Big Pharma, 24, 254, 380 Big Tobacco, 24, 254, 282, 380

384 biological clocks, 334 biological inferiority, 110, 112-113 biomedicalization, 157–158 biomedical protocol, 23 Birmingham, 125 bisexual men, 18, 100, 132, 134, 136, 139, 141-146, 149, 151, 158-160, 173 Black Death, 29, 319, 336, 341, 344, 347 black people, 5, 14-15, 42–44, 48, 110–128 see also people of color black plague, 92-93 Blair, Steven N., 277 blood stations, 225–227, 230, 235 see also China Bloomberg, Michael, 278 Boas, Franz, 115 Bois, W. E. B. Du, 112–117, 123, 125 Bowles, John, 79-80 Broder, Samuel, 203, 205, 206-207, 214 bromodeoxyuridine, 206 Buddhism, 89–90 C Cage, John, 365-366, 368 Caldcleugh, Alexander, 310, 317 capitalism, 3, 15, 244–245, 253– 254, 258, 260 captivity, 52, 56 Carbohydrate Responsive Element Binding Protein (ChREBP), 273 cardiovascular disease, 25, 242, 263, 265, 270–271, 275, 281, 304 Carrasco, Gabriel, 315 Casper, Stephen, 351, 353 Center for Disease Control and Prevention (CDC), 24, 34, 135, 137, 152, 159, 173, 210, 217, 267, 271 Chadwick, Edwin, 249 Charles Rosenberg, 322

Index China AIDS epidemic in Henan, 13, 15, 23, 222–341, 379 blood donors, 224-230 government response, 231-239 Model Villages, 236-237 cholera, 21, 29, 34, 92, 112, 125, 126, 312, 313, 345, 378 Civil War, 31, 44, 329, 338, 343 civilization, 13, 91–94, 308, 310 climate and health Chile, 307-308 Brazil, 309-314, 319 Argentina, 29, 308, 315-318, 319, 321 co-evolution, 302-304 collectivization, 253 colonialism, 3, 13, 31, 49, 64-69, 71, 75, 82-83, 88, 91, 98-99, 105, 244, 309-310, 321, 329-330, 379 combination therapy, 197–199,210– 216 communism, 3, 246 community based participatory research (CBPR), 169-170, 380 definition, 176-178 photovoice, 19, 23, 178-188 principles, 177 limitations, 189-190 confinement, 44, 87–93, 99–102, 105 consilience, 9, 32 constructiveness, 21 contagious diseases, 119, 124-125 see also HIV/AIDS; Ebola; Covid-19; acute infectious diseases cordons sanitaires, 342 correlation, 27, 201, 274 Covid-19, 3, 239, 293, 377-382 stigma and prejudice, 380 Crane, Jasper, 246 criminalization, 87, 105 Crisis, 3, 15, 77, 82, 116, 125, 224, 282, 329, 340, 351, 367, 371, 381

The Shapes of Epidemics and Global Disease Crummett, Lisa, 16, 25, 263 curb disease, 114, 127 cytomegalovirus (CMV), 211 D Darwin, Charles, 310 Day, Thomas, 43–44 de Clercq, Erik, 203–204 de Vasconcelos, Bernardo Pereira, 311 democratic germ theory, 128 Derrida, Jacques, 367 diabetes insulin resistance, 266-268 pandemic, 265-266 prevention, 280-283 research, 275-279 sugar, 25-26, 268-275 type 1 diabetes (T1D), 266 type 2 diabetes (T2D), 25, 265– 267, 271, 274–275, 278–283 diacylglycerol (DAC), 270 disarticulation, 56 discrimination, 6, 18, 87–88, 102, 111, 125, 128, 135, 172–173, 257, 380 diseases emerging, 3, 328, 332–333, 336, 339 new disease, 199, 205, 216, 313, 322, 329, 333, 340 tropical, 26, 205, 354 vector-borne, 346 viral, 199, 336, 339 Disturnell, John, 312–313 Dobzhansky, Theodosius, 304 Douglass, Frederick, 46–47, 53 drug development, 22, 214, 380-381 Drosophila melanogaster, 28, 34, 297–300 Dying Negro, The, 42–44, 58–59 dyslipidemia, 265, 273, 275, 279, 283

385

E Ebola Ebola Virus Disease (EVD), 3032, 329, 338, 293, 343, 346 history, 335-339 historical methods, 351-355 outbreak in 2014, 330-334, 343 teaching notes, 333, 335 West African Ebola Crisis, 329, 351, 353 ecosystems-disease interaction, 7-8, 20, 27 ecology, 28 economy, 245, 252-254 capitalist, 253 global, 78 market, 224, 252-254 plasma, 224, 228, 234-235 political, 248, 258 Elion, Gertrude B., 198 emancipation, 17, 19, 103, 169–171 Embree, Edwin R., 119 embryonic development, 298 environmentalism, 254 epidemic cough, 2 epidemic disease, 1, 4, 6, 8–10, 14, 20, 22–30, 48, 119, 128, 200, 314, 340, 344, 355, 377–380 epidemics co-emergence of, 30–32 compared to endemic, 2 control of, 17-20, 212-217, 382 co-resolution of, 30–32 culture and meaning, 6-7, 10-11 definition, 1-3, 47 emergent, 31, 330 empowerment, 18-19, 143, 154156, 169-171, 176-177, 179, 368 fuel diseases, 23 ideology, 13–15 matter and physicality, 7-8, 20– 21 post-colonial circumstances, 64– 65 shaping of, 11, 13, 20–22, 28

386 social stratification, xvi-xvii perception of, 12-14, 48-49, 56, 322 transformed, 15–17 see also, archaeogenetic; genetics; retrodiagnosis; scientific discovery; epidemiological change, 307 epidemiology, 2, 12, 18, 25–28, 171–172, 242, 252, 267, 332, 381–382 Epstein, Steven, 174 Errázuriz, Eduardo Lira, 315 eugenics, 13 American South, 119 Eugenic Protection Law (EPL), 97–98 Japan, 88, 94-95 expert network, 71-74, 81-83 selves, 66

Index

F fatty liver disease, 265, 271, 273 Federation of Leprosarium Directors (FLD), 102–103 Federation of National Leprosarium Patients (FNLP), 100–103 Fellowship of Churches, 70 first AIDS cases, 201 Fontdevila, Jorge, 17, 132, 138, 140, 143–144, 152 Foucault, Michel, 251–254, 260, 364–365, 369, 375 fraudulent nucleosides, 208 Fresh Air Camp, 124 fruit flies, 27, 297–299, 303

gay-related immune deficiency (GRID), 21 gene therapy, 128 genetics, 6-7, 28, 110, 127, 297-303, 334-338, 355 diverse populations, 303 engineering, 200 mutation, 348, 379 Georgia, 121 germ theory, 111, 117, 128, 250– 251, 293 Gire, Stephen K., 334–335 global disease, 9, 329–330, 344–345, 352 economy, 78 causes of death, 264 health, 31, 223, 227, 252–253, 259, 299 Global Action Plan, 243, 255–256 Global Energy Balance Network (GEBN), 277 globalization, 2, 17, 65, 74–75,82, 252, 258, 307, 330, 332, 377– 378 Goldberger, Joseph, 119 Gomes, José Caetano, 309 government, 65–66 government at a distance, 64–66, 74, 82 governmentality, 65–66, 81–82, 251–254, 260 Graham, Maria, 313–314 Green, Monica H., 9, 30, 328, 330, 332–333, 336, 344, 347 Guinea, 309, 329, 331, 334–336, 342, 344, 351, 354–355 gun violence, 24-25

G Gao, Yaojie, 222, 227–233, 238 Garrett, Laurie, 332 Gasquet, Clélia, 339 gay community, 156, 210, 331, 380 gay medical grapevine, 202

H Hand, Gregory A., 277 Hansen's Disease Prevention Act, 102 Hansen, G. A., 87 health transformations, 183

The Shapes of Epidemics and Global Disease healthcare policies as result of scientific discovery, 127 community, 13, 19, 379 colonial power, 88 discrimination, 6, 10, 17, 87, 102, 104-105, 111, 116, 124-128 expenditures (USA), 263 individual responsibility, 11, 15, 19, 141-144, 158 inequity, 14, 100, 110–111, 113, 115, 379 integrative, 174 infrastructure, 353-354 meaning in context, 18 neoliberalism, 79, 252-253 healthcare workers, 329, 341–342, 348 heart diseases, 113, 128 heterosexualization, 144 Hezel, Fran, 67, 71 high blood pressure, 265 Highland Papua New Guinea, 73 Hirsch, Martin, 213 Hitchings, George H., 198, 208 Hitchings-Elion antimetabolite research program, 211 HIV/AIDS, 134–136 activism, xv-xvii, 32, 173-174, 207, 217, 368-369 Age of Global Health, in the, 224–225 arts, 1, 10, 32-33, 364-374 as “cancer”, 199-202 drug treatment, 197-199, 213, 216 Henan Province, 23-24, 224–225 immigration, 18, 139-143, 158 history, 348-51 liminal spaces, 151-152 poverty, 19, 23-24, 135, 169, 172, 181 prevention, 137–140, 142 stigma and prejudice, 139, 144, 151, 154-156, 159, 368

387

therapy, 22-23 see also alpha interferon, antimetabolite; AZT; combination cocktail; HPA-23; protease inhibitors; reverse transcriptase inhibitor; suramin vulnerable populations, xvi, 17, 132, 137, 157-159, 169, 172, 175, 189, 210 Hoffmann, Jules A., 298 hookworm disease, 113, 120 Hotez, Peter J., 354 HPA-23, 199–206, 216 Huang, Yanzhong, 236, 239 Hudson, Rock, 202–203 human capital, 254 human immune system, 294-297 human immunodeficiency virus (HIV), 132–144 human T-cell lymphotropic virus-III (HTLV-III), 201, 203 humoral immunity, 296 hyperlipidemia, 26, 265 hypertension, 26, 265, 271 hyperuricemia, 275 I Igbo, 53–54, 56–57 immune defense, 28, 294–304 imperialism, 3, 5, 13, 21, 87-88, 91, 96 increased egoism, 77 industrialization, 249, 258 Indy, 52, 303, 317 inequity, 14, 100, 110–111, 113, 115 Infectious Disease Prevention Law (IDPL), 92 infectious diseases, 250, 263, 293– 294, 310, 333, 341, 346, 348, 350 infrastructure boosting project, 232, 236–237 innate immunity, 295, 298

388 insulin resistance (IR), 265–266, 268–271, 273–275 interaction ritual demands, 146, 148 interdependence, 7-8, 30-34, 322 interdisciplinarity, 4-5, 8, 33-34, 381 internal stigma, 184 International Diabetes Federation (IDF), 265 International Health Regulations (IHR), 341 Irarrázaval, Ramón Luis, 314 J Jackson Ward, 116 Japan, 13, 76, 87–106, 226, 380 Japan Leprosy Association (JLA), 100–101, 103 Jahrling, Peter, 336 Jefferson, 113 Jim Crow, 13–14, 110–112, 117, 121, 127 Julius Rosenwald Fund, 119 Justice Department, 70 K Katsuryô, Katakura, 90 Katz, Jonathan D., xvii, 32, 363 Kenny, J. A., 123 Kensuke, Mitsuda, 93–94, 96, 98, 100, 104 Keynesian-style interventionism, 253 Kikwit, 332 King, Nicholas B., 328, 354 Kinshasa, 352 Koch, Robert, 293 Korea, 27, 88, 98–99, 105–106 Kramer, Larry, 331 Krieger, Nancy, 171, 173 Kuper, Adam, 75 Kyoto community, 91 L Lancet, The, 202, 331 Lassa fever, 336, 348

Index Latino 18, 132, 136-139, 144-145, 151-158, 160 Lazarus effect, 215 Le Rodeur, 50–51 Leeuwenhoek, Antonie van, 293 Lemcke, Rudy, 9, 32, 34, 363 leprosy (Hansen’s disease) compensation, 104-106 confinement, 93-96 Federation of National Leprosarium Patients (FNLP), 100-103 Japan, 87-106 Korea, 99 Leprosy Prevention Association (LPA), 96 Leprosy Prevention Law (LPA), 89, 94, 96 Mycobacterium leprae, 87 sterilization, 94-97 stigma and prejudice, 92, 104 Taiwan, 98-99 treatment, 98 see also promin Lesch, John E., 3, 13, 17, 22, 33, 196, 207–208, 211 liberalism, 244, 246, 248, 260 Liberia, 329, 336–344, 351 Liu, Qian, 222–225, 232–238 Liu, Xiaoxing, 15, 23, 222 Locke, John, 244 lockjaw, 28 Louisiana, 117 low density lipoprotein (LDL), 270, 272 Lowe, Edward, 11, 27, 64–65, 68 lymphadenopathy-associated virus (LAV), 201-202 Lynteris, Christos, 328–329 M MacKenna, Juan, 307, 314, 321 Macpherson, Cluny, 73, 77 Macpherson, La'avasa, 73, 77–80 malaria, 5–6, 112, 116–117, 299, 319, 345, 348, 350, 354, 378

The Shapes of Epidemics and Global Disease malignant diseases, 215 Mann, Jonathan, 168 Masayoshi, Yamaguchi, 101 Meiji period, 91 melancholy, 52, 373 Messac, Luke, 223 metabolic disease pandemic, 263, 265, 267, 269, 271 metabolic syndrome (MetS), 25–26, 265–273, 280 methuselah, 303 microbes, 9, 24, 27–29, 293–296, 321–322, 354 microbiology, 16, 110, 117, 127, 250, 336, 350, 381 Micronesia, 64, 67–77, 81–82 Micronesian Independent, 67 Micronesian islands, 12, 64–65, 73, 105 microorganisms, 15, 111, 117, 200, 250–251 Middle Passage, 46-53 Miller, Peter, 64–65, 251 Ministry of Health and Welfare (MHW), 97, 101–103 Mitsuya, Hiroaki, 203 model organisms, 297 modernity, 12, 68–71, 74–83, 88, 242, 244 Monogatari, Oden, 93 monoyoshi, 90–91 Montgomery Advertiser, 119 multi-sectoral action, 257 Murillo, Adolfo, 315 mutualism, 294 mycobacterium avium complex (MAC), 68, 211, 315, 320 Mycobacterium leprae, 87 N National Hansen's Disease Museum, 104 National Health and Nutrition Examination Survey (NHANES), 265, 267, 271

389

National Health Interview Survey (NHIS), 267 natural killer cells, 296 Nazism, 253 neoliberal capitalism, 3, 15, 260 governmentality, 251 political rationality, 251, 254– 255, 257–259 neoliberalism, 79, 143, 160, 245, 251–253 Nesse, Randy, 302 New World, 6–7, 309, 313, 321, 350, 355, 374 New York, 231, 278 New York Times, 71, 76, 276-277, 338, 341 New Zealand, 12, 65–77, 81–82 Non-Alcoholic Fatty Liver Disease (NAFLD), 26, 268, 271, 273 non-communicable diseases (NCDs) cancers, 242 corporate role, 243-249 diabetes, 242 increase in populations, 242243, 264-265 prevention and control, 257259, 280-283 respiratory diseases, 242 North Carolina, 310 Nursing Outlook, 33 O obesity, 2, 26, 265, 270–283 chronic disease, 275 environmental causes, 243-244, 275 government intervention, 280282 individual/non-interventionist narratives, 277-279 metabolic dysfunction, 26, 265272 Oceania, 11, 64–83 Oliver, Denis, 69–74, 79–80 Onchocerca volvulus, 204

390 onchocerciasis, 204 Osborne, Elton S., 119 Ostertag, Wolfram, 206 outbreaks ancient, 21 animal infection, 338 prevention, 339 unexpected, 328 urban, 29, 331 see also epidemic oxidative stress, 269–270, 273 P paid blood donors, 224, 228 pandemic, 2, 9, 31–32, 59, 132,378– 382 see also NCDs; epidemics paradigmatic diseases, 348 paraquat, 27, 79-80 Pasteur, Louis, 293 pathogens, 3, 16, 28, 31, 134, 293– 299 Patterson, Andrea, 1, 14, 110, 377 Pauw, Cornelius de, 309 Peloponnesian War, 242 people of color discrimination, 18, 111-116, 124-129 poverty, 23, 31, 66, 115, 127, 135, 169, 172, 181, 331, 344, 380 stigma and prejudice, 119, 111, 116, 124, 126-128 see also Black people personal protective equipment (PPE), 342 Petty, William, 249 phagocytosis, 296 pharmaceutical citizenship defined as, 154 photovoice, 19, 23, 168, 170, 178– 183, 188–190 see also community based participatory research

Index picturing new possibilities, 181-182 plague, 3, 19, 34, 92–93, 341–346, 352, 355, 379 plasma economy, 224, 228, 234–235 pneumocystis carinii pneumonia, 198, 210, 212 Polynesia, 80 Portuguese America, 321 post-colonial, 12, 64, 67, 74-75, 8182, 329-330 poverty, 10, 23, 48, 115, 121, 135– 136, 172, 249, 331, 339, 344, 380 Prabhu, Krishna, 223 pre-exposure prophylaxis (PrEP), 18, 23, 139, 152–160, 168 PrEP wars, 154 promin, 16, 100 progressive era (U. S. South), 110– 111 protease inhibitors, 196–198, 212– 213 public health community, 111, 254 reflexivity, 12, 82-83, 169 service, 15–16, 111, 117–120, 127, 315 Q quarantine, 96, 342, 355, 377 R race drug, 128 racial discrimination, 111, 124-125, 128 health disparities, 125, 135-137, 169 segregation, 3, 125 racism, 10, 14, 19, 111–112, 115– 116, 127, 135, 169, 368 rational drug design, 206, 216 Read, Ian, 1, 29, 307, 310, 319–320, 377 recalcitrant native, 12, 64–83

The Shapes of Epidemics and Global Disease respiratory diseases bronchitis, 112 influenza, 112 pneumonia, 112 retro-diagnosis, 21 retroviruses, 22, 214 reverse transcriptase inhibitor, 209210 Revista Medica Fluminense, 312 Ridell, Hanna, 92 Riichiro, Sawa, 94 risk groups, 174 ritual [sexual] cruising, 145-148 female ritual demands, 151 interaction demands, 146-148 moral demands, 149-150 required resources, 148-149 Robbins, Roland, 209 Robertson, William, 309, 313 Rockefeller Sanitary Commission, 117, 120 Rodrigues, J. J., 311–312 Roman, Charles V., 116 Rose, Nikolas, 65, 252, 260 Rubinstein, Donald, 71 S Samoa, 12, 27, 64–83 Samoan Health Department, 70 SARS epidemic, 236, 238–239 Schnirring, Lisa, 331 Schweitzer, Albert, 93 scientific discovery, 15-17, 242 see also combination drug therapy; germ theory; promin Sea Surgeon, 52 sedentary behavior, 279 segregation [policies], 16, 90, 94-96, 98-105, 116-117, 121, 127 Sei-I Kai Medical Journal, 91 self-acceptance, 184–186 self-destruction, 46–55, 58 Sensai, Nagayo, 88 servants, 16, 120, 122

391

sexual behavior bisexual, 18-19, 136, 139, 141158 condoms, 147–148, 153, 181– 182 silence during, 139–140 men who have sex with men (MSM), 133-134, 136-158 sexual promiscuity, 18, 139, 152 sexually transmitted infection (STI), 133–136, 153, 155, 160 Shahrestani, Parvin, 3, 6, 13, 16, 27– 28, 33, 293 Shilts, Randy, 196, 202 ship Ruby, 52 SHOWeD technique, 180 sickle cell, 5-6, 114-115 Sierra Leone, 310, 329, 334–338, 342–344, 351 silence signaling trust, 158 Sino-Japanese War, 92 Slaton, Amy, 3, 6, 14, 17–20, 23, 26, 33, 168 slave suicide, 11–12, 43, 47–49, 53, 56–59 slavery, 5, 12, 42–59, 115, 311 enslavement, 5, 52, 56 enslavers, 47, 53–58 sexual and physical abuse, 5152, 56-58 Sloane, Hans, 51, 55 smallpox, 6–8, 21, 29, 31, 34, 123, 242, 319–321, 347–348 Smith, Adam, 244–245, 254 Snow, John, 293 Snyder, Terri L., 11, 42, 44, 48 social determinants, 10 social structures, 19, 169 socialization, 253 societal marginalization, 169 sociocentrism, 77 sociocultural, 18-19, 132, 134, 153154 South Carolina, 50, 53-54 Spanish America, 321 speculum oris, 56–57

392 stigma, 134–140 “filthy” blood disease, 122 humiliating favors, 124 notoriously syphilis-soaked race, 114 see also Covid-19; HIV/AIDS; leprosy; people of color; racism Stiles, Charles Wardell, 120 sucrose, 268–271, 279 sugar sweetened beverage (SSB), 271, 274, 276, 280–281 suicide, 42–54 Suicide Study Group, 70–71, 79 sulfonamide sulfamethoxazole, 211 suramin, 199, 203–206, 216–217 syndemics, 133–137, 158, 160 T table sugar (sucrose), 268–269, 271, 279 Takamatsu Memorial Museum, 104 see also leprosy (Hansen’s Disease) Takemoto, Tina, 32, 363 Technical Report Series (TRS), 277 Teti, Michelle, 3, 6, 14, 19–20, 168 tetanus, 28 Thames River, 42 Thompson, Tommy, 278 Together with treatment as prevention strategy (TasP), 154– 155, 158–159 Tokugawa Period, 90 Toll-like receptor (TLR), 298 Tonga Ilbo, 99 torrid zone, 309, 312–313 transmigration, 54–55 treatment adherence, 133, 136, 153, 157, 175, 183 optimism, 133 Tropic of Capricorn, 307–322 tuberculosis, 113–114, 117, 122– 125, 127, 135, 211–216 Tumor Necrosis Factor (TNF), 298

Index Tuskegee, 5, 113, 115, 123 typhoid, 50, 92, 112, 116–117, 121– 126, 242, 378 U UN Food and Agriculture Organization (FAO), 277 United States, 207, 209, 267, 269, 272, 274, 280–282 urban congregations, 344 urbanization, 29, 258 US Trust Territory of the Pacific Islands (USTTPI), 64, 67, 69, 72–75, 81–82 V vector-borne diseases, 20, 29, 244, 259, 299, 302, 322, 345-346, 378 Venus, 51 very low density lipoprotein (VLDL), 270, 273 Virginia, 50, 58, 123 Virginia Gazette, 58 Virginian-Pilot, 118 von Hayek, Friedrich, 246 W Ward, Martha, 69 Washington Herald, 119 waterborne diseases, 112 web of causation, 171 webs of matter, 20 webs of meaning, 6, 8, 10, 12, 19 Weiner, Michael, 13, 87 white supremacist, 14, 110, 113, 127 White, Geoffrey, 72–73, 79 Williams, George, 302 Wilson, R. M., 99 Wodak, Ruth, 4, 9 Woods-Fildes theory, 207–208 World Health Organization (WHO), 14, 168, 170, 200, 242–243 Y Yang, Joshua S., 14, 26, 242, 258

The Shapes of Epidemics and Global Disease Yarchoan, Robert, 203, 214 yellow fever, 29, 117, 127,308–313, 319, 340, 378 Yersinia pestis, 29, 341, 350 YMCA programs, 69 Yôkuin, 91, 93 Yoshinobu, Hayashi, 101

Yuki, Arai, 96 Z zoonotic disease, 32, 340 reservoir, 333 transfer, 345

393