Eating and Growth Disorders in Infants and Children [1 ed.] 9781452253176, 9780803936836

Citation preview

Eating and Growth Disorders in Infants and Children

Developmental Clinical Psychology and Psychiatry Series Series Editor: Alan E. Kazdin, Yale University

1: CHILD DEVELOPMENT AND PSYCHOPATHOLOGY by Donna M. Gelfand and Lizette Peterson 2: CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY by Magda Campbell, Wayne H. Green, and Stephen L. Deutsch 3: ASSESSMENT AND TAXONOMY

OF CHILD AND ADOLESCENT

PSYCHOPATHOLOGY

by Thomas M. Achenbach 4: INFANT PSYCHIATRY

by Klaus Minde and Regina Minde

5: SUICIDE AND ATTEMPTED

SUICIDE AMONG CHILDREN

AND ADOLESCENTS

by Keith Hawton

6: PSYCHOPATHOLOGY AMONG MENTALLY RETARDED CHILDREN AND ADOLESCENTS by Johnny L. Matson and Cynthia L. Frame 7: HYPERKINETIC CHILDREN

by C. Keith Conners and Karen C. Wells

8: LIFE EVENTS AS STRESSORS IN CHILDHOOD AND ADOLESCENCE by James H. Johnson 9: CONDUCT DISORDERS IN CHILDHOOD AND ADOLESCENCE by Alan E. Kazdin 10: CHILD ABUSE by David A. Wolfe 11: PREVENTING MALADJUSTMENT FROM INFANCY THROUGH ADOLESCENCE by Annette U. Rickel and La Rue Allen 12: TEMPERAMENT AND CHILD PSYCHOPATHOLOGY by William T. Garrison and Felton J. Earls

13: EMPIRICALLY BASED ASSESSMENT OF CHILD AND ADOLESCENT PSYCHOPATHOLOGY by Thomas M. Achenbach and Stephanie H. McConaughy 14: MARRIAGE, DIVORCE, AND CHILDREN'S ADJUSTMENT by Robert E. Emery 15: AUTISM by Laura Schreibman 16: NEUROPSYCHOLOGICAL ASSESSMENT IN CLINICAL CHILD PSYCHOLOGY by George W. Hynd 17: CHILD PSYCHOPATHOLOGY AND THE QUEST FOR CONTROL by Fred Rothbaum and John R. Weisz 18: DELINQUENCY IN ADOLESCENCE by Scott W. Henggeler 19: CHRONIC ILLNESS DURING CHILDHOOD AND ADOLESCENCE by William T. Garrison and Susan McQuiston 20: ANXIETY DISORDERS IN CHILDREN by Rachel G. Klein and Cynthia G. Last 21: CHILDREN OF BATTERED WOMEN by Peter G. Jaffe, David A. Wolfe, and

Susan Kaye Wilson

22: SUBSTANCE ABUSE IN CHILDREN AND ADOLESCENTS by Steven P. Schinke, Gilbert J. Botvin, and Mario A. Orlandi 23: CHILD PSYCHIATRIC EPIDEMIOLOGY by Frank C. Verhulst and Hans M. Koot 24: EATING AND GROWTH DISORDERS IN INFANTS AND CHILDREN

by Joseph L. Woolston

Eating and Growth Disorders in Infants and Children Joseph L. Woolston

Volume 24. Developmental Clinical Psychology and Psychiatry

SAGE PUBLICATIONS

The International Professional Publishers Newbury Park London New Delhi

Copyright © 1991 by Sage Publications, Inc. All rights reserved. No part of this book may be reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, without permission in writing from the publisher.

For information

address:

SAGE Publications, Inc.

2455 Teller Road

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SAGE Publications Ltd.

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Printed in the United States of America Library of Congress Cataloging-in-Publication Data Woolston, Joseph L. Eating and growth disorders in infants and children / Joseph L. Woolston. p. cm.—(Developmental clinical psychology and psychiatry; v. 24)

Includes bibliographical references and index.

ISBN 0-8039-3683-4 (cl).—ISBN 0-8039-3684-2 (pb)

1. Eating disorders in children. 2. Growth disorders. 3. Dwarfism I. Title. II. Series. [DNLM: 1. Child Development Disorders. 2. Dwarfism. 3. Eating Disorders—in infancy & childhood. 4. Growth Disorders—in infancy & childhood. 5. Nutrition Disorders—in infancy & childhood. W l DE997NC v.24 / WS 305.6 W916e] RJ506.E18W66 1991 618.92'8529—dc20 DNLM/DLC

FIRST PRINTING, 1991 Sage Production Editor: Diane S. Foster

91-32898

CONTENTS

Series Editor's Introduction Preface Acknowledgments 1. Overview o f Eating and Growth Disorders Major Controversies General Approach to Treatment Summary 2. Fundamentals of Normal Child D e v e l o p m e n t Biology of Physical Development Phenomenology o f Emotional, Behavioral, and Social

Development Summary 3. Failure to Thrive Natural History Diagnostic Classification and Special Treatment

Issues Summary

ix

xiii

XV

1

2

8

9

11

11

17

19

21

26

30

34

4. Psychosocial Dwarfism Natural History Diagnostic Classification and Special Treatment

Issues Summary 5. Rumination Natural History Diagnostic Classification and Special Treatment

Issues Summary 6. Pica Natural History Diagnostic Classification and Special Treatment

Issues Summary 7. Obesity Natural History Diagnostic Classification and Special Treatment

Issues Summary 8. Benign Nutritional Dwarfing Natural History Diagnostic Classification and Special Treatment

Issues Summary 9. Prepubertal Anorexia Nervosa Natural History Diagnostic Classification and Special Treatment

Issues Summary

37

38

40

41

43

44

46

47

49

49

51

52

53

54

60

62

65

66

67

67

69

70

71

72

10.

Conclusion

73

References

75

Author Index

87

Subject Index

93

About the Author

95

SERIES EDITOR'S

INTRODUCTION

Interest in child development and adjustment is by no means new. Yet, only recently has the study of children benefited from advances in both clinical and scientific research. Advances in the social and biological sciences, the emergence of disciplines and subdisciplines that focus exclusively on childhood and adoles­ cence, and greater appreciation for the impact of such influences as the family, peers, and school have helped accelerate research on developmental psychopathology. Apart from interest in the study of child development and adjustment for its own sake, the need to address clinical problems of adulthood naturally draws one to investigate precursors in childhood and adolescence. Within a relatively brief period, the study of psychopathology among children and adolescents has proliferated considerably. Several different professional journals, annual book series, and handbooks devoted entirely to the study of children and adoles­ cents and their adjustment document the proliferation of work in the field. Nevertheless, there is a paucity of resource material that presents information in an authoritative, systematic, and disseminable fashion. There is a need within the field to convey the latest developments and to represent different disciplines, ix

"

EATING AND GROWTH DISORDERS

approaches, and conceptual views on the topics of childhood and adolescent adjustment and maladjustment. The Sage Series Developmental Clinical Psychology and Psychi­ atry is designed to uniquely serve several needs of the field. The series encompasses individual monographs prepared b y experts in the fields of clinical child psychology, child psychi­ atry, child development, and related disciplines. The primary focus is on developmental psychopathology, which refers broadly here to the diagnosis, assessment, treatment, and prevention of problems that arise in the period from infancy through ado­ lescence. A working assumption of the series is that understand­ ing, identifying, and treating problems of youth must draw on multiple disciplines and diverse views within a given discipline. The task of individual contributors is to present the latest theory and research on various topics, including specific types of dysfunction, diagnostic and treatment approaches, and spe­ cial problem areas that affect adjustment. Core topics within clinical work are addressed b y the series. Authors are asked to bridge potential theory, research, and clinical practice and to outline current status and future directions. The goals of the series and the tasks presented to individual contributors are demanding. W e have been extremely fortunate in recruit­ ing leaders in the fields who have been able to translate their recognized scholarship and expertise into highly readable works on contemporary topics. In Eating and Growth Disorders in Infants and Children, Dr. Jo­ seph L. Woolston examines a topic that encompasses diverse dysfunctions, each with its own corpus of research on epidemi­ ology, etiology, diagnosis, and treatment. Among the disorders considered are failure to thrive, psychosocial dwarfism, rumina­ tion, pica, benign nutritional dwarfing, obesity, and anorexia nervosa. Approaches to understanding eating disorders and de­ velopmental issues serve to introduce the diverse dysfunctions. Subsequent portions of this book focus on the emergence and course o f specific disorders, known or suspected risk factors, descriptive features, and unresolved c l i n i c a l and r e s e a r c h

Series Editor's Introduction

xi

issues. The individual disorders are multifaceted and com­ plex. The book organizes an extraordinary amount of contem­ porary issues in a concise and yet comprehensive fashion. —Alan E. Kazdin,

Ph.D.

PREFACE

Eating and growth disorders in infancy and early childhood are clinically important problems whose study and elucidation will enrich our knowledge in diverse ways. These disorders provide a potential window into the understanding of the complex inter­ play among biological, intrapsychic, and interpersonal processes all unfolding over developmental time. Until recently, eating and growth disorders in this age group have been thought of, and described as, separate and distinct entities with little at­ tempt to group them together in a coherent fashion. In addition, each of the disorders has been studied by quite divergent dis­ ciplines that have tended to concentrate on one level of dysfunc­ tion to the exclusion of the others. For this reason, this monograph has been written with an initial chapter that sum­ marizes, in the briefest terms, normal physical and social/emo­ tional development. I hope this chapter will help the diverse readership to have a common basic understanding of these pro­ cesses. The subsequent chapters on specific disorders are in­ tended to be descriptive overviews of the existing extensive literature. In this way, the monograph is intended to provide a glimpse of the complex process of both normal and disordered eating and growth in the first decade of life. xiii

ACKNOWLEDGMENTS

I am grateful to Alan E. Kazdin, Ph.D., for his encouragement; to my wife, Sara Woolston, for her patience; and to Veronica Alex­ ander, for her secretarial support. I would like to acknowledge the invaluable collaboration with Fred Volkmar, M.D. I dedicate this work to my three mentors, Albert J. Stunkard, M.D., Sally Provence, M.D., and Albert J. Solnit, M.D., who stim­ ulated, nurtured, and supported my investigation in eating and growth disorders.

xv

1

OVERVIEW OF EATING AND

GROWTH DISORDERS

Eating and growth disorders of infancy and childhood are multifaceted phenomena that epitomize the complexity of body-mind-family interactions over time. T h e earliest investi­ gators in this field (e.g., Freud, 1946; Leonard, Rhymes, & Solnit, 1966; Lourie, 1955; Spitz, 1945) began to articulate vari­ ous aspects of these complex disorders. Unfortunately, de­ spite the meticulous nature of the clinical research that characterized the work of these writers, the subsequent re­ search and clinical treatment employed a more reductionistic approach by attempting to define specific pathognomonic signs and etiologic determinants for each syndrome. All too often, investigators responded to the complexity o f these dis­ orders by narrowly focusing upon specific dichotomies of eti­ ology, diagnosis, and treatment. This dichotomous approach obscured the necessity for an inclusive, comprehensive strat­ egy to better understand these complex disorders. In the past 15 years, investigators in early childhood devel­ opment and developmental psychopathology have provided data and techniques that now permit new understanding of eating and growth disorders. Even more important than new 1

2

EATING AND GROWTH DISORDERS

information about developmental sequences (e.g., Greenspan, 1981; Stern, 1985) has been the emergence of the concept of a multifactorial, transactional model of development (Sameroff & Chandler, 1975; Sameroff & Fiese, 1989; Woolston, 1989b). This model replaces the deterministic, linear causality model that postulated that each effect or developmental outcome had a single cause. Instead, the transactional model proposes that each person influences, and is influenced by, a large vari­ ety o f experiences that change continually over time. Al­ though complex and multifactorial, this process includes a sophisticated regulatory system that employs cybernetic fea­ tures of feedback and "feedforward" at multiple levels chang­ ing over time. Just as normal development in general, and normal eating be­ havior and growth in particular, are regulated according to this transactional model, so are the eating and growth disorders. Vir­ tually all of these disorders represent a final common pathway of diverse contributions at all levels of human experience. These contributions frequently include genetics, congenital factors, infant-parent relationships, physical, psychological, cognitive developmental family functioning, and social is­ sues. In turn, the resultant eating disorder may well exacer­ bate some or all of the initiating problems as well as cause new and even more maladaptive disturbances. Eating and growth disorders represent a closed system in which there is feedback between each "unit" of the system (Woolston, 1988).

MAJOR CONTROVERSIES Lumpers Versus Splitters Meaningful research in any natural science is founded upon classification of forms into stable, related groups. Frequently, classification is hampered by ignorance of entities or inaccurate theories that distort observation. Once successful classification

Overview of Eating and Growth Disorders

3

begins, it permits investigation into primary relationships, which then allows for more accurate classification. This syn­ ergy between classification and functional understanding can promote rapid advance of knowledge once this classification process is accurate (Woolston ck Riddle, 1990). The beginning of this process may be marked by a debate between "lump­ ers," who propose to group each new form as variants of ex­ isting, larger categories, and "splitters," who advocate them as separate entities (Holland, 1904). The study of eating disorders of childhood remains in the beginning stage of this process because it has been plagued by a paucity of basic phenomenological data and persistent diagnostic confusion. For example, as a result of a mistaken theoretical framework, failure to thrive (FTT) and psychosocial dwarfism (PSD) are still sometimes used synonymously (e.g., Green, Campbell, & David, 1984; Masten & O'Connor, 1989); the relationship between rumination and gastroesophageal re­ flux (GER) is rarely commented upon and distinctions among rumination, GER, psychophysiological vomiting, and F T T are not delineated. The current official psychiatric diagnostic schemata, the Diagnostic and Statistical Manual of Mental Dis­ eases (third edition, revised; D S M III-R) and the International Classification of Disease—10th Revision—Clinical Modification represent a major advancement by promoting (ICD-10-CM) atheoretical, phenomenologically based diagnostic systems. However, both diagnostic systems ignore important, distinct eating disorders and, therefore, might be considered to err on the side of lumping. D S M III-R lists pica and rumination as the only eating disorders for this age group. ICD-10 includes pica, Kleine-Levin syndrome (periodic somnolence, morbid hunger, and motor unrest), and a general category of feeding disorders but not rumination. In both diagnostic systems, an­ orexia nervosa is considered chiefly a peri- or postpubertal disorder with no mention of a prepubertal variant. In D S M III-R, FTT is not recognized as an entity in its own right but as a variable sequela of Reactive Attachment Disorder. Obesity

4

EATING AND GROWTH DISORDERS

is considered a physical disorder to be listed on Axis III in DSM III-R. Although ICD-10 lists vomiting and obesity asso­ ciated with other psychological disturbances as adult onset disorders, P S D and benign nutritional dwarfing (BND) are not even mentioned as possible diagnoses in either DSM III or ICD-10. The splitter side o f the diagnostic controversy has been promulgated b y recent investigators who have cast aside pre­ mature theoretical constructs and have energetically explored the entire realm of eating and growth disorders in childhood. They have proposed a proliferation of subtypes of F T T (Egan, Chatoor, & Rosen, 1980; Woolston, 1983), obesity (Woolston, 1987), and rumination (Mayes, Humphrey, Handford, & Mitchell, 1988) as well as new diagnostic entities such as B N D (Davies, Apley, Fill, & Grimaldi, 1978), prepubertal anorexia nervosa (Irwin, 1984), and phobic food refusal (Chatoor, Con­ ley, & Dickson, 1988). The next step in the advancement of the study of eating disorders will be to integrate some of these new forms into the phenomenologically based diagnostic systems of DSM and ICD. For example, the next edition of DSM may ex­ pand its restricted diagnostic list to include FTT and a nonspe­ cific eating disorder category (F. Volkmar & L. Mayes, draft section of the DSM IV: Eating disorders in childhood; personal communication, 1991).

Bad Mothers Versus S i c k B a b i e s A second major controversy in eating and growth disorders in childhood is the relative contributions of poor parenting ver­ sus intrinsic problems in the child. In its most hyperbolic form, this dichotomy is expressed by the debate between bad mother­ ing and sick infants. In contradiction to this dichotomy, there is in reality a continuum of parent-infant dyads that range from parents who can successfully nurture no child to children who can be successfully nurtured by no parent. Unfortunately, much

Overview of Eating and Growth Disorders

5

of the past literature of eating disorders has focused on one end of this spectrum to the exclusion of everything else. Once again, the literature of FTT best exemplifies this debate. While the earliest writers (Coleman & Provence, 1957; Spitz, 1946) documented the correlation between environmental depriva­ tion and FTT, later investigators increasingly focused on the psychopathology of mothers. Maternal personality distur­ bances and depression (e.g., Elmer, 1960; Evans, Reinhart, & Succop, 1972; Fischoff, Whitten, & Pettit, 1971; Leonard et al., 1966) have been reported to be so striking in clinical observa­ tions of FTT populations that the need for control groups seemed unnecessary. However, studies that controlled for so­ cioeconomic status and the presence of a clinically ill child did not find specific maternal psychopathology as characteris­ tic of FTT. Instead, a wide variety of stresses impinge on the parents of FTT children. These include poverty (Oatis, Bobo, & Herman, 1982; Pollitt, 1975), maternal attachment distur­ bances (Benoit, Zeanah, & Barton, 1989), marital discord, chronic physical illness, depression, intellectual impairment, recent death of a family member, abuse of alcohol and other substances, and isolation from relatives and the wider com­ munity (Woolston, 1983). Rather less emphasis has been placed on the behavioral characteristics of the child that may contribute to inadequate or inappropriate feeding. Lethargic, ill, or hypersensitive chil­ dren may frustrate the increasingly frantic attempts of par­ ents to feed and comfort them, with these children withdrawing into sleep or vomiting and appearing inconsol­ able (Rathburn & Peterson, 1987). Malnutrition itself may pro­ duce a syndrome of listless irritability, which alienates caretakers, giving them little satisfaction in their attempts to provide nurturance (Casey, Bradley, & Wortham, 1984; Cha­ vez & Martinez, 1979; Kerr, Bogues, & Kerr, 1978; Pollitt, 1973; Powell & Low, 1983). In addition to the effects of malnutrition and congenital physiological and temperamental characteris­ tics, Chatoor and colleagues have suggested that certain infants

6

EATING AND GROWTH DISORDERS

and toddlers develop internalized eating disorders (Chatoor, Dickson, Schaeffer, & Egan, 1985; Chatoor & Egan, 1983). Other eating disorders, including psychogenic obesity, pica, rumination, and prepubertal anorexia nervosa, have raised identical dilemmas of separating the relative contributions of inadequate or noxious caretaking from intrinsically disturbed infants. For disorders in which the interplay between emo­ tional state and physiological disturbance is even more inti­ mately intertwined than in FTT, the controversy between environmental stress (e.g., maternal inadequacies) and intrin­ sic physiological disturbance has been even more intense. For example, the disorder of rumination was definitively de­ scribed by mental health and child developmental profession­ als as the result of inadequate emotional stimulation of the infant. Simultaneously, pediatric surgeons described an ap­ parently identical syndrome named chalasia as a physiological a n d / o r anatomical disorder that was completely uninfluenced by the infant's emotional states. Improved physiological diag­ nostic technology enabled pediatric gastroenterologists to de­ fine a disorder called gastroesophageal reflux (GER), which was held to be a purely physiological disorder. Treatment for these nearly identical but differently named disorders has been narrowly influenced by their namers: rumination is to be treated with emotional a n d / o r behavioral interventions, chalasia by surgery or mechanical means, and GER with med­ ication. Although no research has yet been done to explore the relationships among these disorders, they presumably represent overlapping and interconnected aspects of a general syndrome involving regurgitation in infants and young chil­ dren. Separating the emotional, physiological, and anatomical contributions to this syndrome into mutually exclusive phe­ nomena obviously obscures understanding. Clearly, the gene­ sis of eating and growth disorders in infants and children is the final common pathway of multiple interacting variables including specific characteristics of both the caretakers and the infant.

Overview of Eating and Growth Disorders

7

Organic Versus Nonorganic Etiologies Traditionally, the causes of eating disorders have been dichotimized as organic or nonorganic. Organic etiology was ascribed to a major illness or organ system dysfunction thought to be sufficient to account for growth failure or an eating disorder (Frank & Zeisel, 1988). Obviously, such a term could only could exist if it were paired with its opposite: non­ organic disorders, which have been proposed to be caused by environmentally induced, emotional disturbances. This rigid dichotomy currently persists, although several authors have recognized disorders with a mixture of so-called organic and nonorganic causes (Homer & Ludwig, 1981; Woolston, 1983; Woolston & Forsyth, 1989). Although problems with this artificial dichotomy o f etiol­ ogy apply to all eating and growth disorders in childhood, this organic/nonorganic dichotomy has been best exemplified in the literature about FTT, in which research and treatment has been misled for several reasons. First, the organic / n o n o r ­ ganic dichotomy denied the reality that all FTT has the same organic basis: malnutrition (Bell & Woolston, 1985; Krieger & Chen, 1969; Whitten, Pettit, & Fischoff, 1969). Thus clinicians mistakenly focused upon discovering occult illness to support the "organic" diagnosis. However, such a search is usually fruitless because diseases that lead to growth failure are al­ most always suggested by the initial history and physical (Berwick, Levy, & Kleinerman, 1982; Sills, 1978). Second, this dichotomous concept obscured the fact that children with se­ rious medical illness fail to thrive because of malnutrition (Kappy, 1987) rather than directly from their primary medical disorder. Contrary to the popular belief that weight gain dur­ ing hospitalization rules out major organic disease, such ill children often grow in the hospital because m a n y trained personnel are available to share the burden o f their care (Bell & Woolston, 1985; Berwick et al., 1982; Kotelchuck, 1980). Rather than attempting to diagnose each case of F T T

8

EATING AND GROWTH DISORDERS

as organic or nonorganic, current practice is to evaluate the diagnostic and therapeutic implications of the nutritional, medical, psychosocial, and developmental factors (Rathburn & Peterson, 1987).

GENERAL APPROACH TO TREATMENT Despite the considerable heterogeneity of eating disorders in childhood, they are all characterized by the transactional nature of their etiology and progression. For this reason, as is appropri­ ate for any complex, multifactorial chronic disorder, assessment and treatment must occur in the context of a multidisciplinary team approach (Alvarado, 1982; Berkowitz, 1985; Peterson, Washington, & Rathburn, 1984). Ideally, this team consists of a pediatrician, a nurse, a developmental psychologist, a child psy­ chiatrist, a social worker, and a nutritionist. The team assesses the child's pediatric, developmental, psychiatric, familial, adap­ tive, and nutritional status. Because of the complexity and sever­ ity of these disorders, an inpatient evaluation may be required. A full medical assessment of the child must be performed to evaluate the concomitants and the sequelae of these eating dis­ orders as well as their possible causes. For example, morbid obe­ sity may be associated with such disorders as slipped femoral epiphysis, diabetes mellitus, sleep apnea, and Pickwickian syn­ drome. These serious medical disorders result from obesity and must b e treated vigorously (Woolston & Forsyth, 1989). Because there appears to be a correlation b e t w e e n severe familial disorganization and some eating disorders, the pedia­ trician should evaluate the child for other problems associ­ ated with neglect, such as inadequate immunization, lead poisoning, iron deficiency, and tuberculosis. A careful devel­ opmental, cognitive, and emotional assessment is required to define various psychological/developmental strengths and weaknesses. If the child is older than 36 months, the develop­ mental psychologist should contact the appropriate educators

Overview of Eating and Growth Disorders

9

to assess and enroll the child in an early intervention school program. The child should be evaluated for specific psychiat­ ric disorders, such as attention deficit disorder, anxiety disor­ ders, mood disorders, and oppositional disorder (Woolston & Forsyth, 1989). Engagement of the family is the most important variable in successful treatment. In addition to evaluating all aspects of family functioning, potential mental health and social re­ sources for the family need to be assessed. Such issues as par­ ental psychopathology, social isolation, and unemployment are crucial factors in treatment. The overall nutritional state of the child, the caloric intake for weight maintenance, and per­ haps the nutritional status of other family members should be determined. The daily functioning of the child and family, in­ cluding feeding and other mealtime behavior, must be ascer­ tained and specific behaviors that need to be eliminated or strengthened must be determined. In this manner, the team must evaluate the overall strengths and weaknesses of the child and family to discover the multiple factors for the child's eating and growth disorder. The various factors that contribute to the disorder then must be addressed by each member of the treatment team as is appropriate. Because se­ vere growth and eating disorders threaten to permanently compromise the child's developmental potential, removal of the child from the home sometimes is necessary. Because the problem frequently reemerges when the child returns to the home, however, this most restrictive alternative should b e re­ served as a last and relatively undesirable intervention (Woolston & Forsyth, 1989).

SUMMARY Eating and growth disorders in prepubertal children are complex phenomena that represent the interaction o f multiple levels of organization over time. A l t h o u g h m a n y of these

10

EATING AND GROWTH DISORDERS

disorders have been studied and described for nearly a cen­ tury, advances in understanding and treatment have been slowed by their multifactorial nature. A major thrust of research has mistakenly focused upon narrow, dichotomous debates, which have tended to retard progress. These dichotomous de­ bates have included arguments about under- and over­ inclusiveness of diagnostic definitions, locus o f etiological disturbance in either the child or the caretaker, and relative contributions of medical illness and emotional disturbance. Just as advancement in understanding depends upon integra­ tion of all aspects and levels of risk, so treatment requires a multidisciplinary team approach.

2

FUNDAMENTALS OF NORMAL

CHILD DEVELOPMENT

BIOLOGY OF PHYSICAL DEVELOPMENT Physical growth is a complex, stepwise process that re­ quires the orchestration of hormonal regulatory systems, ade­ quate energy and other nutritional resources, and the necessary antecedent biological events. This last factor repre­ sents the biological expression of the transactional develop­ ment. Ongoing growth is not only dependent upon current and future physiological and nutritional resources but also upon past physiological experiences. In this fashion, environ­ mental events interact with genetic and constitutional homeo­ static mechanisms to produce a particular individual's growth pattern.

Growth (1) Hormonal regulation. In healthy children, statural growth is controlled by the interaction between nutritional stores and the effect of circulating hormones on the skeletal system. 11

12

EATING AND GROWTH DISORDERS

Growth hormone (GH) and thyroid hormone (T4) are the major hormonal determinants of growth rate during the childhood years. The growth spurt and skeletal maturation of adolescence are primarily dependent on gonadal steroids in conjunction with G H and T4. Insulin and glucocorticoid influ­ ence carbohydrate, fat, and protein metabolism, provide sources of energy needed for growth, and exert a permissive influence on the anabolic actions of GH. Whether insulin acts only permissively or whether it also functions as a growth factor is still unresolved because of the inseparable link be­ tween insulin and nutrition (MacGillivray, 1987). Under the influence and control of the limbic cortex and amygdaloid nuclei, the hypothalamus releases two growth hor­ mone controlling hormones that exert opposite influences on growth hormone (GH) release: somatosatin or growth hormone inhibiting factor (GHIF) and growth hormone releasing factor (GRF). GHIF suppresses the GH response to various stimuli such as insulin induced hypoglycemia and thyrotropin releasing hormone (TRH) and induced thyroid stimulating hormone (TSH) release. GRF appears to have a highly specific function of increasing GH release from the pituitary. In children and young adults, approximately 50% to 75% of daily production of G H oc­ curs during the early nighttime hours, following the onset of deep sleep. GH has a wide variety of influences including in­ creasing cellular metabolic activity, stimulating fat metabolism, altering insulin activity, and changing electrolyte and mineral excretion by the kidney. The current hypothesis for GH's spe­ cific mediation of growth is by its stimulation of the production in the liver of several growth factors called somatomedin (SM). In the presence of adequate nutrition and T4, SM induces cellu­ lar enlargement and multiplication. This entire process, like most hormonally regulated systems, employs a cybernetic con­ trol mechanism at each level. (2) Patterns of growth. The dynamics of growth change by orders of magnitude during the course of life. Growth both in

Fundamentals of Normal Child Development

13

length and in weight can be measured in two fashions: total cumulative growth and growth velocity. Total cumulative growth is simply determined by the absolute weight and length, whereas growth velocity is measured by the amount of change in a unit of time (e.g., centimeter of growth per month or year). The initial period of growth during gestation has the high­ est velocity in the course of human development. This growth rate reaches its peak at the beginning of the second trimester when it approaches the equivalent of 144 centimeters per year, which is 6 times the rate of growth during the neonatal period and 14 times the rate during the adolescent growth spurt. In the first year of life, linear growth and weight gain continue at a rate that is still remarkable although less spec­ tacular than that during fetal life. B y 1 year, the normally de­ veloping infant has accumulated generous stores of adipose tissue, has tripled its birth weight, and has grown 25 addi­ tional centimeters, an increase of 5 0 % of birth length. In the second year, there is continued deceleration of linear growth rates; b y the age of 2 years, linear growth has stabilized at a rate that is characteristic of the childhood years (MacGillivray, 1987). Growth velocity for weight gain follows similar patterns. The period of childhood growth, which extends from the age of 2 years to the onset of puberty, is characterized by relatively stable rates of gain in height (5 to 7.5 c m / y e a r ) and weight (2 to 2.5 kg/year). Throughout these years, there is slight deceleration in linear growth rate and slight acceleration in weight gain. The major period of brain growth has already been completed and cellular multiplication in musculoskeletal and adipose tissues continues at a lesser pace than is evident during infancy or ado­ lescence. In the years prior to puberty, there is an increased gain in adipose tissue (MacGillivray, 1987). Adolescence is the last period of major growth; in it, there is attainment of adult stature, sexual maturation, and repro­ ductive function (MacGillivray, 1987). Among healthy chil­ dren, chronological age at the onset of puberty and rate of

14

EATING AND GROWTH DISORDERS

sexual maturation are highly variable. These differences are largely dependent on genetic factors. The individual's sex also plays a role, because the average girl enters and com­ pletes pubertal development one to two years ahead of the average boy. The most accurate criterion for assessment of ad­ olescence is not chronological age but the individual's biolog­ ical age (bone age) and his or her physical stage of sexual maturation, based on Tanner's criteria (Tanner & Whithouse, 1976). While these global trends of growth velocity of length and weight provide an important view of development, the con­ siderable variation o f size among individuals follows a nor­ mal distribution. The physical measurements (height, weight, and head circumference) of an individual can be expressed ei­ ther in terms of percentiles for chronological age, with the range of normal being between the 3rd and 97th percentiles, or in terms of standard deviations (SD) above or below the mean. A variety of published growth curves are widely avail­ able that plot growth for infants and children. One S D ex­ tends from the 16th to the 84th percentile; two SD extend from the 2th to 97th percentile or approximately the 3rd and 97th percentiles on the growth curve. The use of S D provides information on the magnitude of the growth disorder and is particularly helpful in quantifying growth abnormalities in children whose height and weight fall above the 97th or below the 3rd percentile. An increase in the number of SD away from the mean indicates the growth problem is worsen­ ing; a decrease in the number of SD from the mean is synony­ mous with improved growth (MacGillivray, 1987). The growth curves also allow for expression o f an individual's size in terms of height age (HA) and weight age (WA). HA is defined as the chronological age at which the patient's height would fall at the 50th percentile. This is calcu­ lated by drawing a horizontal line from the patient's position on the growth curve to the 50th percentile and dropping a vertical line to age in years. It does not take into account

Fundamentals of Normal Child Development

15

genetic influences on stature and pace of maturation. Never­ theless, it is extremely valuable when used to compare an individual's stature with his or her biological age (i.e, bone age; MacGillivray, 1987). The method for calculating W A is similar to that for HA but is more subject to error. The relationship between chronological age, HA, W A , and bone age in a patient helps delineate the etiol­ ogy of the growth disorder; for example, a 2-year-old with HA = 18 months and W A = 6 months is likely to have a nutritional problem that impairs weight gain more seriously than linear growth. Conversely, a 6-year-old child with HA = 3, W A = 4, and a bone age of 3 may have GH or thyroid deficiency (MacGillivray, 1987). A further refinement of this process is the calculation of percentage of ideal body weight (IBW) for height, age, and sex. Using calculated HA to replace chronological age, the IBW is determined by drawing a vertical line up from the age on the weight growth curve to the 50th percentile curve and then drawing a horizontal line across to determine the weight value. This weight value theoretically represents the weight that is correlated for height but corrected for the individual's partic­ ular stature growth pattern. The percentage of IBW is the quo­ tient of the IBW and actual weight.

Energy Metabolism (1) Energy balance. The dynamics and economics of energy metabolism are intimately linked with growth given that growth cannot occur in the presence of a negative energy bal­ ance. In the most global terms, energy metabolism is de­ scribed by the equation: Energy stored = energy absorbed - energy expended Energy is stored primarily as the complex polymers o f fat, glycogen, and protein. Energy is absorbed in the small intestine

16

EATING AND GROWTH DISORDERS

in the form of glycerides, sugars, and amino acids. Glycerides have approximately twice the energy value for unit volume or weight as sugars and amino acids. These relatively small mol­ ecules are produced from the breakdown of larger molecules that have been ingested, mechanically broken up, and depolymerized. This process of ingestion and digestion re­ quires a complex and well-orchestrated control of the upper gastrointestinal tract including the mouth, esophagus, stom­ ach, and small intestine. After being absorbed through the wall of the small intestine, these small molecules are trans­ ported by the circulatory system to various target organs where they cross the cell membranes and are metabolized or stored. A variety of pathophysiological disorders can inter­ fere with this process at any step from ingestion to cellular storage and metabolism. In the absence of such disease states, virtually all of the variance of energy absorption is defined by differences of energy ingested. Energy expended is traditionally divided into three compo­ nents: Total energy expended = energy of digestion + energy of basal metabolism + energy of activity Except in grossly pathological states, the majority o f the vari­ ance in energy expenditure among individuals is accounted for by the differences in variability in degree of muscular ac­ tivity, especially spontaneous activity (i.e., fidgeting; Ravussin, Lillioja, Anderson, Christin, & Bogardus, 1986). Therefore, the variations in energy stored, especially in fat ac­ cumulation, are described by the equation: Energy stored ρ energy absorbed - energy of activity Stated in other words, most variance in degrees of fatness or thinness is determined by only two variables: caloric intake and caloric expenditure through muscular activity. Very little

Fundamentals of Normal Child Development

17

information is known about the mechanism of regulation of either caloric intake or muscular activity. Because both of these processes tend to be quite stable over time in a particu­ lar individual, presumably such regulatory mechanisms exist. (2) Characteristics of chronic negative energy balance. When ca­ loric expenditure chronically exceeds caloric intake, states of hypocaloric malnutrition occur. The physiology of malnutrition is influenced by the acuity, severity, and type of malnutrition. Degree of malnutrition is categorized by several different classi­ fication systems that are based on general clinical features (Waterlow, 1972) as well as anthropometric measurements (McLaren & Read, 1972). Within the general diagnosis of moder­ ate and severe malnutrition, marasmus and kwashiorkor are two subtypes that are recognized. Marasmus is defined as com­ bined protein calorie malnutrition (PCM) whereas kwashiorkor is a syndrome associated with a relatively specific deficiency of protein. Despite these differences, characteristic physiological adaptations to malnutrition include various neuroendocrine changes (e.g., reduction of the triidothryromine/reverse triidothryromine ratio [Chopra, Chopra, Smith, Reza, & Solo­ mon, 1975; Wartofsky & Bruman, 1982], loss of Cortisol circadian rhythm [Beitins, Kowarski, Migeon, & Graham, 1975], increase in growth hormone [Kaplan, Abrams, Bell, & Conte, 1968; Pimstone, Whattman, & Hansen, 1966; Robinson & Picou, 1977]), hematological abnormalities (hypoproteinemia, various anemias), dermatological changes (loss of adipose tissue, alope­ cia, and loss of hair pigmentation), and emotional/behavioral alterations (lethargy, anhedonia, apathy).

P H E N O M E N O L O G Y OF EMOTIONAL,

BEHAVIORAL, AND SOCIAL DEVELOPMENT

In parallel with rapid changes of physical growth, emo­ tional and behavioral development unfolds in a predictable

18

EATING AND GROWTH DISORDERS

sequence but with great individual variation. In infancy and early childhood, the child's lack of speech has made investi­ gation of this development more challenging. Indeed, many concepts of childhood development were based more on retrospective reconstruction from psychoanalytic treatment of adults and metapsychological speculation than on empirical observation. While this earlier theoretical structure may sometimes have been inaccurate, it promoted the crucial con­ cept that infants and young children are developing individu­ als who have complex and important relationships with caretakers that shape their future lives. The pioneering work of Gesell and Piaget exemplified the use of careful empirical observations to establish the unfolding of development. Cur­ rently, development of behavior is divided into four major domains: personal/social, language, adaptive, and motor. In addition to these empirically definable steps of develop­ ment, the last decade has witnessed an explosion of such em­ pirical investigations into the cognitive and interpersonal development of even the youngest infants. There is now con­ siderable literature about the development of personality and personhood. While this literature remains by definition more speculative, it represents the clinically richest material. In the broadest terms, during the first several months of life, the infant is focused upon homeostasis of state regula­ tion, especially eating, sleeping, and alertness (Greenspan, 1981). In the next 7 to 9 months of the first year of life, the in­ fant is engaged in developing the rudiments of attachment to the primary caretaker. The second and third years of life in­ troduce the challenges related to the infant's definition of him- or herself in relationship to and distinct from his or her important caregivers. The various developmental milestones, including sphincter control, locomotion, language, and con­ ceptual memory, permit and demand this development of the child as a separate but connected person. Slightly later but in an overlapping fashion, in the third, fourth, and fifth years of life, the child expands the psychological realm to include

Fundamentals of Normal Child Development

19

peers and nonprimary caretakers. The child acquires more complex cognitive, moral, and interpersonal skills in interac­ tion with this development. Frequently, the child develops powerful emotional relationships with other adults in addi­ tion to his or her relationship with a single primary caretaker. These experiences may be the anläge of such complex and im­ portant emotions as love, jealousy, rivalry, and guilt. B y the sixth and seventh years o f life, the child experiences enor­ mous maturation in his or her attention span, social aware­ ness, motor skills, and cognitive abilities so that the child can begin the process o f learning to read, write, and figure, partic­ ipate in group games, and value group ideals. T h e child uses the next several years until puberty to develop and consoli­ date these and other skills. In this fashion, although both physical growth and emotional/behavioral development of the infant and child unfold in a predictable, stepwise fashion, the interaction between the person and his or her interper­ sonal environment follows a unique, complex, transactional course.

SUMMARY Normal child development in both physical and emo­ tional/behavioral spheres follows predictable, sequential pat­ terns. Normal eating and growth, as well as eating and growth disorders, are influenced by these established patterns of development. Physical growth is dependent upon the inter­ action between complex neuroendocrinological regulation and nutritional stores. These nutritional stores of energy are primarily determined by the balance between caloric intake and energy expenditure through activity. Abnormalities of growth can b e best documented by deviations from patterns of growth on standardized charts. In a fashion analogous to that of physical growth, emo­ tional/behavioral/social development unfolds in a predictable

20

EATING AND GROWTH DISORDERS

pattern. Progression in these areas of development can be as­ sessed by comparison with expected milestones. E m o t i o n a l / behavioral/social development describes the progressive growth of a socially related and functional human being. Until recently, many researchers and clinicians have un­ deremphasized the interactive nature between these two spheres of development or have proposed undocumented connections.

3

FAILURE TO THRIVE

Failure to thrive (FTT) is a disorder of infancy and early child­ hood characterized b y a marked deceleration of weight gain and a slowing or disruption of acquisition of emotional and social developmental milestones. Deceleration of linear growth and head circumference growth are associated but not primary phenomenon. FTT is a common disorder, occurring at a rate of 1% to 5% of pediatric hospital admissions (Berwick, 1980; Hannaway, 1978; Shaheen, Alexander, Truskowsky, & Barberro, 1968). Surveys of low-income children in primary care suggest that nearly 10% show weight or length below the fifth percentile for age (Koumjian & Marks, 1985; Mitchell, Gorrell, & Greenberg, 1980; Trowbridge, 1984). This common condition is o f great concern because FTT is associated with increased risk for lasting deficits in growth, cognition, and so­ cioeconomic functioning (e.g., Eid, 1971; Elmer, Gregg, & Elli­ son, 1969; Glaser, Heagarty, & Bullard, 1980; Oates, Peacock, & Forrest, 1 9 8 4 , 1 9 8 5 ) . FTT was first described in the English-language medical lit­ erature by Holt (1897, pp. 207-208). He characterized the syn­ drome in the following manner: 21

22

EATING AND GROWTH D I S O R D E R S The history in severe cases is strikingly uniform. The fol­ lowing is the story most frequently told. "At birth the baby was plump and well-nourished and continued to thrive for a month or six weeks while the mother was nursing him; at the end of that period cir­ cumstances made weaning necessary. From that time on the child ceased to thrive. He began to lose weight and strength, at first slowly then rapidly, in spite of the fact that every known infant food was tried. As a last resort the child, wasted to a skeleton, is brought to the hospital."

Despite this 96-year history of study, the understanding of FTT has been marked by confusion and controversy about such basic issues as the definition and the name of the disor­ der (Wilcox, Nieburg, & Miller, 1989). The plethora of syndro­ mic names provide a glimpse into the confused literature: hospitalism (Spitz, 1945), anaclitic depression (Spitz & Wolf, 1946), institutionalism (Provence & Lipton, 1962), environmen­ tal retardation (Coleman & Provence, 1957), maternal depriva­ tion syndrome (Ainsworth, 1962; Bawkin, 1949; Bowlby, 1951), psychosocial deprivation dwarfism (Krieger, 1974), deprivational dwarfism (Silver & Finkelstein, 1967), deprivation syndrome (Krieger & Good, 1970), failure to thrive (Leonard et al., 1966), environmental failure to thrive (Barbero & Shaheen, 1967), and nonorganic failure to thrive syndrome (Togut, Allen, & Lelchuck, 1969). This blizzard of interchangeably used but non­ synonymous terms, which frequently represented the mis­ taken or oversimplified underlying conceptions of the investigators, has created a major obstacle to the course of re­ search (Wilcox et al., 1989). These misconceptions arose out of the multifaceted nature of the syndrome. At different times, the three components of FTT—weight gain deceleration (Frank & Zeisel, 1988), linear growth delay (Silver & Finkel­ stein, 1967), and developmental delays (Provence & Lipton, 1962; Rosenn, Loeb, & Jura, 1980)—were separated so that each was perceived as the central aspect to the exclusion of

Failure to Thrive

23

other parts. In fact, depending upon the focus of the defini­ tion, FTT has been reported as consisting of only one compo­ nent rather than a triad. For example, when the diagnosis of FTT is made on the basis of primary weight gain deceleration, developmental deficits are less evident (Drotor et al., 1985; Field, 1984), and, indeed, in one study using age-matched controls, there were no differences in development test scores between FTT and normally growing infants (Mitchell et al., 1980). A second aspect of this confusion in the understanding of FTT has been the controversy between the contribution of emotional deprivation and that of malnutrition. From the ear­ liest observers to present-day clinicians, the correlation be­ tween emotional misery and growth problems has been obvious. Perhaps too simplistically, some investigators ar­ gued that such disorders were directly caused by misery, me­ diated by some effect on the mind acting directly upon the body, without requiring such external factors as altered calo­ ric intake. The starkest presentation of the argument has been the the­ oretical debate of the importance of love versus food in the etiology of FTT. Widdowson (1951) articulated the "love ver­ sus food" argument in her article aptly named "Mental Con­ tentment and Physical Growth." According to this thesis, mental contentment in infants and young children was cre­ ated by a loving relationship with a mothering figure. This psychic state produced an unnamed physical process that caused growth. While a minimal nutritional state was obvi­ ously required for life, mental contentment was held to be more crucial then caloric intake for growth. While she pur­ portedly demonstrated the central role of "mental content­ ment" in her report, the methodology of her naturalistic experiment was so severely flawed as to render it worse than useless: She had no documentation of what the children actu­ ally ate. Studies by Engle, Reichsman, and coworkers (Engle & Reichsman, 1956; Engle, Reichsman, Harway, & Hess, 1986;

24

EATING AND GROWTH DISORDERS

Reichsman, Engle, Harway, & Escalona, 1958) of an infant fed through a gastric fistula have been used to support the "men­ tal contentment" argument. This infant became apathetic and stopped gaining weight shortly after her mother became se­ verely depressed and withdrew from her emotionally. Al­ though these workers have provided an exhaustively documented, 28-year longitudinal study that has provided in­ valuable insights into eating behaviors, they never docu­ mented the subject's caloric intake! Thus the investigators assumed that their subject stopped her weight gain solely be­ cause o f her anaclitic depression induced by her mother's withdrawal. They did not explore the more plausible explana­ tion for the weight gain deceleration that her mother fed her less. Early clinical experience indicated that some infants with FTT who were given a normal caloric intake did not gain weight at their expected rate. These observations were used to bolster the argument that calories alone were not sufficient for weight gain. However, studies o f malnourished children have demonstrated that they have supracaloric requirements before catch-up growth is possible (Casey & Arnold, 1985; Goldbloom, 1982). In addition, Whitten et al. (1969) reported that even grossly understimulated infants with FTT gained weight rapidly if given enough food. From a different per­ spective, Provence and Lipton (1962) described how psy­ chosocial deprivation caused infantile depression and developmental delay without deceleration o f weight gain. The persistence of this debate about love versus food has several origins. First, FTT is a syndrome with physical (weight gain and growth deceleration) and b e h a v i o r a l / e m o ­ tional (developmental delays) components. The overwhelming evidence indicates that inadequate caloric intake is the primary cause of growth deceleration while emotional and socioeco­ nomic deprivation is the primary cause of the developmental delays (Casey, Bradley, & Wortham, 1984). However, the depressionlike symptoms associated with FTT probably re­ duce the infant's interest in feeding, rendering the infant

Failure to Thrive

25

harder to feed. Similarly, the significant malnutrition associ­ ated with FTT can produce a state of apathetic withdrawal. To further complicate matters, a small group of severely de­ prived and abused young children have a disruption of pitu­ itary function even in the presence of adequate nutrition. Although these children represent a clearly defined and dis­ tinct diagnostic syndrome of psychosocial dwarfism (PSD; Powell, Brasel, Raiti, & Blizzard, 1967), their symptoms are persistently confused with those of FTT. For example, Green et al. (1984) and Ferholt et al. (1985) argued that, based on their observations of children with apparently psychosomatic growth failure, a "very slow rate of linear growth can be un­ derstood as a neuroendocrine concomitant of a severe depres­ sive disorder in a person who is still growing" without regard to nutritional state. Apparently influenced by Green et al. (1984) and Ferholt et al. (1985), Masten and O'Connor (1989) described a case study of a young girl who developed a growth disturbance beginning at age 15 months in response to gross psychosocial deprivation. Masten and O'Connor (1989, p. 278) report that "Sara's history and course are also consistent with the clinical picture of 'psychosocial dwarfism.' " Although these authors presented their patient's height and weight growth charts, they made no comment on her degree of malnutrition. Calculated from their data, her significant linear growth delay did not begin until she was 24 months of age at which time she was 79% of ideal weight for her height and age. Using McLaren and Read's (1972) nomogram for calculating de­ gree of protein calorie malnutrition (PCM), the patient would have been classified as having moderate PCM. Similarly, her lin­ ear growth catch up followed her weight gain acceleration. Nev­ ertheless, these authors never mentioned any aspect in the patient's nutritional status or caloric intake in the case discus­ sion. Instead, they postulated that "Sara's growth retardation may have been secondary to depression caused by the loss of primary caregivers at a sensitive age in a potentially vulnerable child" (Masten & O'Connor, 1989, p. 278). Thus, although the

26

EATING AND GROWTH DISORDERS

primacy of PCM in the growth disturbances found in FTT has been well established, the confusion about the relative contri­ butions of love versus food continues in the literature.

NATURAL HISTORY Developmental Evolution and Outcome FTT is a disorder with an onset in the first 3 years of life. Typically, infants who h a v e the onset of F T T before the end of one year o f life are m o r e likely to h a v e been actively de­ prived of food or to have primary physiological disorders that interfere with caloric intake. W h e n the initial onset of FTT occurs in older infants and toddlers, it is m o r e likely that there are active interactional difficulties b e t w e e n the child and primary caregiver that manifest as an eating dis­ order. Frequently, a y o u n g infant w h o presents with F T T will respond rapidly to adequate feeding. However, the same s o c i a l / f a m i l i a l conditions that are associated with such acute malnutrition may also b e associated with chronic emotional and physical deprivation and poor infant­ caregiver relationships. Therefore, infants w h o s e initial epi­ sode o f F T T is rapidly ameliorated b y refeeding m a y develop a second episode of FTT that is characterized b y a more chronic and internalized eating disorder. These tod­ dlers and young children resist ingestion of adequate caloric intake and show secondary stunting of linear growth and head circumference as a result of chronic malnutrition. The developmental outcome of children with FTT is re­ markably heterogenous, perhaps because o f the heterogeneity of the syndrome. Significant variables that influence outcome include general factors such as socioeconomic status, mater­ nal education, parental mental illness, and family social func­ tioning. Because these factors are risk factors both for FTT

Failure to Thrive

27

and for poor developmental outcome, they probably mediate their influence somewhat independently of FTT per se. Risk factors that are more directly linked to FTT include degree and chronicity of malnutrition, degree and chronicity of de­ velopmental delay, severity and duration of the dysfunction in the infant-caretaker relationship, and severity of the major medical disorder. Problems associated with FTT such as phys­ ical abuse, medical neglect, educational neglect, and social isolation interact with the general and specific risk factors to influence developmental outcome.

Epidemiology As indicated in the introduction, FTT is a common disorder ranging from l % - 3 % of inpatient pediatric admissions to 10%­ 15% of some outpatient populations. Few data exist on histor­ ical trends for shifting prevalence of FTT. Sex ratio is reported to be approximately equal, although studies of older infants indicate a slight preponderance of boys.

Etiology (1) Social and family factors. Although FTT occurs in children of all social strata, it is more common in families where func­ tioning is compromised by poverty, unemployment, social dislocation and isolation, and parental mental illness. As with any complex, multifactorial disorder, most infants develop relatively normally in conditions characterized by many of these risk factors while a minority develop an e a t i n g / g r o w t h disorder such as FTT. On the other hand, some infants de­ velop FTT despite the apparent absence of any of these risk factors. Thus social and family risk factors are just that: risk factors rather than specific etiological agents.

28

EATING AND GROWTH DISORDERS

(2) Genetic factors. Virtually nothing is known about what, if any, genetic factors exist in various forms of FTT. Obviously, there are important genetic contributions to various mental disorders that can influence caretaker adequacy. (3) Temperament and psychogenic factors. Because the etiol­ ogy of FTT is a multifactorial process, virtually a n y temper­ ament or psychological factor that interferes with somatic homeostasis a n d / o r attunement between infant and care­ taker m a y well disrupt feeding and cause inadequate calo­ ric intake. In young infants, the two most c o m m o n such difficulties are marked irritability or apathy. Both of these states are themselves the result of multiple underlying fac­ tors including basic psychophysiological temperament, nu­ tritional state, physical health, and affective interaction with the primary caregiver. This last factor has been the focus o f considerable research as the major etiological fac­ tor in the development of FTT. Investigators have postu­ lated that any emotional a n d / o r behavioral disturbance in the primary caretaker that causes her to be physically a n d / o r emotionally absent will result in the state of apa­ thetic depression in the infant. Alternatively, emotional dis­ turbance in the caregiver that results in the infant's experiencing constant anger, rejection, irritability, or hatred will cause the infant to b e irritable, difficult to soothe, a n d / o r withdrawn. As Chatoor, Dickson, Schaeffer, and Egan (1985) have emphasized, the type of psychological disturbance in the infant is strongly influenced b y the de­ velopmental stage of the infant. For example, these writers have suggested that, for some infants with an onset of F T T in the first year, the primary disturbance originates from a failure in attachment to a nurturant primary caretaker. In contrast, toddlers and young children w h o develop F T T m a y experience a failure in appropriate separation and in­ dividuation from their caretakers. According to these au­ thors, this latter group of children b e c o m e stuck in a battle

Failure to Thrive

29

over the ingestion o f food as a misplaced focus for the normal developmental process of b e c o m i n g separate individuals. Al­ though the paucity of data prevents us from evaluating the clinical importance o f clear diagnostic separation b y develop­ mental stage of onset, there is no doubt that infants, toddlers, and young children may have a variety of emotional distur­ bances that are influenced by their developmental stage and that can interfere with caloric intake. In addition to developmentally determined emotional dis­ turbances, Chatoor et al. (1988) have reported several cases of young children who develop FTT as a result of specific trau­ matic experiences. These authors report that clearly defined choking events can trigger phobic food refusal. The relation­ ship between gastroesophageal reflux, which is commonly as­ sociated with aspiration and choking, and phobic food refusal remains to be explored. (4) Organic factors. Clinicians in the past have sometimes overemphasized the importance of the search for occult or­ ganic factors, as has been demonstrated b y the low yield from exhaustive testing (Sills, 1978). A major impetus for this ex­ cessive use o f laboratory testing has been the misconception of the organic/nonorganic dichotomy. To be sure, the number of primary medical illnesses that can be associated with FTT is extensive. However, a thorough pediatric history, physical examination, and minimal screening laboratory tests usually identify physical illnesses that are contributing to FTT. These screening tests include complete blood count, lead level and free erythroyoctye protoporphyrin, tuberculosis skin test (PPD), urinalysis and urine culture, and a sweat test in popu­ lations predisposed to cystic fibrosis (Frank & Zeisel, 1988). Some organic factors may be caused by the malnutrition as­ sociated with FTT as well as aggravating its course. Malnutri­ tion suppresses immune functions so that children with FTT are at risk for chronic respiratory and gastrointestinal infec­ tions. The illnesses that these infections produce interfere

30

E A T I N G AND G R O W T H D I S O R D E R S

with the infant's ability to ingest adequate calories, which ex­ acerbates the infant's state o f malnutrition. Similarly, infants with FTT are at risk for vitamin and mineral deficiencies, es­ pecially in terms of calcium, iron, and zinc. These deficiencies result in blood dyscrasias and metabolic disturbances that worsen the infant's clinical state. In addition, the mineral deficiencies and malnutrition increase the risk of lead toxicity because lead absorption is significantly increased in these de­ ficiency states. Perhaps most important in evaluation of or­ ganic factors is the concept that illnesses that coexist with FTT belong in a continuum, from those that actually cause malnu­ trition (e.g., malabsorption) at one end to those that are caused by malnutrition (e.g., immunosuppression; Woolston, 1985) at the other.

DIAGNOSTIC CLASSIFICATION AND

SPECIAL TREATMENT ISSUES

The literature on F T T has ranged from the view that F T T was solely the result of emotional deprivation of the infant to the concept of multiple subtypes based upon a variety of phe­ nomenological (Woolston, 1983) and theoretical schemata (Chatoor et al., 1985; Freud, 1946). Although some of these subtyping classifications eventually may hold merit, there cur­ rently is insufficient data to support such a refined classification. Rather than a categorical approach to F T T diagnostic classi­ fication, a multiaxial, dimensional approach appears to be warranted at this time (Woolston, 1985). The crucial axes on which to evaluate an infant with FTT include age of onset and duration of FTT, degree of malnutrition, degree of linear growth and head circumference stunting, presence of other physical illness, developmental delay, and level of family functioning. Age of onset is important in understanding both the genesis of FTT as well as its prognosis. FTT with onset in the first 12

Failure to Thrive

31

months of life in the absence of any concurrent medical illness is almost always a feeding disturbance resulting from the infant's either being deprived of adequate caloric intake or being so fussy and irritable that feeding is nearly impossible. In the former situation, the infant will rapidly gain weight when offered enough food. Thus, if the factors that contributed to the inadequate caloric intake can be ameliorated, infants with this pattern of FTT have an excellent prognosis. Simi­ larly, most infants who have severe problems with establish­ ment o f basic physiological homeostasis will develop more effective state regulation by the second and third years of life. However, the presence of other risk factors on the multiaxial approach to F T T puts such infants at high risk for poor devel­ opmental outcome. Calculation of the degree of malnutrition is crucial in all as­ pects of the clinical management of FTT including diagnosis, prognosis, and treatment. Frequently, the severity of the mal­ nutrition is associated with the severity of the other risk fac­ tors that are influencing the FTT. T h e degree of malnutrition affects the severity of medical complications associated with FTT, ranging from acute immunosuppression to permanent interference with brain growth. Calculation of degree of mal­ nutrition is essential for the correct nutritional treatment re­ quired for compensatory catch-up growth. T o achieve such catch-up growth, the infant needs supraordinary daily caloric intake. These special nutritional requirements expressed as calories per kilogram of body weight can b e estimated as fol­ lows (MacLean, de Romana, & Masse, 1980): K c a l / k g = 120 Kcal x I B W current weight According to this formula, most children will require 1.5 to 2 times the caloric intake normally recommended for their age to achieve optimal catch-up growth (Casey & Arnold, 1985; MacLean et al., 1980; Peterson et al., 1984). Depending on the severity of the initial deficit, the infant may require up to 2

32

EATING AND GROWTH DISORDERS

weeks of refeeding to initiate catch-up growth (Casey & Arnold, 1985; Ellerstein & Ostrov, 1985). Accelerated growth must then be maintained for 4 to 9 months to restore a child's weight for height (Casey & Arnold, 1985). Because the infant will regain weight growth more rapidly than height, the care­ takers may become concerned that the child is becoming obese and prematurely stop dietary treatment (Frank & Zeisel, 1988). The degree of height and head circumference growth stunt­ ing provides important data about the chronicity and severity of the malnutrition (McLaren & Reed, 1972). Generally, such stunting is associated with a poorer growth prognosis, be­ cause such growth arrest is both difficult to overcome as well as being strongly associated with long-standing psychosocial deprivation. Stunting of head circumference growth is espe­ cially ominous because it reflects structural alterations in brain size (Stoch, Smythe, & Moodie, 1982). If nutritional in­ terventions are delayed or inadequate, deficits in head cir­ cumference may be lifelong, even if weight and length deficits may be largely restored (Ashem & Jones, 1978; Engsner & Vahlquist, 1975; Stoch et al., 1982). An important caveat in the calculation of growth stunting is consideration of intrauterine growth retardation (IUGR) and prematurity. IUGR is defined as both weight and height less than the 10th percentile for gestational age (Frank & Zeisel, 1988). The growth prognosis for children with a history of IUGR varies with the nature of the prenatal insult. Infants with IUGR who are underweight as compared with their length or head circumference have the best prognosis for later growth. Presumably, such infants have been poorly nourished during the end of gestation and can regain adequate weight for height by appropriate caloric intake. In contrast, infants with IUGR whose weight and length are equally delayed fre­ quently remain small despite intervention. These infants have often suffered a variety of systemic intrauterine pathological

Failure to Thrive

33

events including exposure to teratogens, infections, and chro­ mosomal abnormalities (Frank & Zeisel, 1988). Infants who were born prematurely may appear to be growth delayed simply because they are being evaluated by chronological age of birth rather than by gestational age. The age used to evaluate height and weight should be calculated by subtracting the number of weeks since birth (Frank & Zeisel, 1988). Such corrections should be made for head cir­ cumference until 18 months after birth, for weight until 24 months, and for height until 40 months (Brandt, 1979). Obvi­ ously, children with IUGR and prematurity may develop F T T in addition to their preexisting conditions. In fact, because both conditions are commonly associated with such risk fac­ tors for FTT as maternal substance and alcohol abuse, family dysfunction, and maternal mental illness or poor competence, infants with prematurity or IUGR are at higher risk for devel­ oping FTT than are full-term, normally developed neonates. Thus, while the diagnosis of either of these conditions by no means precludes the diagnosis of FTT, prematurity and IUGR must be taken into account when assessing the infant's degree of growth delay. The presence of other medical disorders associated with FTT is a c o m p l e x p h e n o m e n o n that covers the c o n t i n u u m from illnesses like malabsorption that directly cause malnu­ trition to recurring infections secondary to malnutrition in­ duced immunosuppression (Frank & Zeisel, 1988). At one time, researchers and clinicians alike attempted to rigidly dichotomize b e t w e e n children w h o were "only" malnour­ ished (so-called nonorganic failure to thrive) and children who had a p r e s u m a b l y etiological medical illness (organic failure to thrive). This rigid dichotomy served to obscure both evaluation and treatment and thus has been discarded (Frank & Zeisel, 1988). Rather than focusing only on a disor­ der that causes the malnutrition, the clinician must evaluate a child with F T T as being at high risk for chronic infectious

34

EATING AND GROWTH DISORDERS

illnesses, elevated blood levels of heavy metals, and mineral deficiencies. As with the other factors in the multiaxial approach to diag­ nosis and assessment of FTT, developmental delay is an im­ portant, multiply determined, and transactional risk factor. Both malnutrition and emotional deprivation are indepen­ dently associated with developmental delay (Frank & Zeisel, 1988). Obviously, when they are combined, they are potent risk factors. In addition, developmental delays themselves may contribute to the infant's feeding problems. Level of family functioning is a crucial variable in assess­ ment and treatment of FTT. The clinician must come to under­ stand which of myriad family dysfunctions is contributing to the infant's failure to ingest adequate calories. Earlier re­ searchers had wondered about a specific type of family and especially maternal problem. No such specific dysfunctions have been found for children with FTT as a group. However, many reports have described specific family-related problems that appear to be directly related to specific infants with FTT. Thus the absence of a prototypical family dysfunction that is related to most cases of FTT should not discourage the clini­ cian from the search for sources of family problems for a spe­ cific child with FTT. Such an exploration is crucial because the ongoing nutritional supplementation and emotional stim­ ulation must b e done in the context of the child's family. Fre­ quently, the family problems that contributed to the infant's FTT will serve as roadblocks to effective treatment.

SUMMARY Failure to thrive (FTT) is a common and serious eating and growth disorder of infancy and early childhood. Despite ex­ tensive research, considerable confusion remains over the di­ agnostic criteria that define this syndrome. Current practice supports the concept that F T T is characterized by a marked

Failure to Thrive

35

deceleration of weight gain and a slowing or disruption of emotional/behavioral/social developmental milestones. Both deceleration of linear growth and head circumference are as­ sociated but not primary phenomena. Past efforts were fo­ cused upon differentiating FTT associated with physical illness (so-called organic FTT) and FTT not associated with such illness (so-called nonorganic FTT). However, F T T is now understood to result from insufficient caloric intake that may or may not be associated with physical illnesses. These illnesses may contribute to the child's ability to eat and / o r may be caused by the infant's malnutrition. After extensive searches for specific family and social factors that cause FTT, current research indicates that a plethora of risk factors inter­ act together to influence the child's caloric intake and behav­ ioral development.

4

PSYCHOSOCIAL

DWARFISM



Psychosocial dwarfism (PSD)—also called a variety of other names, including deprivational dwarfism (Drash, Greenberg, & Mooney, 1986), emotional deprivation (Powell et al., 1967), ma­ ternal deprivation (Patton & Gardner, 1963), psychosocial short stature (Tanner, 1973), and psychosomatic dwarfism (Ferholt et al., 1985)—is a syndrome of deceleration of linear growth combined with characteristic behavior disturbances (sleep disorder and bizarre eating habits), both of which are revers­ ible by a change in the psychosocial environment (Green et al., 1984; Money & Wolff, 1974; Powell et al., 1967; Silver & Finkelstein, 1967). The deceleration of linear growth is re­ markable in that it occurs in the absence of weight gain decel­ eration. In this way, PSD is quite distinct from growth stunting secondary to malnutrition (FTT) but rather resembles primary hypopituitarism (Blizzard, 1973; Powell et al., 1967). The most common characteristic abnormal behaviors include polyphagia, gorging, vomiting, stealing and hoarding food, and eating from garbage pails and animal food dishes. Other behaviors reported include polydipsia including drinking stagnant water, toilet bowl water, and dishwater. Various sleep disorders have been described such as initial onset insomnia 37

38

EATING AND GROWTH DISORDERS

and night wandering (Drash et al., 1986; Green et al., 1984). These sleep disturbances may be related to growth delay be­ cause it interferes with the major nocturnal pulsatile release of growth hormone (Money & Wolff, 1974). Children with PSD may exhibit a variety of unusual patterns of relatedness and problems with behavior including aggressiveness and impulsivity. Both specific language delays and delays in gen­ eral intellectual development have been reported (Drash et al., 1986; Ferholt et al., 1985). Unfortunately, PSD has been confused with FTT to such a degree that research has been greatly confused. A n example of the persistent nature of this diagnostic confusion between PSD and FTT is presented in a recent, comprehensive review article on PSD (Green et al., 1984). Although the authors con­ cisely defined P S D as not including malnutrition as directly contributory, and although they quoted Blizzard's (1973) clear distinction between P S D and FTT, they used the term failure to thrive as a synonym for PSD in several places in their literature review, discussion of etiology, and summary.

NATURAL HISTORY Epidemiology and Developmental Course PSD apparently is a rare disorder so that virtually all of the available literature consists of case reports or small case se­ ries. Incidence, prevalence, sex ratio, and sociodemographic features are unknown. The age of onset is unclear but report­ edly is between 18 months and 48 months. Blizzard (1973) ar­ gued that the onset must occur after 24 months to reliably distinguish it from FTT. Developmental outcome appears to be highly variable al­ though limited outcome data are available. Outcome appears to be highly contingent upon the adequacy o f the child's psy­ chosocial environment. Hospitalization or removal to a less

Psychosocial Dwarfism

39

noxious home environment is presumed to be ameliorative because these are associated with reversal of some of the neu­ roendocrine, growth, and behavioral concomitants of the dis­ order (Hopwood & Becker, 1979; Powell et al., 1967). If the child is returned to the noxious home environment, the vari­ ous gains that have been achieved may be arrested or re­ versed. Behavioral disturbance, developmental delays, and short statue are possible long-term sequelae. In addition, de­ layed puberty may occur (Howse et al., 1977; Money & Wolff, 1974).

Etiology (1) Social and family factors. The literature is virtually unani­ mous in describing parental psychopathology that results in maltreatment of the child (e.g., Ferholt et al., 1985; Powell et al., 1967) including overt abuse a n d / o r neglect (Drash et al., 1986; Ferholt et al., 1985). This maltreatment may include sib­ lings (Hopwood & Becker, 1979). Several reports have indi­ cated that both the parental psychopathology and the maltreatment of the child may be obscured in initial office visits. The parents have been reported to withhold clinical in­ formation and to be uncooperative with treatment (Hopwood & Becker, 1979). The frequent association of parental psycho­ pathology and the reversal of the associated features with change in environment appear to be quite convincing. How­ ever, because no studies have been reported that control for such basic variables as socioeconomic class, the validity of these findings should be viewed as preliminary. (2) Organic and genetic factors. Much of the research on P S D has focused on neuroendocrine abnormalities found in the syndrome in an attempt to unravel the relationship between growth rate and neuroendocrine changes. Unfortunately, these investigations have led to the discovery of no pathognomonic

40

EATING AND GROWTH DISORDERS

or consistently abnormal findings, with the possible exception of depressed somatomedin levels (Green et al., 1984). The ab­ normalities in hormonal levels and hypothalamic functioning have been found to normalize partially or completely follow­ ing the subjects's removal from the inimical environment. This normalization may occur in several weeks or require as long as two years, depending on the specific endocrine distur­ bance and the type of specific medical, hormonal, or psychiat­ ric treatment (Green et al., 1984). In addition to this great variability in the normalization of endocrine abnormalities, none of the abnormal hormonal findings correlates specific­ ally with growth failure. Growth failure has occurred with normal endocrine values, and catch-up growth has occurred with subnormal values (Green et al., 1984). The mechanisms causing the growth failure in P S D are thus, as yet, unknown. The explanation for the rarity of P S D even among children exposed to maltreatment is a complete mystery. Possible fac­ tors may include genetic vulnerability to a disruption in the rate or rhythm of growth hormone production or some spe­ cific type of psychosocial deprivation that causes such neuro­ endocrine dysfunction. However, the unraveling of these mysteries awaits better designed studies that have larger sam­ ple sizes and use matched controls.

DIAGNOSTIC CLASSIFICATION

AND SPECIAL TREATMENT ISSUES

PSD involves several factors: reversible neuroendocrine and growth dysfunction, b e h a v i o r a l disturbances and develop­ mental delays, and presumably a noxious psychosocial envi­ ronment. Evaluation of the neuroendocrine and growth dysfunction is important in the differential diagnosis of other disorders that are associated with short stature as well as in monitoring the response to treatment. These other disorders involving short stature include primordial dwarfism, IUGR

Psychosocial Dwarfism

41

with persistent small size, hypopituitarism from a variety of etiologies, constitutional delayed growth, Turner's syndrome (XO chromosomal pattern), osteochondrodystrophies, and growth stunting secondary to chronic malnutrition with or without chronic disease. P S D is virtually unique in being re­ versible with a change in living situation and in the absence of any signs of physical illness except growth delay. Like short stature, the behavioral disturbances and devel­ opmental delays found in P S D serve as important factors in helping to monitor response to treatment as well as in repre­ senting serious aspects of the disorder that must b e ad­ dressed. A careful psychiatric evaluation of the child is required that assesses for the presence of bizarre and disrup­ tive behaviors as well as for problems in normal social relat­ edness. A developmental assessment must evaluate both for specific delays, especially in language, and for general devel­ opmental delays. In older children, psychoeducational testing is helpful to assess specific intellectual, academic, and adap­ tive functioning. Psychotherapeutic and educational interven­ tions should b e guided by these findings. Evaluation and intervention to ameliorate the psychosocial adversity is both the most important as well as the most difficult task (Hopwood & Becker, 1979). According to all reports, care­ takers of a child with PSD may be actively uncooperative in the assessment and treatment phases. Ideally, the caretakers can be engaged in the appropriate individual and family psychothera­ pies. In addition, they can use various social supports such as home aides and support groups. In the event of active treatment refusal, which may result in permanent damage to the child, the treaters must consider removal of the child from the home.

SUMMARY Psychosocial dwarfism (PSD) is an apparently rare growth disorder characterized by primary deceleration of linear

42

EATING AND GROWTH DISORDERS

growth combined with characteristic behavioral disturbances. Both of these aspects of PSD are reversible b y a change in the psychosocial environment. The deceleration of linear growth is remarkable in that it occurs in the absence of weight gain deceleration. In this way, PSD is quite distinct from the growth stunting that occurs late in the course of FTT but resembles primary hypopituitarism. PSD apparently occurs in neglected and abused children whose neuroendocrine regula­ tion is susceptible to disruption. Primary caretakers of chil­ dren with P S D are alleged to be abusive and resistent to obtaining treatment.

5

RUMINATION

Rumination, also k n o w n as merycism or psychogenic vomiting, is a relatively rare s y n d r o m e in w h i c h previously ingested food is voluntarily regurgitated, rechewed, and partially swallowed (Richmond, Eddy, & Green, 1958). In the process of this regurgitation, the infant loses a considerable a m o u n t of food and so b e c o m e s malnourished ( R i c h m o n d et al., 1958). According to C a m e r o n (1925), The infant appears w i t h d r a w n and apathetic except when in the act o f ruminating. At those times, the in­ fant lies with an expression o f supreme satisfaction u p o n its face, sensing the regurgitated milk and sub­ jecting it to innumerable sucking and chewing m o v e ­ ments. . . . It is very evident that achievement of his purpose produces a sense of beatitude while failure re­ sults in nervous unrest and imitation.

43

44

EATING AND GROWTH DISORDERS NATURAL HISTORY

Developmental Evolution and Outcome Because rumination is apparently a relatively rare disorder, virtually all of the information about the phenomenology must be derived from single case reports or small case series (e.g., Mayes et al., 1988; Sauvage, Leddet, Hameur, & Barthelemy, 1985; Winton & Singh, 1983) without comparison groups (Holvoet, 1982). In otherwise normally developing in­ fants, the age of onset is in the first year of life, whereas in mentally retarded individuals, the age of onset can extend into adulthood (Mayes et al., 1988). In some unknown propor­ tion of cases, the disorder remits spontaneously, while in oth­ ers, the course may be malignant, marked by aspiration, severe malnutrition, growth failure, developmental delay, and death. Some authors (Mayes et al., 1988) have proposed two diagnostic subgroups, psychogenic and self-stimulatory, to capture the difference in the course of retarded and non­ retarded individuals. However, the relatively small sample size appears to make diagnostic subtyping premature.

Epidemiology Very little is known about the incidence and prevalence of rumination although the most severely affected cases, which are the ones that have been reported, are rare. The sex ratio of the disorder is also unclear, although one case series (Mayes et al., 1988) reported a male predominance.

Etiology (1) Social, family, and genetic factors. Several authors have proposed that an adverse psychosocial environment is central

Rumination

45

to the development of rumination in otherwise normal infants (e.g., Hollowell & Gardner, 1965; Mayes et al., 1988; Rich­ mond et al., 1958). The most common environmental factor cited in the genesis of rumination is an unsatisfactory mother­ infant relationship that causes the infant to seek an internal source of gratification. This turning inward by the infant has been proposed to occur because the environment is more stimulating than the infant can tolerate (Flanagan, 1977), be­ cause the environment is not gratifying enough (Menking, Wagnitz, Burton, Coddington, & Solos, 1969; Richmond et al., 1958), or because the environment is too stimulating with neg­ ative effects (Ferholt & Provence, 1976; Hollowell & Gardner, 1965). Aside from these proposed family factors, no informa­ tion has been reported about more general sociodemographic features. Similarly, the role of genetic factors is unknown. (2) Psychogenic factors. Learning theorists have explained ru­ mination in terms of the reinforcing response that it elicits. These proposed feedback mechanisms include positive rein­ forcement when a desired event such as pleasure or attention follows rumination and negative reinforcement when an un­ desired event such as anxiety is reduced or removed. A more sophisticated theory involves combining the concept of posi­ tive and negative reinforcement by proposing a change in the valence of the behavioral consequences. For example, conse­ quences that are normally behavior suppressing m a y ac­ quire behavior reinforcing characteristics if other, more usually positive, consequences are lacking (Winton & Singh, 1983). These concepts of the operant conditioning psycho­ genic factors in rumination are useful as the theoretical un­ derpinnings of certain behavioral treatments of rumination. (3) Organic factors. The role of organic factors in rumination remains obscure but some authors have argued that rumina­ tion is totally the result of physical disorders including hiatal

46

EATING AND GROWTH DISORDERS

hernia and other esophageal abnormalities (Astley, 1956; Botha, 1962; Herbst, Friedland, & Zboralske, 1971). The rela­ tionship between the syndromes of rumination and gas­ troesophageal reflux (GER) is unknown although high rates of association have been reported (Shepherd, Wren, Evans, Lander, & Ong, 1987). GER, or chalasia, is the syndrome of re­ gurgitation of the stomach contents into the mouth and esopha­ gus, apparently as a result of hypomobility of the gastric fundus and delayed gastric emptying rather than a weakened esopha­ geal sphincter (Hillemeier, Lange, McCallum, & Gryboski, 1981; Papaila et al., 1989). A possible but untested hypothesis is that GER is the physiological substrate upon which various psy­ chosocial disruptions or deviant operant conditioning act so that rumination develops (Woolston, 1989a).

DIAGNOSTIC CLASSIFICATION

AND SPECIAL TREATMENT ISSUES

Rumination appears to require three factors: an impaired ability of the infant or retarded person to regulate his or her internal state of satisfaction, a physical propensity to regurgi­ tate food, and a learned association that regurgitation helps relieve the internal state of dissatisfaction. The assessment of the child must include an evaluation of each of these factors as well as the medical sequelae of rumination such as malnu­ trition and aspiration. Obviously, these medical sequelae will influence the vigor of the intervention as well as serving as a baseline by which to measure the child's response to treatment. The assessment of the infant's capacity to regulate his or her internal state must include a general developmental as­ sessment to evaluate for serious d e v e l o p m e n t a l delay as well as hyperirritability states. In addition, the mother-infant relationship must be carefully examined for clues to stimuli that are noxious or disruptive to the infant.

Rumination

47

The child's propensity to regurgitate can b e best evaluated by procedures developed for GER including esophageal pH moni­ toring, scintigraphic gastroesophageal reflux scan, endoscopy, and gastric emptying studies (Arosu et al., 1980). In addition, various radiological procedures that evaluate esophageal abnor­ malities should be considered. The learned aspect of rumination, especially in retarded in­ dividuals, may be crucial. After careful evaluation of this fac­ tor, various behavioral interventions must be considered, especially if there are serious medical complications. These interventions include aversive techniques in which a noxious stimulus is paired with rumination (Glasscock, Friman, O'Brien, & Christopherson, 1986; Singh, Manning, & Angell, 1982) and nonaversive techniques such as differential rein­ forcement of other incompatible responses (Mestre, Resnick, & Berman, 1983) and holding (Whitehead, Drescher, & MerrillCorbin, 1985).

SUMMARY Rumination, also known as merycism or psychogenic vom­ iting, is a relatively rare syndrome in which previously in­ gested food is voluntarily regurgitated, rechewed, and partially swallowed. In the process of this regurgitation, the infant loses a considerable amount of food and so m a y be­ come malnourished. Rumination typically occurs in otherwise normally developing infants or mentally retarded individuals of all ages. Like other eating disorders, considerable confu­ sion exists about its relationship with other diagnostic enti­ ties. For example, gastroesophageal reflex (GER), the physiological propensity to reflex the stomach contents into the esophagus and mouth, may be related to the development and continuation of rumination. Investigators have typically advocated for only one type of etiology depending upon their area of interest. Surgeons and pediatricians have emphasized

48

EATING AND GROWTH DISORDERS

the physical contributions including GER and anatomical ab­ normalities. Child psychiatrists have focused upon inade­ quate or adversely stimulating environments provided by caretakers. Behavioral psychologists have described specific learning paradigms that seem to sustain rumination. Current understanding indicates that rumination requires all three factors: a physical propensity to regurgitate food, an impaired internal state of satisfaction, and a learned behavior habit pat­ tern.

6

PICA

Pica, the persistent ingestion of nonnutritive substances, is an eating behavior that has been documented for centuries (Lacey, 1990). Despite this long history and despite the significant health hazards associated with this disorder, surprisingly little is known about it. Even the definition has been unclear, with disagreements about the types of substances ingested, the person's degree of control over the behavior, and its relationship to normal eating behavior (Lacey, 1990). Indeed, the confusion in the literature reflects the broad diversity of the disorder, which includes normally developing toddlers mouthing paint chips, rural pregnant women eating clay or starch, severely re­ tarded adults eating feces, and normally developed, anxious adults chewing pencil erasers, fingernails, and ice.

NATURAL HISTORY Developmental Evolution and Outcome In many ways, the heterogeneity of pica precludes a coher­ ent statement about age of onset or developmental outcome. 49

50

EATING AND GROWTH DISORDERS

Because in the pediatric literature great attention has b e e n paid to the p h e n o m e n o l o g y of lead poisoning, pica has be­ come s y n o n y m o u s with eating paint chips. For these chil­ dren, pica has been reported to b e more c o m m o n in situations of relative environmental deprivation (Madden, Russo, & Cataldo, 1980) or parental p s y c h o p a t h o l o g y . In this population, pica begins in the second and third y e a r of life and may continue into midchildhood. In a second pop­ ulation, young pregnant w o m e n , the onset of pica begins with the first pregnancy in late adolescence or early adult­ hood and m a y continue intermittently for several decades. Pica in mentally retarded individuals begins in childhood and may diminish after middle age ( M c A l p i n e & Singh, 1986). In this population, the risk of pica appears to b e re­ lated to the degree o f retardation so that the most severely retarded are most likely to have the disorder (Danforth & Huber, 1982). Pica in chronically anxious children or adults has never been studied or described in the literature. In this last group, a possible relationship between pica, trichotillo­ mania, and other compulsive behavior disorders has never been investigated.

Epidemiology Incidence and prevalence figures for such a heterogenous disorder are difficult to interpret. However, among specific at-risk populations, pica has been reported to be quite com­ mon. Halstead (1968) summarized findings from research studies that indicated that pica occurred in 2 5 % to 3 3 % of young children and 4 0 % to 5 0 % of poor black pregnant woman. Pica among institutionalized retarded adults has been reported to range from 9% (McAlpine & Singh, 1986) to 26% (Danforth & Huber, 1982).

Pica

51

Etiology (1) Social and family factors. Numerous studies have docu­ mented that the eating of specific substances such as clay and starch has been strongly influenced by cultural and family factors (Lacey, 1990) because various social groups, especially poor and rural people, regard the eating of certain nonnutri­ tive substances as acceptable. In addition, toddlers who are poorly supervised and understimulated are at high risk for in­ gesting inappropriate materials like paint chips. (2) Other factors. Except as mediated by mental retardation, there are no known genetic factors in the etiology of pica. Boredom, anxiety, and depression may exacerbate pica but lit­ tle has been reported about such associated psychopathology. Iron deficiency is sometimes associated with pica but the di­ rection of the causal association is unclear (Vyas & Chandra, 1984).

DIAGNOSTIC CLASSIFICATION

AND SPECIAL TREATMENT ISSUES

W h i l e the extraordinary diversity of this disorder m a k e s any useful classification schema unlikely, the r e m a r k a b l e prevalence and seriousness of its medical complications re­ quire a thoughtful, vigorous approach. These medical compli­ cations include heavy metal poisoning, mineral/vitamin deficiency, parasite ingestion, and intestinal obstruction. For toddlers and young children with a history of pica, a careful evaluation of the home environment and family functioning is required. In addition, these children should be evaluated for cognitive and psychiatric impairments. Pregnant women with pica presumably have more voluntary control over their

52

EATING AND GROWTH DISORDERS

eating. A careful assessment of their cultural and nutritional beliefs is essential so that nutritional counseling can be help­ ful. Severely retarded individuals presenting with pica should be assessed for access to noxious materials and provided with sufficient supervision to prevent the pica. .

SUMMARY Pica, the persistent ingestion of nonnutritive substances, is a complex phenomenon that is difficult to confine to a single, syndromic complex because persistent confusion exists about the types of substances that are ingested, the degree of volun­ tary control over the behavior, and the relationship to normal eating behavior. Pica occurs in four rather distinct population groups, which may or may not be related. In one population, pica occurs in the first and second years of life in normally developing but somewhat poorly stimulated and supervised toddlers. The very serious and substantial sequelae of lead poisoning may occur in this group as a result of ingestion of paint chips. A second population consists of adolescent and young adult pregnant women who eat a variety of substances including clay and starch. Those eating practices are usually culturally accepted and under voluntary control. Such pica may result in heavy metal poisoning, nutrient deficiency, and intestinal obstruction. A third population is mentally retarded individuals of all ages. These individuals may ingest almost any substance at hand, including feces. The fourth population is normally developed children and adults who chew on and ingest various substances during periods of anxiety. Assess­ ment and treatment of pica is strongly influenced by the spe­ cific population in which it occurs.

7

OBESITY

Considerable attention in the literature has been focused on the eating disorders of early childhood that result in growth failure, such as FTT, PSD, and rumination. In contrast, the eating disorders that result in excessive weight gain have been virtually ignored. D S M III-R has reinforced this preju­ dice by refusing to classify any form of obesity as an eating disorder (American Psychiatric Association, 1987). Instead, it describes obesity as a physical disorder. In conjunction with this lack of interest in the obesity of early childhood, there are many widely held misconceptions about its etiology, course, and even heterogeneity of subtypes. This state of clinical in­ difference about the fundamentals of infantile obesity makes a scientific strategy for intervention difficult. The first step in the elucidation of any new field of study is the construction of an operational definition that is phenome­ nologically reliable and valid. In the study of obesity, there needs to be an easy, accurate, reliable method of defining the clinical condition. Because obesity denotes being excessively fat, the operational definition must differentiate the condition of having excessive adipose tissue for chronological age from simply being heavy for chronological age as a result of large 53

54

EATING AND GROWTH DISORDERS

muscle mass or skeletal frame. Triceps skin fold thickness (Garn & Clark, 1976) and an obesity index using weight gain, suprailiac skin fold, and waist circumference (Crawford, Kel­ ler, Hampton, Pacheo, & Huenemann, 1974) are two well­ standardized measurements that appear to satisfy the requirements for a useful, operational definition of obesity. A simpler, if slightly less valid, measure of obesity is defined by exceeding 120% of ideal body weight (IBW) for height for a given age and sex. Specifically, IBWH is calculated by divid­ ing actual weight by the expected weight for a given age and sex and height percentile.

NATURAL HISTORY Developmental Evolution and Outcome The study of the natural history of obesity in infancy and early childhood is in its beginning stages. Data about the typi­ cal course of this disorder are contradictory. The most widely held belief is that obesity of early onset is a chronic and stead­ ily progressive disorder with very few remissions. Compared with 14% of average or lightweight infants, 3 6 % of infants who exceeded the 90th percentile in weight were reported to be overweight as adults (Charney, Chamblee, McBride, Lyon, & Pratt, 1976). Eid (1970) found that infants who were gaining weight rapidly were four times more likely to be obese b y age 8 than infants who were gaining weight at a normal rate. This grim prognosis has been buttressed by a network of theory and experimental data about fat cell proliferation in early childhood and its deleterious impact on appetite and weight gain later in life. However, more recent workers (Poskitt, 1980; Shapiro, Crawford, & Clark, 1984) have reported that obesity in infancy is a poorer predictor of later childhood obe­ sity than was believed previously. Poskitt (1980) showed that the relative risk of an overfat infant becoming an overfat

Obesity

55

5-year-old was about 2.5 times that for a normal infant. Of 203 children, 4 0 % were overweight (110% IBW) or obese (120% IBW) as infants. B y age 5 years, 13.5% were overweight, and 2.5% were obese. Most overweight infants did not become overweight children, but 6 0 % of the 27 overweight 5-year­ olds also were overweight in infancy. Shapiro, Crawford, and Clark (1984) studied 450 six-month-old infants w h o m they followed for 8 years. They found that, o f the 26 children (17 boys and 9 girls) who were obese at 6 months, fewer and fewer remained obese at subsequent annual measurements, until only one remained obese at 9 years. In contrast, infants who were not obese at 6 months but who later became obese at ages 4 to 8 years were much more likely to be obese at 9 years. This rather poor correlation between obesity in infancy and obesity in later childhood calls into question the notion of re­ lentlessly progressive obesity that is triggered by fat cell pro­ liferation in infancy or early childhood. Rather than there being a critical phase in infancy for fat cell proliferation, it is more likely that the degree and duration of obesity are the major determinants of total adipose cell number in man (Kirt­ land & Gurr, 1979; Knittle, Timmers, Ginsberg-Fellner, Brown, & Katz, 1979). Poskitt (1980) reported that very little multiplication of adipose cells takes place in infancy. T h e nat­ ural increase in size of those adipose cells present at birth is sufficient to account for almost all of the increase in fat stored in the first year without any increase in cell number.

Epidemiology The incidence and prevalence of obesity in early childhood is not nearly as well studied as obesity in adulthood. The few studies indicate that the prevalence rate of obesity is 5%-10% of preschool-aged children (Maloney & Klykylo, 1980). Occasion­ ally, "epidemics" of infantile obesity have been reported with

56

EATING AND GROWTH DISORDERS

prevalence rates of 16.7% of infants under 12 months of age (Shukla, Forsyth, Anderson, & Marwah, 1972). These epidem­ ics appear to be caused by culturally determined misinforma­ tion or fads about infant feeding practices (Shukla et al., 1972; Taitz, 1971). The well-publicized and best documented epi­ demic occurred in England between 1960 and 1975 (Taitz, 1971). At that time, English parents were encouraged to fol­ low the maxim: "One cannot overfeed a young baby." Parents commonly used full cream milk powder with added sucrose as baby formula and, in many parts of England, mothers were encouraged to introduce solids at a very early stage. By 1973, the dangers of infantile obesity and hypertonic dehydration were well publicized. Between 1971 and 1976, the rate of 6­ week-old infants being fed unmodified milk powder went from 90% to 0%, and the rate of infants above the 50th percentile in weight went from 79% to 43% (Taitz, 1971). In a closely analo­ gous fashion, nonorganic failure to thrive has been reported to occur as a result of parental misconceptions about diet (Pugliese, Weyman-Daum, Moses, & Lifshitz, 1987; Woolston, 1983). In a more classic picture, obesity appears to be related to cultural prac­ tices given that it covaries with social class. Obesity in females is nine times more common in working­ class families than in middle- and upper-class families (Stunkard, D'Aquill, Fox, & Filion, 1972). The prevalence of obe­ sity is linked to the socioeconomic status of the parents almost as strongly as it is to the subject's own social class (Goldblatt, Moore, & Stunkard, 1965). This finding argues that socioeco­ nomic status is linked to obesity in a causal, rather than a sim­ ple associative, manner, perhaps mediated through culturally determined eating habits and dietary misconceptions.

Etiology (1) Genetic and familial factors. A family-line analysis of obe­ sity indicates that there is a strong correlation between the

Obesity

57

fatness of parents and their children. For example, by age 17, the children of obese parents have three times the chance of being obese as the children of lean parents. If one sibling is fat, there is a 4 0 % chance that a second sibling will be fat (Garn & Clark, 1976). If two siblings are fat, there is an 8 0 % chance that the third sibling will be fat. While these data seem to support a genetic basis for obesity, one must keep other nongenetic, but family-related, factors in mind. The same study reporting the sibling data also indicates that, if one spouse is fat, there is a 3 0 % chance that the other spouse also will be fat (Garn & Clark, 1976). Obviously, this finding can­ not be explained b y genetic factors. The familial factors related to infantile obesity are less clear. Poskitt (1980) reported that there was no significant differ­ ence between the number of overweight and normal weight infants with one or both parents overweight. But, by 5 years of age, 78% of the overweight and only 3 5 % of the normal weight children had at least one parent overweight. This was a significant difference and showed that the relative risk of a child's being overweight with at least one parent overweight was more than five times that of a child with two normal weight parents. Well-designed genetic studies involving monozygotic/di­ zygotic concordance (Stunkard, Foch, & Hrubec, 1986) and adoption samples (Stunkard, Sorenson, et al., 1986) support a strong genetic contribution to all forms of body habitus rang­ ing from fatness to thinness. (2) Temperament and psychogenic factors. Although tempera­ ment has become a focus of study in pediatrics and child psy­ chiatry (Thomas & Chess, 1977), it has been generally neglected in research about childhood onset obesity. This lack of investigation is surprising because temperament could poten­ tially be associated with the development and course of obesity in three separate ways: (a) etiology (e.g., low activity out­ put), (b) correlates or consequences (e.g., social undesirability

58

EATING AND GROWTH DISORDERS

might result in negative peer interactions and social with­ drawal), and (c) problems in management (low persistence would interfere with treatment compliance; Carey, Heguik, & McDewitt, 1988). Because temperament has been demon­ strated to have a major genetic determination (Wilson & Mathany, 1986), it may be one mediating factor for the ge­ netic contribution of obesity. To date, one study has demon­ strated an association between eight difficult temperament characteristics and rapid weight gain and obesity in middle childhood (Carey et al., 1988). Studies of overt psychopathology in obese adults have been as contradictory as studies of other aspects of obesity. Although m a n y authors have reported no objective data in­ dicating an increased incidence of p s y c h o p a t h o l o g y in obese adolescents and adults (McCance, 1 9 6 1 ; Shipman & Plesset, 1963), other authors such as Bruch (1973) and Stunkard (1975) have reported just the opposite. Silverstone (1969) attempted to reconcile these discrepant reports b y differentiating b e t w e e n late onset obesity secondary to a gradual accumulation o f fat and early onset obesity charac­ terized b y a sudden increase in fatness that was the result of anxiety-driven overeating. Very little is k n o w n about p s y c h o p a t h o l o g y in infantile obesity. In one of the few re­ ports about this problem, Kahn (1973) described a sample of 73 obese children less than 3 years old. He found 3 2 % o f these young children showed a sudden weight gain associ­ ated with a major and traumatic separation from their pri­ mary caretakers. This report is suggestive of a discrete s y n d r o m e related to traumatic separation that results in a sudden onset o f obesity. A second type of psychogenic obesity of infancy and early childhood occurs in the context of a disorganized family in which the child's needs are poorly perceived and even more poorly differentiated (Christoffel & Forsyth, 1985). Typically, any sign of distress in the infant or toddler is responded to b y feeding a n d / o r neglect.

Obesity

59

The observed psychosocial characteristics parallel features described in failure to thrive of psychosocial origin (Barbero & Shaheen, 1967; Leonard et al., 1966). Children with this form of psychogenic obesity are from families in which there is severe disruption and disorganization. Factors that contrib­ ute to and are an expression of family dysfunction include separation of the parents, alcohol or drug abuse by the par­ ents, and failure to maintain a stable and constant living envi­ ronment. There often is denial of the severity, or even the existence, of the problem, and there often is poor medical care, failure to follow through with management plans, and, sometimes, hostility toward health professionals. The com­ mon behavioral outcome is the parents' inability to set limits, which also is evident in other parent-child interactions. Ma­ ternal depression is clearly evident in some cases. Severe family disorganization, in addition to being related to the etiology of obesity, presents a major obstacle to treatment. Case reports (Boxer & Miller, 1987; Woolston & Forsyth, 1989) describe a high level of parental noncompliance, direct under­ mining, and a lack of participation in the treatment of the child. (3) Organic factors. One of the primary foci of clinicians who are exploring the etiology of infantile obesity is the discovery of specific organic dysfunctions that produce endogenous obesity. This endogenous form of obesity is in contradistinc­ tion to exogenous obesity, in which there is no physical dys­ function other than consuming excess calories. Endogenous forms are caused by discrete genetic, endocrinological, or neurological syndromes, including Prader-Willi, Klinefelter's, Fröhlich's, Lawrence Mood Biedl, Kleine-Levin, and Mauriac syndromes. Of special research interest is the finding that Pra­ der-Willi syndrome appears to be associated with a micro de­ letion of the proximal long arm of chromosome 15, band q 11.2 (Donlon, 1988). In a surprising and currently inexplicable turn of events, Angelman syndrome, or the "happy puppet"

60

EATING AND GROWTH DISORDERS

syndrome, appears to be associated with the same micro dele­ tion (Donlon, 1988). Although these endogenous causes of obesity are fre­ quently searched for as an etiology for obesity in early child­ hood, they are quite rare. In addition, a clinical rule o f thumb distinguishes between exogenous and endogenous obesity. Children with endogenous obesity are usually below the 25th percentile in height and have delayed bone age, whereas chil­ dren with exogenous obesity are above the 50th percentile in height and have advanced bone age.

DIAGNOSTIC CLASSIFICATION

AND SPECIAL TREATMENT ISSUES

One of the most obvious explanations for the contradictory results of various studies in regard to developmental course and etiology is that obesity in this age group is a heteroge­ neous syndrome. Many authors (e.g., Maloney & Klykylo, 1983; Stunkard, 1975, 1980) have identified multiple factors that contribute to the development of obesity, including emo­ tional, socioeconomic, genetic, developmental, and neurologi­ cal factors. Although preliminary attempts have been made to subdi­ vide forms of juvenile onset obesity into phenomenologically homogeneous groupings (Woolston, 1988; Woolston & Forsyth, 1989), such attempts are probably premature. Many of the same issues related to diagnostic classification of FTT apply to obe­ sity. Fundamentally, all forms of obesity have the same organic basis: caloric intake that exceeds caloric expenditure. Like FTT, there are a multitude of primary medical illnesses that are asso­ ciated with obesity. However, because it is the excess caloric in­ take that actually mediates the obesity, there frequently are psychosocial components to even so-called endogenous obesity. The data base of obesity of early childhood is too small to per­ mit construction of clinically useful categories. Instead, like FTT,

Obesity

61

a multiaxial list of major risk factors is more helpful. These should include age of onset and duration, degree of obesity, fam­ ily history of obesity, presence of a medical illness or syndrome associated with obesity, and type of family functioning. In a similar fashion to FTT, obesity that is associated with an acute onset in the first 12 months has an excellent progno­ sis because the treatment is simply a matter of reducing the infant's caloric intake to recommended level for height and age. However, this benign condition can become much more problematic if there are other risk factors such as severe fam­ ily dysfunction, a strong family history for obesity, or a medi­ cal syndrome associated with obesity. The longer the obesity persists beyond infancy and the later is its onset in childhood, the more persistent it is likely to be. The degree of obesity, expressed either as a percentile of ideal body weight for height and age or as a Ζ score, predicts prognosis in that the degree of obesity m a y reflect the serious­ ness of the underlying risk factors. More important, the de­ gree of obesity helps guide the clinician regarding the likelihood of serious medical sequelae of obesity such as slipped femoral head epiphysis, sleep apnea, Pickwickian syndrome, hypercholesterolemia, and diabetes mellitus. In addition, the degree of obesity must guide the nutritional in­ tervention. Caloric restriction below the recommended amounts for height, age, and sex is rarely indicated. Instead, the primary goal is to arrest continued weight gain until the child's height and weight are proportional. Family history of obesity is important for both genetic and family-cultural reasons. Regardless of the mode of action, obe­ sity that is related to the influence of family history alone has a slow, gradual onset in middle childhood and is frequently per­ sistent into adulthood. New data indicate that children with a positive family history for being overweight as their only risk factor may have a relatively good response to brief, family-based behavioral intervention. Using a prospective, randomized con­ trolled experimental design, Epstein, Valoski, Wing, and

62

EATING AND GROWTH DISORDERS

McCarley (1990) demonstrated that an 8-week behavioral inter­ vention program for both the obese child and his or her parents significantly reduced the obesity in the child at the end of the 10-year follow-up. In the absence of other risk factors, children with this pattern of obesity rarely become morbidly obese and so rarely develop the major medical complications of severe obesity. As indicated earlier, children with obesity as part of a primary medical syndrome are usually below the 25th percentile in height and are frequently cognitively impaired. Level of family functioning may be crucial in both the genesis of obesity as well as its treatment. Severely dysfunctional fami­ lies provide the child with an environment of emotional neglect, a sense of abandonment, and no limit setting around the use of food. A small number of children who grow up in such environ­ ments develop a pattern of enormous caloric intake and a rapid onset of severe obesity, usually beginning between age 3 and 5 years. These children are at high risk for poor developmental outcome because the constellation of risk factors conspire to produce a powerfully negative synergistic spiral. These children usually have low self-esteem, which is exacerbated by their obe­ sity. They are likely to suffer the most serious medical complica­ tions of obesity. Most important, they are at high risk because the only effective intervention for treatment of obesity is medi­ ated through the family system. This intervention includes the orchestration of appropriate medical and mental health services, effective limit setting, and the development of more positive self-esteem and emotional security. Unfortunately, the very risk factor that contributed so heavily to the genesis of the disorder, family dysfunction, makes intervention difficult (Woolston & Forsyth, 1989).

SUMMARY Obesity in infancy and early childhood is a heterogeneous s y n d r o m e that has been relatively neglected in the eating

Obesity

63

disorder literature. The development of obesity is influenced by the interplay of social, familial, emotional, and physical factors. Analogous to FTT, obesity has been subtyped accord­ ing to the presence or absence of physical disorders that are associated with obesity. Much less attention has been given to the different roles of genetics, cultural eating habits, and psy­ chogenic factors.

8

BENIGN NUTRITIONAL

DWARFING

Benign nutritional dwarfing (BND) is a disorder of school-age children and young adolescents in which maladaptive eating patterns unaccompanied b y psychiatric or medical disorders result in a marked slowing of weight gain for at least one year followed by a deceleration o f linear growth. Delayed puberty may b e associated with this disorder. Because the subnormal weight gain in such children is accompanied by a proportion­ ate decline in growth velocity, body weight for height deficits are frequently not evident. Therefore, children with B N D do not present with emaciation as is commonly observed in cases of severe malnutrition. Although dwarfing, secondary to chronic malnutrition in childhood, is as old as humankind, BND is a relatively newly described disorder (Apley et al., 1971; Davis et al., 1978; Lifshitz et al., 1987; Pugliese et al., 1983). While various authors report various different motiva­ tions for the inadequate caloric intake, all reports have been consistent in describing an absence of weight loss (as opposed to a slowing of weight gain) and an absence of body image distortion. A recent, well-controlled study found virtually no differences in various measures of psychological functioning 65

66

EATING AND GROWTH DISORDERS

between children with B N D and matched constitutionally growth delayed or familial short-statured children (Sanberg et al., 1991).

NATURAL HISTORY Developmental Evolution and Outcome Typically, the age of onset for B N D is middle childhood to early adolescence (8-14 years), although some authors have included children as young as 2 years (Davis et al., 1978) and as old as 15 (Lifshitz et al., 1971). Although the consequences of chronic insufficient caloric intake can include delayed puberty and permanent short stature, children with B N D frequently respond to relatively straightforward nutritional counseling with an increase in caloric intake that is sufficient enough to reinitiate normal growth. There are no reports of associated development or psychiatric disorders either during the course of B N D or as its sequelae.

Epidemiology Because of the relatively recent reporting of B N D , satisfac­ tory data on its incidence and prevalence do not exist. In most reports of B N D , there is a slight predominance of boys to girls.

Etiology (1) Social, family, genetic, and psychogenic factors. B N D is characterized by the absence of social or familial dysfunction that typifies other eating and growth disorders. There are no reports that indicate any particular parental psychopathology

Benign Nutritional Dwarfism

67

or genetic factors. Some reports have described special nutri­ tional concerns (Pugliese et al., 1983) and chronic nonspecific feeding disturbances (Davis et al., 1978). The only psycho­ genic factors reported to be related to B N D are inaccurate nu­ tritional beliefs about weight gain or special dietary needs. (2) Organic factors. As indicated earlier, inadequate caloric intake to maintain normal weight gain is the only known or­ ganic factor. Various mineral and vitamin deficiencies may complicate the inadequate caloric intake (Lifshitz et al., 1971). One report (Lifshitz et al., 1971) has speculated that some pa­ tients with B N D may be physiologically predisposed to be sa­ tiated with a smaller caloric intake than "normal" individuals.

DIAGNOSTIC CLASSIFICATION

AND SPECIAL TREATMENT ISSUES

B N D is characterized by chronic inadequate caloric intake as a result of mistaken nutritional beliefs. While a variety of medical and psychiatric disorders may result in chronic mal­ nutrition, children with B N D have normal physical and psy­ chiatric examinations except for a history of weight velocity deceleration, followed by growth velocity deceleration. A careful history of growth and of dietary beliefs and eating habits is crucial to establish the diagnosis and guide the inter­ vention. The treatment of B N D should focus on nutritional counseling of the child and parents. Follow-up visits should be scheduled to ascertain weight gain.

SUMMARY Benign nutritional dwarfing (BND) is a disorder of school­ age children and young adolescents in which maladaptive

68

EATING AND GROWTH DISORDERS

eating patterns, unaccompanied by psychiatric or medical dis­ orders, result in a marked slowing of weight gain followed b y a deceleration of linear growth. B N D is distinguished from anorexia nervosa by the absence both of weight loss and of psychiatric disturbance. Because B N D is a relatively newly described disorder, little is known about its epidemiology or course. Apparently, B N D is frequently responsive to nutri­ tional counseling and brief family or parent therapy.

9

PREPUBERTAL ANOREXIA

NERVOSA

Prepubertal anorexia nervosa has all of the essential features of typical adolescent onset anorexia including intense fear of be­ coming fat, disturbance of body image, significant and defined weight loss, and a refusal to maintain a minimum normal body weight. The only modifications of the standard diagnostic cri­ teria are those required by the physical characteristics of prepu­ bertal children. Obviously, because these children are prepubertal, amenorrhea is not a meaningful criterion. In addi­ tion, because prepubertal children have a smaller percentage of body fat than adolescents, a smaller percentage of weight loss will have a greater physiological impact. This relatively greater deleterious effect of weight loss is sometimes compounded by the fact that prepubertal children are more concrete in their thinking, so that they more frequently generalize their patholog­ ical eating to include their fluid intake (Irwin, 1984). Although prepubertal anorexia nervosa was reported in the same year (Collins, 1894) that adolescent onset anorexia nervosa was first described (Gull, 1964), substantial case re­ ports did not occur until nearly 70 years later (e.g., Halmi, 69

70

EATING AND GROWTH DISORDERS

1974; Reinhart, Kenn, & Succop, 1972; Shafi, Salquero, & Finch, 1975). Indeed, full recognition of the special characteristics of prepubertal anorexia nervosa awaited reports in the 1980s to es­ tablish this as a relatively rare but bona fide form of anorexia nervosa (Irwin, 1984; Jacobs & Isaacs, 1986; Russell, 1985).

NATURAL HISTORY Developmental Evolution and Outcome Because relatively few cases of prepubertal anorexia nervosa have been reported, conclusions about any aspect of natural history remain tentative. However, existing reports support the notion that prepubertal anorexia carries all of the possible negative sequelae of adolescent anorexia nervosa. In addition, the experience of an episode of acute malnutrition severe enough to cause significant weight loss in a prepuber­ tal child will likely have a deleterious effect on growth (Rus­ sell, 1985).

Epidemiology Although anorexia nervosa is a relatively rare disorder, pre­ pubertal anorexia is considerably rarer. In a summary of 23 series of case reports, including a total of 893 cases, Irwin (1984) reported that 5% of the patients were under age 13 and 1% were under age 10. The sex ratio and sociodemographics appear to be similar to the more typical anorexia nervosa.

Etiology (1) Social, family, and genetic factors. Current published re­ ports indicate that the same types of social and family factors

Prepubertal Anorexia Nervosa

71

are implicated in the genesis of prepubertal anorexia nervosa as with more typical anorexia nervosa. These factors include being middle or upper-middle class and having an enmeshed, intrusive family communication style. Like social and family factors, genetic factors may play an important role in anorexia nervosa regardless of the age of onset (Garfinkel & Garner, 1982; Morgan & Russell, 1975). (2) Psychogenic factors. Although numerous theories exist about various psychogenic factors related to anorexia nervosa, all remain relatively speculative. Children with pre­ pubertal onset anorexia express fewer concerns about sexual maturity (Jacobs & Isaacs, 1986) than those with older age onset anorexia. In addition, prepubertal children with an­ orexia nervosa have less cognitive ability to understand vari­ ous concepts of nutritional counseling. Some of the emotional and social goals in the treatment of adolescent anorexia re­ lated to differentiation from the family m a y be inappropriate for a prepubertal child. (3) Organic factors. As with other forms of anorexia nervosa, there are no known organic factors related to etiology. Acute malnutrition has a variety of important consequences for neu­ roendocrine functioning and growth.

DIAGNOSTIC CLASSIFICATION

AND SPECIAL TREATMENT ISSUES

Prepubertal anorexia nervosa is a primary psychiatric eat­ ing disorder with well-described physical, genetic, psycholog­ ical, behavioral, and family characteristics. The prepubertal age o f onset in this typically adolescent and adult disorder is the main stumbling block to accurate diagnosis and treat­ ment. Generally, clinicians who typically treat anorexia nervosa have little knowledge about the special cognitive,

72

EATING AND GROWTH DISORDERS

emotional, or physical needs of prepubertal children. Analo­ gously, clinicians who treat prepubertal children have little experience in the diagnosis or treatment of anorexia nervosa. Once these obstacles have been overcome, the diagnosis and treatment is at once as straightforward and as difficult as in more typical anorexia.

SUMMARY Prepubertal anorexia nervosa has all of the essential features of typical adolescent onset anorexia nervosa including intense fear of becoming fat, disturbance of body image, and significant and defined weight loss with a refusal to maintain a minimum normal body weight. Although all forms of anorexia nervosa can be devastating disorders, prepubertal onset anorexia may be especially deleterious because prepubertal children have less fat stored so that they become physically debilitated more rapidly. In addition, severe malnutrition at this earlier phase of develop­ ment may delay or prevent secondary sexual development. Pre­ pubertal onset anorexia raises the question of the presumed primacy of adolescent developmental issues as essential etiolog­ ical factors.

10

CONCLUSION

Eating and growth disorders of infancy and childhood repre­ sent a complex constellation of syndromes that epitomize the interactions of all levels of human development. For this rea­ son, the study of these disorders poses an exciting challenge to the further understanding of human biology. The conflu­ ence of significant conceptual and technological advance­ ments now permits more rapid progress in this field. Methodological, statistical, and technical innovations allow for the simultaneous study of interactions ranging from the biochemical to the sociological. T h e concepts of transactional risk model and developmental psychopathology have guided investigators to rely on empirical data without losing an ap­ preciation for multilevel, systems interactions. The influence and direction of this research will establish more clearly de­ fined stable syndromes that do not obscure the reality by oversimplification. The benefits of this research will be im­ provement in strategies to alleviate the human misery associ­ ated with these disorders as well as better understanding of normal development and resilience.

73

REFERENCES

Ainsworth, Μ. D. S. (1962). The effects of maternal deprivation: A review of findings and controversy in the context of research strategy. In Deprivation of maternal care: A reassessment of its effects (Public Health Papers, No. 14; pp. 97-167). Geneva: World Health Organization. Alvarado, P. J. (Ed.). (1982). Failure to thrive in infancy and early childhood: A multidisciplinary team approach. Baltimore, MD: University Park Press. American Psychiatric Association. (1987). Diagnostic and statistical manual of mental disorders (3rd ed., rev.). Washington, DC: Author. Apley, J . , Davies, J . , Davis, D. R., & Silk, B. (1971). Dwarfism without appar­ 64,135-138. ent physical cause. Proceedings of the Royal Society of Medicine, Arosu, T. S., Wyllie, R., Fitzgerald, F. J . , Franken, Ε. A, Siddiqui, A. R., Leh­ man, G. Α., Eigen, Η., & Grosfeld, J. L. (1980). Gastroesophageal reflux in infants and children: Comparative accuracy of diagnostic methods, journal of Pediatrics, 96, 798-803. Ashem, B., & Jones, M. (1978). Deleterious effects of chronic undernutrition 19,23-31. on cognitive abilities. Journal of Child Psychology and Psychiatry, Astley, R. (1956). Radiology of the alimentary tract in infancy. London: Edward Ar­ nold. Barbero, G. J., & Shaheen, E. (1967). Environmental failure to thrive: A clinical review. Journal of Pediatrics, 71, 639-644. Bawkin, H. (1949). Emotional deprivation in infants. American Journal of Dis­ 63,30-40. eases of Children, Beitins, F. Ζ., Kowarski, Α., Migeon, C. ] . , & Graham, G. C. (1975). Adrenal function in normal infants and in marasmus and kwashiorkor. Journal of Pe­ diatrics, 86, 302-308. Bell, L. S., & Woolston, J. L. (1985). The relationship of weight gain and caloric intake in infants with organic and non-organic failure to thrive syndrome. Journal of the American Academy of Child Psychiatry, 24, 447-452.

75

76

EATING AND GROWTH DISORDERS

Benoit, D., Zeanah, C. H., & Barton, M. L. (1989). Maternal attachment distur­ 10,185-202. bances in failure to thrive. Infant Mental Health Journal, Berkowitz, L. (1985). Comprehensive pediatric management of failure to thrive: An interdisciplinary approach. In D. Drotar (Ed.), New directions in failure to thrive: Implications for research and practice (pp. 193-210). New York: Plenum. Berwick, D. M. (1980). Nonorganic failure to thrive. Pediatrics in Review, 1, 265-270. Berwick, D. M., Levy, J. C , & Kleinerman, R. (1982). Failure to thrive: Diag­ nostic yield of hospitalization. Archives of Diseases in Children, 57, 347-351. Blizzard, R. M. (1973). Discussion: Plasma somatomedin activity in children with growth disturbances. In S. Raiti (Ed.), Advances in human growth hor­ mone research (NIH Publication No. 74-612, pp. 124-125). Rockville, MD: De­ partment of Health Education and Welfare. Botha, G. S. (1962). The gastroesophageal function. Boston: Little, Brown. Bowlby, J. (1951). Maternal care and mental health. Bulletin of the World Health 3,355-534. Organization, Boxer, G. H., & Miller, B. D. (1987). Treatment of a 7-year-old boy with obesity­ hypoventilation (Pickwickian syndrome) on a psychosomatic inpatient unit. Journal of the American Academy of Child and Adolescent Psychiatry, 5,798-805. Brandt, L. (1979). Growth dynamics of low birthweight infants with emphasis on the perinatal period. In F. Faulkner & J. Tanner (Eds.), Human growth: Neurobiology and nutrition. N e w York: Plenum. Bruch, Η. (1973). Eating disorders: Obesity, anorexia nervosa and the person within. N e w York: Basic Books. Cameron, H. D. (1925). Forms of vomiting in infants. British Medical Journal, 1, 872-876. Carey, W. B., Heguik, R. L . , & McDewitt, S. C. (1988). Temperamental factors associated with rapid weight gain and obesity in middle childhood. Devel­ opmental and Behavioral Pediatrics, 9, 194-198. Casey, P. H., & Arnold, W. C. (1985). Compensatory growth in infants with 78,1057-1060. severe failure to thrive. Southern Medical Journal, Casey, P. H., Bradley, R., & Worthham, B. (1984). Social and nonsocial home 73,348-353. environment of infants with organic failure to thrive. Pediatrics, Charney, E . , Chamblee, H., McBride, M., Lyon, B., & Pratt, R. (1976). The childhood antecedents of adult obesity: Do chubby infants become obese adults? New England Journal of Medicine, 295, 6-9. Chatoor, I., Conley, C , & Dickson, L . (1988). Food refusal after an incident of choking: A post-traumatic eating disorder. Journal of the Academy of Child and Adolescent Psychiatry, 27,105-110. Chatoor, I., Dickson, L., Schaeffer, S., & Egan, J. (1985). A developmental clas­ sification of feeding disorders associated with failure to thrive: Diagnosis and treatment. In D. Drotar (Ed.), New directions in failure to thrive: Implica­ tions for research and practice (pp. 235-258). N e w York: Plenum. Chatoor, I., & Egan, J. (1983). Nonorganic failure to thrive and dwarfism due to food refusal: A separation disorder. Journal of the American Academy of Child Psychiatry, 27,294-301.

References

77

Chavez, Α., & Martinez, C. (1979). Consequences of insufficient nutrition on environ­ child character and behavior. In D. A. Levitsky (Ed.), Malnutrition, ment, and behavior. New York: Cornell University Press. Chopra, I. J., Chopra, U., Smith, S., Reza, M., & Solomon, D. H. (1975). Recip­ rocal changes in serum concentrations of 3, 3', 5' Triiodothyromine (reverse T3) and 3, 3', 5 Triiodothyromine (T3) in systemic illness. Journal Clinical Experimental Medicine, 41,1043-1049. Christoffel, Κ. Κ., & Forsyth, Β. W. C. (1985). The ineffective parent, childhood obesity syndrome [Abstract]. From the 25th Annual Meeting of the Ambula­ tory Pediatric Association. Coleman, R. W., & Provence, S. (1957). Environmental retardation in infants living in families. Pediatrics, 19, 285-292. Collins, W. J. (1894). Anorexia nervosa. Lancet, 1,202-203. Crawford, P. B., Keller, C. Α., Hampton, M. C , Pacheo, F. R., & Huenemann, R. L. (1974). An obesity index for six month old children. American Journal of Clinical Nutrition, 27, 706-711. Danforth, D. E . , & Huber, A. M. (1982). Pica among mentally retarded adults. American Journal of Mental Deficiency, 87,141-146. Davis, R., Apley, J., Fill, G., & Grimaldi, C. (1978). Diet and retarded growth. 1,539-542. British Medical Journal, Donlon, T. A. (1988). Similar molecular deletions on chromosome 15q 11.2 are encountered in both the Prader-Willi and Angelman syndromes. Medical 80,322-328. Genetics, Drash, P. W., Greenberg, Ν. E . , & Mooney, J . (1986). Intelligence and person­ ality in four syndromes of dwarfism. In D. B. Cheek (Ed.), Human growth: Body composition, cell growth, energy and intelligence. Philadelphia: L e a and Febiger. Drotor, D., Malone, C. Α., Devost, L . , Brickell, C , Mautz-Clumpner, L . , Negray, J., Wallace, M., Woychik, J., Wyat, B., Eckerle, D., Bush, M., Finlon, Μ. Α., El-Amin, D., Nowark, M., Satola, J., & Pallotta, J . (1985). Early pre­ ventive intervention in failure to thrive: Methods of early outcome in fail­ ure to thrive. In D. Drotar (Ed.), New directions in failure to thrive: Implications for research and practice (pp. 119-138). N e w York: Plenum. Egan, J., Chatoor, I., & Rosen, G. (1980). Nonorganic failure to thrive: Patho­ genesis and classification. Clinical Proceedings of the Children's National Med­ ical Center, 3 4 , 1 7 3 - 1 8 2 . Eid, Ε . Ε . (1970). Follow-up study of physical growth of children who had ex­ cessive weight gain in the first six months of life. British Medical Journal, 2, 72-76. Eid, Ε. Ε . (1971). A follow-up study of physical growth following failure to thrive with special reference to a critical period in the first year of life. Acta Pediatric Scandinavia, 60, 39-48. Eilerstein, N. S., & Ostrov, Β. E. (1985). Growth patterns in children hospital­ ized because of caloric deprivation failure to thrive. American Journal of Dis­ 139,164-166. eases in Children, Elmer, E . (1960). Failure to thrive: Role of the mother. Pediatrics, 25, 717-725.

78

EATING AND GROWTH DISORDERS

Elmer, E . , Gregg, G. S., & Ellison, P. (1969). Late results of the "failure of thrive" syndrome. Clinical Pediatrics, 8, 584-589. Engle, G. L . , & Reichsman, F. (1956). Spontaneous and experimentally in­ duced depression in a n infant with gastric fistula: A contribution to the problems of depression. Journal of the American Psychoanalytic Association, 4, 428-453. Engle, G. L., Reichsman, F . , Harway, V. T., & Hess, D. W. (1986). Monica: In­ fant feeding behavior of a mother gastric fistula-fed as an infant: A 3 0 year longitudinal study of enduring effects. In E. J. Anthony & G. H. Pollack (Eds.), Parental influences in health and disease (pp. 29-89). Boston: Little, Brown. Engsner, V., & Vahlquist, B. (1975). Brain growth in children with protein en­ ergy malnutrition. In M. Bazier (Ed.), Growth and development of the brain. N e w York: Raven. Epstein, L. H., Valoski, Α., Wing, R. R., & McCarley, S. (1990). Ten-year fol­ low-up of behavioral, family-based treatment for obese children. Journal of the American Medical Association, 264,2519-2523. Evans, S. L., Reinhart, J. B., & Succop, R. A. (1972). Failure to thrive: A study of 4 5 children and their families. Journal of American Academy of Child Psy­ chiatry, 11, 440-459. Ferholt, J., & Provence, S. (1976). Diagnosis and treatment of an infant with psychophysiological vomiting. The Psychanalytic Study of the Child, 31, 439­ 461. Ferholt, J. B., Rotnem, D. C., Genel, M., Leonard, M., Carey, M., & Hunter, D. Ε. K. (1985). A psychodynamic study of psychosomatic dwarfism: A syn­ drome of depression, personality disorder and impaired growth. Journal of the American Academy of Child Psychiatry, 24, 49-57. Field, M. (1984). Follow-up developmental status of infant hospitalized for nonorganic failure to thrive. Journal of Pediatric Psychology, 9, 241-256. Fischoff, J., Whitten, C. F., & Pettit, M. D. (1971). A psychiatric study of moth­ ers of infants with growth failure secondary to maternal deprivation. Jour­ nal of Pediatrics, 79,209-215. Flanagan, C. H. (1977). Rumination in infancy: Past and present. Journal of the American Academy of Child Psychiatry, 16,140-149. Frank, D. Α., & Zeisel, S. A. (1988). Failure to thrive. Pediatric Clinics of North America, 35,1187-1206. Freud, A. (1946). The psychoanalytic study of infantile feeding disturbances. The Psychoanalytic Study of the Child, 2,119-132. Garfinkel, P. E., & Garner, D. M. (1982). Anorexia nervosa: A multidimensional perspective. N e w York: Brunner/Mazel. G a m , S. M., & Clark, D. C. (1976). Trends in fatness and the origins of obesity: Ad Hoc Committee to Review the Ten-State Nutrition Survey. Pediatrics, 57, 443-456. Glaser, Η. Η., Heagarty, Μ. C , & Bullard, D. Μ. (1980). Physical and psycho­ logical development of children with early failure to thrive. Journal of Pedi­ atrics, 73, 690-698.

References

79

Glasscock, S. G., Friman, P. C , O'Brien, S., & Christopherson, E. R. (1986). Varied citrus treatment of rumuninant gagging in a teenage with Batten's 17,129-133. disease. Journal of Behavior Therapy and Psychiatry, Goldblatt, P. B., Moore, Μ. E., & Stunkard, A. J . (1965). Social factors in obe­ 192,1039-1044. sity. Journal of the American Medical Association, Goldbloom, R. B. (1982). Failure to thrive. Pediatric Clinics of North America, 29, 151-165. Green, W. H., Campbell, M., & David, R. (1984). Psychosocial dwarfism: A critical review of the evidence. Journal of the American Academy of Child Psychia­ try, 23,39-48. Greenspan, S. I. (1981). Psychopathology and adaptation in infancy and early child­ hood: Principals of clinical diagnosis and preventive intervention. New York: In­ ternational University Press. Gull, W. W. (1964). The address in medicine. In M. R. Kaufman & M. Heiman (Eds.), Evolution of psychosomatic concepts (pp. 104-131). N e w York: Interna­ tional University Press. Halmi, K. (1974). Anorexia nervosa: Demographic and clinical features in 94 cases. Psychosomatic Medicine, 36,18-25. Halstead, J. A. (1968). Geophagia in man: Its nature and nutritional effects. American Journal of Chemical Nutrition, 21,1384-1393. Hannaway, P. (1978). Failure to thrive: A study of 100 infants and children. Clinical Pediatrics, 9, 69-99. Herbst, J., Friedland, G. W., & Zboralske, F. F. (1971). Hiatal hernia and rumi­ 78,261-265. nation in infants and children. Journal of Pediatrics, Hillemeier, A. C , Lange, R., McCallum, R., & Gryboski, J. (1981). Delayed gas­ tric emptying in infants with gastroesophageal reflux. Journal of Pediatrics, 98, 190-193. Holland, W. J. (1904). Splitters and lumpers. In W. J. Holland, The moth book: A popular guide to a knowledge of moths of North America (pp. 112-113). N e w York: Doubleday, Page. Hollowell, J. G., & Gardner, L. I. (1965). Rumination and growth failure in male fraternal twin: Association with disturbed family environment. Pediatrics, 36, 565-571. Holt, L. E. (1897). The diseases of infancy and childhood. New York: Appleton. Holvoet, J. F. (1982). The etiology and management of rumination and psy­ chogenic vomiting: A review. Monograph of the American Association of Men­ tal Deficiency, 5,19-77. Homer, C , & Ludwig, S. (1981). Categorization of etiology of failure to thrive. American Journal of Diseases of Children, 135, 848-851. Hopwood, N. J . , & Becker, D. J . (1979). Psychosocial dwarfism: Detection, 3,439-447. evaluation and management. Child Abuse and Neglect, Howse, P. M., Rayner, P. H., Williams, J. W., Rudd, Β. T., Bertrande, P. V., Thompson, C. R. S., & Jones, L . A. (1977). Secretion of growth hormone in normal children of short stature and in children with hypopituitarism and 6,347-359. interuterine growth retardation. Clinical Endocrinology,

80

EATING AND GROWTH DISORDERS

Irwin, M. (1984). Early onset anorexia nervosa. Southern Medical Journal, 77, 611­ 614. Jacobs, B. W., & Isaacs, S. (1986). Prepubertal anorexia nervosa: A retrospec­ tive controlled study. Journal of Child Psychology and Psychiatry, 27, 237-250. Kahn, Ε. J . (1973). Obesity in children. In N. Kiell (Ed.), The psychology of obe­ sity: Dynamics and treatment. Springfield, IL: Charles C Thomas. Kaplan, S. L . , Abrams, C. A. L . , Bell, J. J . , Conte, F. Α., & Grumbach, Μ. Μ. (1968). Growth and growth hormone: I. Changes in serum growth hormone following hypoglycemia in 134 children with growth retardation. Pediatric Research, 21,43-63. Kappy, M. S. (1987). Regulation of growth in children with chronic illness: Therapeutic implications for the year 2000. American Journal of Diseases in Children, 141, 489-493. Kerr, M., Bogues, J., & Kerr, D. (1978). Psychosocial functioning of mother of malnourished children. Pediatrics, 62, 778-788. Kirtland, J., & Gurr, Μ. I. (1979). Adipose tissues hypercellularity: A review. 2. The relationship between cellulocity and obesity. International Journal of Obesity, 3,15-55. Knittle, J. C , Timmers, Κ., Ginsberg-Fellner, F . , Brown, R. E., & Katz, D. R. (1979). The growth of adipose tissues in children and adolescents. Journal of 63,239-246. Clinical Investigation, Kotchelchuck, M. (1980). Nonorganic failure to thrive: The status of interac­ tional and environmental theories. In B. W. C a m p (Ed.), Advances in behav­ ioral pediatrics (Vol. 1). Greenwich, CT: JAI. Koumjian, L. L., & Marks, R. (1985). Catching up! Annual Report for Failure to Thrive Program in Massachusetts, 1985. Boston: Massachusetts Department of Public Health, Division of Family Health Services, Statistics and Evaluation Unit. Krieger, I. (1974). Food restriction as a form of child abuse in ten cases of psy­ 13,127-133. chosocial deprivation dwarfism. Clinical Pediatrics, Krieger, I., & Chen, Y. C. (1969). Calorie requirements for weight gain in in­ fants with growth failure due to maternal deprivation, undernutrition and congenital heart disease. Pediatrics, 44, 647-654. Krieger, I., & Good, Μ. H. (1970). Adrenocortisol and thyroid functioning: The deprivation syndrome. American Journal of Disease in Children, 120, 95-102. Lacey, E. P. (1990). Broadening the perspective of pica: Literature review. Pub­ 105,29-35. lic Health Reports, Leonard, M. F., Rhymes, J. P., & Solnit, A. J. (1966). Failure to thrive in infants: A family problem. American Journal of Diseases in Children, 111, 600-612. Lifshitz, F . , Moses, N., Cervantes, C , & Ginsberg, L . (1971). Nutritional dwarfing in adolescents. Seminars in Adolescent Medicine, 3, 255-266. Lourie, R. (1955). Treatment of psychosomatic problems in infants. Clinical Proceedings of the Children's National Hospital, 2,146-148. MacGillivray, Μ. H. (1987). Disorders of growth and development. In P. Felig, J. D. Baxter, A. C. Broadus, & L. A . Frohman (Eds.), Endocrinology and me­ tabolism (2nd ed., pp. 1581-1628). N e w York: McGraw-Hill.

References

81

MacLean, W. C , de Romana, G. L . , & Masse, E. (1980). Nutritional manage­ ment of chronic diarrhea and malnutrition: Primary reliance on oral feed­ 97,316-323. ing. Journal of Pediatrics, Madden, Ν. Α., Russo, D. C., & Cataldo, M. F. (1980). Environmental influences on mouthing in children with lead intoxication. Journal of Pediatric Psychology, 5, 207-216. Maloney, M. J . , & Klykylo, W. M. (1983). An overview of anorexia nervosa, bulimia and obesity in children and adolescents. Journal of the American Academy of Child Psychiatry, 22, 99-107. Masten, A. S., & O'Connor, M. J. (1989). Vulnerability, stress and resilience in the early development of a high risk child. Journal of the American Academy of Child and Adolescent Psychiatry, 28,274-278. Mayes, S. D., Humphrey, F. J., Handford, Η. Α., & Mitchell, J. F. (1988). Rumi­ nation disorder: Differential diagnosis. Journal of the American Academy of Child and Adolescent Psychiatry, 27,300-302. McAlpine, C , & Singh, N. (1986). Pica in institutionalized mentally retarded persons. Journal Mental Deficiency Research, 30,171-178. McCance, C. (1961). Psychiatric factors in obesity. Dissertation for diploma in psychological medicine, University of London. McLaren, D. S., & Read, W. E. (1972). Classification of nutritional status in early childhood. Lancet, 2,146-148. Menking, M., Wagnitz, J. G., Burton, J. J., Coddington, R. D., & Solos, J. (1969). Rumination: Near fatal psychiatric disease of infancy. New England Journal of Medicine, 280,802-804. Mestre, J. R., Resnick, R. J., & Berman, W. F. (1983). Behavior modification in 22,488-491. the treatment of rumination. Clinical Pediatrics, Mitchell, W. G., Gorrell, R. W., & Greenberg, R. A. (1980). Failure to thrive: A study in a primary care setting. Epidemiology and follow-up. Pediatrics, 65, 971-976. Money, J., & Wolff, G. (1974). Late puberty, retarded growth and reversible 9,121-134. hyposomatotropisism (psychosocial dwarfism). Adolescence, Morgan, H. G., & Russell, G. F. M. (1975). Value of family background and clinical features as predictors of long-term outcome in anorexia nervosa: Four-year follow-up study of 41 patients. Psychological Medicine, 5,355-372. Oates, R. K., Peacock, Α., & Forrest, D. (1984). Development in children fol­ lowing abuse and nonorganic failure to thrive. American Journal of Diseases 138,764-767. in Children, Oates, R. K., Peacock, Α., & Forrest, D. (1985). Long-term effects of nonor­ 75,36-40. ganic failure to thrive. Pediatrics, Oatis, P., Bobo, R., & Herman, D. (1982). Nutritional status of hospitalized children (Effect of socioeconomic status). Pediatric Research, 4 , 5 8 3 . Papaila, J. G., Wilmont, D., Grosfeld, J. L., Rescorla, E . J., West, K. W., & Vane, D. W. (1989). Increased incidence of delayed gastric emptying in children with gastroesophageal reflux. Archives of Surgery, 128, 933-936. Patton, R. G., & Gardner, L. I. (1963). Growth failure in maternal deprivation. Springfield, IL: Charles C Thomas.

82

EATING AND GROWTH DISORDERS

Peterson, Κ. E., Washington, J., & Rathbun, J. M. (1984). Team management of failure to thrive. Journal of the American Dietetic Association, 84, 810-815. Pimstone, B., Whattman, W . , & Hansen, J. W. (1966). Growth hormone and kwashiorkor: The role of protein in growth hormone homeostatis. Lancet, 2, 779-780. Pollitt, E . (1973). Behavior of infants in causation of nutritional marasmus. American Journal of Clinical Nutrition, 26, 264-270. Pollitt, E. (1975). Failure to thrive: Socioeconomic dietary intake, and mother­ 34,1593-1597. child interactional data. Federation Proceedings, Poskitt, Ε. Μ. E. (1980). Obese from infancy: A re-evaluation. Topics in Pediatrics, 1, 81-89. Powell, R., Brasel, J. Α., Raiti, S., & Blizzard, R. M. (1967). Emotional depriva­ tion and growth retardation simulating idiopathic hypopituitarism: I. Clin­ ical evaluation of the syndrome. II. Endocrinological evaluation of the 276,1271-1278,1279-1283. syndrome. New England Journal of Medicine, Powell, F . , & Low, J. (1983). Behavior in nonorganic failure to thrive. Journal of 4,26-33. Developmental and Behavioral Pediatrics, Provence, S., & Lipton, R. C. (1962). Infants in institutions. N e w York: Interna­ tional Universities Press. Pugliese, Μ. T., Lifshitz, F., Grad, G., Fort, P., & Marks-Katz, M. (1983). Fear of obesity: A cause of short stature and delayed puberty. New England Jour­ nal of Medicine, 309,513-518. Pugliese, Μ. T., Weyman-Daum, M., Moses, N., & Lifshitz, F. (1987). Parental health beliefs as a cause of nonorganic failure to thrive. Pediatrics, 80, 175­ 182. Rathburn, J. M., & Peterson, Κ. E . (1987). Nutrition in failure to thrive. In R. J Grand, J. L. Sutphen, & W. H. Dietz, Jr. (Eds.), Pediatric nutrition: Theory and practice. Boston: Butterworth. Ravussin, E . , Lillioja, S., Anderson, Τ. E . , Christin, L., & Bogardus, C. (1986). Determinants of 24-hour energy expenditure in man: Methods and results using a respiratory chamber. Journal of Clinical Investigation, 78,1568-1578. Reinhart, J . B., Kenn, Μ. D., & Succop, R. A. (1972). Anorexia nervosa in chil­ dren: Outpatient management. Journal of the American Academy of Child Psy­ chiatry, 11,114-131. Reichsman, F., Engle, G. L., Harway, V., & Escalona, S. (1958). Monica, an infant with gastric fistula and depression: An interim report on her development to age four years. American Psychiatric Association, Psychiatric Research Report, 8, 12-63. Richmond, J. B., Eddy, E . , & Green, M. (1958). Rumination: A psychosomatic syndrome of infancy. Pediatrics, 22, 49-55. Robinson, H., & Picon, D. (1977). A comparison of fasting plasma insulin and growth hormone concentrations in m a r a s m i c , kwashiorkor, m a r a s m i c ­ kwashiorkor and underweight children. Pediatric Research, 11, 637-640. Rosenn, D., Loeb, J . S., & Jura, Μ. B. (1980). Differentiation of organic from non-organic failure to thrive syndrome in infancy. Pediatrics, 66, 698-704.

References

83

Russell, G. F. Μ. (1985). Premenarchal anorexia nervosa and its sequelae. Jour­ nal of Psychiatric Research, 19, 363-369. Sameroff, A. J . , & Chandler, M. (1975). Reproductive risk and the continuum of caretaking causality. In F. Horowitz (Ed.), Review of child development re­ search (Vol. 4, pp. 197-244). Chicago: University of Chicago Press. Sameroff, A. J . , & Fiese, Β. H. (1989). Conceptual issues in prevention. In D. Shaffer, I. Philips, & N. Enzer (Eds.), Prevention of mental disorders, alcohol and other drug use in children and adolescents (pp. 23-53). Rockville, MD: U.S. Department of Health and H u m a n Services, Public Health, Alcohol, Drug Abuse and Mental Health Administration. Sanberg, D. E . , Smith, M. M., Fornai, V., Goldstein, M., & Lifshitz, F. (1991). Nutritional dwarfing: Is it a consequence of disturbed psychosocial functioning. Unpublished manuscript. Sauvage, D., Leddet, L . , Hameur, L . , & Barthelemy, C. (1985). Infantile rumi­ nation: Diagnosis and follow-up of twenty cases. Journal of the American 24,197-203. Academy of Child Psychiatry, Shaft, M., Salquero, C , & Finch, S. (1975). Anorexia a deux: Psychopathology and treatment of anorexia in latency age siblings. Journal of the American Academy of Child Psychiatry, 14, 617-632. Shaheen, E . , Alexander, D., Truskowsky, M., & Barberro, G. (1968). Failure to thrive: A retrospective profile. Clinical Pediatrics, 71, 255-260. Shapiro, L. R., Crawford, P. B., & Clark, M. J. (1984). Obesity prognosis: A lon­ gitudinal study of children from age six months to nine years. American Journal of Public Health, 74, 968-972. Shepherd, R. W . , Wren, J . , Evans, S., Lander, M., & Ong, Τ. H. (1987). Gas­ troesophageal reflux in children: Clinical profile, course, and outcome with active therapy in 126 cases. Clinical Pediatrics, 26,55-60. Shipman, M. G., & Plesset, M. (1963). Anxiety and depression in obese dieters. Archives of General Psychiatry, 8, 530-535. Shukla, A „ Forsyth, Α. Α., Anderson, C. M., & Morwah, S. M. (1972). Infantile overnutrition in the first year of life: A field study in Dudley, Worcester­ 4,507-515. shire. British Medical Journal, Sills, R. H. (1978). Failure to thrive: The role of clinical and laboratory evalua­ tion. American Journal of Diseases in Children, 132, 967-969. Silver, Η. K., & Finkelstein, M. (1967). Deprivation dwarfism. Journal of Pediat­ rics, 70,317-324. Silverstone, J. T. (1969). Psychological factors in obesity. In I. M. Baird & A. N. Howard (Eds.), Obesity: Medical and scientific aspects (pp. 45-55). London: Liv­ ingston. Singh, N., Manning, P. J . , & Angell, M. L. (1982). Effects of an oral hygiene punishment procedure on chronic rumination and collateral behaviors in monozygous twins. Journal Applied Behavioral Analysis, 15, 309-314. Spitz, R. A. (1945). Hospitalism. Psychoanalytic Study of the Child, 1, 53-74. Spitz, R. (1946). Hospitalism: A follow-up report. Psychoanalytic Study of the Chüd, 2,113-117.

84

EATING AND GROWTH DISORDERS

Spitz, R. Α., & Wolf, Κ. M. (1946). Anaclitic depression: An inquiry into the genes of psychiatric conditions in early childhood: II. Psychoanalytic Study of the Child, 2,313-339. Stern, D. S. (1985). The interpersonal world of the infant: A view from psychoanaly­ sis and developmental psychology. New York: Basic Books. Stoch, M., Smythe, P., & Moodie, A. L. (1982). Psychosocial outcome and CT findings after gross undernourishment during infancy: A 20-year develop­ mental study. Developmental Medicine and Child Neurology, 24, 419-436. Stunkard, A. J. (1975). Obesity. In M. Reiser (Ed.), American handbook of psychi­ atry. N e w York: Basic Books. Stunkard, A. J. (1980). Obesity. In Η. I. Kaplan, A. M. Freedman, & B. J. Sad­ ock (Eds.), Comprehensive textbook of psychiatry (Vol. 3, pp. 1872-1881). Balti­ more, MD: Williams & Wilkins. Stunkard, A. J., D'Aquill, E . , Fox, S., & Filion, B. D. L. (1972). Influence of so­ cial class on obesity and thinness in children. Journal of the American Medical Association, 221, 579-584. Stunkard, A. J., Foch, Τ. T., & Hrubec, Z. (1986). A twin study of human obe­ sity. Journal of the American Medical Association, 256, 51-54. Stunkard, A. J., Sorenson, Τ. I. Α., Hanis, C , Teasdale, T. W., Chakroborty, R., Schull, W. J., & Schulsinger, F. (1986). An adoption study of human obe­ 314,193-198. sity. New England Journal of Medicine, Taitz, L. (1971). Infantile overnutrition among artificially fed infants in the Sheffield region. British Medical Journal, 1, 315-316. Tanner, J. M. (1973). Resistance to exogenous human growth hormone in psy­ chosocial short stature (emotional deprivation) [Letter to the editor]. Jour­ nal of Pediatrics, 82,171-172. Tanner, J. M., & Whithouse, R. H. (1976). Clinical longitudinal standards for height, weight, height velocity, weight velocity, and stages of puberty. Ar­ 51,170-179. chives of Diseases in Children, Thomas, Α., & Chess, S. (1977). Temperament and development. N e w York: Brun­ ner/Mazel. Togut, M., Allen, S., & Lelchuck, L. (1969). A psychological exploration of the nonorganic failure to thrive syndrome. Developmental Medicine and Child Neurology, 11, 601-607. Trowbridge, F. L. (1984). Prevalence of growth stunting and obesity: Pediatric nutritional surveillance system. Morbidity and Mortality Weekly Report, 32, 23-76. Vyas, D., & Chandra, R. K. (1984). Functional implications of iron deficiency. In A. Stekel (Ed.), Iron nutrition in infancy and childhood (pp. 45-59). N e w York: Raven. Wartofsky, L . , & Bruman, K. D. (1982). Alterations in thyroid function in p a ­ tients with systemic illness: The "euthyroid sick syndrome." Endocrine Re­ view, 30,177-181. Waterlow, J. C. (1972). Classification and definition of protein-calorie malnu­ trition. British Medical Journal, 3, 566-569.

References

85

Whitehead, W. E . , Drescher, W. M., & Merrill-Corbin, E. (1985). Rumination syndrome in childhood treated by increased holding. Journal of Pediatric Gastroenterology and Nutrition, 4, 550-556. Whitten, C. F., Pettit, M. G., & Fischoff, J. (1969). Evidence that growth failure from maternal deprivation is secondary to undereating. Journal of the Amer­ 209,1675-1682. ican Medical Association, Widdowson, Ε. M. (1951). Mental contentment and physical growth. Lancet, 1, 1316-1318. Wilcox, W. D., Nieburg, P., & Miller, D. S. (1989). Failure to thrive: A continu­ 28,391-394. ing problem of definition. Clinical Pediatrics, Wilson, R. S., & Mathany, A. P. (1986). Behavioral-genetics in infant tempera­ ment: The Louisville twin study. In R. Plomin & J. Dunn (Eds.), The study of temperament: Changes, continuities and challenges (pp. 81-97). Hillsdale, NJ: Lawrence Erlbaum. Winton, A. S. W . , & Singh, N. (1983). Rumination in pediatric populations: A behavioral analysis. Journal of the American Academy of Child Psychiatry, 22, 269-275. Woolston, J. L. (1983). Eating disorders in infancy and early childhood. Journal of the American Academy of Child Psychiatry, 22,114-121. Woolston, J. L. (1985). Diagnostic classification: The current challenge in fail­ ure to thrive syndrome research. In D. Drotar (Ed.), New directions in failure to thrive: Implications for research and practice (pp. 225-233). New York: Ple­ num. Woolston, J. L. (1987). Obesity of infancy and early childhood. Journal of the American Academy of Child and Adolescent Psychiatry, 26,123-126. Woolston, J. L. (1988). Theoretical considerations of the adjustment disorders. Journal of the American Academy of Child and Adolescent Psychiatry, 27, 280­ 287. Woolston, J. L. (1989a). Eating disorders in infancy and early childhood. In B. J. Blinder, B. F. Chaitin, & R. Goldstein (Eds.), The eating disorders (pp. 275­ 285). New York: Spectrum Medical. Woolston, J. L. (1989b). Transactional risk model for short and intermediate term psychiatric inpatient treatment of children. Journal of the American 28,38-41. Academy of Child and Adolescent Psychiatry, Woolston, J. L . , & Forsyth, B. (1989). Obesity of infancy and early childhood: A diagnostic schema. In Β. B. Lahey & A. E. Kazdin (Eds.), Advances in clin­ ical child psychology (Vol. 12, pp. 179-192). New York: Plenum. Woolston, J. L . , & Riddle, M. A. (1990). The role of advanced technology in in­ patient child psychiatry: Leading edge or useful aid. Journal of the American Academy of Child and Adolescent Psychiatry, 29, 905-908.

AUTHOR INDEX

Abrams, C. A. L . , 17

Ainsworth, M. D. S., 22

Alexander, D., 21

Allen, S., 22

Alvarado, P. J., 8

American Psychiatric Association, 3,

53

Anderson, Τ. E . , 16

Anderson, C. M., 56

Angell, M. L . , 47

Apley, J . , 4, 65, 66, 67

Arnold, W. C , 24, 31, 32

Arosu, T. S., 47

Ashem, B., 32

Astley, R., 46

Barbero, G. J., 22, 59

Barberro, G., 21

Barthelemy, C , 4 3

Barton, M. L., 5

Bawkin, H., 22

Becker, D. J., 39, 41

Beitins, F. Ζ., 17

Bell, J. J . , 17

Bell, L. S., 7

Benoit, D., 5

Berkowitz, L . , 8

Berman, W. F., 4 7

Bertrande, P. V., 39

Berwick, D. M., 7, 21

Blizzard, R. M., 2 5 , 37, 38, 39

Bobo, R., 5

Bogardus, C., 16

Bogues, J., 5

Botha, G. S., 4 6

Bowlby, J., 22

Boxer, G. H., 59

Bradley, R., 5, 24

Brandt, L., 33

Brasel, J. Α., 2 5 , 3 7 , 39

Brickell, C., 22

Brown, R. E., 55

Bruch, Η., 5 8

Bruman, Κ. D., 17

Bullard, D. M „ 21

Burton, J. J., 4 5

Bush, M , 22

Cameron, H. D., 4 3

Campbell, M., 3, 25, 37, 38, 4 0

Carey, M., 2 5 , 37, 3 9

Carey, W. B., 58

Casey, P. H., 5, 24, 31, 3 2

Cataldo, M. F . , 50

Cervantes, C , 6 5 , 66, 6 7

Chakroborty, R., 57

87

88 Chamblee, H., 54

Chandler, M., 2

Chandra, R. K., 51

Charney, E . , 54

Chatoor, I., 4, 6 , 2 5 , 3 0

Chavez, Α., 5

Chen, Y. C , 7

Chess, S., 57

Chopra, I. J., 17

Chopra, U., 17

Christin, L . , 16

Christoffel, Κ. Κ., 58

Christopherson, Ε. R., 47

Clark, D., 5 4 , 5 7

Clark, M. J . , 5 4 , 5 5

Coddington, R. D., 4 5

Coleman, R. W., 5, 22

Collins, W. J., 6 9

Conley, C , 4 , 2 5

Conte, F. Α., 17

Crawford, P. B., 54, 55

Danforth, D. E . , 50

D'Aquill, E . , 56

David, R., 3 , 2 5 , 3 7 , 3 8 , 4 0

Davies, J . , 65

Davis, D. R., 65

Davis, R., 4, 65, 66, 67

d e Romana, G. L . , 31

Devost, L . , 22

Dickson, L . , 4 , 6 , 25, 30

Donlon, Τ. Α., 59, 6 0

Drash, P. W., 37, 38, 39

Drescher, W. M., 4 7

Drotor, D., 22

Eckerle, D., 22

Eddy, E . , 43, 45

Egan, J., 4 , 6 , 2 5 , 3 0

Eid, Ε. Ε., 2 1 , 54

Eigen, Η., 4 7

El-Amin, D., 22

Eilerstein, N. S., 32

Ellison, P., 21

Elmer, E . , 5 , 2 1

Engle, G. L., 2 3 , 2 4

EATING AND GROWTH

DISORDERS

Engsner, V., 32

Epstein, L. H., 6 1 , 62

Escalona, S., 24

Evans, S. L . , 5, 46

Ferholt, ] . , 45

Ferholt, J. B., 25, 3 7 , 3 9

Field, Μ., 22

Fiese, Β. Η., 2

Filion, Β. D. L . , 56

Fill, G., 4, 65, 66, 6 7

Finch, S., 70

Finkelstein, M., 22, 3 7

Finlon, Μ. Α., 2 2

Fischoff, ] . , 5, 7 , 2 4

Fitzgerald, F. J . , 4 7

Flanagan, C. H., 45

Foch, Τ. T., 57

Fornai, V., 66

Forrest, D., 21

Forsyth, Α. Α., 5 6

Forsyth, Β. W. C., 58

Forsythe, B., 7, 8, 9 , 5 9 , 6 0 , 6 2

Fort, P., 56, 67

Fox, S., 56

Frank, D. Α., 7, 2 2 , 2 9 , 3 2 , 33, 34

Franken, Ε. Α., 47

Freud, Α., 1, 30

Friedland, G. W . , 4 6

Friman, P. C , 4 7

Gardner, L. I., 37, 45

Garfinkel, P. E . , 71

Garn, S. M., 54, 57

Garner, D. M., 71

Genel, M., 2 5 , 3 7 , 3 9

Ginsberg, L., 6 5 , 6 6 , 67

Ginsberg-Fellner, F., 55

Glaser, Η. H., 21

Glasscock, S. G., 4 7

Goldblatt, P. B., 56

Goldbloom, R. B., 24

Goldstein, M., 66

Good, Μ. Η., 22

Gorreil, R. W., 2 1 , 2 3

Grad, G., 56, 6 7

Author Index Graham, G. C., 17

Green, M., 43, 4 5

Green, W. H., 3, 2 5 , 37, 3 8 , 40

Greenberg, Ν. E . , 37, 38, 3 9

Greenberg, R. Α., 21, 23

Greenspan, S. I., 2 , 1 8

Gregg, G. S., 21

Grimaldi, C., 4, 6 5 , 66, 67

Grosfeld, J. L . , 4 6 , 4 7

Grumbach, Μ. Μ., 17

Gryboski, J., 46

Gull, W . W., 69

Gurr, Μ. I., 5 5

Halmi, K., 69, 7 0

Halstead, J. Α., 5 0

Hameur, L . , 43

Hampton, M. C., 54

Handford, Η. Α., 4 , 4 4 , 4 5

Hanis, C , 57

Hannaway, P., 21

Hansen, J. W., 17

Harway, V., 24

Harway, V. T., 2 3

Heagarty, M. C., 21

Heguik, R. L., 5 8

Herbst, J., 46

Herman, D., 5

Hess, D. W., 23

Hillemeier, A. C., 4 6

Holland, W. J . , 3

Hollowell, J. G., 45

Holt, L . E . , 21

Holvoet, J. F . , 43

Homer, C., 7

Hopwood, N. J . , 3 9 , 4 1

Howse, P. M., 3 9

Hrubec, Z., 57

Huber, A. M., 5 0

Huenemann, R. L . , 5 4

Humphrey, F. J., 4 , 4 4 , 4 5

Hunter, D. Ε. K., 2 5 , 37, 39

Irwin, M., 4, 69, 7 0

Isaacs, S., 70, 71

Jacobs, B. W . , 70, 71

Jones, L. Α., 3 9

Jones, M., 32

Jura, Μ. B., 22

Kahn, Ε. J., 5 8

Kaplan, S. L . , 17

Kappy, M. S., 7

Katz, D. R., 5 5

Keller, C. Α., 54

Kenn, Μ. D., 70

Kerr, D., 5

Kerr, M., 5

Kirtland, J., 5 5

Kleinerman, R., 7

Klykylo, W. M., 5 5 , 60

Knittle, J. C., 55

Kotchelchuck, M., 7

Koumjian, L. L., 21

Kowarski, Α., 17

Krieger, I., 7, 22

Lacey, E. P., 4 9 , 51

Lander, M., 4 6

Lange, R., 46

Leddet, L . , 4 3

Lehman, G. Α., 4 7

Lelchuck, L . , 22

Leonard, M., 2 5 , 3 7 , 3 9

Leonard, M. F . , 1 , 5 , 2 2 , 5 8

Levy, J. C., 7

Lifshitz, F. 5 6 , 65, 66, 67

Lillioja, S., 16

Lipton, R. C., 22, 24

Loeb, J. S., 2 2

Lourie, R., 1

Low, J . , 5

Ludwig, S., 7

Lyon, B., 54

MacGillivray, Μ. H., 1 2 , 1 3 , 1 4 , 1 5

MacLean, W . C., 31

Madden, Ν. Α., 50

Malone, C. Α., 22

Maloney, M. J., 5 5 , 6 0

Manning, P. J . , 47

90

EATING AND GROWTH DISORDERS

Marks, R., 21

Marks-Katz, M., 5 6 , 67

Martinez, C , 5

Masse, E . , 31

Masten, A. S., 3, 2 5

Mathany, A. P., 58

Mautz-Clumpner, L . , 22

Mayes, S. D., 4 , 4 4 , 45

McAlpine, C , 5 0

McBride, M., 54

McCallum, R., 46

McCance, C , 58

McCarley, S., 61, 62

McDewitt, S. C , 5 8

McLauren, D. S., 17, 2 5 , 32

Menking, M., 45

Merrill-Corbin, E., 47

Mestre, J. R., 47

Migeon, C. J., 17

Miller, B. D., 59

Miller, D. S., 22

Mitchell, J. F . , 4 , 4 4 , 4 5

Mitchell, W. G., 2 1 , 2 3

Money, J . , 37, 38, 39

Moodie, A. L . , 32

Mooney, J., 37, 38, 39

Moore, Μ. E . , 5 6

Morgan, H. G., 71

Morwah, S. M., 56

Moses, N., 6 5 , 66, 6 7

Negray, J . , 22

Nieburg, P., 22

Nowark, M., 22

Oates, R. K., 21

Oatis, P., 5

O'Brien, S., 47

O'Connor, M. J., 3, 25

Ong, Τ. H., 4 6

Ostrov, Β. E., 32

Pacheo, F. R., 54

Pallotta, J., 22

Papaila, J. G., 46

Patton, R. G., 37

Peacock, Α., 21

Peterson, Κ. E . , 5, 8, 31

Pettit, M. D., 5

Pettit, M. G., 7, 24

Picon, D., 17

Pimstone, B., 17

Plesset, M., 5 8

Pollitt, E . , 5

Poskitt, Ε. Μ. E . , 54, 55, 5 7

Powell, F., 5

Powell, R., 2 5 , 37, 39

Pratt, R., 54

Provence, S., 5 , 2 2 , 24, 4 5

Pugliese, Μ. T., 56, 65, 6 7

Raiti, S., 2 5 , 37, 39

Rathburn, J. M., 5, 8 , 3 1

Ravussin, E . , 16

Rayner, P. H., 3 9

Read, W. E . , 17, 2 5 , 32

Reichsman, F., 23

Reinhart, J. Β., 5 , 7 0

Reischman, F . , 2 3 , 2 4

Rescorla, Ε. J., 4 6

Resnick, R. J., 4 7

Reza, M., 17

Rhymes, J. P., 1, 5, 22, 5 8

Richmond, J. B., 43, 45

Riddle, Μ. Α., 3

Robinson, H., 17

Rosen, G., 4

Rosenn, D., 22

Rotnem, D. C , 25, 37, 39

Rudd, Β. T., 39

Russell, G. F. M., 70, 71

Russo, D. C , 5 0

Salquero, C , 70

Sameroff, A.J., 2

Sanberg, D. E . , 66

Satola, J . , 22

Sauvage, D., 4 3

Schaeffer, S., 6, 2 5 , 3 0

Schull, W. J . , 57

Schulsinger, F . , 57

Shafi, Μ., 70

Author Index Shaheen, E . , 2 1 , 2 2 , 59

Shapiro, L. R., 5 4 , 55

Shepherd, R. W., 46

Shipman, M. G., 58

Shukla, Α., 56

Siddiqui, A. R., 47

Silk, B., 65

Sills, R. H., 7 , 2 9

Silver, Η. K., 2 2 , 3 7

Silverstone, J. T., 58

Singh, N., 43, 4 5 , 47, 50

Smith, Μ. M., 66

Smith S., 17

Smythe, P., 32

Solnit, A. J., 1, 5 , 2 2 , 5 8

Solomon, D. H., 17

Solos, J., 45

Sorenson, Τ. I. Α., 57

Spitz, R. Α., 1, 22

Spitz, R., 5

Stern, D. S., 2

Stoch, M , 32

Stunkard, A. J., 5 6 , 5 7 , 5 8 , 60

Succop, R. Α., 5, 70

Taitz, L., 56

Tanner, J. M., 14, 37

Teasdale, T. W., 57

Thomas, Α., 5 7

Thompson, C. R. S., 39

Timmers, Κ., 5 5

Togut, Μ., 22

Trowbridge, F. L . , 21

Truskowsky, M., 21

Vahlquist, B., 32

91 Valoski, Α., 61, 62

Vane, D. W., 46

Vyas, D., 51

Wagnitz, J. G., 4 5

Wallace, M., 22

Wartofsky, L . , 17

Washington, J., 8, 31

Waterlow, J. C., 17

West, K. W., 46

Weyman-Daum, M., 65

Whattman, W., 17

Whitehead, W. E., 47

Whithouse, R. H., 14

Whitten, C. F., 5 , 7 , 2 4

Widdowson, Ε. M., 2 3

Wilcox, W. D., 22

Williams, J. W., 39

Wilmont, D., 46

Wilson, R. S., 58

Wing, R. R., 61, 62

Winton, A. S. W., 43, 45

W o l f K . M., 22

Wolff, G., 37, 38, 39

Woolston, J. L . , 2 , 3 , 4 , 5, 7, 8, 9 , 3 0 ,

56, 59, 60, 62

Worthham, B., 5, 24

Woychik, J . , 22

Wren, J . , 46

Wyat, B., 22

Wyllie, R., 4 7 7

Zboralske, F . F., 46

Zeanah, C. H., 5

Zeisel, S. Α., 7, 2 2 , 2 9 , 3 2 , 33, 34

SUBJECT INDEX

Anorexia nervosa, prepubertal, 3 , 4 , 6, 69-72

Growth: hormonal regulation of, 11-12 patterns of, 12-15

Benign nutritional dwarfing, 4, 65-68 Classification: major controversies, 2-8 bad mothers versus sick babies, 4-6 lumpers versus splitters, 2-4 organic versus nonorganic etiolo­ gies, 4-6 Developmental sequences, 1 - 2 , 1 7 - 1 9

Malnutrition, 5, 7 , 1 7 , 30-33 Medical problems associated with eating disorders, 8 - 9 , 2 9 - 3 0 , 3 9 ­ 4 0 , 4 5 - 4 6 , 5 1 - 5 2 , 59-60, 61-67 Obesity, 3 , 4 , 6, 8 , 5 3 - 6 3 Parental psychopathology, 4-5 Phobic food refusal, 4 Psychosocial dwarfism, 3, 37-42

Energy balance, 15-17 Failure to thrive, 3, 4, 7, 21-35

Reaction attachment disorder, 3 Rumination, 3, 4, 6 , 4 3 - 4 7

Gastroesophogeal reflux, 3, 6, 46-47

Transactional model, 2

93

ABOUT THE AUTHOR

Joseph L. Woolston (M.D.) is Associate Clinical Professor of Child Psychiatry at the Yale Child Study Center and the Med­ ical Director of the Children's Psychiatric Inpatient Service at Yale New Haven Hospital. He received his B.A. in biology from Yale College in 1970 and his M.D. from the University of Pennsylvania School of Medicine in 1973. He completed his medical internship at the University of Pennsylvania Presby­ terian Medical Center in 1974, his psychiatric residency at Stanford University School o f Medicine in 1976, and his child psychiatry residency at the Yale Child Study Center in 1978. He has been on the faculty of the Yale Child Study Center since the completion of his child psychiatry residency. His current research interests include eating and growth disor­ ders in children, phenomenology and treatment of psychiatri­ cally hospitalized children, and the application of systems theory to various complex processes of clinical psychiatry and natural evolution.

95

NOTES