Mercury and Social Anxiety; Why Limiting Your Exposure to Mercury Can Ease Shyness, Anxiety and Depression

Citation preview

Mercury and Social Anxiety Why Limiting Your Exposure to Mercury Can Ease Shyness, Anxiety and Depression

© 2013 Mary Hammond. All rights reserved.

For You No more wasted years

Table of Contents PROLOGUE – QUIET MARY THE HISTORY OF MERCURY HYSTERIA AND THE NERVOUS TEMPERAMENT IN THE 1800’S MERCURY AND DEPRESSION IN THE LIFE OF JACK LONDON PATHOLOGICAL SHYNESS IN INDUSTRY MERCURY IN THE FOOD CHAIN EXCESSIVE CONSUMPTION IDIOSYNCRATIC SENSITIVITY EPILOGUE – A NATURAL “HI” A SPECIAL NOTE FOR THE OVERWEIGHT AND HYPERTENSIVE UNITED NATIONS 2013, MINAMATA REFERENCES

Prologue – Quiet Mary I remember being part of a group when I was small, running around in a pack with the other neighborhood kids, up and down the streets, in and out of each other’s houses, not different, not special in any way. It was a belonging without any thought. But somewhere along the way I got lost. I became the quiet girl on the outside of the group. My heart would pound in my ears when it was my turn to stand in front of the class and present a current event. I would have pored through the newspaper the evening before and found a small piece, a column as short as I felt I could get away with, a little piece of newspaper no more than one and a half inches wide, less than three inches long, and I would have practiced and practiced presenting it. I can still remember being so nervous in class knowing it would soon be my turn, not able to concentrate on anything else except that, and then getting up standing in front of the other children holding my news story, summarizing it for the class, my skin getting redder and hotter and always my heart pounding away, I can see it all still, as if I was there, the classroom, the chalkboard, the chairs, the children sitting on the rug in front of me... the memory is burned into my mind’s eye. At the end of the year in fourth grade I brought my yearbook up to my teacher and he drew a little cartoon of a beard and a pair of glasses to represent himself, signing it “to noisy Mary”. He hadn’t meant to hurt me, but I was crushed with the sudden understanding of how he saw me, the knowledge that while I felt like I knew him, he did not feel like he knew me. And it went on like that, my life, with me on the sidelines, taking other people in, but not able to extend myself. I was terribly shy all through my school years. By the time I got to college, I was even worse than I had been in elementary school. Around this time I started to have terrible problems with prolonged blushing. I tried my best to be invisible, but inevitably, I would be called on to speak in class and no matter how hard I fought to be easy, my body would betray me. I would feel my face getting warm, and then it would build and build and build until the fact that I was turning so red was now the problem, a self-perpetuating loop of hot embarrassment which would last for five or ten minutes. I met someone in college who I really liked, but one day he put it to me straight. “I need someone who is going to be able to help me in the world,” he said. He had trotted me out to meet his friends, one after another, little tests of social facility that I was doomed to fail. I had been out of college for a few years, floating in a legal assistant job

and doing fairly well with the people in the small office I worked in, when my ability to overcome the limitations of my social anxiety was put to its most extreme test. I took the law school aptitude test “just to see”, and it came back with an exceptionally high score. I knew I didn’t have the right personality to be an attorney—but there was an offer of a scholarship. I had painted myself into a corner by creating an opportunity for myself that I couldn’t refuse. Of course it went badly. Law school was a repeat of college, but I imagined that it was worse because I was a bit older than the other students and I told myself that was the reason I didn’t fit in. In reality, I was too anxious to become a part of any social group, and I watched as they formed and closed with me standing in my usual place, on the outside, walking alone, studying alone, finding quiet places on the grass with a nice view to eat alone, and etcetera, etcetera. I wasn’t happy about it, and I tried to find a way out of my selfimposed isolation through self-help books, but they didn’t really help in the long run. Yes, I could see that I was focusing too much on myself and how uncomfortable I was and that it was my anxiety that was making other people uncomfortable with me, and not any greater failing, but it didn’t do me any good to know that. After all the work that it took me to get through law school and to pass the bar, I quit law entirely after my first experience in front of the Court of Appeals. I had chosen appellate law because I liked the research and writing involved, but mostly because it required much less face time in court. That face time, however, when it finally came, involved trying to present a case in front of 3 justices at once, each one of whom broke into my statement of the case with questions, trying to guide the argument to his own position. I had prepared for weeks, but there was no way to prepare for this experience. It was simply beyond me. The last 4 years had been a calamitous confrontation with my own weakness. It didn’t matter in the least how smart I was, and I told myself that I should have known better than to even have tried. I had gotten married recently. Against all odds I had found someone who put up with my tendency to fall apart and run off at the slightest emotional challenge, and I was expecting our first child. So I turned away from the world and tried to be kind to myself. I had grown up and found a nice life for myself with a really respectable, successful and self-confident man, and I kept expecting that I would break out of my shell and grow into a more mature sense of self confidence myself, but if anything, I got worse. I couldn’t even take a proper photograph any longer, I couldn’t stand the attention or the intensity of the camera, and I hated the crazy, trapped look I

would have in the photographs that I hadn’t been able to avoid. I thought I was irreparably damaged from childhood and I would have to learn to accept that I wasn’t ever going to improve. I wasn't asking for much any longer, I just wanted to be able to say "hi" in a natural way to people I might pass walking the dog, but I was always awkward. Still, I was grateful for my children and my husband and the life I was able to live away from the bigger world. My entire life had been difficult for me, but having decided to accept myself as I was, I felt that it was as good as it could be. There were still moments that were very difficult for me, children’s birthday parties (which I couldn’t escape attending) were an unexpected source of ongoing pain, but on the whole, in a life which had been terribly painful, really, these were the good years. So I took it in stride when I started to have physical problems. The first was a permanent sunburn in my blush areas, my face and chest. I tried wearing broad brimmed hats everywhere, even into the ocean, and I tried having the redness lasered away, but without much success. I had a series of miscarriages, one, two, three in a row, I developed high blood pressure, and an apparent case of tendonitis that seriously hampered my ability to walk for an entire year. I fell down the stairs and starting holding onto the rail walking the risers one at a time, one step down, the other foot to meet it, walking down the stairs like an old woman. I went to doctor after doctor, telling them the pain in my ankles, the high blood pressure, they all started at once, but I couldn’t engage any one of them in consideration of an underlying cause. They blamed my high blood pressure on my increasing weight and age. I blamed my swollen painful legs on the blood pressure medication. My life was going well, I had a lot to be thankful for, but I found myself increasingly fragile emotionally. Depressed. My hands looked like an old woman’s. They would fall numb now and then while I slept and I’d wake with them curled in hard at the wrists. My handwriting, never good, was falling apart. I was losing words. My appetite was out of control. I exercised as much as I could, I ate as healthy as I could, lots of fresh fruit and vegetables and plenty of fish, and I started taking a variety of vitamins, trying to find my way back to health. And, just to make sure I wasn’t harming myself in the trying, I had a hair test analysis performed. What came back shocked me. I was off the charts high for mercury.

The History of Mercury “I tell you that they take quicksilver and sulphur, and mix them together with water and make a drink of them, and they drink it and say it increases their life and they live longer by it, and they do it twice in the week and sometimes twice in the month. And you may know those people use this drink from their infancy so as to live longer, and without mistake those who live so long use this drink of sulpher and quicksilver.” - Marco Polo, 1298

Natural mercury belts are found in areas where the world’s tectonic plates have been forced together and pushed up to build mountains, a process known as orogeny from the Greek words “oros” and “genesis” for “mountain” and “creation”. It is the same process which forms volcanoes and hot springs, and in this process rock and other material from deep within the earth is pushed up to the surface. A natural mercury belt runs from the most northern point of Alaska down along the coast of North America to the southernmost point of South America.1 There is a massive belt which runs from the western Mediterranean through the Himalayas and into Central Asia. At times, hotspots underlying the earth’s mantle push up isolated mountains or volcanoes that are not necessarily on tectonic plate boundaries. Mercury occurs naturally in these areas, most often in ore form as cinnabar, but also in its silvery liquid state, lying at the surface in small rocky crevices awaiting chance discovery. 500 years ago, mercury mining in the western world was dominated by the Fuggers, an exceptionally wealthy German banking family who had negotiated mining rights throughout Europe in collateral for loans they had made. They had control of Idrija, the mercury mine in the Austrian Alps where a craftsman had discovered the liquid metal at a local spring where he was working. He had placed a wooden tub under a dripping spring to test it for water fastness, and on returning in the morning, had found the tub so heavy with quicksilver that he could barely move it.2 The little river Idrijca which ran through the town was full of fine, fat trout which were said to taste as they should, even though the bottom of the river was “entirely a quicksilver ore.”3

The Fuggers also had a controlling interest in the Almaden mercury mines in Spain, and through the Spanish government, an interest in the Huancavelica mine in the Peruvian Andes. The miners who worked the mines suffered a variety of serious health related complaints, and they were subject to strange forms of mental despair, introversion, depression, alcohol abuse and hallucination. Somehow, at around this same period of time, even though the problems suffered by the miners were not unknown, mercury began to be used as a medicine to be taken internally. How did it happen? In all began in the Eastern world, where an idea had taken hold among Chinese mystics that mercury could restore life and prolong health. In the 3rd century, Qin Shi Huang, the First Emperor of a united China drank a potion containing mercury in an attempt to achieve immortality. He died instead, at the age of 49. According to the cautionary 9th century book, Classified Essentials of the Mysterious Tao of the True Origin of Things, drinking mercury in the quest for longer life was a fatal mistake made by many privileged Chinese throughout the centuries.4 Qin Shi Huang was buried in a massive underground tomb whose very construction gave

evidence of his life beyond death fascination with mercury. Within the tomb, “mercury was used to simulate the hundred rivers, the Yangtze and Yellow River, and the great sea, and set to flow mechanically.”5 Meanwhile, people in the Western world were aware of mercury, and quite transfixed with the way in which it interacted with other metals and might be used to increase wealth. Mercury has a unique ability to dissolve most lesser metals and to unite with gold and silver to form an amalgam. When the amalgam is heated, the mercury vaporizes, leaving only the pure metal behind—a process which facilitates the recovery of gold and silver from common ore. Mercury was rarely used in Western medicine, and when it was, its use was limited to external remedies. Preparations made from cinnabar had been used as a topical treatment of various skin conditions and venereal diseases—Celsus included a reference for it in his de Medicina written in 30 AD—but the venereal diseases of the time were not as severe as they would later become, and most conditions still responded to other, more common, plant and herb based treatments. The two worlds came together in the Arab empire, an orogeny of ideas which pushed up something new, “alkimia” as it was known in Arabic, or alchemy—the science of metal and of man. The tenth century history T’ai P’ing Kuang Chi, contains an allegorical story about the meeting of the two worlds. In the story, a young Chinese scholar named Tu Tzu Chun, meets an old man at a Persian bazaar who is willing to pay him handsomely to create an immortality elixir using an alchemical procedure. An illustration in the book shows the old man standing in front of a furnace spewing out purple vapor, and the story contains a poetic but quite accurate account of the emotional torments suffered by those exposed to mercury in vapor form. After ingesting certain drugs and sitting down to gaze in meditation at a blank wall, Tu found himself undergoing the torments of a variety of Buddhist hells, and was eventually reincarnated in another body before breaking the spell by a burst of uncontrollable emotion. Having failed to master these terrifying apparitions, Tu awoke, and the experiment which would have gained hsien immortality for both him and the old Persian ended in failure.6

Warnings abounded, but the temptation of prolonged life was enough to deafen the ears of even the wisest men. Roger Bacon, the thirteenth century friar and philosopher, embraced the promise of alchemy with wholehearted enthusiasm. He reasoned that the shortening of man’s lifespan after the “Fall” (before which, it was believed, a man might live for a thousand years), was due to a gradually increasing accumulation of inherited “corruption” which might be remedied, and he was convinced that alchemy

could be used not only to produce gold, but also to prolong a man’s life span by a hundred years or more. In an address to Pope Clement IV he stated, It will give the prolongation of human life. For that medicine which would remove all the impurities and corruptions of baser metal, so that it should become the purest gold, is considered by the wise to be able to remove the corruptions of the human body to such an extent that it will prolong life for many centuries.7

In response to the Pope’s request that Bacon put his ideas into writing, Bacon generated a series of “works” in the year 1267, culminating in his Opus Tertium, in which he restated his firm belief that “alchemy not only procures wealth, but, in conjunction with experimental science, it can prolong life.” He had spread his knowledge of the mysteries of alchemy piecemeal through each of his works in order to guard the secret from the “vulgar”, and he expressed his desire for a personal audience with the Pope in which he would speak using a simple code in which the names of the Sun and Moon and each of the planets would stand for a particular metal, so that the word Sun would stand for gold, the word Moon for silver, and the word Mercury would stand for quicksilver.8 The raw material of the alchemical elixir would be referred to as “stones”, and “prepared stone” would refer to the elixir itself.9 Bacon wrote about the art of using quicksilver in the creation of gold and silver to demonstrate the use of his code, writing that “Sun and Moon are made artificially in several ways. One way is from Mercury and sulphur, which are the constituent parts of all metals. Others try to convert Mercury alone into Sun and Moon.” He set down his secrets of life extension in a separate letter which went into greater detail on the extent to which a man could prolong his life, the reasons for keeping the secret from the “common rabble”, and his use of code and other methods to safeguard the secret of the elixir which he had named “Stone” in code, but which he now referred to as the “Philosopher’s Egg”.10 And so quicksilver, the substance capable of removing the impurities and corruptions of baser metals, came to be known as mercury, and mercury combined with sulphur became known as the Philosopher’s Stone, a substance purportedly capable of prolonging life by removing the corruptions of the human body, and yet, the myth of the Philosophers Stone had grown so much larger than the reality that this truth was overlooked by all but a few. Two things happened at the end of the 15th century to change the physicians’ cautious approach to mercury—sailors returning from Christopher Columbus’ journey to the New World introduced syphilis to the

Old World, renewing interest in the earlier mercurial treatments for venereal diseases recommended by Celsus, and Theophrastus Bombast von Hohenheim was born. Theophrastus’ father was a doctor who had been appointed as the physician of the town of Villach in Carinthian Austria. The Fuggers ran a school at Villach where they trained overseers for their mines. Theophrastus attended the school, and worked later at the Fugger’s laboratories studying metals and their compounds. He was hardworking, brilliant, but aggressively antagonistic to the medical authority of the time. He disagreed with the teachings of the Arabic physician Avicenna who in 1025 had also prescribed the use of mercury as an external treatment for venereal disease but who had cautioned against its internal use. While Theophrastus was still a student at the school in Villach, he threw Avicenna’s Canon of Medicine into a bonfire, a stunt he would repeat for dramatic effect in later lectures. It was the custom of the time to choose a Latin name to be known by, and the name Theophrastus chose was Paracelsus, meaning, literally, Better than Celsus! Paracelsus carried a sword with him which he kept by his side night and day, a talisman with a secret compartment containing what he considered to be a source of supernatural power. “He maintained that his sword, which he had received as a present from an executioner in Germany, imprisoned in its handle a familiar genie called Azoth” wrote his secretary Operin. And it is true—in portraits of Paracelsus carrying his sword, the inscription “Azoth” can be clearly seen on the knob at the hilt of the sword. The Arabic word for mercury, alzauq, latinized to azoth, was used interchangeably to refer to the Philosophers’ Stone, and also as the poetic word for mercury. 11 Was there mercury in the secret compartment in the handle of the sword as the pommel advertised? Almost certainly. Paracelsus announced that he had found the philosophers stone. He had worked with mercury at the Fugger’s labs, investigating its ability to transform and form amalgams with other metals, but he believed that “the business of alchemy is not to make gold but to prepare remedies for human ills.”12 Paracelsus was the man who first introduced mercury to the Western world as a medical treatment to be taken internally. Paracelsus was outspoken in his contempt of the long established medical doctrines of his day, especially that of humoral pathology, a doctrine whose fundamental ideas had been held for over 2,000 years. The doctrine of the four humors held that all illness was a result of an imbalance in the four “humors” of the body, yellow bile, black bile, pleghm and blood,13 in relation to the four elements of fire, earth, water and air and the four corresponding elementary qualities, heat, dryness, cold and moisture.

As you can see from the diagram above, blood and its corresponding element air were considered to be both hot and wet. Yellow bile and its corresponding element fire were both hot and dry, and so forth. Treatment of patients was the result of years of careful study in the methods by which medication, diet (hot food or cold food) and exercise regimens could be implemented to correct the imbalance. Paracelsus’ denial of the existence of the humors outraged the medical profession of the time. “A crowd of physicians,” he said, “rise up against me. From them come the names bile, melancholy, phlegm, and blood. But who has seen bile in Nature? How can phlegm resemble one of the elements? How does blood resemble air? You say this is a vice of the blood, and that of the liver; but what, I pray you, has given you such lynx eyes as to know so well that the blood or the liver is the cause when you are utterly ignorant of the nature of the blood?”14 The medical establishment of the time did rise up against Paracelsus in defense of their specious humoral philosophy, quite successfully boycotting any publisher who agreed to publish his work, and condemning his mercurial prescriptions as “poison”. Abrasive, lacking in personal hygiene

and socially tactless (by his own admission), Paracelsus fired back that the physicians were unqualified to use poisonous mercurial ointments and fumigations, which they frequently did, being unschooled in mercury’s proper safe dose and the manner in which to render it safe. He made an argument which is still in use today15, that it is the dose that makes the poison. If you wish justly to explain each poison, what is there that is not poison? All things are poison, and nothing is without poison; the Dosis alone makes a thing not poison. For example, every food and every drink, if taken beyond its Dose, is poison; the result proves it.16

Few people were exposed to his work during his life-time. Due to the physicians successful publishing boycott, the great majority of Paracelsus’ works were not published until years after his death, and, during his brief position as a lecturer at the University of Basel in Switzerland, his students could not handle his “strange ways.”17 Later researchers have speculated that his erratic behavior was due to the results of mercury poisoning, but some of his strange ways were due, no doubt, to the fact that he drank so excessively. According to his secretary Operin, he drank “night and day” so that “it was almost impossible to find him two successive hours except completely drunk,” and he would often “arrive drunk at the hall where he gave his courses, holding in one hand the famous sword and with the other leaning against a pillar.”18 He would lecture angrily and insultingly against the medical establishment, assuring his students that “every little hair on my neck knows more than you and all your scribes, and my shoe buckles are more learned than your Galen and Avicenna, and my beard has more experience than all your high colleges.”19 Disappointed, antagonized and misunderstood, and laboring under a cloud of suspicion in the death of his benefactor (who he had treated with mercury), Paracelsus left the city suddenly and resumed his earlier travels. He had a genuine affection for the common man, and he lived among them in relative obscurity, open to “the humble contribution of tavern keepers and gypsies,” and lecturing to the barber-surgeons. In contrast to the educated doctor-physicians of the day who studied illness and prescribed medications according to ancient Aristotelian philosophical doctrines, the barber-surgeons were the men who were not allowed to prescribe medications, but who performed the “dirty” work of caring for the physical body, men who, in addition to haircutting and shaving, would pull teeth, lance boils, give enemas, perform bloodletting, leeching and surgery. One barber-surgeon of the time was Leonardo

Fioravanti, and he was about to bring mercury as an internal remedy directly to the people. In 1541, the year Paracelsus died at the age of 48, ill and prematurely old, Fioravanti was a 24 year old Italian barber surgeon with a checkered past whose chance impersonation of a physician had gone so well that he decided to act the part. He advocated a return to the wisdom of the natural world, a strong medicine which would purge the stomach in the same way that a sick dog or cat will eat grass to make itself vomit and evacuate.20 Fioravanti was aware of the emetic and laxative actions of mercury taken orally, and the theory he proposed, that pollution of the stomach was the cause of all diseases, fit the remedy perfectly. Echoing Paracelsus in his outspoken criticism of the four humors, he wrote, When I saw an anatomy done, I never saw phlegm, choler, melancholy, or vital spirits, or any of those other fabulous things that the physicians dream up. I saw the tongue, lungs, heart, liver, spleen, ventricle, diaphragm, bowels, kidneys, bladder, nerves, veins, tendons, flesh, skin and bones, but I never saw those imaginary things.21

Fioravanti’s words (a repackaging of Paracelsus’ words really) resonated with the people of the time and he began to publish books containing his remedies. He told everyone that he had found the secret of making the philosophers stone, and the foremost of Fioravanti’s remedies was his “pietra filosofale”, a mercury-sulfur compound.22 He worked with pharmacies to produce his patented medicines and had a brisk mail order business sending remedies to England as early as 1568. The physicians held the line that surgeons might use mercury as an external remedy, however questionable that use might be23, but they objected that when surgeons prescribed mercury to be taken orally, they were encroaching upon the physician’s domain and violating the law. The physicians charged that Fioravanti was poisoning his patients and asked that he be thrown in jail for prescribing medicine without a license. Having earlier claimed that he had discovered a secret known to no one else, he wrote from jail in his own defense that, My method is founded upon the true doctrine of Hippocrates, which Avicenna understood poorly. But the moderns, such as Ramon Lull, Arnald of Villanova, Abacue the Jew, Paracelsus, Cornelius Celsus, and Philip Ulstadius, understood it well and used the same methods.”24

Fioravanti had charged that the physicians had made a case against him due to no more than professional jealousy, and the jurists of the day must have agreed, as they solved the problem neatly by accrediting Fioravanti as a physician. The repeated attacks left him disheartened and depressed, however, and in an ending common in those who are chronically exposed to mercury, he became both “combative and reconciled to defeat,”25 and Fioravanti faded away from view. His books did not, however. They were amazingly popular, and more than 83 editions of his works were published in Italy and throughout Europe for a span of nearly 200 years. Seeing the chance to profit themselves, apothecaries and pharmacists in England soon began to prepare and sell Fioravanti’s remedies on their own. The genie had come out of the sword, so to speak, and was free to wreak havoc in the world. The doctor-physicians took up where Fioravanti left off, satisfying the desire of the people for mercurial cures and patenting their own mercury compound pills, a practice which was far more lucrative than the practice of medicine alone. The two most well-known of these physicians were the French physician Augustin Belloste, and the English physician Thomas Dover, who was known as Dr. Quicksilver. The French military physician Augustin Belloste created a fabulously popular proprietary mercury-purgative blend pill, the composition of which he kept secret. He had begun using mercury pills in 1681 as a 27 year old physician at a military hospital in the French Alps. The treatment was a great success, but as Belloste was still a young man, he was not able to promote his mercurial treatments until much later.26 In 1725, at the age of 70, he published The Hospital Surgeon, a reprint of an earlier book in which he included several new essays relating the many occasions on which he had used his mercury-purgative blend pills in the treatment of various diseases with great success. Experience being the strongest of all proofs, I thought it might not be improper to relate some cures performed at different times, on different subjects, and in different disorders. Were I to publish all those which I have performed in the space of the three and forty years that I have made use of mercury, a very large volume would hardly contain them.27

Belloste distinguished himself from past physicians with his statements that mercury taken internally was preferable to ointments or lotions, “render’d wholesome by the ferment of the stomach” in the same way that you can safely eat a poisonous snake that could kill you with a bite,28 and with his belief that larger doses of mercury were less harmful than smaller

doses, as “when some pounds of it are swallow’d, if it meets with no stop in the intestines, it quickly passes through, retaining the same weight it had when it was taken.”29 Mercury was not only beneficial in the treatment of venereal diseases, he wrote, but a miracle cure useful for itch, pimples, worms, running sores, kidney stones, early cases of gout, rheumatism, sciatica, carcinomas, liver and breast tumors, small pox, leprosy and plague. On preventing plague he advanced several theories of plague, each of which would be best met with the use of mercury. For example, under the theory of contagion he wrote, This system, which carries with it greater probability than any other which has been advanced upon the subject, authorises the use of mercury, as an internal specific, and as a preservative, when worn on the surface of the body. A most illustrious sovereign prince has worn it about him for more than fifty years, to preserve him from this disease. He is now above fourscore, and never had it. I always wear mercury about me: I am an old man, yet never had the disease.30

Belloste’s book and its glowing praise of mercury as a “miracle of nature” and a “gift of providence” was published widely throughout Europe, with translations in English, German and Italian. But a perception that the use of mercury as a medication was useless at best, and dangerous at worst, was an ever present undercurrent. Daniel Defoe wrote in his History of the Plague in London in 1722 that physicians making false claims: not only robbed and cheated the poor people of their money, but poisoned their bodies with odious and fatal preparations; some with mercury, and some with other things as bad, perfectly remote from the thing pretended to, and rather hurtful than serviceable to the body in case an infection followed.31

Soon after Belloste’s death in 1730, English physician Thomas Dover (aka Dr. Quicksilver) published his own book on mercury, The Ancient Physician’s legacy to his country.32 Whether by design or coincidence, Dover’s book echoed Fioravanti’s and Paracelsus’ precepts that no medical education could be complete without many years of travel, that purging and vomiting are remedies of the natural world, that doctors long complicated prescriptions were designed to increase their profit, and that doctors who rejected mercurial cures were hypocrites who were using it already in other forms. Like Fioravanti, Dover appended testimonial letters from grateful patients, and like Fioravanti, he had many powerful enemies. Dover confronted his enemies in like manner, stating that their notion

that “quicksilver is poison” was a failure of natural philosophy due to their limited experience in travel. Nonchalantly dismissing the concerns of his detractors, he wrote, “Let them take a trip to Hungary, and visit the mines where the quicksilver is dug; they may there see slaves working entirely naked, to prevent them stealing this precious jelly of metals, as it may be called; yet every day swallow so much that they buy a choppin of drink with it at night.”

In reality, it was well known that the health of the quicksilver miners in Hungary was “extremely impaired”, that the miners working with the “virgin” liquid quicksilver were more likely to suffer nervous disorders, such as tremors and convulsions than those mining the cinnabar ore. Even rats did not last long, as, “even these vermin are seized with the like convulsive disorders as the men are subject to, which soon kills them.”33 Nevertheless, Dover asserted confidently that quicksilver had never harmed any patient, and that no harm could come from the use of it. He wrote that purging with mercury would free the intestines from “filth and impurities,” and in cases of impacted bowel, he advised confidently that “you need go no further for the cure of this fatal disease, than to take a pound, or a pound and half of crude mercury.”34 Answering accusations that he had caused the death of many of his patients, he claimed the accusations were all lies, or malicious rumors. (“I know very well, I am no sooner called to a patient, but it is reported immediately he is dead, and I have killed him.”) 35 Nevertheless, neatly shifting the burden for any calamitous effect off of himself and onto his patients, Dover noted a single “caution”, that, there is a great difference in the several constitutions of mankind; and therefore it must be left to every man’s discretion, as to the quantity he is to take of each of 36

these medications.”

Belloste was a better writer than Dover, and much more persuasive in his glowing accounts of miracle cures, with the result that his second edition of the Hospital Surgeon would be printed and reprinted for more than 50 years, with translations in Italian, German and English. Dover’s book, on the other hand, was the subject of immediate rebuttal and criticism. One physician, Daniel Turner, published a book declaring that Dover’s practice of recommending large quantities of crude quicksilver was “repugnant” and he included letters from physicians who had attended cases of fatal mercury

poisoning caused by following Dover’s advice. 37 It might have appeared that Turner was a caring physician, trying to save lives needlessly endangered by mercurial treatments, but his motives in denouncing Dover were far from impartial. Turner used his book as an opportunity to praise Belloste’s pill as “a very good one,” and to promote his own pill as similar to it in all respects. If Monsieur Bellost in his life-time, or his assigns, since his death, endeavor to persuade us, that nobody besides themselves, knows how to mix crude quicksilver with some purging ingredients, and to incorporate the same into a pill, they ought to be convinced of their mistake, and I can assure our pharmaceutical gentlemen, if they will but take the same pains in reducing the quicksilver by the help of a little turpentine, into as fine moleculae, as Belloste’s compounder had done, and after as thoroughly incorporate the same, with the purging ingredients, as I have already observed, will have, though not perhaps Belloste’s individual, yet a pill that in all respects comes up to it in its virtues.38

Belloste had promised he would eventually make the secret composition of his compound mercury-purgative pill public, but he had recanted shortly before his death, citing his family’s need for the income their production would generate. Belloste’s son, Michel-Antoine Belloste, was granted a patent to continue to manufacture the pills, which he did with great success for many years.39 Newspaper advertisements and instructions for the use of Belloste’s pills were published at least as late as 1819, after which the formula was published, with the result that many, many different forms of mercury pills began to be compounded, joining the already existing blue pill Barbarossa, the Neapolitan Renaudot pills, grey powder (Hydrargyrum cum Creta, or mercury with chalk, reputed to be “advantageously exhibited in cases of diarrhea in children”), Ward’s white drops (mercury dissolved in nitric acid with a solution of carbonate of ammonia), Addison’s pills, Baillie’s pills, Plummer’s pills, Guy’s Hospital pills, and Boerhaave’s red pill, to name just a few.40 The lack of viable alternatives in illness, the desperate outcry for a solution, and the opportunity for huge profits all worked together to create an incredible prevalence of mercury in medicine. An iatrogenic illness is one caused unintentionally by a doctor in the course of treatment of another illness. Not surprisingly, in the later part of the 1500’s, just as mercury began to be used as an internal remedy, a new illness began to occur in sporadic outbreaks and epidemics throughout the world, a non-contagious disease most frequently associated with or following directly after some

other infection or disease. It was the same in every country in which it occurred, manifesting with psychological symptoms of irritability, restlessness, insomnia and depression, and neurological symptoms of tingling and numbness of the fingers, toes, hands and feet, and progressing to swelling, pain and contraction of the limbs.41 In the years 1828 and 1829 an epidemic of the disease swept through Paris, affecting between 40,000 and 50,000 people.42 It was named Acrodynie from the Greek words for extremity and pain, and its name would be used again, but not until the early 1900’s when another terrible epidemic began a 50 year sweep through the children of the world, a mysterious nervous affectation presenting with painful hands and feet.

Hysteria and the Nervous Temperament in the 1800’s “Take the silver tear instead, from my full eye.” - Emily Dickinson

People in the 1800s were afflicted with many strange illnesses, including inexplicable episodes of temporary paralysis and loss of vision. They were taking a lot of mercury in the treatment of various illnesses, and while we know now that mercury is a potent neurotoxin capable of causing exactly that sort of nerve dysfunction, physicians at the time had no explanation for paralysis or blindness without an apparent physical cause. It was clearly a pseudo-paralysis and not structural in nature, said the physicians, who had seen more than one afflicted patient regain function when threatened or otherwise sufficiently motivated.43 It was a form of “hysteria”, they decided, and they described it alternately as a perversion of the mental disposition the nervous were prone to, or as a jealous thirst for attention—a case in which the afflicted were either deceiving themselves, or attempting to deceive others. Hysteria could present in symptoms as diverse as pain, cough, convulsive attacks, fainting fits, difficulty swallowing, vomiting, asthma, hiccups, heart palpitations, a constant feeling of the need to urinate, delirium, coma, or catalepsy. Catalepsy is a strange disease in which there is a sudden suspension of the action of the senses and of volition—cataleptics display no will of their own and will hold any position they are placed into, remaining frozen rigidly in place, except that certain meaningful or sudden stimuli, such as music, touch, or a ball being thrown directly at them, can cause a reactive response.44 Acknowledging that the “multitude and apparent incongruity” of the symptoms of hysteria have “perplexed and bewildered observers,” physician Julius Althaus explained that it all makes sense if you view hysteria as an exaggeration of normal physical reactions. Giving the example of an impressionable woman, or one who has recently suffered some stress or illness, he stated: Tell this woman suddenly that the house is on fire, or that she has lost a near relation, and you may be sure to observe some of or all of the following symptoms. She perceives a feeling of constriction in the epigastrium, oppression on the chest, and palpitations of the heart; a lump seems to rise in her throat and gives a feeling of suffocation; she loses her power over her legs, so that she is for the moment unable to move; and she wrings the hands in a spasmodic manner.

Let these symptoms increase in degree of intensity, and you have the well-known signs of hysteria, which I have just classified under the four heads of functional spasm and paralysis, anaesthesia and hyperaesthesia, and which result from painful impressions being transmitted to the emotional part of the brain.45

Hysterical paralysis could appear as hemiplegia (one-sided paralysis), paraplegia (paralysis of the lower extremeties), or a more general paralysis which might affect not only the voluntary muscles of the extremeties, but also the involuntary muscles of the pharynx, vocal cords, diaphragm, bladder, rectum and heart. Terrifying instances of individuals suffering from “hysteria” being presumed dead and buried alive were “by no means rare.”46 Fairly early on, the famed German neurologist Moritz Romberg had published his findings that excitability of the neuronal reflex arc was increased in cases of hysteria, but later physicians, such as Althaus, dismissed this purely structural explanation, feeling that Romberg “did not lay sufficient stress on the emotional character of the disease.” They couldn’t explain the “infinite variety of symptoms”, the “causation and progress of hysteria” without reference to what they believed was its essentially emotional character. In one published study, Oscar Clayton, the master of a charitable institution for girls aged 9 to 14 told the story of a “hysterical affection of the vocal apparatus” which occurred in the fall of 1841 when a considerable number of girls at the institution were afflicted with a short hacking cough and slight fever. The illness had been sweeping through the school repeatedly since the beginning of the year. This time, however, the coughing was so loud that it disturbed and alarmed the neighborhood. Clayton was at his wits end. He believed that the coughing this time was markedly “hysterical and imitative” and he decided to test whether “a strong mental impression” might shock the girls out of their hysteria. Assembling the children, he told them that he would have to apply a red-hot iron to the throats of all the girls who were not “quite well” the next morning. The next day all but two were “quite well”, but soon all relapsed, and their throats were blistered with a spatula wrapped in silk and heated in boiling water, which, “with some” succeeded in removing the symptoms. This affection, like most of the hysterical family, although for the most part involuntary, still to a certain extent was controllable by a strong effort of the will; although such effort was extremely painful, giving rise to spasmodic catchings of the breath. Not that I believe the children were guilty of any trick, but that, on the contrary, they were very glad to be relieved.47

Hysteria had become a catch-all diagnosis for a condition of disordered function that the doctors had no other explanation for, and rather than admitting this failure of understanding to themselves or others (in an ironic parallel to the diagnosis of hysteria which they themselves crafted, a case either of fooling themselves, or fooling others), the doctors blamed the patients for their state of ill-health. Most physicians of the day thought hysteria was the result of mental weakness, the case of a patient brooding over and magnifying disagreeable sensations that a mentally stronger person wouldn’t pay much attention to. But at times the tragic results of an unheeded case of hysteria gone wrong would impress itself so strongly upon the physician involved, that he would publish his experience. Such was the case with Dr. Robert Foss, who was called in to see a 19-year-old girl in the throes of an hysterical convulsion, “throwing her arms and legs about, laughing and crying alternately.” The girl had been having these fits for more than a year, and all of the medical men who had been called in to see her had told her father she was simply suffering from hysteria, and would soon be well again. Dr. Foss “expressed a similar opinion, believing that it was a case more for moral than medical treatment,” but within 3 hours, the girl had died. Her grief stricken father demanded an autopsy to discover the cause of death, but no obvious cause was found. In relating the case and one similar to it, Foss warned his fellow physicians that hysteria was not all in the mind, that when convulsions were present, it was a physical, life threatening condition.48 The cause of the disordered function so often labeled as hysteria was clear, at least, to a vocal minority. In July of 1847, surgeon Richard Storrs decried the increasing use of mercury as a medicine, citing 8 cases of hemiplegia and paraplegia owing to the use of mercurial treatment which he had personally observed. In general, he found weakness, pain, or numbness preceding paralysis of the extremities49, often accompanied with loss of bladder control, and loss of speech. Of the 8 patients surveyed, all either died or suffered permanent disability. Storrs told his fellow physicians that they would stop flattering themselves on the success of their mercurial treatments if they would stop overlooking the shortened lives, ruined constitutions, and disabled limbs, the “lasting monuments of the carelessness, the willfulness, or the ignorance of the practitioner.”50 A young girl of the same age in time as the Clayton girls was growing up in Massachusetts, but in slightly more favorable circumstances. Emily Dickinson was the middle child in a socially prominent family in Amherst Massachusetts, and she was looking forward to a bright future. On May 7, 1845, at the age of 14, Emily Dickinson wrote to a friend, “I am growing

handsome very fast indeed! I expect I shall be the belle of Amherst when I reach my 17th year. I don’t doubt that I shall have perfect crowds of admirers at that age. Then how I shall delight to make them await my bidding, and with what delight shall I witness their suspense while I make my final decision.” But it was not to be. She would change. The bright confident young Emily Dickinson would become so pathologically shy and reclusive in later years that she rarely left the house. She would not delight at crowds of admirers, she would speak to visiting friends from behind a closed door. She would change, or something would change her, so that she would become a tormented soul living in the shadows who would treat children to candy from her second story window showing only an arm and lowering a bucket like Dr. Seuss’ ruined Onceler. On May 16, 1848, at the age of 17, Dickinson wrote, “I had not been very well all winter, but had not written home about it, lest the folks should take me home.” No recluse yet, she added that a friend had notified her parents who came and fetched her home immediately. “Have you so treacherous a friend?” she asked. “I could not bear to leave teachers and companions before the close of the term and go home to be dosed and receive the physician daily . . . . Haven’t I given a ludicrous account of going home sick from a boarding school? Father is quite a hand to give medicine, especially if it is not desirable to the patient, and I was dosed for about a month after my return home, without any mercy, till at last out of mere pity my cough went away.” The historical record is silent on the nature of the medication young Emily received in 1848, but it is likely that her doctor prescribed some form of mercurial treatment. There was a lot of talk among the physicians in New England around that time about the value of using mercurials in the treatment of coughs and fevers. In 1845, another New England physician, Dr. Hubbard of Maine, spoke before the Philadelphia College of Physicians about his success using sub-sulphate of mercury in the treatment of scarlet fever and croup. He presented the case of a 12 year old girl racked with violent nightly coughing fits and spasmodic breathing who he treated with enough mercury to cause vomiting, with great success. Stating emphatically, “I know of no other emetic substance that would have effectively met such a case,” and that “in this form and condition of croup, my experience furnishes me with no substitute for the turpeth mineral,” he recommended the dose be “larger than is usually recommended”, and proclaimed it “entirely safe.”51

There was a growing movement among physicians in the late 1840’s towards the use of mercurials in the treatment of resistant coughs, traditionally as a pill or ointment. 52 In 1842 a study was published in the Provincial Medical Journal stating that although the majority of doctors had considered mercury to be “decidedly injurious” before that point, that more recently many well respected physicians had found it to be a useful adjunct, helpful in arresting the course of disease and gaining time for the application of other remedies. From the undoubted testimony and high talent of the authors above mentioned, and from the numerous well marked cases which they have detailed, little question can exist but that in some cases of incipient consumption, the production 53 of ptyalism is attended with the happiest result...

The amount and method of mercury employed varied widely between physicians, but it was generally believed that in order for treatment by mercury to be effective it had to reach a point of ptyalism, the excessive salivation caused by a course of mercury54, to the point at which the mouth became sore from the effects.55 Sometimes the parents took matters into their own hands, giving their children calomel (a form of mercuryl chloride) before calling the doctor.56 Many pharmacists of the time had found it to be much more profitable to deal with their clients directly and there was “a continuous undercurrent of medical practice over the counter . . . either with or without the aid of the physician’s prescriptions on file.”57 In 1844, Elisha Bartlett, a respected physician, professor and member of the Massachusetts House of representatives wrote this about the widespread use of calomel in medicine, Almost every ailment to which the body is subject—functional or organic—trifling or grave—chronic or acute—each of these ailments can be removed in only one way,--by the restoration of the bilary secretion,--by inducing the liver “to act”; and this can be accomplished with certainty, only by one infallible remedy— calomel. This substance is proclaimed to be, not only the most efficacious and important article in the material medica, but, also, one of the safest and most inoffensive. It is constantly administered—on all occasions—in all diseases—and in all their stages. It has, literally, in some instances, been made an article of daily food—sprinkled upon buttered bread, and mixed with it before baking.58

It is likely that Emily Dickinson’s father dosed her with mercurials. In addition to it being the practice of the time, the nature of her later illnesses

suggests it as a strong possibility. Like a pointillist painting composed of small dots of color, if you look at the individual events up close, you may not see anything meaningful,.. you may not see evidence of mercury, but when you step back and look at the entirety of her life and the physical symptoms Dickinson suffered in the context of the historical time she lived in--the coughs that wound in death, the consumption and the scarlet fever that could quickly carry you away, the growing concensus among physicians on the efficacy of mercury, coupled with the fact that her father was aggressive with medication and the strongest remedy available at that time was mercury, in the form of calomel (Hg2Cl2) and mercuric chloride (HgCl2 or corrosive sublimate)--when you step back and look at the whole picture, it comes into focus, and I believe that enough is known to strongly suggest that Dickinson was treated with mercury. It was, in fact, after this episode of illness and the long period of being “dosed” that Dickinson, formerly a bright young girl who wanted nothing more than to stay in school surrounded by her friends, began to change into the troubled woman she would become. The first indication of an “excitation” of her temperament appeared in the May 16, 1848 illness/dosing letter, in which Dickenson wrote of thoughts “crowding thick and fast, like lightnings” and a feeling of desolation. Undoubtedly, this increasing intensity and introversion contributed to her poetry, but at great price. Dickinson became so pathologically shy that she was virtually agoraphobic, and her physical health was impacted as well. She later wrote that her sister “ ‘cannot see why I don’t get well.’ This makes me think I am long sick, and this takes the ache to my eyes.” By the time Dickinson had reached her early 30’s in 1863, she had increasing difficulty with her vision, an affliction which at that time in history was usually addressed with mercury. If Dickinson received this treatment from her local physicians, it unsurprisingly did little to halt the deterioration of her vision. In 1864, desperate for some improvement in her condition, she traveled to a nearby city to obtain treatment from the preeminent opthamologist of his day, Dr. Henry Ward Williams, the author of Treatment of Iritis without Mercury (1856). Under Dr. William’s care, Dickinson slowly improved, but it appears the improvement may have been due to a lack of harmful treatment rather than to any proactive treatment, as not long after her treatment was concluded, Williams published a new edition of his book on Opthamology in which he included a section on psychosomatic photophobia, an intense sensitivity to light he claimed affected women of “hysterical temperament”, and which was amenable to “nonspecific” treatments.59 Poor Emily. How humiliated she must have been by this if, as is likely, it came to her attention. By the 1886 edition of

his book, Williams had designated this form of intense photophobia as “hysterical hyperaesthesia,” a heightened sensitivity without a physical cause. In the late 1800s, these cases of impaired vision without apparent cause were increasingly diagnosed as “hysterical” or psychological in origin, a “conversion” of anxiety into physical symptoms. In a case study of hysterical blindness published in 1876, the physician Junius Hardwicke was called upon to attend a 16 year old girl with “obstinate vomiting”, tics, violent emotional outbursts, difficulty swallowing, refusal to eat, disturbed sleep and an intense sensitivity to light which had progressed to a state of temporary blindness. Although Hardwicke stated that he knew “[t]his young lady is of a very kind and amiable disposition; neither deceitful, perverse, nor obstinate, and is not at all fanciful or even troublesome” he nevertheless concluded that “her youth and some peculiarities about her seemed to point more to hysteria than anything else.” It should be noted that nausea, tics, emotional outbursts, inflammation of the mucosal lining of the mouth and esophagus, loss of appetite, restless sleep and photophobia are all known symptoms of mercury poisoning. Hardwicke’s treatment of the unfortunate girl consisted of threatening to send for a “galvanic [electroshock] apparatus” and some unnamed but even more feared instrument to induce her to swallow and eat, and a variety of medicines which included perchloride of hydrargyrum, or mercuric chloride.60 Hysterical blindness is now considered an outdated diagnostic term. The preferred term for the presentation of “apparent” neurological symptoms following a traumatic or anxiety provoking event is Conversion. Incredibly, Conversion is still listed in the Diagnostic and Statistical Manual of Mental Disorders today, and the presentation of possible symptoms listed thereunder reads like a study on mercury toxicity, including such symptoms as impaired coordination, weakness or paralysis of a limb, tremor, gait problems, impaired vision and hearing, and loss or disturbance of touch or pain sensation.61 In our modern age, mercury is known to cause visual disturbances, from increased sensitivity to light, to constriction of the visual field, deteriorating vision and even blindness; and failing vision due to mercury is not a thing of the past. A study published in the British Journal of Opthamology in 2006 tells the story of a 36 year old man with progressive peripheral neuropathies who was referred to an eye clinic for deteriorating vision and difficulty reading. MRI imaging revealed no structural abnormality of the optic nerves, cerebrum or cerebellum, but electroretinography revealed optic neuropathy, or damage to the nerves of the cerebral visual pathway. He was discovered to have markedly high mercury levels due to the consumption of

10 to 12 servings of Red Snapper a week, which was calculated to contain more than 24 times the safe level of mercury recommended by US FDA guidelines.62 When the introverted and reclusive Emily Dickinson died in 1886 at the age of 54, more than 800 poems were found in her room neatly bundled into booklets. The period of her greatest introversion and social withdrawal was also the most productive period of her artistic life. She had been ill for the preceding 2 years, with symptoms of headache and nausea, and she lapsed into coma in the end. Her physician listed the cause of death as Bright’s disease, a general diagnosis including symptoms of kidney disease and hypertension. Bright’s disease, known today as glomerulonephritis, consists of a swelling and inflammation of the endothelial cells lining the inside of the kidneys’ glomerular capillaries, resulting in closure and atrophy of the tubules and most cases of primary hypertension show this renal lesion to some extent.63 Significantly, glomerulonephritis can be experimentally induced in rats by injections of mercury.64 There is little direct evidence of mercury poisoning in Emily Dickinson’s life, but the circumstantial evidence is compelling. She is a perfect example of the type of pathological shyness, vision problems and kidney disease which mercury is known to cause. Her mother was troubled throughout her life with mystery illnesses as well, “suffering intensely from acute neuralgia”, which is a severe pain caused by damaged nerves. The physical symptoms of so-called hysteria were often due to a functional disorder of the nervous system, but what of the “nervous temperament” itself? In 1878 American neurologist George Beard observed a strange disorder in a cluster of French Canadians and lumberjacks living near Moosehead Lake in Northern Maine. The afflicted individuals had such an exaggerated startle reflex that they would react abnormally and excessively to any sudden or unexpected noise. They would take advantage of this sensitivity in each other by playing tricks designed to startle and frighten each other into jumping and yelling and hitting. Because the syndrome was clustered in a remote location, and fifteen of the cases had occurred in 4 families, Beard believed the condition to be a hereditary disease. They came to be known quite famously as the Jumping Frenchmen of Maine, and, although their reactions when startled could be quite angry and violent, most of them described themselves as shy.65 Beard and others described them as “modest, quiet, retiring, deficient in power of selfassertion and push.”66 When given a command while under the effect of the startle, the lumbermen would immediately comply, often repeating the command word for word. The unthinking compliance demonstrated by the Jumping Frenchmen of Maine calls to mind the cataleptics who have lost all

capacity for self-willed movement, but who will follow the “command” of another person by holding any position they are placed into. Trying to make sense of the phenomenon, and in direct contradiction of Beard, later physicians would suggest psychiatric diagnoses; a form of mass hysteria.67 Another argument made against Beard’s genetic theory of the Jumping Frenchmen was the existence of isolated pockets of similar disorder which took place elsewhere in the world during the same time period. In Indonesia, for example, the natives were often afflicted with a “nervous complaint” they called lâtah, which was identical in every way to the nervous condition found in the Jumping Frenchmen of Maine.68 The Indonesian natives considered lâtah to be a disease, but it was considered to be a curious culturally based social phenomenon by visiting Europeans and later researchers.69 One man who disagreed that lâtah was cultural in origin was Hugh Clifford, a British Colonial Official who had lived among the Malays for many years in the late 1800’s. He believed that lâtah was no more than an extreme exaggeration of the startle effect, and that anyone trying to figure out the pathology of lâtah should begin by analyzing the common startle or jump. Most human beings can be made to start or ‘jump’ involuntarily at a sudden noise, such as that caused by the loud slamming of a door, and Malays are peculiarly liable to these temporary nervous surrenders of self-control and of will-power, for in this light these involuntary movements must be regarded. The man who is the victim or a sudden fright or nervous shock loses for a moment all control over his body, as completely as does the Malay on whom latah has won its firmest grip. The difference which exists between him and the latah man is only one of degree, and that difference may often be more trifling than that which separates one latah subject from another. Imagine a start or ‘jump’ infinitely prolonged, and you have the lâtah state, about which so much has been said and written.70

Furthermore, Clifford asserted, there was something about Malaysia itself that seemed to cause lâtah. It was Clifford’s experience that every European who spent time in the Malay Peninsula would “within a year or two” become nervous and “jumpy”. “He starts violently at any sudden noise; finds it difficult to control the trembling of his hands in moments of strong excitement; and is generally less master of his will, and over the movements of his body, than is his wont.”71 There is a spectrum of increasing nervousness with concomitant violence in reactive response which travels from the common startle effect through exaggerated startle to

lâtah which, in advanced cases, was known to culminate in outbreaks of rage.72 The description of the lâtah afflicted as quiet, reserved, or silent men who gave no indication that they were differently constituted to their neighbors until they were provoked bears a strong enough parallel to the commonly heard statement “he was quiet and kept to himself” in response to senseless acts of violence in this country as to warrant further research. There has not been sufficient research to determine the cause of lâtah, but the excitation and deadening of the nerves caused by mercury exposure is known to cause an exaggerated startle effect. Results of testing on nerve cell membranes show that mercury can cause a profound modulation of the neural circuitry responsible for the regulation of behavior,73 and that animals poisoned with mercury have impairments in skin and hearing sensitivity so that weaker stimuli which would ordinarily have prepared the animal for a second stronger stimuli go unnoticed with an accompanying exaggeration of response to the second stimuli.74 There are more things than genes which run commonly through a family, group or area, there are habits of common practice and routine, there is a common place and time. The Malay Peninsula is located on a seismically active volcanic belt with thick seams of coal and other minerals, such as quicksilver which was actively mined in the late 1800’s. There are a connected series of thermal springs passing nearly the entire north south length of the peninsula, and hot mud swamps, which would have exposed the bathers to high levels of mercury vapor.75 Add to that the Malaysian fascination with mercury, their practice in the 1800’s of using quicksilver to harden bullets so that they would be able to pierce an elephant’s skull, and their practice of filling the cavities of the dead with quicksilver before burning them on funeral pyres, and you have a massive cultural exposure. Finding mercury exposure in the case of the Jumping Frenchmen is only a little more difficult. The entire state of Maine is located on a natural orogenic belt,76 however, and recent environmental monitoring assessments have found elevated concentrations of mercury in a “locus” in northern Maine. Researchers believe that there must be a bedrock source of mercury in northeastern Maine which is released from storage into the rivers during periods of high runoff.77 Before the mid-1800s, quicksilver in its native liquid state had rarely been found outside of Bavaria, but with the painstakingly thorough geological investigations spurred on by the California gold rush, it was suddenly found in many places in California and its neighboring states. For example, in 1860, “quicksilver was found in small pools upon the surface of the rocks, and in others it was obtained from the rocky bed of a small stream near at hand, on merely removing the sand which concealed it.”78 If native quicksilver lurked in cavities and crevices

of rock in the inaccessible mountains above the streams leading to Moosehead Lake in Maine, the globules could easily have washed into the river and floated for many miles downstream to the areas worked by the shy and easily startled lumberjacks.79 And of course, the State Board of Health of the State of Maine was very busy in the late 1800s, trying to fight epidemic small pox in the lumber camps in Northwestern Maine, getting the men vaccinated, washing down the cabins, and disinfecting the men themselves, hair, beard, body and clothes, with bichloride of mercury.

Mercury and Depression in the Life of Jack London “All right,” said I; “but put some corrosive sublimate on it just the same.” - Jack London

In July of 1897, the steamship Umatilla left San Francisco crowded with miners headed for the gold fields of the Canadian Yukon. On board was a young Jack London hoping, as they all were, to find his fortune. The Alaskan Gold Rush had begun in the summer of 1880 when a local Indian Chief brought prospectors Joe Juneau and Richard Harris to what is now called Gold Creek in the aptly named City of Juneau. Soon the Indian village and surrounding area were crowded with the tents and huts of miners in search of gold. Early on one prospector, John Treadwell, began to stake claims in the surrounding areas and to develop his property with water powered mills running heavy steel stamps to crush gold ore and wash it over mercury coated copper sheets. In this way the fine gold particles would form an amalgam with the mercury making it easier to harvest. Treadwell started with a five stamp mill but within seven years he had expanded the mill to an incredible two hundred and forty stamps, and he ran them day and night with the exception of the 4th of July and Christmas.80 By the 1895 publication of Miner Bruce’s Field Guide to Alaska, which Jack London studied before his trip, there were several more stamp mills in operation within a four mile radius of Juneau, six along Gold creek, and one at Sheep Creek, and these stamp mills along with the more traditional in-ground Treadwell and Mexico mines located across the bay, were all leaching mercury into the local rivers and bays. The story of Jack London’s journey reads like one of his later novels, with feats of daring, strength and courage at every turn, but London “brought nothing back from the Klondike but my scurvy”. Imaginings of the frozen North, and its lack of fresh fruit and vegetables encourage a quick diagnosis of scurvy when fatigue, sore gums and loose teeth appear, but was it scurvy? Or could it have been a physical disorder resembling scurvy? One of the most well known of the physical signs of mercury exposure is stomatitis, or inflammation of the lining of the mouth, resulting in sore gums and loose teeth. 50 years before, during the California gold rush, a similar disorder was often seen, a Californian “miners’ scurvy”. An article published in 1850 in the Daily Alta California described the process in which miners separate the

finer pieces of gold from gravel, silt and clay using quicksilver to form an amalgam of one part gold, eight parts mercury, which is then heated to volatize the mercury, leaving only the gold. When the gold amalgam is heated in an open ladle, the article warned, “the mercury escapes in fumes and minute globules, and charges the atmosphere, which is inhaled by the operator and those in the immediate vicinity, inducing prompt and severe sore mouth, spongy gums, trembling, ulcerations, and swelling of limbs, paralysis and death.” The article continued on to state “There is much reason to suspect that some of the Californian “miners’ scurvy” may be veritable mercurialization by inhalation.”81 In February of 1898 there were so many cases of scurvy reported at Dawson in the Yukon that The San Francisco Call ran an article titled “Dawson’s Scurvy Plague”. Scores of miners in the town of Dawson and its vicinity were afflicted with the disease—needlessly—according to Klondiker Chris Solid, who stated that “there is absolutely no need of any one at Dawson getting the scurvy. I could live there a lifetime and never be troubled with it.” Solid continued on to say that the situation at Dawson was quite good, with provisions such as milk and butter available at regular summer prices and relating that the cost of supplies had actually fallen, perhaps because the gold rush was already tapering off, and in many gulches and streams the prospectors were finding nothing except light “flake” gold, “almost impossible to save except with quicksilver.”82 Evidence that London was aware of the use of quicksilver in amalgamating flake gold appears in his fiction. In his novel Burning Daylight, a crotchety old miner advises the "chechaquos" or newcomers that they won’t go home with much gold if they are too proud to use quicksilver to go after the “flour” gold.83 Although London was in the Yukon from August of 1897 to May of 1898, he wasn’t roughing it in a miners’ camp in one unbroken stint of time. After staking a claim in mid-October, he traveled to the nearby city of Dawson to register it, and remained there for nearly two months, not returning to his camp on Upper Island between the Stewart and Henderson creeks until December 7th. Kid Hargrave, one of the miners at London’s camp, wrote that in the early spring of ’98 before the ice went out, he was suffering so badly from scurvy “from the many months lack of fresh meat” that London broke an arduous trail through the snow and ice, eighty miles each way, to bring in a moose.”84 This would have been an effective cure as almost all other animals synthesize their own vitamin C in great amounts— one of the reasons Arctic Eskimos can survive without fruits and vegetables in their diet. London’s actions and Kid’s statement suggest they had heard word of the groundbreaking work of Dr. Thomas Barlow, who had recently given

lectures on his discovery that fresh milk and raw meat were effective against scurvy.85 Regardless of London’s apparent vitality in the early spring of ’98 and his access to fresh meat, by late spring he was suffering so badly from what he believed to be scurvy that a doctor in a nearby camp took him on a raft to nearby Dawson to get medical care. From Dawson he sailed for home, taking the long route by river raft to the coast of Alaska, too disabled to make his way back out on foot. He had a small bag of gold dust in his possession which was not worth even a fraction of the $1,000 he had spent on supplies. Traveling down the river on the first stage of his journey home from Dawson, London wrote in his journal: Given some fresh potatoes & a can of tomatoes for my scurvy, which has now almost entirely crippled me from my waist down. Right leg drawing up, can no longer straighten it, even in walking must put my whole weight on toes.86

In the summer of ’98 as London made his way back home, gold had become very difficult to find in the Canadian Yukon, and the miners turned their attentions to Alaska. Thousands of miners descended on Kobuk, one of the three rivers feeding into the Kotzebue Sound in North Western Alaska. The demand for quicksilver in Alaska grew so high that its price skyrocketed.87 By 1899 the miners were dying in droves of apparent cases of scurvy and black leg, a disease in which “the legs swell up and turn black, the teeth loosen and fall out while you lose flesh rapidly.”88 Kotzebue was one of the hardest hit areas. A miner from Kotzebue described his symptoms as follows: Our arms and legs swelled terribly, turned black, our teeth became so loose you could easily pull them out. My limbs are all drawn up, but I am doing well and can walk a short distance without crutches.89

The Indians, who had always before managed to live quite well without access to fresh fruit and vegetables, were also dying of a disease “resembling” scurvy. In October 1900 an article appeared stating that “Whole tribes are being decimated by a peculiar disease somewhat similar to a very virulent attack of scurvy. Out of one tribe of one hundred Indians thirty-three of the males died within two weeks. Others were sick and altogether the Indians were in a terrible condition.”90 Not only were the Indians frequently hired on to help with prospecting, the mercury used in mining was unquestionably contaminating the fish which served as the Indian’s nearly exclusive food source.

The whole of the state of Alaska and the area comprising the Canadian Yukon is a massive orogenic zone. In the 1880’s the White river, so called for its “muddy white hue,” carried the mineral effluent of “Mount Smokey” an active volcano, roaring down from its source in the Wrangell Volcanic Field in Eastern Alaska into the Canadian Yukon.91 An active geothermal area runs east to west from the Canadian Yukon to the mercury rich hot springs and volcanic maar lakes of the Seward Peninsula which borders the Kotzebue Sound. The naturally high levels of mercury emission in the Yukon and Western Alaska were compounded exponentially by the use of quicksilver in gold retrieval. Graphing of ice core data measuring atmospheric mercury over the past 270 years shows the gold rush was responsible for a tremendous amount of mercury introduced into the environment, rivaled only by the poisonous outpourings of volcanoes, and the increasing pollution of our own modern age.92

It is interesting to note that both London and the miner from Kotzebue

mention the contraction of their limbs, which is not a symptom of scurvy, but which is an iconic symbol of the tragic results of advanced mercury poisoning. And there is evidence to suggest that London himself, although he spoke of his “scurvy” later became aware that mercury poisoning and scurvy share similar symptoms. In his short story The Lost Poacher, written not long after London’s return from Alaska, the following dialogue appears: "Why, the quicksilver gets into your blood; I think that's the way. And your gums all swell like you had the scurvy, only worse, and your teeth get loose in your jaws. And big ulcers form, and then you die horrible. The strongest man can't last 93 long a-mining quicksilver.

Jack London experienced two major bouts of depression in his lifetime. The first, on his return from Alaska, was easily explained away as due to the circumstances of his life. He was weakened and ill from his adventure in the Yukon, his beloved step-father, John London, had died while he was away, he had spent all of the money he had borrowed from his step-sister and was unable to repay it, and he didn’t want to be a laborer anymore, but his career prospects were bleak. His earliest letter still in existence to his friend Anna Strunsky, written in November of 1898, read “Forgive me for not writing, for I have been miserable and half sick. So nervous this morning that I could hardly shave myself.” In March of 1900 he wrote to her again, decrying the fact that he had once had “unfailing nerve” but that now he was increasingly nervous and timid.94 His fortune would soon turn. Much like Emily Dickinson, Jack London, in the period of his nervous introversion “focused more intently, and began hewing unique art forms of unmistakable purity.”95 He slept little, and worked constantly at his writing, with great success. Jack London’s awareness of the dangers of quicksilver makes what happened next difficult to understand. Perhaps London didn’t make the connection between quicksilver and the particularly poisonous form of mercury known as corrosive sublimate. Whatever the reason, whether he thought the difference in form rendered corrosive sublimate something which he could control safely, he began to use it freely, and with complete abandon. In 1907 Jack London began a long journey through the South Sea tropics and mercury jumped out of the hands of his fictional characters and into his own life. The voyage of his sailing vessel, the Snark, was intended to last seven years, and London, always the master of his own destiny, set out to master navigation, dentistry and medicine, with sea charts, dental tongs, a skull to practice pulling teeth from, and a medical chest well stocked with corrosive sublimate.96

The Snark landed at Hawaii, the Marquesa Islands, and Tahiti before the crew ran into trouble, contracting “Solomon sores” or “yaws”, a tropical bacterial infection transmitted by skin-to-skin contact. London, the selfprofessed amateur physician, described the sores as follows: “A mosquito bite, a cut, or the slightest abrasion, serves for the lodgment of the poison with which the air seems to be filled.”97 It is most likely they picked up the infection from a French sailor they picked up in Tahiti, who had “a vile skin disease.” London, after reading through all of the medical books he had brought along, proceeded to treat the sailor, “taking care afterwards always to use a thorough antiseptic wash” on his hands.98 Soon the entire crew of the Snark was afflicted with Solomon sores. London “nursed” his “on a diet of corrosive sublimate.”99 In the meantime, in my amateur M.D. way, I did my best. I read through all the medical works on board. Not a line nor a word could I find descriptive of my affliction. I brought common horse-sense to bear on the problem. Here were malignant and excessively active ulcers that were eating me up. There was an organic and corroding poison at work. Two things I concluded must be done. First some agent must be found to destroy the poison. Secondly, the ulcers could not possibly heal from the outside in; they must heal from the inside out. I decided to fight the poison with corrosive sublimate. The very name of it struck me as vicious. Talk of fighting fire with fire! I was being consumed by a corrosive poison, and it appealed to my fancy to fight it with another corrosive 100

poison.

London felt fully confident in his medical self-education, especially when four of his five ulcers healed, and the remaining sore decreased dramatically in size, but the rest of the crew remained hesitant, one after the other refusing London’s offer to mix up some corrosive sublimate to wash their cuts with. Soon, however, their infections proved too much to bear, and they surrendered to his treatment. On reaching the Solomon Island of Santa Anna, they encountered a trader who was afflicted not only with yaws, but who had a paralyzed arm as well. Paralysis was a common native disease on Santa Anna, explained the trader, as he was helped down the ship’s ladder, “his dead arm dropping, bump-bump, from step to step.”101 Interestingly in light of the paralysis (a late stage symptom of mercury exposure), and much to London’s satisfaction, a missionary confirmed that yaws was quite common in the Solomons and that corrosive sublimate was what they used in treatment.102 After the missionary’s confirmation, London was unstoppable, applying “antiseptic treatment” at the slightest indication. The entire crew of the Snark had been so unnerved by the encounter with the

dead-armed man that whenever they saw “a particularly horrible case” of an islander with yaws, London wrote, “we retire to a corner and deluge our own sores with corrosive sublimate.” Soon the crew began to suffer from depression, “everybody had fever, everybody had dysentery, everybody had everything.” Wada, the ship’s cook, and Tehei, one of the crew, fell into a bad “funk” and “prayed dolorously and cried for hours at a time.” Finally, Wada “went daffy” and ran off from the Snark one day when it docked on the island of Ysabel, “going ashore for good in a driving rain-storm, between two attacks of fever, while threatened with pneumonia.”103 “He never did think much of my medicine,” London concluded. After the corrosive sublimate was accidentally left behind and another crew member had “lost his wits altogether”, London admitted defeat. “With the exception of the insanity cases,” he wrote, “I’m the worst off on board.”104 Among my minor afflictions, I may mention a new and mysterious one. From the past week my hands have been swelling as with dropsy. It is only by a painful effort that I can close them. A pull on a rope is excruciating. The sensations are like those that accompany severe chilblains. Also, the skin is peeling off both hands at an alarming rate...105

Admitting that he had failed in his doctoring of the yaws and the “lunacy cases” and fearing that he had contracted leprosy, London made plans to catch a steamer to Australia to seek proper medical care. “Ten skins have peeled off my hands and the eleventh is now peeling,” he wrote worriedly as they sailed. In the meantime the crew was not faring much better. Henry, one of the Tahitian sailors, developed rheumatism in his back, Tehei became “more lunatic than ever,” and Nakata, the cabin boy, became so ill they believed he had ptomaine poisoning (what we now call food poisoning), an affliction in which the body attempts to purge itself of a toxin by vomiting and diarrhea—nature’s cure.106 Jack London entered the hospital in Sydney in 1909 suffering from yaws, malaria, anal fistula, sloughing “silvery” skin, and swollen painful hands. He spent 5 weeks in the hospital, during which time he was cured of the yaws and was successfully operated on to repair the fistula,107 and his malarial attacks began to lessen in intensity. He next spent the next five months “miserably sick in hotels” not well enough to make the voyage home. The doctors had diagnosed the silvery sloughing skin as psoriasis but held out no hope for a cure of it beyond that which might occur spontaneously. They could not ascertain what was causing London’s hands

and feet to become so swollen and painful. The mysterious malady that afflicted my hands was too much for the Australian specialists. It was unknown in the literature of medicine. No case like it had ever been reported. It extended from my hands to my feet so that at times I was as helpless as a child. On occasion my hands were twice their natural size, with seven dead and dying skins peeling off at the same time.108

The most the doctors could say was that neither the sloughing silvery skin nor the problems with London’s hand and feet were caused by tropical parasite, and that therefore they most both be “nervous” in nature. The San Francisco newspapers gleefully trumpeted, “Jack London A Nervous Wreck” and London made plans to return home to California in the hopes of regaining his nervous equilibrium.109 The leading specialist in the hospital in Sydney had told London that “not only has he never observed anything like this, but that not a line has been written about it by other observers.” That was untrue, however, as over 100 years earlier an English Physician, John Pearson, had written up his observations of similar symptoms in what he termed mercurial erethism, a state in which the body begins to show signs of a dangerous, potentially fatal, hypersensitivity to mercury.110 Pearson’s observations of the “mercurial eczema” accompanying the state of mercurial erethism included the symptoms London experienced of redness, swelling and tenderness of the extremities followed by “desquamation” or peeling off of thin layers of skin in “whitish scales.”111 Not only that, but London’s mystery illness shared many similarities with a peculiar dysfunction of the nervous system which Australian physicians specializing in the diseases of children had been seeing for at least the last ten years. In 1914, too late to help Jack London, Dr. H. Swift of Adelaide, Australia presented a paper on 14 cases he had observed of the condition, which he called erythroedema after the characteristic “redswelling” of the hands and feet. 112 It soon became apparent that, except for the fact that it was children who were affected, the disease was similar to the epidemic of acrodynia which had occurred in France in 1828, a painful affliction of the extremities coupled with a red rash and disorders of the nervous system.113 The names erethroedema, dermatopolyneuritis, and trophodermatosis were tossed around before the disease became known again as acrodynia, as it had been in France, or more commonly, pink disease, after the pink or red coloration that often preceded the worst of the symptoms. The afflicted children, generally 2 to 6 years in age, displayed a

characteristic withdrawal, depression and irritability. As one physician put it, The advances of the infant’s mother often seem no more welcome than those of a stranger. I have seen infants almost in extremis from infection or severe anemia, who still maintained an active interest in their surroundings. To watch the child with acrodynia is to receive a very deep impression of a primary emotional 114 disorder.

The children had a characteristic frown of such complete misery that psychoanalysts believed they were suffering from a depressive psychosis which would be comparable to melancholia with suicidal tendencies in an adult.115 The condition had distinctive physical symptoms as well, including insomnia, anorexia, an intense aversion to light, swollen, red hands and feet (the skin of which would begin to thicken and scale or peel off in flakes), and in the more severe cases, loss of teeth, “glove and stocking” loss of sensation, “a peculiar stiff gait in walking” and pseudo paralysis (in a characteristic “drawn-up” flexion position), with a death rate estimated at 20 to 30%.116 Autopsies routinely revealed degeneration of the nervous system and demyelization of peripheral nerves.117 When some researchers began to consider the possibility that mercury poisoning was the fundamental cause of acrodynia, there was tremendous resistance to the idea for the simple reason that mercury was so commonly given to children, and if mercury was the cause, the doctors reasoned, there would be many more cases of acrodynia. Millions of these treatments were produced each year, and as a rule they were not prescribed by doctors, but were bought directly from chemists' shops as the result of aggressive advertising campaigns directed at mothers. The powders, consisting mostly of calomel mixed with sugar, were recommended for safe teething, peaceful nights, and superior strength and health—to be taken on alternate days for the entire duration of teething.118 Acrodynia continued to afflict young children well into the 1950’s before the causative role of mercury in the form of calomel in worm and infant teething and soothing treatments, use of mercurial ointments, and local treatment with corrosive sublimate was recognized.119 In the end it was not the physicians who called a halt to the scourge of acrodynia, or the government health agencies (“there is not yet definite evidence to justify general publicity”). After many years of researchers’ warnings and government inaction, a coroner listed the cause of death of two children not as acrodynia, but as chronic mercurial poisoning, and the manufacturers began to withdraw mercury from their infant products. When acrodynia

virtually disappeared, the cause was undeniable in retrospect.120 But that discovery was many years in the future yet, so that when London returned home to California in 1909 and came upon a book by a surgeon with the United States Army who had been afflicted with a similar illness in the tropics, London thought that he had found the answer to his affliction. The book’s author, Colonel Charles Woodruff, believed his illness had been caused by the destructive effects of tropical light.121 Woodruff had found that his men suffered a near universal neurasthenia in the tropics, including loss of appetite, trouble concentrating in the young, memory loss in the old, vasomotor disturbances, visual disturbances with presbyopia apt to become more marked, and increased rates of depression, suicide and insanity.122 The mild cases recovered quickly on return home, but in the older or weaker men, their “exhaustion” was liable to progress to the point where recovery was no longer possible. Not at all suspecting the possible contribution of the Navy’s longstanding mercurial treatment of tropical diseases,123 Woodruff formed long complicated Darwinian arguments to suggest that the constellation of symptoms suffered by his men was due to a lack of evolved ability to tolerate the tropical sun. Strangely, Woodruff found that men who drank more alcohol were more likely to survive their tropical sojourns. 11% of the abstainers died, while only 2% of the excessive drinkers did.124 It all made sense to London. Back home in the temperate California climate, the pain and swelling in his hands slowly resolved and his silvery skin disappeared, bolstering London’s belief that he had found the answer to the cause of his terrible and mysterious illnesses—the destructive power of strong, tropical light. He told anyone who asked, and more, that ultra-violet rays caused men who had not evolved to withstand the tropical sunlight to become “nervous” and “irritable” and drove them to drink. London had started drinking as a form of self-medication on the Snark, insisting that it had helped him, and that it eased the “gasping” and “trembling” of his hard working crew.125 Back at home, he continued to drink, at first to fight the insomnia that began to trouble him, then to “loosen up” his brain enough to work, and lastly to fight a searing depression, an unbearable appreciation of a “truer order of truth”, a cruel and bleak “white logic.”126 London’s physical condition had forced him to withdraw from his adventuring, but he threw himself into ranching with similar passion, “bound”, as one article stated, “to make as much of a success in farming as he has in journalism.”127 He purchased several failing ranch parcels in the Northern California area of Glen Ellen and created one larger ranch he called Beauty Ranch. He had a vision of a manmade utopia. He was determined to bring the soil back to a healthy state using crop rotation and

the manure of his livestock. He brought in purebred goats and hogs and cattle, and bought a prize winning, grand champion Shire stallion, Neuadd Hillside, to found his very own English Shire stable. Years before, around the same time an epidemic of hysterical blindness was sweeping through women of nervous temperament in the United States, an epidemic called the blind staggers had begun to sweep through the horses. Characteristic symptoms of the disease included loss of appetite, grinding of the teeth, difficulty swallowing, depression, weakness, impaired vision, sensitivity to light, staggering gait, and contraction (drawing up) of the muscles of the neck, back and loins, progressing to partial or complete paralysis and death. “Some horses—those of a nervous temperament— become very violent” stated an 1887 article in the Pacific Rural Press, “but others remain very quiet.”128 Autopsies revealed inflammation and degeneration of the brain and spinal column, and the disease was initially identified as infectious cerebrospinal meningitis. This identification was later disproven and in 1903 the experts concluded that the “epidemics are cause by some poisonous substance contained in the forage.”129 Their conclusion was based on experiments conducted by the veterinarian Dr. Leonard Pearson who had proven the influence of contaminated food by placing fresh food on top of the food at a stables in which there had been an outbreak of the disease. No new cases of disease occurred while the horses were eating the fresh food, but once the old food was reached, fifty nine horses soon developed the disease. The experts did not discover the agent of the disease, but suspected a toxic mold or fungus.130 Understandably, then, when Jack London began to make renovations to his ranch property, he was considerably concerned with preventing similar diseases from taking hold in his own animals. As a part of his renovations he converted unused stone winery buildings into a stables and designed a unique hog yard of concrete and stone. Every feature of the hog yard was designed to facilitate cleanliness and sanitation, and “a system of flushing and antiseptizing” was used in both the stables and the barns.131 In fact, London was so concerned with sanitation that he required all visitors who entered the hog yard to apply a “germicide solution to the soles of their shoes so that no contamination may be conveyed to his swine.”132 What germicide and antiseptic did he use? London’s fictional characters were great fans of the use of corrosive sublimate. In 1910 his Burning Daylight mused that “ “They sure wouldn’t bat an eye if I called for a glass of corrosive sublimate,”133 in Adventure (published 1911) “the house-boy, brought him corrosive sublimate and water, and he took a thorough

antiseptic wash,” and in “The End of the Story” (written in 1911134) London wrote the story of a camp doctor in the Yukon who is asked to make a 100 mile journey in 50 degree below weather to save the life of a man who has been savagely mauled by a panther. The doctor is told that the man has been “washed clean with bug-killin’ dope before we stitched” and that the dressing which had been used on the wounds was “Corrosive, sublimate, regular solution."135 Corrosive sublimate was, in fact, at that time the preferred and recommended disinfectant for use in protecting livestock from infectious disease. As far back as 1872, corrosive sublimate was recommended by Our Home Journal as “the best liniment for cuts, galls, spavin, poll-evil, fistula, or any other of the external diseases that animals are liable to.”136 And in 1873, if a horse was infected with poultry lice, it was recommended that 32 grains of bichloride of mercury be dissolved in one pint of cold water, and that the mixture be applied to the horse with a brush to a part of the horse’s body “everyday till all has been gone over with the brush.”137 In a 1903 article on prevention of the spread of disease in hogs, veterinarians advised that railroad cars transporting stock hogs be disinfected with corrosive sublimate “each time before it is loaded”, with the helpful comment that “sublimate is not costly and can be purchased at almost any drug store” and a reminder that “all kinds of stock and also men may carry the infection from one spot to another.”138 In 1906 the agricultural department of the University of California published a circular recommending that stables be treated with chemical disinfectants to prevent the spread of contagious diseases. Two substances were listed as “far more efficient than others”, “cheap and obtainable at any drug-store”, carbolic acid and bichloride of mercury or corrosive sublimate. The circular noted that corrosive sublimate, although it “is poisonous and must be used with great care”, has the advantage of being odorless. The circular also recommended that whatever disinfectant was used, it should be used often, and in sufficient quantity to thoroughly saturate all surfaces, that it should be scrubbed into the floor and lower parts of the walls with a broom, and applied to every crevice and recess, the ceilings and upper parts of the walls with a spray pump.139 This recommendation from the University of California must have been particularly persuasive for London, a one-time student at the University of California at Berkeley. You might, by this time be wondering if a close examination of the life of any famous person of this time period would reveal the use and influence of mercury, and that is pretty much correct. Abraham Lincoln took “blue pills” containing mercury as his “usual medicine”, quitting them finally because he said they made him “cross.”140 Louisa May Alcott, the author of

Little Women, was treated with repeated doses of mercuric chloride after contracting typhoid pneumonia during the civil war, an episode which left her temporarily unable to walk, and “permanently poisoned.”141 Howard Hughes, perhaps the most famous recluse of all time, was sent off to camp by his germ phobic mother with a suitcase full of “patent medicines” after which he experienced an episode of “hysterical” paralysis. Most interesting in Hughes’ case is that after his mother died, his teachers noticed a marked decrease in his intense shyness.142 Jack London had two episodes of serious depression in his lifetime. The first episode corresponded roughly to the period after his return from the Yukon and was easily attributed to the circumstances of his life. The second came over him for no obvious reason. “In vain do I ask myself why I should be sad” he wrote, “My life has indeed fallen in pleasant places. Not a hundred men in a million have been so lucky as I. Yet, with all this vast good fortune, am I sad.”143 Mercury poisoning is known to cause depression, and some researchers have suggested that in cases of episodic depression, or of depression without an apparent cause, chemical poisoning should be eliminated before other courses of treatment are pursued. In London’s case, he blamed his depression on his drinking and made a heroic and very public effort to stop drinking with the publication of his John Barleycorn, or, Alcoholic memoirs in 1914, in which he asked with painful openness, “if [drinking] could get such sway over me, a non-alcoholic, what must be the sufferings of the true alcoholic, battling against the organic demands of his chemistry while those closest to him sympathise little, understand less, and despise and deride him!”144 London’s success over his drinking problem was not followed by renewed health as he had hoped, however, but rather by a quick decline into further ill health, gastric pain, appendicitis, rheumatism, insomnia, and an increasing tendency to anger. His wife Charmian wrote of London’s episodes of “catastrophic red wrath,” “mental fury” and “increasing fervor and violence” in the last year of his life.145 As they said in the Rural Press article, some horses remain very quiet, but some horses become “very violent.”146 Some of the small children with acrodynia appeared to have “rage attacks.”147 In the end there was pain, pain so bad that London would not walk one block, and death from uremia, at the age of 40. Many historians have speculated that London’s early death from uremia was related to kidney damage incurred by his heavy use of corrosive sublimate on the Snark journey, but none have mentioned the possible continuing intoxication in the course of his agricultural work. And yet, one thing is without dispute, London’s champion Shire stallion Neuadd Hillside died on October 22, 1916, one month precisely before London did, “shaking

all over” before he lay down and died. Next, London’s horse Prince developed an “incurable rheumatism” and could not be used.148 Did Nueadd Hillside and Prince die of mercury poisoning due to the over liberal use of corrosive sublimate in their stables and in their care? Both horses are buried in a wooded ravine at the Beauty Ranch, and if they were to be exhumed, a mercury test of their remains would provide a definitive answer.149

Jack London with a vibrant Nueadd Hillside in 1916

After London’s death, his wife wrote: “Even with modern familiarity with body chemistry, scientists are not able to determine with exactitude the nature of the toxins that produce uremia. ‘A gastro-intestinal type of uremia,’ the doctors pronounced Jack's disorder. The symptoms had been present for a long time—stomachic disturbances, insomnia, sporadic melancholia, dysentery, rheumatic edema in ankles, and dull headaches alternating with the speeding up of his mental enginery.”150

Pathological Shyness in Industry “But above all things the patient shows evidences of psychic disturbances which are peculiar to mercury poisoning—Erethismus mercuriales.” - Ludwig Teleky

Modern occupational and vocational medicine had its origins in the quicksilver mines of Huancavelica in the Peruvian Andes, the Almaden quicksilver mine in Spain, and the mercury mines of Idrija. In Peru, local Indians were forced to work a 2 month turn or “mita” in Huancavelica, “la mina de la muerte”. Working in the mines was so dangerous to the health of the workers that when the surrounding population began to dwindle in the early 1600’s, De Jeria, the “protector” of the Indians attempted to persuade the King of Spain to cease operations with a purely financial argument. De Jeria argued that to ignore the tremendous loss of life in favor of the economic gain from mercury mining would eventually lead to the economic collapse of Peru, as “without them there will be neither quicksilver, nor silver, nor the common good, nor Peru.”151 The symptoms of acute mercury poisoning; tremors, excessive salivation, ulcers of the mouth, restlessness and depression were well known to the miners, and those who were rendered unable to work would retreat to the lowlands for a remedy which consisted of heaving drinking and sweating. Eventually the mita was abolished on humanitarian grounds, and by the year 1740, a mining guild had been formed to improve working conditions in the mine, an action which sent ripples through the rest of the world, so that by the year 1754 Austrian physician Giovanni Antonio Scopoli was appointed to oversee the health of workers in the mercury mines of Idrija.152 One of the symptoms of mercury poisoning Scopoli expressly noted was the “unusually sad mental state of these workers.” He also noted that those workers with the worst symptoms of mercury toxicity were those that drank the most alcohol, and he drew the conclusion that alcohol must intensify the effects of mercury poisoning.153 It wasn’t only miners who suffered from mercury poisoning. Workers in many occupations were exposed to mercury during the course of employment, including artisans using the method of gold plating known as fire gilding, makers of thermometers, barometers, mercury vacuum pumps and other scientific instruments, and mirror silverers. In the mid 1800’s the German physician Adolph Kussmaul was instrumental in bringing public attention to industrial mercury poisoning among the workers who applied mercury solutions in silvering the back of mirrors. Kussmaul described the

mental “intensity” of habitual mercury exposure, stating that it precedes the physical effects by weeks, “or sometimes for years.” Essentially the condition is characterized by great mental excitability of the patient to external impressions. Every unexpected or perplexing event excites him to the highest degree. The visit and conversation of the physician puts him into a state of complete bewilderment, even to syncope; the adult patient grows pale, and stammers in answering the simplest questions. To perform his allotted task requires the greatest effort, or is even impossible if he sees or thinks that he is being watched. There is also great solicitude and a feeling of anxiety without any reason for it. There is sleeplessness, or sleep which is restless, frequently broken, and disturbed by frightful dreams, headache and palpitation. In the severer forms there are frequently hallucinations, usually of a frightful nature. When perplexed or excited, traces of tremor are often perceptible in a slight twitching of the muscles of the face at the corner of the mouth.154

Kussmaul noted that the physical disturbances of mercury poisoning do not occur until the second stage, manifesting initially as a tremor which “comes on as a slight quivering, perceptible especially on speaking, and increases in violence until complete convulsive twitchings are produced.” He also noted that in the more severe cases, “paralysis of the affected limbs always occurs.” The publication of Kussmaul’s findings in 1861 led to regulations in Germany forcing a switch to an alternative mirror making process.155 The greatest mercury using industry of the time, however, was felt hat making. Hat makers were exposed to mercuric nitrate in the course of refining fur pelts into felt, a process which has been traced to the middle of the seventeenth century, when it was a secret in the hands of a few French workmen who carried “le secret” to England with them in 1685. Mercurialism in hatters was first officially described in 1829,156 a description which obviously resonated with the people of the time as the phrase “mad as a hatter” went what was the equivalent of going viral in those days, sweeping into the popular lexicon that very same year as popular slang referring to a crazy person.157 The United States was somewhat behind the rest of the world in the regulation of industrial poisons, and mercurial tremors had not been officially noted in hatters until 1860 when J. Addison Freeman, M.D., published a paper briefly discussing the subject in Transactions of the Medical Society of New Jersey. No mention was made of their pathological shyness until 1910 when Mrs. Lindon W. Bates, the Chairman of the National Civic Federation’s Committee upon Dangerous and Unhealthy Industries conducted a study on poisoning in mercury-using industries in

and around New York City. 158 Mrs. Bates’ goal was to impress upon the community as a whole that it was in their own best interest to treat the health of local labor as an asset worth protecting. Bates and her chief medical inspector were granted open access to the factories of New York, Brooklyn and Yonkers as the factory managers underestimated the impact their study would make. Bates related that the factory managers didn’t really take their committee seriously and stated that they “seemed to consider the study the whim of time encumbered women.”159 The early emotional effects of mercury poisoning were easily overlooked for a variety of reasons. Firstly, the men themselves often failed to attribute changes in their nervous condition to the effects of mercury, and they tended not to seek professional medical attention until they reached the stage at which their mercurial tremors interfered with their ability to perform their jobs. Secondly, the doctors were generally satisfied to make diagnoses based on objective symptoms, and did not, as a rule, find it necessary to question their patients emotional well-being. The general feeling was that if these patients were anxious or depressed, that could just as easily be explained by the stress of their difficult lives and the impact of their physical condition upon their financial circumstances. It was a gray area, unclear and hard to define, and as one physician stated, “The objective symptoms are sufficiently apparent, so that one needs no subjective examination.”160 Lastly, the essential character of the pathological introversion of mercury poisoning is a desire to go unnoticed. Mrs. Bates herself noted that when she first toured the factories, the disability of the workers was not immediately apparent. But the managers were well aware of the situation. In one factory, the foreman pointed out two men who could not lift a glass of water to their own lips, cautioning Mrs. Bates not to look too obviously at them “as they were sensitive to the trouble and would begin to visibly shake.”161 Bates inspected the medical records of physicians in areas surrounding the mercury using factories in the greater New York area, but she found that the records were most often brief and lacking in personal history. Very few addressed the early psychic disturbances of chronic mercurialism that she had come to expect based on her familiarity with Kussmaul’s work. Bates began to interview the hatters and their families and to ask the questions that the physicians had neglected to ask. In doing so, she found that mental and nervous irritations were the first symptoms to be experienced, and that “melancholia will be found at all stages running like the very thread upon which the experiences are strung together.”162 Her comprehensive case studies contain many notations of emotional disturbance which the afflicted workers and their families felt were due to occupational mercury exposure:

Their minds are not right...Man has suspicious and vicious tendencies—has thought of suicide...Over a year nervous...Suicidal tendencies. Isolates himself from other members of the family...”dead like” in his actions...memory perceptibly failed...The first effects that are noticeable are mental. When complaints are received in the shop about the quantity or quality of the work he becomes extremely nervous and is unable to do as well as usual...quite unable to utter even the ordinary salutation, although he made desperate efforts to do so...Very nervous and irritable for a few months. Can’t stand the “racket” of company at the house...His nerves were so unstrung that he feared everything and everybody.163

The men Bates interviewed had progressed to the advanced stages of mercury poisoning, they were prematurely aged, they had high blood pressure, and they suffered from difficulty walking and speaking. In the most severe cases, the men had tremors so severe that they could not feed themselves and episodes of paralysis as well as blindness. One man told Bates “I used to have fits of vomiting and weak spells, when I couldn’t see at all.” Another told Bates that he had been nearly blind for almost a year, but that his sight had gradually returned after eight years away from the shop. Others showed her that they could not walk up or down stairs, or had arms they could not move.164 In return, Bates was their champion. She argued that the cost of a process so harmful to the health of the workers should not be born as a tax on the workers and their families, “but upon the industry profiting at their peril” in the form of mandated improvements in working conditions and health care.165 She also addressed the long standing prejudice that mercury workers were responsible for the worst of their symptoms due to heavy drinking, stating “I personally do not believe that alcoholism has anything to do with making men more susceptible to the poison.”166 Using statistics to show the patterns of the disease, she proved that men who did not drink at all were not spared the worst effects of mercury poisoning, and her case studies were filled with the tragic stories of men who did not drink, or who hardly drank at all. Among the men who did drink heavily, a great many felt that “they had to take something to ‘brace’ them before they could start for work,” and that drinking provided a steadying effect which initially gave temporary relief from their symptoms.167 Following up on this testimony, Bates introduced the concept, so foreign to the medical authorities up to this point, that perhaps it was the symptoms which caused the drinking, and not the other way around.

If any excess is characteristic of a large body it is reasonable to seek its cause in some common predisposition. The “symptoms” reviewed earlier gave as the very first influence in all mercury-contact a marked mental depression. The late William James, of Harvard, in writing upon liquors, declares that its great hold upon mankind lies not in its physical but its quick mental reaction.168

Mrs. Bates’ study was read at the National Conference on Industrial Diseases held in 1912, but not memorialized, unless it was in the statement that future investigators “should refrain from any conversation with the employees except by the specific permission of the employer” and that the need for reform “requires a trained mind to ascertain the necessary facts...and should not be undertaken by those who are easily fatigued or confused.”169 The conference leaders had little respect for Mrs. Bates and the time encumbered women of the National Civic Federation, in other words. They did respect the Germans for their lead in health and safety in industry, however, and a paper on mercury poisoning which had been published that same year by the German physician Ludwig Teleky, was translated into English, and included as the sole authority on Mercury Poisoning in the book Diseases of Occupation and Vocational Hygiene published in the United States in 1916. 170 Teleky wrote that the mental disturbances experienced by workers exposed to mercury consists of “a peculiar form of stimulation and timidity and are evident more especially when the patient is in the presence of strangers.”171 Teleky’s research included an examination of workers in the sciences, men with higher income and social standing than the hatters, whose emotional difficulties were not as easy to explain away. He recounted the subjective experience of his mercury poisoned patients in their own powerful words. One labworker described his shyness in this way: As a general thing I am a very energetic person and have taken part in many functions, but while affected with mercury poisoning I felt oppressed and uncomfortable, and was as shy as in my later boyhood days, in the presence of grown people.

172

A technologist involved in the design of scientific instruments described his experience in this way: An invention had been completed, strangers came, and it was decided to demonstrate to them the manufacture of the respective commodity. As long as I

was conscious of the fact that these people were standing behind I could not proceed to move a finger.173

Teleky recounted a similar report made by a French author on the working conditions of felt hat makers in France. The hatters, sitting and drinking in a lounge were so affected by the presence of a stranger in their midst that not one of them was able to lift a glass of wine to their mouths.174 In a follow up study on industrial poisons published in 1925, Dr. Alice Hamilton of Harvard University corroborated the findings of earlier researchers of the typical findings of anxiety, excitability and shyness in the hatter’s trade. Now that the industry was subject to regular investigation, hatters throwing down their tools and saying angrily that they could not work if they were watched was no longer just an anecdote. The hatters, she wrote, “described themselves as easily upset, easily angered or embarrassed, especially if spoken to quickly; while others were timid, full of vague fears.” Among the mercury miners and metallurgists in California this symptom of mercurialism is very familiar and the men recognize it in themselves as well as others. They describe an increasing shyness, anxiety, embarrassment at being noticed, loss of self-confidence, or irritability which is very marked if the man is spoken to suddenly or asked to do something unusual. Some men are obliged to give up their work because they can no longer take orders without losing their tempers; or, if they are foremen, they have no patience with the men under them. Sometimes insomnia is the chief complaint, or bad dreams, or depression and loss of memory.175

“For a long time,” wrote Teleky, “these psychic manifestations were regarded as hysterical in nature, but this view has long since been dispelled.” One of the strangest features of mercurial poisoning which doubtless contributed to diagnoses of hysteria in the past is the difference in loss of function between intentional and habitual or reactive movements. Teleky had found that workers so affected with mercury poisoning that they could not lift a glass to their own lips, or who had difficulty in walking, could still carry on a line of work to which they had become “accustomed through years of practice.” Even those patients who were so severely affected by mercury poisoning that, if they fell to the ground could not rise without assistance, as each intentional movement would cause convulsion muscular contractions—even that class of patients was able to continue to work at their regular occupations in the factory.176 Dr. Hamilton of Harvard University also found that patients with

advanced mercury poisoning retained the ability to continue performing habitual tasks long after they had lost the ability to perform intentional movements without great difficulty. In several instances described to me a workman who was still capable of carrying on his trade, the motions of which had become almost automatic, was not able to reach his bench alone, but had to be guided there by a fellow workman. In Orange, New Jersey, there was a famous case of “hatter’s shakes” in a man who kept on at work long after he had developed severe tremors. He could not feed or dress himself, and the only way he could get to work was by pushing a baby carriage before himself to steady his gait. When he reached the plant he was guided to his bench and then he could carry on the work familiar to him through years of practice.177

These real life examples of the sort of inexplicable inconsistencies of function caused by mercury help us to understand why these patients were so often believed to be either faking their symptoms or laboring under a form of mental delusion. A modern day example would be Desiree Jennings, the 25 year old cheerleader who suffered severe neurological dysfunction 10 days after having a seasonal flu shot. Although medical experts had diagnosed her condition as an exceptionally rare 1 in a million reaction to the mercury contained in the flu shot, the fact that Desiree could not properly speak or walk, but could run and talk properly while running or walking backwards caused many to believe her story was a hoax.178 Significantly, Teleky made the point that the more subtle emotional effects of mercurialism are not found in acute cases of catastrophic poisoning which develop quickly, but rather in those cases in which there are repeated exposures to smaller doses over time with progression to physical signs only in more marked cases. “We must conclude that the smallest amount of mercury taken continuously over a long period of time will eventually produce manifestations of the disease” he wrote, factoring the length of exposure over time into the Paracelsian notion that the dose makes the poison. The elimination of mercury is slow and not continuous.179 If the amount of mercury to which an individual is exposed exceeds the amount which that person is able to eliminate, no matter how small the difference, the amount of mercury in the body will eventually increase to a toxic level. It is not surprising that in a past world beset by terrible illnesses without genuine remedies, emotional difficulties were often borne without question, and accounts of changes in personality were not common—but they do exist. One notable case is that of Niccolo Paganini, the famed violin

virtuoso who suffered from chronic mercury poisoning due to “murderous doses” of mercury taken during a 5 year period spanning from 1823 to 1828. Unsurprisingly, Paganini suffered many of the well-known physical effects of mercury poisoning such as failing eyesight, deteriorating handwriting, and the loss of his teeth—but more interestingly, for our purposes, he also experienced documented changes in his personality. Before his mercurial treatments, Paganini had been an “ambitious and self confident man”, and afterwards he became nervous about appearing in public, shy and reclusive. He became “easily startled by sudden noises, and nervous if he could not actually see the person he was talking to”.180 Other researchers have called into question the reclusive tendencies of well known scientists known to have worked closely with mercury, such as Isaac Newton and Blaise Pascal.181 Exposure over time is not the only factor in mercury toxicity which is often overlooked. As was the case with Desiree Jennings, there is also a tremendous difference in individual susceptibility. Recall the English physician, John Pearson, who in 1807 described a subset of patients suffering an abnormal sensitivity to mercurial treatments, which he termed mercurial erethism, erethism meaning simply, an excessive sensitivity to stimuli.182 In 1818, a physician named Bateman had a serious reaction to a mercurial ointment he used to treat himself for impairment of vision in his right eye, as was the approved medical custom of the time. Neither Bateman nor his medical advisors recognized the symptoms of his sensitivity to mercury, and he felt that better awareness of the possibility of such a sensitivity would have prevented “consequent repetition of the dose of the poison.” He wrote up his experience in the hope of saving others from the “suffering and danger” he had experienced. Following the usual and expected tenderness of his gums, Bateman began to experience severe symptoms including sweating, a “harassing” cough, retching and flatulence, accelerated heart rate, weakness, confusion, depression in the power of speaking, inability to eat, a sensation of globus,183 coldness of the extremities, oedema of the lower limbs, and such anxiety and dread that sleep would lead to “sinking to immediate death” that he slept in fitful bursts of only minutes at a time. Interestingly, in light of previous accounts, Bateman first experienced an increasing “depression of muscular power” which was initially alleviated by liberal drinking of spiced wine, but which progressed to the point at which three glasses of brandy in the course of five minutes did not produce relief.184 A full year after the attack Bateman related that he continued to suffer muscular weakness, high blood pressure, fatigue and “aching of the limbs induced by very moderate exertions in

walking.”185 Another physician who experienced a case of mercurial erethism in his own practice attempted to educate his colleagues about the possibility of sensitivity to mercury by republishing Pearson’s work in a series of articles in the Provincial Medical Surgical Journal in 1848. W.S. Oke, M.D. had treated a captain of a cavalry unit for constipation with a calomel-purgative compound, 3 grains to be taken every 2 hours until the bowels moved. After the man had taken “about 4” doses, he began to have a bad reaction to the medication. “I found him greatly depressed, pale, pulseless, and sighing, with remarkable inquietude, and pain of the feet—in short, it was evidence the mercury had brought him to an alarming state of erethism.”186 In 1884, the physician W.E, Green presented an “unusual” case of a woman with mercury sensitivity to the British Medical Association. The woman had bought a pot of dandruff cream containing 40 grains of white precipitate per ounce and had applied it one time on the day before seeking medical attention. At first she suffered swelling and blistering of her fingers which progressed to swelling of the head so extreme that both of her eyes were swollen shut. “The next day,” read the doctor, “all the symptoms were increased, and the chin hung down upon the left side like a great pendulous bag.” When the swelling subsided, the skin desquamated between the fingers and over the whole scalp. A colleague affirmed the uniqueness of the woman’s reaction, stating that he had never seen a case of similar reaction to a mercurial ointment, “which is not usually an irritating application.” Interestingly, the doctor was aware of the possibility of an idiosyncratic sensitivity to mercury. I at once asked the patient as to whether she knew that she was peculiarly susceptible to the influence of mercury. She said “Yes;” that some years since, in Germany, her medical man had prescribed an ointment for a small sore behind the ear, and one slight application of it had produced an exactly similar condition to her present one; that he had ascribed it to the use of a mercurial ointment, and cautioned her to never make use of any preparation containing it.187

Teleky confirmed the opinion of earlier researchers. “From experience gained in the therapeutic use of mercury,” he wrote, “we have come to know that great differences exist among individuals in regard to receptiveness for mercury.” As evidence, he related the case of a 20-year-old girl who died after a single application of only 5 grams of blue ointment (containing about 1.5 grams of mercury) with all the manifestations of acute mercurial poisoning, diarrhea, bloody stools, and degeneration of the kidneys.188 In another case he noted that he had observed “extraordinary receptivity in a

strong 17-year old girl who became affected with mercurialism a short time after beginning work in a hat factory.” Although she did not come into contact with mercury or mercurial compounds with the exception of a daily visit to the felting division to bring water to the workmen, she began to suffer from diarrhea, soreness of the mouth, psychological disturbances and tremor within 4 months. In contrast, “the parents and grandparents of the girl although engaged in hat making and rabbit hair cutting (contractors) were never, as far as could be determined, affected with mercurialism.”189 Hamilton also noted the difference in susceptibility between individuals, including a story of two barometer makers who slept in a room with a pot of quicksilver on the stove. One of the men was only “slightly” affected, and the other “was made tremulous for life.”190 Hamilton did not mention the relative ages of the two men. In addition to the individual differences in susceptibility to mercury there are differences in the rate of recovery, in which age is an important factor. Physical symptoms of mercury exposure are slow to resolve, and may be permanent in those over 50. The good news is that the emotional disturbance of mercury exposure “vanishes completely when the patient is kept from mercury”. 191 The disordered emotions seen after exposure of the central nervous system to mercury is a neuropsychological syndrome affecting the mental processes of the mind, of the mind, but not existing only in the mind. Mercurial erethism, or the reaction of sensitive individuals to sustained low doses of mercury, has a physical basis and is “characterized by irritability, personality change, loss of self-confidence, depression, delirium, insomnia, apathy, loss of memory, headaches, general pain, and tremors.”192 Review of the recent biomedical literature reveals the awareness in medical researchers of the “mental” or “behavioral” symptoms that accompany mercury exposure. The following are excerpts quoted verbatim from recent scientific abstracts.

“ The importance of excluding mercury toxicity in patients with psychiatric and 193

neurological disorders is stressed.”

“In our patients, tension, nervousness, agitation, and depression were observed, and outbursts of anger without apparent cause were noted”194 “a case of mercury poisoning in a 12-year-old girl with prominent psychiatric manifestations is presented”195 “we present a case of 50 year-old man [chronically exposed to mercury] with a 3month history of severe frontal headache episodes and vision loss together with a history of asthenia, anorexia, muscle pain, fatigue and neuropsychiatric symptoms”196

”Herein we report a case of cutaneous Hg granuloma resulting in chronic painful local wounds and systemic toxicity in the form of abdominal pain, visual disturbances, and psychiatric abnormalities.”197 “study suggests a relationship between pre- or postnatal exposure to methylmercury and psychiatric symptoms among the general population in 198 Minamata” “developmental MeHg exposure produced perseverative responding or altered the sensitivity of behavior to its reinforcing consequences”199 “All psychological parameters were in highly significant correlations with 200 mercury levels and length of occupational exposure.” “[chemical workers exposed to mercury] suffered from elevated clinical levels of psychiatric symptomatology, including anxiety, depression and phobic 201 avoidance.” “Among chronically poisoned workers [at a light bulb factory], 76 (98.70%) displayed neuropsychological alterations, 69 (75.82%) suffered from neurological impairments, 62 (68.13%) showed pathological findings under clinical examination, and 59 (63.96%) displayed psychiatric disorders.”202 “Nine persons exposed to inorganic mercury had "erethism" and xenophobia in addition to non-specific features of central nervous system poisoning... unique alternation between outbursts of [rage] and deep depression.”203 “Forty-three patients with methylmercury poisoning were studied; 74·4% showed some degree of depression. Their blood levels of mercury were higher than the average values for the whole group, and considerably higher than the blood levels of the non-depressed patients...”204 “occupational exposure to mercury vapors, even at low levels, is likely to be associated with neurological and psychological symptoms”205 “Classical mercury poisoning is characterized by a triad of signs, namely tremors, erethism and gingivitis. Mercurial erethism, which is characterized by behavioral and personality changes such as extreme shyness, excitability, loss of memory, and insomnia are also observed.”206 “ex-miners [with past mercury exposure] tend to be more introverted and sincere, more depressive, more rigid in expressing their emotions and are likely to have more negative self-concepts than controls”207 “The mercury-exposed workers had introvert behavior”208 “personality changes [in patient with elemental mercury intoxication] including depression, anxiety, desire to be alone, lack of interest and sensitivity to physical problems 209 “Chronic subtoxic levels of inorganic mercury appear to produce mild changes in short-term nonverbal recall and heightened distress generally, and particularly in categories of obsessive compulsion, anxiety and psychoticism”210

“Mercury is a well-known neurotoxin implicated in a wide range of neurological or psychiatric disorders”211

If that doesn’t convince you, here’s something that will. The United States Environmental Protection Agency and the World Health Organization both recognize excessive shyness as a result of mercury exposure.212 Sit with that thought for a moment. If you are anything like me at all, up to this point you have been interested and wondering if it could all be true, but at this moment your previous understanding of the world has collapsed like a house of cards, and you are stunned into a silence of the mind.

Mercury in the Food Chain “It’s time to end the madness about mercury levels in canned tuna. No one is at risk from the minute amounts of mercury in canned tuna. This is the conclusion of the FDA and the public health community."- Dave Burney, US Tuna Foundation

Now that you have become aware of the ability of mercury to produce neuropsychological changes in your emotional state, it is time to examine the ways in which mercury has entered the food chain. Primarily the most significant food chain contamination is that of fish as the result of industrial pollution, but there have also been many instances of mercury poisoning due to intentional use of anti-insecticidal and anti-fungal mercurials in agriculture, both on plants and on animals, which have introduced mercury into the food chain.213 And mercury in the soil in areas contaminated by past mining activities has poisoned both animals and crops, so that in certain areas of China, for example, rice has been found to be a significant source of methyl mercury.214 Farmers discovered and embraced the anti-insecticidal and anti-fungal properties of quicksilver and corrosive sublimate from the mid 1800’s onwards. Corrosive sublimate was widely used to seal pruning cuts on fruit trees and quicksilver was mixed into the soil around California grape vines to successfully fight the aphid which had devastated French vineyards.215 So much quicksilver had been lost in the amalgamating process during the California gold rush, that minute globules of the liquid metal could be found in every pan of sand taken from the Marin coast.216 Mercury was used in industry, especially in pulp paper mills and in chlor-alkali plants manufacturing chlorine (for use in bleaching textiles and paper), and caustic soda, or lye (for use in making soaps and other cleaning products).217 Beginning in 1932 the Chisso Corporation in Minamata, Japan began dumping the waste mercury from its chlor-alkali plant into the river emptying into Minamata Bay. Over time the mercury began to accumulate in the sludge of the sheltered fishing bay. Engineers at the time believed that inorganic mercury was insoluble and biologically insignificant. They did not know that bacteria in the sediment could transform the relatively inert inorganic mercury into a much more toxic form of organic mercury which would then be able to enter the food chain. This methylated mercury, or methylmercury, entered the food chain from the bottom up, first contaminating the plankton and sea plants, then contaminating the plant-

eating fish, then the small predatory fish eating fish, increasing in concentration in each “link” as it made its way up the food chain, so that a large predatory fish might contain much, much more mercury than the surrounding waters. Beginning in the 1950s the wildlife in the area around Minamata bay began to be affected. First, the fish themselves were affected, and many were found floating nearly dead in the bay. Next, the animals which ate the fish were affected. Crows fell dead from the sky, and cats staggered erratically by the waterside, plummeting suddenly into the water, “dancing” cats, in a rash of cat suicides.218 In the meantime, as the poisoning of Minamata Bay was continuing unnoticed, agriculturalists were beginning to use toxic organic forms of mercury as antifungal treatments to preserve seed grain for planting.219 Rats which ate the seed grain died of mercury poisoning, and the predatory birds which ate the rats suffered the same fate. Inevitably, human tragedy followed. In 1955 the first of 3 serious mercury poisoning events occurred in Iraq following the use of treated seed grain to make bread.220 After the second mass poisoning, the countries which had sold the seed grain to Iraq decided to place a bright pink dye on the treated seed to warn that it was not safe to consume.221 In late April of 1956 the poison in Minamata began to reach a critical point in the villagers who lived off of the fish of the Bay. Shizuko Tanaka, a 5 year old girl who lived just yards from the seashore, was the first to arrive at the Chisso Corporation’s hospital with the symptoms of a “strange disease.” She couldn’t walk and her speech was incoherent. Shizuko’s 3 year old sister Jitsuko was soon ill with the same symptoms, as was the neighbor’s 5 year old girl. The neighbor and her two sons fell ill next. As more villagers began to fall ill, there was a lot of fear in the village that the illness was contagious. Strangely, the people noticed around this same time that almost all of the staggering “suicidal” cats had disappeared.222 By early May, so many of the villagers had been afflicted that the Chisso hospital director reported an epidemic of an unknown disease of the central nervous system. Doctors offered a number of possible diagnoses including encephalitis, alcoholism, and cerebral palsy. The symptoms of the disease included numbness of the extremities, lack of coordination, sensory disturbance, weakness and tremor, speech disturbance, a stumbling gait, disturbances of sight and impaired hearing, and progression in the worst cases to general paralysis, difficulty swallowing, convulsions and death. Pathological findings included lesions in the cerebral cortex, cortical damage of the cerebellum and damage to the peripheral nerves.223 In July a

two year old girl named Mayumi Sakamoto entered the hospital blind and pale, salivating, unable to walk or swallow well, and suffering from convulsions. She died in the hospital. Her mother was devastated by Mayumi’s death but tried to console herself with her newborn daughter Shinobu. Unfortunately, not only is the immature nervous system more sensitive to the toxic effects of mercury, mercury in the mother’s body is passed preferentially into the fetus, so that children born to apparently unaffected mothers could be born with devastating developmental disabilities such as cerebral palsy and mental retardation. Shinobu was severely affected.224 The devastating illness continued to sweep through the village, gaining force, so that within 5 months, it was bringing down the strong and healthy adult men and women of Minamata. One morning in September of 1956, the fisherman Sohachi Hamamoto, a strong and muscular man who had been perfectly fine the evening before, woke up “crazy”. He swung slowly up, and then he stared all the way around him. He could not hear very well. Even when [his son Tsuginori] told him the time, he could not understand. When he tried to get up and go to the toilet his feet did not work right. Also, he could not get his zoris on correctly. When Tsuginori told him he’d better not go fishing that day, he got angry: “What in the hell have you all ever 225

been able to do without me?”

Sohachi continued to get worse, and on the fourth day his family hospitalized him. He kept getting worse. They moved him to a separate room and tied his limbs down with bandages. Even so, he craze danced, he said words that did not come out as words, he salivated, he convulsed.226

Before Sohachi died, 7 weeks later, his wife had developed such severe symptoms that she was not even aware she had lost her husband. She would linger on, however, bedridden for 9 years until her death. Their daughter devoted those years of her life to her invalided mother’s care, and their son, Tsuginori, developed lifelong speech impediments and movement disorders. When Tsuginori told his family’s story later in court, he testified, “I would ask for nothing else if only I could return to my former body.” Minamata was a tragedy of global proportions. The afflicted suffered greatly, were dealt with poorly, struggled for recognition of their plight and were lied to for years about remedial measures taken to address the

situation. A Chisso corporation doctor had proven to the company that its effluent was causing the poisoning in Minamata in October 0f 1959, yet the company continued to discharge mercury, albeit diverted to the Minamata river on the other side of town and out into the Sharanui sea.227 Chisso told the doctor to stop conducting experiments, and Cat no. 400, the animal whose death and autopsy verified the poisonous nature of the effluent, disappeared. The official results of the cat autopsies did not surface for 40 years.228 It is, perhaps, obvious that Chisso was not running the only chlor-alkali plant in the world. In 1962 a chlor-alkali plant in Dryden, Ontario began to discharge mercury into the Wabigoon-English river system in Northwestern Ontario, and the Canadian Indians of the Grassy Narrows First Nation and the Whitedog Independent Nations who lived off of the fish from the river began to experience the symptoms of acute mercury poisoning; “numbness and paresthesias of the extremities, dysarthria, coordination disturbances, ataxia, and impairment of hearing.”229 In an accusation reminiscent of the moral judgments made against the mercury miners and the hatters, the Indian communities were told that their neurological problems were the result of alcohol abuse. Tourists who visited the area, a popular fishing spot for the well-to-do, were not told about the mercury unless they specifically asked, “but,” said Eugene Smith, the photojournalist who wrote the foremost book on the tragedy at Minamata, “how would they know to ask?” When Smith asked the manager of the Tourist Association office in Kenora (the launching spot for the English-Wabigoon tourist camps) about mercury levels in the fish, the answer he received was, “Why that problem they had over in Japan, that was marine fish. This is river fish so it’s not the same problem at all!” When Smith challenged the man—stating that there is little difference between marine and river fish if the mercury levels are comparable—he answered, “Science is so advanced that they detect almost anything. I bet they could detect mercury in your shoe there.”230 Environmental mercury contamination had become a big problem in Sweden as well. Birds of prey which had eaten rats which fed on mercury treated seed grains were falling dead from the sky, and elevated concentrations of mercury had been found in fish in Swedish rivers, lakes and coastal waters in close proximity to chlor-alkali plants and pulp paper mills. It was the Swedish who discovered, in 1967, that inorganic waste mercury was being methylated by bacteria in the aquatic sediment into the more toxic organic form.231 Sweden reacted swiftly, prohibiting fishing in areas where the mean mercury concentration was greater than 1.0 parts per million (ppm) and advising that only two meals a week should be consumed of fish containing between 0.2 and 1.0 ppm of mercury.232 In doing so, the

Swedish scientists rather pointedly voiced their opinion that the United States was not recognizing its own problems with mercury contamination.233 The United States would not be able to ignore its own problems for long. A Canadian scientist found large quantities of methyl mercury in the Great Lakes. NBC News reported that “If no more mercury were dumped into the lakes it would take 100 years to be rid of what’s already there,” and stating, “we must all live with some methylmercury in our bodies.”234 A veterinarian who oversaw a sales ban on contaminated chickens, which had been given mercury treated seed grain mixed in with their normal grain, warned others against what had become a standard practice. “Seed grain treated with organo-mercurial fungicides is frequently left over at the end of seeding operations. Unused, treated seed is fed to livestock, including poultry, frequently with no apparent ill effects.”235 In 1969 in Alamogordo, New Mexico, Ernest Huckleby purchased grain from the Golden West Seed Company to feed his hogs. As part of his purchase he was also given some "waste" grain which included some seeds, dyed pink in warning, which had been treated with a mercuric fungicide. Unaware of the danger, Huckleby fed the mercury treated seed grain to a hog which he later slaughtered and fed to his wife, who was 3 months pregnant, and to his three children, 20 year old Dorothy Jean, 13 year old Amos, and 8 year old Ernestine. Within 3 months the children had developed “ataxia, agitation, visual impairment, and impaired consciousness.”236 When born, baby Michael was severely neurologically impaired—blind, subject to convulsive seizures, and only minimally aware of his environment. 8 year old Ernestine became blind, unable to sit unsupported or to roll over, unable to hold objects, incontinent and unable to speak. 13 year old Amos became functionally blind, with sensory degradation and impaired coordination. 20-year-old Dorothy Jean Huckleby suffered from tunnel vision, slurred speech, impaired coordination and numbness and tingling in her extremities.237 Dorothy Jean later sued the Federal government alleging the government was negligent in oversight of the warning label on the treated seed as the label was insufficient to apprise the Golden West Seed Company of the possibility of food-chain poisoning. 238 She was unsuccessful. The judge expressed his regret that in following the law, he was not able to reach a finding in Dorothy Jean’s favor. Perhaps the government would help her, he added. Most countries had restricted the use of organic mercurial fungicides in reaction to the mass poisonings, but legal maneuvers stalled the deregistration of organomercurial fungicides in the United States, and it continued to be used as a seed treatment.239 Mercury headlined the news in the United States throughout 1970.240 Commercial fishing was banned in the Ontario waters of Lake St. Clair

because the mercury levels in walleyes in the lake exceeded the 0.5 parts per million government “action level.”241 Striped bass, catfish and sturgeon tested high in California, and a task force there recommended that the public be advised to eat California sport fish no more than one time per week.242 And in December of 1970, Bruce McDuffie, a chemistry professor at New York State University analyzed cans of tuna he had purchased at a local grocery store. His discovery that the tuna exceeded the governments’ action level prompted the recall of over 1,000,000 cans of tuna. The “solid white” albacore tuna, a larger, longer lived fish, had the highest mercury levels. Albacore tuna has an annual migration pattern starting in the waters off of Japan, and ending in the waters off of the coast of Southern California, where the United States Tuna Foundation is headquartered. In January, a pod of 28 pilot whales beached themselves and died on San Clemente Island, 60 miles off the Southern California coast. The whales were found to have liver mercury concentrations ranging from 8.5 parts per million (ppm) in the juvenile animals to 23.9 ppm in the mature female animals. Researchers were reluctant to reach a conclusion about whether or not the animals’ high mercury levels had anything to do with their beaching, as very little research on the subject had previously been performed. Because parts per million is a figure based on a proportional relationship, or ratio, the mercury level of animals of different sizes can be compared without reference to size. Experiments investigating the effect of methylmercury on hogs had found that hogs begin to show signs of illness at liver concentrations of 6.5 ppm, and are considered near death at 30 ppm, but higher levels had been found in the livers of apparently normal California sea lions and Alaskan fur seals.243 If nothing else, the study was a good demonstration of the way in which mercury builds up in the larger, longer lived animals, and a warning that whale meat, popular in some cultures, can be very dangerous to eat.244 The events of 1970 and 1971 concluded with the third and most serious mercury treated seed grain poisoning in Iraq, a disaster in which thousands were hospitalized with mercury poisoning and hundreds, mostly children, died.245 The result was a flurry of research articles in the early ‘70’s attempting to discover the extent of the problem of mercury in the food chain, trying to answer the question that was being raised by an increasingly hysterical public, do the rest of us have anything to worry about? Frederick Stare, the Chairman of the Department of Nutrition at the Harvard University School of Public Health held himself out as the voice of reason. He scoffed at the alarm of his colleagues, stating that “The discovery of mercury levels in some tuna and much swordfish that exceed the FDA ‘interim guideline’ has sent a panic wave through the ranks of

many who ought to know better. Personally, I think this arbitrary guideline could be at least twice as high as it is.” He continued on to state that the attention being given to mercury contamination in fish was “unfortunate” when so many people were dying of heart disease.246 Academic debate on the subject stalled. No one seems to have been willing to question Stare’s obvious motivations to make light of the mercury scare. The first obvious motivation: an all too human inclination to professional jealousy. Stare was, after all, a heavily titled academic, affiliated with Harvard University and known as America’s top nutritionist, and yet it was not he, but an unknown chemistry professor from a lesser university who sounded the warning. The second obvious motivation: conflict of interest. Stare had longstanding financial ties to the food industry, from whom he had received millions of dollars in funding for his Department of Nutrition, and he held a long term position on the board of Directors of the Continental Can Co.247 Nevertheless, Stare managed to throw a chill on the hysteria about mercury levels in fish and to redirect the attention of the nation back to his unquestioned area of expertise, heart disease. In 1979, after much deliberation and cost benefit analyses weighing the risk of increased mercury exposure in the average consumer against the economic interests of the US Tuna Foundation, the FDA neatly solved the problem of “over detection” by raising the action level to 1.0 parts per million.248 This was the same action level which had been enacted by the Swedish government, but it came without advisement to limit consumption. In the early 1980’s studies began to be published finding that eating fish reduced mortality from coronary heart disease. And that was pretty much the last word in the public discourse on the dangers of mercury in the food chain, the last nail in the coffin, and the issue lay fallow for 20 years. A couple of long term studies were run on mother infant pairs in the high fish eating populations of the Seychelles in the Indian Ocean and the Faroe Islands in the North Atlantic, and the results were interpreted to mean we didn’t have anything to worry about, not really.

Excessive Consumption “Clogged with yesterday's excess, the body drags the mind down with it.” - Horace, Roman Poet 65-8 BC

Some people with fair skin have a noticeable problem with facial redness, or erythema. The cause of this facial redness, commonly called rosacea, is unknown, but it is theorized that hyper-responsive sensory nerves play a central role. Over time, fixed changes in the vasculature of the skin can occur leading to persistent facial redness.249 In 1992 a 46 year old woman consulted a physician for treatment of reddened skin. In the course of treatment the physician learned that the woman had been eating a diet high in fish for the past two years, and a hair mercury test was performed that revealed a staggeringly high hair mercury concentration of 67.8 parts per million. (Average hair mercury concentrations in the US adult population range from 0.47 ppm to 3.8 ppm.250) The woman’s physician advised her to reduce her fish intake but, “while she indicated that she did try to cut back somewhat on her fish consumption, she considered fish to be essential to her health and continued her practice of daily fish consumption.”251 If this woman’s facial redness was a sign of mercurial erethism, a sign that mercury was beginning to act as a poison in the woman’s body, it was an accurate one, as within the next few years she began to experience the usual symptoms of advanced mercury poisoning, including inflammation of the lining of the mouth and tremor. This time a blood mercury test was performed which revealed mercury concentrations of 125 microg/L, which translates into a substantially reduced, but still quite high hair mercury concentration of 37.5ppm.252 Unable to believe that her habit of daily fish consumption could be anything other than nutritious and healthful, the woman contacted the Agency for Toxic Substances and Disease Registry (ATSDR) in 1999 “to obtain assistance in determining the source of the mercury.” The ATSDR reviewed the woman’s case and concluded that “excessive” fish consumption was the problem. It appeared obvious that her excessive fish diet was the likely source of the mercury identified in the sample. She was advised to visit an occupational and environmental medicine specialist for proper evaluation of her problem and to substantially reduce her consumption of fish.253

In the years 1999 and 2000, the National Health and Nutrition Examination Survey (NHANES) conducted a survey of blood mercury concentrations among 1,709 women of childbearing age. In a move that shocked the government out of its complacency, the EPA announced that based on the distribution of blood mercury levels and the number of US births, more than 300,000 newborns were being born each year exposed in utero to levels of methylmercury carrying an increased risk of adverse neurodevelopment effects.254 The blood mercury levels of the women tested ranged from levels that were non-detectable at the 5th percentile, 0.6 microg/L at the 50th percentile, and 6.7 microg/L at the 95th percentile, which would correspond to hair mercury levels of 0.18 ppm at the 50th percentile and 2.01 ppm at the 95th percentile. Current research suggests subtle developmental deficits can result where maternal hair mercury concentrations are greater than 5 ppm, and that clinically obvious neurological deficits, such as delayed walking, appear at levels above 10 ppm.255 As the government prepared to issue new warnings about mercury in fish, the three big fishing industry groups, the National Food Processors Association, the National Fisheries Institute and the US Tuna Foundation wrote a letter to the FDA commissioner arguing that a broad advisory would not only expose the industry to consumer litigation and economic hardship, it “could have an irreversible impact on American dietary habits, profoundly affecting consumers and producers of seafood and resulting in significant segments of the population turning away from the proven health benefits of fish consumption.” The advisory committee appeared to agree, and the 2004 FDA/EPA advisory was issued based solely on protection of the fetal/immature nervous system, with a warning that women who are or may become pregnant, nursing mothers and children reduce consumption of high mercury fish. Intentionally, no advisory was issued for the general population. The vast majority of people in the United States eat fish an average of one fish meal a week, or less. The interests of protecting the health of the majority of Americans—who were considered not to eat enough fish to reap the cardiac benefits modest consumption of fish can provide—was weighed against the interests of the much smaller percentage who eat fish several times a week or more and who run a significant risk of overexposure to methylmercury. The Alaskan Division of Public Health followed up on the FDA/EPA decision with a commentary published in the March 2005 issue of the American Journal of Public Health, stating that if generic fish advisories might have adverse public health consequences because of decreased fish consumption, the obvious solution would be human

biomonitoring.256 We have our cholesterol and other indicators of potential health risk tested every year, afterall, to alert our physicians of possible problems. It wouldn’t be difficult at all to include a test for methylmercury. In August of 2005, the Wall Street Journal published the story of Matthew Davis, a 10 year old boy who had eaten three to six ounces of solid white albacore tuna each day for over a year. He was a child, and therefore intended to benefit from the fish consumption advisory, but his parents hadn’t gotten the message. Matthew, formerly a bright and active child, had developed problems with coordination and concentration. He couldn’t focus in school, he could no longer properly catch a football, and his fingers had started to curl in. A specialist diagnosed Matthew with a learning disability, but the truth was that he had mercury poisoning, with blood levels of twice the safe level. The Davises had been very happy about Matthew’s fish eating habit, believing that it was “brain food” and would help his intellectual development. When asked about Matthew’s case, the US Tuna Foundation’s executive director, David Burney responded flatly, “There is no connection between a learning disability and mercury.”257 It’s worth noting that awareness of the true nature of Matthew’s problem did not come about through a physician’s diagnosis, but rather by chance, when Matthew’s father read an article in The San Francisco Chronicle on the high mercury levels of a San Francisco physician’s “coastal affluent” clientele who had a habit of eating expensive high mercury varieties of fresh fish, such as swordfish, bluefin and albacore tuna and shark.258 Recognizing his son’s problems in the symptoms described, the Davises brought the issue to the attention of the doctors themselves, and neurological tests confirmed their suspicions. A “pescetarian” diet, in which the only source of animal protein is that from seafood, is the choice of more and more health and weight conscious eaters these days.259 It’s a step on the path to vegetarianism for the animal lover,260 and a convenience for those living alone. Clearly, increasing numbers of people are exposing themselves to a potentially dangerous level of methyl mercury in their diets. If the doctors hadn’t suspected the possibility of mercury poisoning in a person officially recognized as subject to potential risk, however, how likely is it that they would suspect mercury poisoning in adult men? In 2009 an article was published on two cases of “fish faddism” causing low-level mercury poisoning in two otherwise healthy men, a 38 year old marine engineer and a 46 year old CEO, who had dedicated themselves to a high fish diet in the pursuit of better health.261 Both men had developed vague symptoms which included aches and pains, diarrhea, abdominal pain, and overwhelming fatigue. Both men also underwent a series of advanced diagnostic tests which consistently returned

with normal results, but they persisted in their feeling that “something was wrong.” The older of the two men began to complain of numbness in his lower back, hips and thighs, and this paresthesia, a telling symptom of advanced mercury poisoning, was attributed erroneously to degenerative disc disease and treated accordingly. He was also “generally worried” and suffered from disturbed sleep, and frequent panic and anxiety attacks. Ultimately, questioning revealed that both men had been eating a diet in which the sole source of animal protein was canned tuna and fresh shark. The younger man had a blood mercury level of 17.8 microg/l (corresponding to 5.34 ppm hair) and the older man had a blood mercury level of 26.3 microg/l (corresponding to 7.89 ppm hair). Both patients regained their physical and emotional well-being within 12 months after they were advised to discontinue eating fish—at which point they were encouraged to return fish to their diet in “modest” amounts and to avoid “excess” fish intake.262 The study concluded that “Fish as a 'good' dietary component can turn noxious in excess.” History repeats itself. 100 years ago the medical community had wildly conflicting views on the general effect of smoking on health. When it began to become apparent—as early as 1908—that increasing rates of cancer were linked to smoking, the focus was on the harmful effects of “excessive” smoking and measures were taken to limit the exposure of the young.263 Doll and Hill published their groundbreaking statistical study proving the connection between smoking and lung cancer in England in 1950, but it was not addressed publicly until 1954 when Iain Macleod, the Minister of Health, eventually held a press conference on the subject. Using dismissive language and smoking as he approached the podium, Macleod stated that ‘It is desirable that young people should be warned of the risks apparently attendant on excessive smoking’, but he insisted ‘the time has not yet come when the Ministry should offer public warnings against smoking’.264 In 1957 the US Surgeon General Leroy Burney joined the discussion, confirming that researchers in the United States had also found “there is an increasing and consistent body of evidence that excessive cigarette smoking is one of the causative factors in lung cancer.”265 Throw the word “excessive” around, implying that average people have nothing to fear, and kowtow to industry in an uneven fight between industry and the individual, and you have the makings of a disaster. If you take one thing away from this chapter, let it be this—that as a result of increased mercury in the environment, it is possible to build up a toxic amount of mercury in your body, either by consuming fish in an above average frequency or amount, or through regular consumption of the more contaminated large predatory fish. There are other ways in which you can

be exposed to deleterious amounts of mercury, and the first signs of the problem will be emotional. If hair mercury concentrations in the United States average between .47 and 3.8, that means mathematically that between 1 and 2% of the population have hair mercury concentrations at or over 7.5 ppm, as did the the 46 year old CEO of the “fish faddism” study, and as I did, the author of this book. That is an enormous number of people. The government has determined that modest fish consumption is healthy and beneficial, but, except in the case of pregnant women and children, they haven’t made an effort to inform the public that there is a certain level of fish which is considered “excessive” and potentially harmful to your health and emotional well-being. And what’s more, what’s ironic and tragic, out here in the real world, when our health declines, we tend to throw more fish at the problem, thinking we are doing ourselves some good. The physician’s aren’t checking,266 and, to paraphrase W.E. Smith, if we haven’t been told eating too much fish can be dangerous, how would we know to tell our physicians to look out for the signs of our excess? Methyl mercury is a potent neurotoxin which can easily cross the bloodbrain barrier and penetrate into the brain and the central nervous system. For the most part, methyl mercury toxicity is reversible through natural elimination. It has a half-life of 70 days, so that if you have a significant amount of methyl mercury in your body, you would need to complete at least five half-lives, or 50 weeks, in order for your mercury levels to drop sufficiently to regain your sense of physical well-being.267 In all but the most severe cases you will regain your sense of emotional well-being at a much earlier point than that at which physical symptoms resolve, and it is, in fact, the first sign that you are regaining your health. As Leys stated in his description of infantile acrodynia, the earliest symptoms are emotional, and the earliest symptom of recovery is an improvement in mood and interest “although full health may still not be regained for many months.”268 There are certain factors which can lead to impaired mercury excretion, however. Unlike elemental mercury, which is poorly absorbed by the body and tends to pass right through the intestinal tract, methyl mercury absorption is very high, around 90 to 95%. It is so easily absorbed that it tends to be repeatedly reabsorbed from the small intestine in the process of the body’s attempts at elimination.269 Preliminary studies have found that certain strains of intestinal microflora demethylate the methyl mercury in the gastrointestinal tract, converting it back to inorganic mercury which is less easily absorbed by the body and therefore more likely to be eliminated.270 Supporting this theory is that mice given antibiotics to suppress their intestinal microflora while given methyl mercury had higher tissue levels of

methyl mercury as a result.271 Slowly, slowly, in ways we do not yet fully understand, demethylation is taking place throughout our bodies, so that even if you were to stop eating fish tomorrow, inorganic mercury levels in your tissues and organs would continue to rise for some time. Demethylation is a good thing in the intestinal tract, but a bad thing if it occurs within your brain, because although methyl mercury can pass in and out of the brain through the bloodbrain barrier, inorganic mercury cannot. If demethylation of methyl mercury to inorganic mercury takes place in the brain, the mercury cannot get back out, and it will be stuck there for years, maybe forever. Recall the tragic story of Ernestine Huckleby, the 8 year old girl who was poisoned by methyl mercury contaminated pork. She never did recover, but suffered from quadriplegia, blindness and severe mental retardation until her death at age 30. Even though it had been 22 years since the time of her exposure, an autopsy revealed high levels of inorganic mercury in her brain. (1,974 ppb as compared to 38.5 in a control subject). The researchers concluded that the biotransformation of methyl to inorganic mercury, after the methyl mercury had crossed the blood-brain barrier, accounted for its persistence in the brain and was likely responsible for causing part of the brain damage.272 Another source of inorganic mercury that can enter into and persist in the brain is that which is due to the inhalation of mercury vapor, the type of mercury exposure experienced most often in the course of employment. In one such case, a man who was exposed to metallic mercury during the course of his employment in 1968, developed clinical signs of neurotoxicity from which he slowly recovered over a period of six months after stopping his employment. He subsequently developed “admittedly odd” and neurotic behavior and became an alcoholic. He never returned to work and died 16 years later, in 1984. Residual behavioral disturbances are rare except in the case of severe intoxications, however, and as was the case with the hatters, reviewing physicians declined to find that the mercury had caused a deterioration of the man’s psychological state. He might have had an underlying personality problem, they said, which was exacerbated by his physical ordeal and his financial problems.273 An autopsy performed at his death, however, confirmed that a large proportion of nerve cells in all brain regions still contained granules of mercury.274 In another case a man was exposed to mercury vapor during the course of his employment in 1973. Physicians treating him administered a mercury chelating agent and assumed based on tests of urinary mercury excretion that he had achieved total body clearance of mercury within 3 years. As in the previous case, this man also developed serious psychological problems and never returned to work. An autopsy performed 17 years after the initial

exposure revealed mercury in the majority of his nerve cells and in the cells of his other organs.275 Clearly, inorganic mercury in the brain can produce major and long lasting behavioral changes in cases of severe intoxication. But what of that from chronic low level exposure—such as that from dental amalgams? According to the World Health Organization, the most significant source of inorganic mercury exposure in the general population is that from mercury amalgam fillings. Amalgam restorations continuously release elemental mercury vapor which is inhaled and absorbed by the body and distributed to tissues including the brain. The level of mercury vapor released is small but measurable, and autopsy studies have found a significant correlation between the number of amalgam surfaces and concentrations of I-Hg in the brain. 276 Whether the average daily mercury uptake from amalgam fillings is dangerous to your health is another hotly debated issue, but there is a general agreement that certain factors can increase the rate of mercury outgassing significantly, such as “excessive” gum chewing, nightly teeth grinding, and hot drinks.277 Psychological testing of women with and without amalgam fillings has shown that women without amalgams score significantly higher on controlling anger, and that women with amalgams were less happy and showed significantly higher scores for anxiety.278 But the real danger of amalgam is in the placement and removal of the fillings, so much so that studies suggest that placement and removal of amalgam fillings in pregnant and nursing women would subject their unborn and newborn children to dangerously high levels of inorganic mercury.279 And of course, the dental workers, who are present at all placement and removals, are the persons most at risk, making mercury exposure a possible psycho-organic explanation for the historically high suicide rate among dentists.280 In a large scale study studying the effects of alcohol on dentists, abstainers were found to have significantly higher urinary mercury concentrations than drinkers, a result which the study authors believed reveals a protective effect of alcohol.281 This theory is bolstered by a Swedish study in which an increased exhalation of mercury was found in the breath after alcohol intake.282 But the findings might just as easily have revealed a tendency of the subjects to retain rather than eliminate the mercury to which they were exposed. And if so, perhaps the vulnerability of that subset of dentists to the effects of the mercury might have lead to their increased drinking. The predictable frequency with which those exposed to high levels of mercury turn to alcohol is an area of mercury exposure which, like so many others, requires more research.

Strangely, or perhaps not so strangely, dentists dropped out of the first ranking for suicide among occupations in the 1980’s with much less suicide in younger dentists around the same time that dentists began to take more precautions to limit their mercury exposure. When dentists’ suicide rates fell, veterinarians took the pole position—veterinarians—who still use mercurial treatments on animals.283

Idiosyncratic Sensitivity First to fall over when the atmosphere is less than perfect, Your sensibilities are shaken by the slightest defect, You live your life like a canary in a coal mine -The Police, Canary in a Coalmine

By far the largest source of mercury pollution caused by mankind in recent years is that caused by coal burning power plants. Recent legislation enacted by the EPA, the Mercury and Air Toxics Standards (MATS) act, will require coal burning power plants in the United States to spend billions of dollars to upgrade their mercury capture equipment to reduce emissions by the year 2017. The new rule will eliminate 90% of the 53 tons of mercury emitted annually by coal fired power plants in the United States, that is, if the industry fails in its attempts to overturn the legislation.284 Of course, mercury in the atmosphere doesn’t respect national boundaries and the coal burning power plants in other countries, such as China, have a much higher emission rate which also contributes to the amount of mercury in the atmosphere worldwide.285 When the bleach and caustic soda chlor-alkali manufacturing plants of the last century were dumping their mercury waste into the bays and oceans, there was an expectation that the waste would be dispersed and degraded to a point of harmlessness. That expectation proved incorrect when methylation by bacteria in the aquatic sediment caused the mercury to become concentrated to dangerous levels in the aquatic food chain and returned to us on our dinner tables. But what of mercury that is emitted into the atmosphere? Is global dispersal sufficient to render the toxin harmless? The ability of mercury to break into infinitesimally small orbs which “are never lost, but, one way or other, meet and incorporate again,” has been understood for hundreds of years. Among all the wonders of this unaccountable liquid, that which to me seems most remarkable is, that although it is the most ponderous thing in the world, it is immediately converted into the lightest, which is smoke, in which it presently flies up quite dissolved; and then that same smoke, which is so light, in a moment returns again to such a weighty thing as mercury is; for as soon as the smoke of that metal meets with a solid body up above, or comes into a cold region, it immediately falls again, converted into quicksilver.286

The mercury will eventually return to earth and sea in mercury

contaminated rainwater to undergo, ultimately, the process of methylation through which mercury enters the food chain. But there is also evidence that people, plants and animals in areas in close vicinity to the point sources of mercury discharge, such as coal burning power plants, mercury recycling centers and chlor-alkali plants, are exposed to the contaminant in a more concentrated form. Mercury levels in the lichen of trees downwind from a chlor-alkali plant have been found to be as high as 3.66 ppm with levels decreasing exponentially with distance. The sphere of increased mercury deposition has been estimated to extend more than 2 miles, and animals raised downwind of power plants have been found to have increased mercury accumulation in their organs.287 Not surprisingly, wildlife is beginning to show the effects of increased mercury pollution. Raccoons in high mercury areas have been determined to be potentially dangerous sources of contamination for man and other high level predators, with mercury concentrations over the 1.0 ppm government action level for seizing commercial fish.288 In 1989 mercury was found to be responsible for the death of a critically endangered Florida panther, an important breeding female in a closely monitored conservation effort. On autopsy, the panther was found to have mercury levels of 110 ppm in her liver and 130 ppm in her fur.289 In an ironic parallel to successful high-end consumers eating too much expensive large predatory fish, researchers found that panthers in the most contaminated area of the Everglades, who were successful enough in hunting to catch and consume a diet heavy in raccoons, were far more at risk of potentially fatal mercury contamination than panthers with a “diversified diet.”290 In addition to the unfortunate death of one of the panthers, researchers discovered that high mercury levels were affecting both panther reproductive rates and the rate of cub survival. The higher the mercury levels in the blood of lactating female panthers, the less likely their cubs were to survive to 6 months of age. It is a pattern that is playing out in many areas of the animal kingdom, with adverse effects found not only in reproductive rates and offspring survival, but also in the behavior of the offspring in such varied species as water snakes, mice and birds.291 Two studies examining the behavioral effects of environmentally “relevant” levels of mercury on birds demonstrate the nervous over stimulation of the senses which human beings are known to experience at low levels of mercury exposure. Mallard ducklings whose parents were given feed containing either .5 or 3 ppm of mercury were hyper-responsive in a test of avoidance of a frightening stimulus (an excessive startle effect), and Nelson Sparrows with higher blood mercury levels were found to sing faster, higher pitched songs.292

Other studies demonstrate the deficits in social interaction that accompany a higher relative level of exposure. In the case of the Common Loon, as their mercury levels rise, the loons make fewer nesting attempts, have lower nest attentiveness and lower nest fidelity. Their chicks spend less time interacting with their parents.293 In the highly social prairie vole, elevated mercury levels have been shown to cause male prairie voles to isolate themselves rather than interact with unfamiliar same sex prairie voles. The study authors noted that these characteristics, social avoidance and a male-oriented bias, are two of the hallmark characteristics of autism, and support the use of prairie voles as model animals in which to study autism.294 Clearly mercury pollution is becoming an increasing factor in our lives, and one of which we should be aware. Not only is there an increasing amount of mercury in fish, that fish is being used in fish meal to feed poultry and swine. There is mercury in pig manure.295 Cattle are being grazed in areas near power plants. Crops are being grown in areas downstream of contaminated historical gold mining areas. Chinese herbal medicines and imported skin lightening creams contain mercury.296 And mercury is sprinkled throughout homes and burned in candles as a part of the religious ceremonies of some cultural groups.297 Some of these sources are major, and some minor, but they are all cumulative, part of a problem grown so large that the countries of the world have gotten together to begin to formulate a solution. In January of 2013, 147 countries including the United States adopted the Minamata Convention on Mercury, a legally binding treaty designed to reduce global mercury emissions which will be ratified in October of 2013, in Japan. The treaty incorporates goals for reduced emissions from power plants, strategies to reduce the amount of mercury used by small scale gold miners, plans to phase mercury out of many products, including dental amalgams, and plans to work with medical personnel so that they are better able to recognize and treat the effects of mercury poisoning.298 The human brain contains billions of neurons, which communicate with each other through long-range axons. Mercury damages the brain by causing the degeneration of both the neurons and the long-range axons. The brain attempts to compensate for the damage through the increased production of short-range axons, and the increased production of glial cells, the non-neuronal cells which provide support and protection for the neurons. At levels lower than that which would result in overt damage to the physical structure through which the signals are passed, mercury can cause alterations in the signals themselves. Neurons pass signals to other cells by the release of electrical signals that induce voltage changes in the

receiving cells, or through the release of chemical signals that bind to the receptors in the receiving cells. Mercury binds to these receptors, preventing the uptake of the intended chemicals, disrupting critical messaging within the brain and central nervous system and causing changes which can result in neurological and psychiatric disorders.299 One such change which has proven effects on mood and behavior are changes to the brain’s dopamine system. Neurochemical alteration in the dopamine system by organomercurials has been proven to decrease prosocial interaction in both sexes, and to make males more prone to asocial or antisocial acts.300 Remember the cataleptics you read about in Chapter Two? Dopamine receptor agonists, drugs which bind to dopamine receptors by mimicking other chemicals, have been used to cause drug induced catalepsy.301 Mercury in the environment is increasing at an alarming rate and contributing to increased levels of emotional and behavioral pathology in the over-exposed. Those people who are sensitive to the effects of mercury will begin to experience the emotional and behavioral effects of mercury exposure at a much lower level than the average person factored into statistical adverse effect models. From the earliest days, when the voices of the proponents of mercury use drowned out the dire warnings of the critics, there were people whose disastrous reactions to relatively modest doses stood outside of the norm. In 1884, the physician W.E, Green presented an “unusual” case of a woman with mercury sensitivity to the British Medical Association. The woman had bought a pot of dandruff cream containing 40 grains of white precipitate per ounce and had applied it one time on the day before seeking medical attention. At first she suffered swelling and blistering of her fingers which progressed to swelling of the head so extreme that both of her eyes were swollen shut. “The next day,” read the doctor, “all the symptoms were increased, and the chin hung down upon the left side like a great pendulous bag.” When the swelling subsided, the skin desquamated between the fingers and over the whole scalp. A colleague affirmed the uniqueness of the woman’s reaction, stating that he had never seen a case of similar reaction to a mercurial ointment, “which is not usually an irritating application.” Interestingly, the doctor was aware of the possibility of an idiosyncratic sensitivity to mercury. I at once asked the patient as to whether she knew that she was peculiarly susceptible to the influence of mercury. She said “Yes;” that some years since, in Germany, her medical man had prescribed an ointment for a small sore behind the ear, and one slight application of it had produced an exactly similar condition to her present one; that he had ascribed it to the use of a mercurial ointment, and

cautioned her to never make use of any preparation containing it.302

Back in the day of widespread acrodynia, the doctors were slow to believe the first rumblings that mercury was the cause of the disease. There was an extraordinary prevalence of the use of mercury in infancy in those days. One study found that 48% of all mothers surveyed had used teething powders containing calomel, and that an additional 4% had used “grey powder” or mercury and chalk. “The powders had often been given every week from a very early age.”303 The vast majority of children tolerated the mercury without any problem. Only a tiny fraction of children given mercurial teething and soothing powders developed a clinical case of acrodynia—only 1 in 500 of all children developed acrodynia.304 Yet, ten years after the manufacturers ceased production of mercurial teething powders, and acrodynia virtually disappeared, the results showed “how correct earlier authors had been in their belief that chronic mercury poisoning was the main, if not the only, cause of pink disease.”305 The arguments against mercury exposure as a cause of autism and the related autism spectrum disorders are based on the same line of reasoning as that which was used against mercury as a cause of pink disease. Mercury in the environment is widespread, and whether it is introduced before birth through maternal consumption of seafood or amalgam fillings, after birth through childhood vaccines, or through any of the many varied sources of mercury in the atmosphere, the incidence of autism is still relatively small. In 2011, a brilliant study was published by two Australian researchers testing the hypothesis that a genetic sensitivity to mercury underlies autism. The researchers reasoned that if sensitivity to mercury is a genetically heritable trait, the descendants of pink disease survivors, a group of people confirmed as having a hypersensitivity to mercury, should include a higher than normal number of grandchildren with autism spectrum disorders. And that is exactly what they found. 1 in 25 grandchildren of pink disease survivors had been diagnosed with an autism spectrum disorder, as compared to 1 in 160 in the general population, a statistically significant finding.306 Arguments made against clinical toxicity at comparatively low levels of mercury exposure suffer from the same failure to recognize that some people are more at risk. Recent research has proven this to be true beyond any doubt. Variations in your genetic code influence the way your body handles the mercury you are exposed to. A study using blood samples from 2,926 mercury exposed adult twins living in Australia found a strong genetic correlation of 83% and a weaker environmental correlation of only 34%,

showing that variations in your genes affects mercury concentrations in your body to a greater extent than environmental exposure.307 Furthermore, researchers have identified specific differences in the DNA sequence between individuals which affect the body’s reaction to mercury exposure in the genes GSTT1, GSTM1, GSTA1, GSTP1, GCLC and MT, with dual gene combinations causing a synergistically negative effect on the body’s ability to handle and dispose of mercury.308 The study was performed on a group of 324 medical students in Austria. It is a near certainty that a study on a more diverse group would find even more variation. There are inconsistencies in the toxic dose levels in different geological areas.309 Taking, for the sake of argument, the number of children affected by acrodynia as a starting point, 1 in 500, with roughly half of all children exposed, a rough extrapolation would be that 1 in 250 people have a genetic sensitivity to mercury. The United States, with a population of 315,000,000 people would have 1,260,000 people with an unusual sensitivity to mercury. Think of the number of people you went to high school with, and do the math. The first effects of mercury on the human nervous system are an over stimulation of the sensory nerves causing an exaggerated response to external stimuli, which translates into excessive shyness and an often crippling over-awareness of social cues. As exposure increases, the damage caused can sometimes lead to higher levels of thought and artistic achievement. Emily Dickinson’s thoughts crowded “thick and fast, like lightnings.” Jack London experienced a “truer order of truth.” Elderly people with lesions in the frontotemporal lobe have displayed sudden artistic brilliance. 310 Autopsy on Einstein’s brain revealed the increased glial cell to neuron ratio that is typical of the pathogenesis of mercury exposure.311 Mercury is very likely the secret behind the well understood but unexplained phenomenon of the tortured genius. The Urban dictionary defines “tortured genius” in this way: “You are smart. Brilliant in fact. And while it's a blessing, it's also a curse. Your head is filled with everything - grand ideas, insufferable worries, and a good deal of angst.”312 You may not be the person you think you are. It’s time to find out.

Epilogue – A Natural “Hi” My life used to be so small. I had tried to come to a mature acceptance of my unchangeable introversion, but it bothered me that I wasn’t able to say "hi" in a natural way to people I might pass walking the dog. I had lowered my expectations of what was possible for me. I wasn’t trying to be somebody special out in the world any longer, but was it too much to ask for a natural “hi”? I practiced it, the way I once used to practice presentations in front of the class, the way I once practiced my argument for the court of appeals, trying to relax as someone was about to pass, and my “hello” was sometimes better and sometimes worse, sometimes very quiet and meek when I did not mean it to be, but always, there was a forced quality to it. When I got the high mercury test results, I stopped eating fish. Over the months that followed, I began to research the effects of mercury on the body, and what I discovered shocked me. One after another of the physical problems I had were attributable to mercury. And there was something else. I was beginning to feel easier out among other people. I had passed by one or two references to mercury as a cause of excessive shyness buried in the studies I had read, and now, realizing the significance of what I had seen, I went back and looked them over again. I had a hard time at first, coming to terms with the fact that the knowledge had been there all along, for a hundred years or more, and that I had suffered so needlessly; all those years of pain and anguish, all those hard things that could have been easier, the best parts of my life over and wasted. Then I began to look around me, and it seemed as if all I could see was all the ways in which the world could be a better place. And so this book was born. To save you. I saw improvement in my social anxiety within 3 months of restricting my mercury exposure. Within 5 months I had achieved not only a natural “hi”, but a George Clooney-esque ability to banter, and I have experienced the unexpected pleasure of not having to notice other people so much, to be able to move among them without having to be on high alert. Already I am losing touch with how anxious I used to feel around other people, struggling to find words to describe the sense of overwhelming... what? Tension? Inability to relax? I can’t explain how nervous I used to feel. I was quiet and introverted among people, I had tremendous anxiety in groups and conversations with strangers was difficult for me and forced, and at times that basic nervousness bled through into my life at home, especially if I had extended myself too far out in the world. I remember, 20 years ago, exactly where I was, sitting in my car waiting

to make a left hand turn on a red light, on my way to the Home Depot, and thinking that I knew it was going to be very bad that day, that I could hardly stand the thought of having to go into that store and walk through the people that would be there. I remember thinking that it wasn’t always so bad and wondering why, what made the difference, between this day, which was going to be a very bad day, and other days when I was less... nervous? Anxious? Words fail me in the description of that peculiar state of mind in which it was just going to be “too much” to interact with other people. I remember also, how I got through it, I remember walking the wide aisles with my cart, avoiding looking other people in the eye, so wound up that I could barely stand it. I didn’t want to see them seeing me, to notice what they thought of me, to read everything into their slightest gestures or expressions, to see how they saw me but were pretending not to, to register their opinion of my clothes or posture or figure in the merest change in arc of the cast of a glance past and through me. I couldn’t stand all that information coming at me, the judgments and cruel thoughts, and everything that is part of an ordinary crowd. I would do what I had to do, try as hard as I could to be invisible and get through it unscathed. But inside I was a free person; smart, artistic and strong-willed, reckless, in my younger, lonelier, more tumultuous days, flirting with destruction, wantonly. How could I be both of these people at once? The girl who would turn red, eyes down, one of those people you would feel sorry for having to watch speak in class, an awkward, struggling, lost person, and the other as well? It’s a “peculiar form of stimulation and timidity” to quote Teleky. And to be free of that is incredible, unexpected, and an unimaginable gift.

A Special Note for the Overweight and Hypertensive If, having read of the habitual incidence of anorexia that accompanies severe mercury poisoning, you think this book must not apply to you, think again. There is almost no research into long term chronic low level mercury exposure and obesity. A study was published in 2011 which found a link between central obesity and elevated mercury levels in Korean men aged 40 to 65 living in coastal areas313, but other than that, most of the evidence is anecdotal, meaning that people have noticed a link, but have not performed the research to either confirm or deny it. The most confounding aspect of the symptoms of mercury poisoning is that it runs the gamut from stimulation to deadening, so that chronic low level exposure can cause over awareness of social cues resulting in pathological shyness and a more serious exposure can cause the inability to perceive and process social cues which is the hallmark of autism. In a similar manner, I believe that chronic low level exposure can result in increased appetite and a more serious exposure can cause anorexia. I believe that all of us who suffer from problems with our weight have had the experience of anxiety or depression driving us to the cupboard, as well as the experience of a much greater emotional upset causing us to lose our appetite altogether. I have always had a tendency to gain weight, and I have been on many diets in my life beginning from the time I was still a teenager. The difference between my early life and my later life was in my ability to diet. When I was younger, I had the strength of mind and will power to do whatever I had to do to stay slim. I would fast if the pounds had slipped on, so much so that one summer, when I counted up afterwards, I had eaten on average, only every other day. Or I would exercise, bicycle for an hour, have lunch of an orange and tuna with crackers. But as I got older, in the last ten years, I reached a point at which I wasn’t able to diet anymore. I would resolve to diet, and by the end of the first or second day, my diet would end in tears and self-hatred. I would fight so hard, fight the first, the second, the third, the fourth, the fifth impulse to break my diet, and then, somehow, I would have given in without even having formed the decision to give in. I tried everything which had ever worked for me before, and more, including weightwatchers on line and in person. I had become hypertensive at the same time my weight began to escape me, and I had to sit in front of doctor after doctor trying to impress on me the wisdom of losing weight, as

if I didn’t know that I should. As if I didn’t know how, in the most mechanical sense. In the first half of my adult life, my experiences with overeating were most often of an emotional nature, and the problem, I found, with eating to solve your emotional problems is that it works. I’m not advising it, but let’s be honest, you and I, and say what other people have been reluctant to say. It leaves you suffering from the consequences of poor health and increased social insecurity, but at least at the moment, it helps. And in some of the bad moments, you decide that feeling better in the present is of overriding importance. I was not significantly overweight during this portion of my life. I would put it on, but I could take it off. But episodically and with increasing frequency in the second half of my adult life I began to experience something different, a greatly increased and driving appetite, sometimes coupled with the troubling sense, even if I had eaten enough to feel quite full, that I hadn’t eaten the right thing to satisfy my hunger. As I began to experience this kind of hunger, I found that I could no longer control myself, and I joined overeaters anonymous in a state of despair. I was not successful there either. In the twelve step programs there is a saying that “knowing why is the booby prize”, but let me offer this to you as a possible explanation. There is a nerve, called the vagus nerve, which is the major neural connection between the gastrointestinal tract and the central nervous system. This nerve controls feelings of hunger and satiety, down to and including the feeling that you have eaten the “right” things your body needs. Is it possible that a low level of over-stimulation to this nerve might cause excessive hunger, and that an excess of stimulation to it might deaden it sufficiently to cause anorexia? Recent research suggests that the answer is “yes,” although researchers are not yet quite sure why. They speculate that electrical stimulation of the vagus nerve may alter the secretion of hormones associated with hunger or satiety.314 Other research has shown that high hair mercury concentrations may indicate an increased risk of metabolic syndrome.315 When I began to write this book I considered it a placeholder, the first book which I would write to fill in time until I was able to successfully resolve my weight problem and my hypertension. I had convinced myself beyond any doubt that I had found an answer which would lead to regaining my health. The only questions I had were, how long would it take? And would the damage which I incurred to cause my high blood pressure be reversible? I was sure that it would take some time. At this point in time, in the spring of 2013, I have been limiting my mercury exposure for 9 months, and I have seen definite measureable improvements in both my appetite and my blood pressure. Give me a couple more years and I am

convinced that I will have the basis for a compelling personal anecdote of success, but is that enough to base a book on? I am not sure—in my opinion there just isn’t enough research out there yet to support a book. Of course, as the saying goes, absence of evidence is not evidence of absence. Over the next few years you might see more research linking methyl mercury, hypertension and heart disease. There have been several studies finding a link in the last few years, including one in which increased methyl mercury exposure in Faroese whaling men 30 to 70 years of age was found to promote the development of high blood pressure and cardiovascular disease.316 In another study, accumulation of mercury in the body was found to be associated with an increased risk of heart attack.317 Much more recently answering studies finding no link have been published, but if you examine them closely, you can see that they have focused on subjects with relatively mild mercury exposure, and have made adjustments for “lifestyle risk factors” such as body mass.318 If, as was found in the Korean study, cardiovascular disease is “increased by mercury exposure via an obesityrelated mechanism”, then making adjustments for “lifestyle risk factors” would lead researchers to an erroneous conclusion. It is widely accepted that mercury exposure can cause high blood pressure, and there are a countless pediatric studies warning physicians to look to mercury exposure in the case of unexplained hypertension in children and adolescents.319 The current accepted thinking is that, for some unknown reason, this effect occurs only in children and adolescents. But then again, who’s checking?320 I believe that the study of mercury caused hypertension should begin with an investigation into the well-known phenomenon of white coat hypertension, a phenomenon in which patients display heightened blood pressure when checked by their doctor, but not at home in selfmeasurement. This heightened physical reactivity in the case of close scrutiny by a relative stranger calls to mind the many reports that the hatters shakes would intensify when they knew they were being observed, and Kussmaul’s statements that the mirror silverers found it very difficult to meet with their physicians, that they would grow pale and stammer in response to even the simplest questions. Intriguingly, recent studies have found that patients with white coat hypertension are more likely to enter eventually into a state of sustained high blood pressure.321

United Nations 2013, Minamata Convention

References [1] http://earthquake.usgs.gov/research/structure/crust/maps.php original upload english wikipedia 22 April 2005 by SEWilco. This image is in the public domain because it contains materials that originally came from the United States Geological Survey, an agency of the United States Department of Interior [2] Keyssler, J. Georg. (1757). Travels through Germany, Bohemia, Hungary, Switzerland, Italy, and Lorrain: giving a true and just description of the present state of those countries ... Illustrated with copper-plates, engraved from drawings taken on the spot. 2nd ed. London: Printed for A Linde and T. Field, p 375 [3] Ibid., p 376 [4] Needham, Joseph. Science in Traditional China. Cambridge, Massachusetts: Harvard University Press, 1981. Print. [5] Sima Qian, Shiji, Chapter 6; The Terracotta Army, Carelli F, Br J Gen Pract. 2008 Apr;58(549):289 [6] Needham, Joseph. Science in Traditional China. Cambridge, Massachusetts: Harvard University Press, 1981, pp 75-76 [7] Ibid., pp 82-83 [8] And so quicksilver, which had been named hydrargyros from the Greek words “hydr” and “argos” meaning “water” and “silver”, the source of the element’s identifier, Hg, came to be known more commonly as mercury. [9] Bacon, Roger, Part of the Opus Tertium of Roger Bacon: Including a Fragment Now Printed for the First Time. Aberdeen: University Press, 1912. [10] Bacon, Roger, Roger Bacon's Letter Concerning the Marvelous Power of Art And of Nature And Concerning the Nullity of Magic. Easton Pa, The Chemical Publishing Co., 1923. [11] Haq, Syed Nomanul (1995). Names, Natures and Things: The Alchemist Jabir Ibn Hayyan and His Kitab Al-Ahjar [12] Paracelsus : I., Scarlett EP, Can Med Assoc J., 1941 May;44(5):510-3; [13] In 1921 the Swedish physician Fahraeus suggested that the four humors might have been based upon the observation of blood which, when left standing will separate into 4 different layers colored black, red, whitish and yellow. [14] Paracelsus and Van Helmont, Mercier CA, Proc R Soc Med. 1916 9 (Sect Hist Med): pp. 1-8, p. 3 [15] Literally still in use today. In a case before the Mine Safety and Health Administration (MSHA) in 1995 a mine operator cited Paracelsus to assert that the MSHA had to prove that a hazardous level of mercury was present in order to find a violation in maintaining office and eating areas exposed to mercury on an ongoing basis. In 1997 the court ruled against the mine operator, upholding the MSHA’s position that mercury is a toxic material as a matter of law. Regulating mercury in miners' eating areas, Malecki MR, Public Health Rep 1998 Mar-Apr;113(2):179-81. [16] Sigerist, Henry E. Four Treatises of Theophrastus von Hohenheim called Paracelsusa. paperback edition 1996. Baltimore, Maryland: The John Hopkins University Press, 1941. Print. Seven Defensiones, pp.20-22

[17] Ibid p 35 [18] The Lure of Medical History, Paracelsus, Oliver J., Cal West Med. 1928 Jan;28(1):723 [19] Paracelsus and Van Helmont, Mercier CA, Proc R Soc Med. 1916;9(Sect Hist Med):18; Jacobi, Jolande. Paracelsus, Selected Writings, New York: Pantheon, 1951. pp. 79-80. Print. [20] All information on Leonardo Fioravanti is derived from the kindle edition of William Eamons excellent study, The professor of Secrets: Mystery, Medicine, and Alchemy in Renaissance Italy (2010). Direct quotations will be identified by location as they arise. [21]Eamon, William (2010) The Professor of Secrets: Mystery, Medicine, and Alchemy in Renaissance Italy, National Geographic, Washington DC, kindle ed, location 667. [22] Ibid., location 3043, 3054, 4412, 5319 [23] A physician who had taken the name Mercurialis commented on the increasing use of mercury in 1572. “Modern surgeons are likely to prefer diluted quicksilver to all other medicines,” he wrote. “While the Greek writers did not recommend it, nor did Galen know of its wonderful capabilities, yet the Arabs did, Avicenna in particular. There are some who fear the use of mercury, persuaded in their view by reasons that are not bad. It is hazardous, for the affected parts are close to the brain, and there is danger that such a poisonous medicine might reach the brain.” Sutton, Jr. M.D., Richard L, 1986, Sixteenth Century Physician and His Methods, Mercurialis on Diseases of the Skin, The First Book on the Subject (1572). Kansas City, Missouri: The Lowell Press. Print. p 80 [24] Eamon, William (2010) The Professor of Secrets: Mystery, Medicine, and Alchemy in Renaissance Italy, National Geographic, Washington DC, kindle ed, location 4242. [25] Ibid., location 4344 [26] Belloste, Augustin. The Hospital Surgeon Vol II. 2nd ed. London, Printed for John Clarke: Reproduction from Countway Library of Medicine, 1733. Print. [27] Ibid., p 8 [28] Ibid., p 54 (“The viper, which by sending its poison into the blood through a puncture of the skin, excites such fatal symptoms, is of no ill consequence if eaten.”) [29] Ibid., p 63 [30] Ibid., pp 70-71 [31] History of the Plague in London, Daniel Defoe, 1894, kindle ed. Location 593-98 [32] Dover, Thomas. The ancient physician's legacy to his country. 2nd ed. London, printed for the author: Reproduction from Countway Library of Medicine, 1732. Print. P. 74 [33] Keyssler, J. Georg. (1757). Travels through Germany, Bohemia, Hungary, Switzerland, Italy, and Lorrain: giving a true and just description of the present state of those countries ... Illustrated with copper-plates, engraved from drawings taken on the spot. 2nd ed. London: Printed for A linde ... and T. Field ....p 380 [34] Dover, p. 138; A remedy which would persist. See A. F. M. Willich, "The Domestic Encyclopaedia 1802, London, B. McMillan, Vol3"on Iliac passion (“Hence we are firmly persuaded, that, in similar cases, no other remedy can with advantage and safety be employed, than frequent doses of castor-oil; and, if this fail to procure relief, that quicksilver, in a native state, is the only medicine on which any reliance can be placed.”) [35] Dover, Thomas. The ancient physician's legacy to his country. 2nd ed. London, printed

for the author: Reproduction from Countway Library of Medicine, 1732. Print. pp. 140-142 [36] Ibid., p 149 [37] Turner, Daniel. The ancient physicians legacy impartially surve'yd; and his practice prov'd repugnant. . London, Printed for John Clarke: Reproduction from British Library, 1733. Print [38] Ibid., pp vii, 156-158 [39] Benjamin Franklin took Belloste’s pills in 1776 for an episode of gout he experienced while living in Paris, of which he wrote “I applied to a physician, who ordered me Mr. Bellosto's pills and an infusion of a root called - . I took the infusion a while, but it being disagreeable, and finding no effect, I omitted it. I continued to take the pills, but finding my teeth loosening, and that I had lost three, I desisted the use of them.” The Writings of Benjamin Franklin Pertaining to Medicine and The Medical Profession, Theodore Diller, Aesculapian. 1909 June; 1(3-4): 156–197. Losing teeth is a common symptom of mercury poisoning. [40] Augustin Belloste (1654-1730), de la chirurgie militaire à la thérapeutique mercurielle (2001) Clair P , Jean-Marie Le Minor JM, Revue d'histoire de la pharmacie, Vol 89 : 331 pp. 369-380 ; Medical Lexicon, a Dictionary of Medical Science, Robley th Dunglison MD, 8 ed. Philadelphia: Blanchard and Lea, 1851 [41] Weston, William. Acrodynia, Chapter XXXIV of ABT's Pediatrics Vol II. Philadelphia: W.B. Saunders Company, 1923. pp 986-993; Teale, T. Pridgin. (1830). A treatise on neuralgic diseases, dependent upon irritation of the spinal marrow and ganglia of the sympathetic nerve. Philadelphia: E. L. Carey and A. Hart ; Ozanam, J. Antoine François. (1835). Histoire médicale générale et particulière des maladies épidémiques: contagieuses et épizootiques : qui ont régné en Europe depuis les temps les plus reculés jusqu'a nos jours. 2e éd., rev., corr. et considérablement augm [42] Medical Lexicon, a Dictionary of Medical Science, Robley Dunglison MD, 8th ed. Philadelphia: Blanchard and Lea, 1851 [43] A Lecture on the Pathology and Treatment of Hysteria., Althaus J., Br Med J. 1866 Mar 10;1(271):245-8 [44] Think of the cataleptics of the Robin William’s movie Awakenings. The real life counterparts of the Awakenings cataleptics were survivors of an epidemic of an atypical form of encephalitis which swept through the world from 1915 to 1926. The cause is unknown, except that many sufferers had suffered from sore throats prior to be stricken. Wikipedia, Encephalitis Lethargica and Awakenings. It was at first considered to be hysterical in nature. Medical Lexicon, a Dictionary of Medical Science, Robley Dunglison MD, 8th ed. Philadelphia: Blanchard and Lea, 1851 [45] A Lecture on the Pathology and Treatment of Hysteria., Althaus J., Br Med J. 1866 Mar 10;1(271):245-8. [46] Hartmann, M.D., Franz. Buried Alive, An Examination Into The Occult Causes of Apparent Death, Trance and Catalepsy. . Boston: Occult Publishing Co., 1895. 13-14. Print. [47] Some account of an hysterical affection of the vocal apparatus, with several cases., Clayton O, Med Chir Trans. 1843;26:115-9 [48] Notes of a Fatal Case of Hysteria., Foss RW, Br Med J. 1872 Jul 6;2(601):9-1 [49] Chronic inorganic mercury induced peripheral neuropathy., Chu CC, Huang CC, Ryu SJ, Wu TN, Acta Neurol Scand. 1998 Dec;98(6):461-5.

[50] On Paralysis from the Effects of Mercury as a Medicine., Storrs R, Prov Med Surg J. 1847 Jul 28;11(15):398-401 [51] On the Effects of the Sub-Sulphate of Mercury, (Turpeth Mineral,) As An Emetic, Hubbard. Prov Med Surg J, 1846 Jun 24;10(25):288-9 “I have given it in much larger doses than are usually directed” [52] A Case of Chronic Inflammation of the Larynx, in which Laryngotomy and Mercury were successfully employed., Hall M., Med Chir Trans. 1819;10(Pt 1):166-75 ”the original disease was subsequently removed by the mercurial action”; Case of Cynanche Laryngea, in which Tracheotomy and Mercury were successfully employed, with Remarks, Porter WH, Med Chir Trans, 1821;11(Pt 2):414-39 “Many instances of the efficacy of mercury in the cure of chronic inflammation of the larynx, without resorting to any previous operation, have come within my own knowledge.”; Dr. Chambers on Mercury in Phthisis., Chambers R, Prov Med Surg J (1840). 1840 Nov 21;1(8):133-4 “a valuable auxiliary in a disease that has hitherto baffled human ingenuity”; On the Symptoms and Treatment of Incipient Phthisis, Durrant CM. Prov Med J Retrosp Med Sci. 1842 Sep 3;4(101):431-5, (“blue pill was prescribed in grain doses three times a day; this speedily excited mild salivation which was gently kept up for some days. Under this treatment the symptoms rapidly disappeared”; California Digital Newspaper Collection—Pacific Rural Press, Vol 4, No 22, 30 Nov 1872, The Way to Treat Consumption “An obstinate dry cough accompanied by emaciation, debility and fever, is very successfully treated by half an ounce of cod liver oil three times a day after meals, in a draught containing one fifteenth of a grain of bichloride of mercury.”) [53] On the Symptoms and Treatment of Incipient Phthisis., Durrant CM, Prov Med J Retrosp Med Sci. 1842 Sep 3;4(101):431-5 [54] Pathogenesis of mercurial salivation in chronic mercurial poisoning, KASAI T. Jpn J Pharmacol. 1955 Sep;5(1):17 [55] Case of Cynanche Laryngea, in which Tracheotomy and Mercury were successfully employed, with Remarks, Porter WH, Med Chir Trans, 1821;11(Pt 2):414-39 “the moment his mouth became sore, there seemed to be a decided amendment in his respiration”; A Specific for Ptyalism, Styrap J, Br Med J. 1876 Dec 2;2(831):711 [56] Pathology and Treatment of Croup., Bird J, Lond J Med. 1852 Jan;4(37):13-22, “[Oct 21st] his mother gave him some calomel with camphor... [Oct 24th] I was called in to see him.” [57] Haller, John S. Jr., American Medicine in Transition 1840-1910. Urbana, Chicago, London: University of Illinois Press, 1981. 268. Print. [58] Bartlett, Elisha, An Essay on the Philosophy of Medical Science, Philadelphia, 1844. [59] Practical Guide to the Study of the Diseases of the Eye, Williams 1886, pp. 262-263; Emily Dickinson's Ophthalmic Consultation With Henry Willard Williams, MD., Blanchard DL, Arch Ophthalmol. 2012 Dec 1;130(12):1591-5 [60] Case of Hysterical Blindness, Junius Hardwicke, Br Med J. 1876 May 6; 1(801): 562– 563. [61] Conversion Disorder, Diagnostic and Statistical Manual of Mental Disorders fourth edition (DSM-IV) [62] Diet-related mercury poisoning resulting in visual loss, Saldana M, Collins CE, Gale R, Backhouse O, Br J Ophthalmol. 2006 Nov;90(11):1432-4. [63] Experimental Glomerulonephritis, Bell ET, Clawson BJ, Hartzell TB, Am J Pathol. 1925 May;1(3):247-258.7.

[64] One of the first of many such experiments, Glomerulonephritis with - and 1C-globulin deposits induced in rats by mercuric chloride, Bariety J, Druet P, Laliberte F, Sapin C. Am J Pathol, 1971 Nov;65(2):293-302. [65] Remarks upon jumpers or jumping Frenchmen, Beard G, 1878, Journal of Nervous and Mental Diseases 5:526 [66] Observations on a Latah-like disorder in Maine by George M. Beard, M.D., published in the Journal of Nervous and Mental Disease in 1878-1880, [No authors listed], J Nerv Ment Dis. 1980 Apr;168(4):207-8. [67] An Exaggerated Startle Reflex Resembling a Kicking Horse, Rabinovitch R, Can Med Assoc J. 1965 Jul 17;93(3):130. [68] Swettenham, Frank. Vocabulary of the English and Malay Languages. 8th Ed. Vol II. Snanghai, Hongkong, Singapore & Yokohama: Kelly & Walsh, Limited, 1910. P 73; Clifford, Hugh. Studies in Brown Humanity Being Scrawls and Smudges in Sepia, White and Yellow. London: Grant Richards, 1898, Ch 12 Some Notes and Theories Concerning Latah pp 186-201; Swettenham, F. Athelstane. (1913). Malay sketches. [4th ed.] London: Lane, Ch IX Latah pp 64-82. [69] Winzeler, Robert L. Latah in Southeast Asia. Cambridge: University Press, 1995. 1112. [70] Clifford, Hugh. Studies in Brown Humanity Being Scrawls and Smudges in Sepia, White and Yellow. London: Grant Richards, 1898, p 196 [71] Ibid., p 198 [72] Amok is a Malaysian word meaning to engage in furious conflict, and to make an onslaught with the object of ruthless and indiscriminate slaughter. Clifford, Hugh, Swettenham, Frank. A Dictionary of the Malay Language. Part I. The Letter "A". Taiping, Perah: Printed for the Authors at the Government Printing Office, 1894. P. 47; Clifford, H. Charles. (1926). In a corner of Asia: being tales and impressions of men and things in the Malay Peninsula. New York: R. M. McBride pp 127 “Now, I am afflicted from my birth by the disease which we name lâtah—not the nervousness such as old women have that makes them to follow any example which may be set to them by a passing stranger, no matter how foolish or unseemly the act to which they are tempted, but lâtah of the lesser sort, which causeth me, when suddenly startled, to do violent deeds almost unknowingly, without taking thought for the consequences.”; Clifford, Hugh. (1913). Malayan monochromes. New York: E. P. Dutton and company, p 251 “He feared that the old fellow might be on the brink of one of those nervous outbreaks which, with his countrymen, are apt to culminate in amok-running.” [73] Excitable membranes--object for evaluating the effect of heavy metal pollution., SRózsa K, Salánki J, Acta Biol Hung. 1987;38(1):31-45 [74] Cutaneous and auditory function in rats following methyl mercury poisoning, Wu MF, Ison JR, Wecker JR, Lapham LW. Toxicol Appl Pharmacol, 1985 Jul;79(3):377-88. [75] Keane, A.H. Eastern Geography. A Geography of the Malay Peninsula, Indo-China, the Eastern Archipelago, The Phillippines, and New Guinea. Second Edition revised. London: Edward Stanford, 1892, pp 67, 130; Logan, J.R. The Journal of The Indian Archipelago and Eastern Asia. Vol III. Singapore 1849. P 283, 389, 399, 525. “The hot swamp...is said by the Malays to have a bottom of hot mud and water throughout. The water must rise from more than one place, and the quantity discharged is considerable, as, where it flows out beneath a bridge across the road, it formed a running stream three feet broad and three inches deep. Every day there is probably discharged about ten thousand cubic feet, and as it has a temperature of 110 ° the quantity of heat that it conducts from

the interior to the atmosphere must in the course of ages be great.”; Brooke, Margaret, My Life In Sarawak, London: Methuen, 1913, pp 287-289 [76] Migration of the Acadian Orogen and Foreland Basin Across the Northern Appalachians of Maine and Adjacent Areas, Bradley DC, Tucker RD, Lux DR, Harris AC, McGregor DC, 2000 USGS “A zone of active deformation migrated across Maine and adjacent parts of New England and Canada from early Ludlow through Givetian time. Initially, the orogen was a narrow belt, but it widened over time, eventually encompassing the entire state of Maine.” p49 [77] Background mercury concentrations in river water in Maine, U.S.A., Peckenham JM, Kahl JS, Mower B. Environ Monit Assess, 2003 Dec;89(2):129-52. [78] California Digital Newspaper Collection—Sacramento Daily Union, Vol 18 No 2776, 18 Fed 1860, The Late Quicksilver Discoveries; California Digital Newspaper Collection— Daily Alta California, Volume 3, Number 12, 13 January 1852 Valuable Discovery. “Native quicksilver has been discovered about a quarter of a mile from this city. It is oozing through the red clay, and already several pounds have been dipped up.”; California Digital Newspaper Collection—Sacramento Daily Union, Volume 18, Number 2761, 1 February 1860, Discoveries in Napa “The quicksilver is found in the open spaces of a lime rock through which the vein runs. When the rock is shaken the little globules of quicksilver fly out.”; California Digital Newspaper Collection—Sacramento Daily Union, Volume 46, Number 7137, 18 February 1874 Oregon Items “A person may take any piece of the ore and knock it against the table and hundreds of minute globules of the liquid silver will jar out of it.” [79] Mercury Contamination from Hydraulic Placer-Gold Mining in the Dutch Flat Mining District, California, Hunerlach MP, Rytuba JJ, Alpers CN, USGS Water-Resources Investigations Reopert 99-4018B, p182 citing Bowie, AJ 1905, A practical treatise of hydraulic mining in California, “minute globules of quicksilver reported floating in surface waters as much as 20 miles downstream of mining operations”. [80] Bruce, Miner (1895). Alaska: its history and resources, gold fields, routes and scenery. Seattle, Wash.: Lowman & Hanford stationery and printing co., pp 32-35 [81] California Digital Newspaper Collection - Daily Alta California, Vol 1, No 29, 28 Aug 1850, Amalgamation of Gold by Mercury [82] California Digital Newspaper Collection – San Francisco Call, Vol 83, No 100, 10 Mar 1898, Returning Miners Find Gold; California Digital Newspaper Collection – Los Angeles Herald, Vol 25, No 146, 23 Feb 1898, Weather in Alaska [83] “Laugh, you-all, laugh! That's what's the trouble with you-all. You-all think goldhunting is the only way to make a stake. But let me tell you-all that when the big strike sure does come, you-all'll do a little surface-scratchin' and muck-raking, but danged little youall'll have to show for it. You-all laugh at quicksilver in the riffles and think flour gold was manufactured by God Almighty for the express purpose of fooling suckers and chechaquos. Nothing but coarse gold for you-all, that's your way, not getting half of it out of the ground and losing into the tailings half of what you-all do get. London, J. (1910). Burning Daylight. New York,: Grosset & Dunlap, p 67 [84] The Book of Jack London, Charmian London, New York, The Century Co. 192, pp. 233-234, 242-243 [85] The Bradshaw Lecture on Infantile Scurvy and its Relation to Rickets, Thomas Barlow, Br Med J. 1894 November 10; 2(1767): 1029–1034. “we now knowthat fresh uncooked meat and fresh milk are antiscorbutic as well as, though perhaps not in so rapid a way, as fresh vegetables and fresh fruit juices

[86] The Book of Jack London, Charmian London, New York, The Century Co. 192, p. 254, quoting London’s journal entry of June 15, 1898. [87] “Money is no object in the purchase of these articles and it is not an uncommon occurrence to see men offer $3 a pound for quicksilver and as much for copper plate.” California Digital Newspaper Collection – Sacramento Daily Union, Vol 98, No 12, 2 Sept 1899, May Miners From Alaska [88] California Digital Newspaper Collection – San Francisco Call, Vol 86 No 125, 3 Oct 1899, Gold Found on Kotzebue Sound [89] California Digital Newspaper Collection – Los Angeles Herald, No. 330, 26 Aug 1899 – Kotzebue Victims [90] California Digital Newspaper Collection - San Francisco Call, Vol 87 No 148, 26 Oct 1900, Disease Among Indians [91] Bruce, p 49; Mount Churchill. (2013, March 15). In Wikipedia, The Free Encyclopedia. Retrieved 17:45, April 3, 2013 [92] Ice core mercury deposit graphic--Atmospheric mercury deposition during the last 270 years: a glacial ice core record of natural and anthropogenic sources, Schuster PF, Krabbenhoft DP, Naftz DL, Cecil LD, Olson ML, Dewild JF, Susong DD, Green JR, Abbott ML, Environ Sci Technol. 2002 Jun 1;36(11):2303-10. [93] The Lost Poacher The Youth's Companion - March 14, 1901. Mercury was so commonly used in medicine during London’s lifetime that it is not surprising that it found its way into his life-based fiction. The Plague Ship, published in 1897 contains 2 mentions of the use of calomel, and A Thousand Deaths, published in 1899, mentions the use mercurial compounds. [94] London, C. Kittredge. (1921). The book of Jack London. New York: The Century co.. pp. 263, 335 [95] Ibid., p 259 [96] London, J. (1913). The Cruise of the Snark. New York: The MacMillan Co, pp 308309 [97] Ibid., p 263 [98] Ibid., pp 314; In 1888 a “fearful experiment” demonstrated that “[w]ashed with soap and with carbolic acid, with any and all of the disinfectants in common use, our hands will still remain scientifically unclean.” It was only with bicholoride of mercury or corrosive sublimate that perfect cleanliness could be attained. California Digital Newspaper Collection—Clean Hands, Daily Alta California, Vol 42, No 14340, 9 Dec 1888 [99] London, J. (1913). The Cruise of the Snark. New York: The MacMillan Co, pp 262263, 275, 282 [100] Ibid., pp 315-317 [101] Ibid., pp 320-322 [102] Ibid., p 324; The standard of care in the treatment of yaws during the time period of London’s visit to the Protectorates was a mercurial ointment applied twice a day. Remarks on the Bacteriology and Treatment of Yaws (Framboesia Tropica), Robertson A, The British Medical Journal 5 Oct 1907, pp 568-569 [103] Pneumonia and other lung disorders are commonly seen in cases of mercury exposure, Pneumonitis after inhalation of mercury vapours, Glezos JD, Albrecht JE, Gair RD, Can Respir J. 2006 Apr;13(3):150-2; The chronic toxicity of inorganic mercury in

goats: clinical signs, toxicopathological changes and residual concentrations, Pathak SK, Bhowmik MK. Vet Res Commun. 1998 Feb;22(2):131-8. [104] London, J. (1913). The Cruise of the Snark. New York: The MacMillan Co, pp 328333 [105] Ibid., p 333 [106] Ibid., p 335, 339 [107] If Jack London drank corrosive sublimate, as he hinted that he had with his comment of fighting yaws from the inside out, it would explain not only the anal fistula, but also London’s later attack of appendicitis, as both fistula and appendicitis have been observed secondary to mercury taken internally. Intraperitoneal mercury granuloma, Crickelair GF, Hiratzka T, Ann Surg, 1953 Feb;137(2):272-5. [108] London, J. (1913). The Cruise of the Snark. New York: The MacMillan Co, p 338 [109] California Digital Newspaper Collection—San Francisco Call, Vol 106 No 7, 7 June 1909, Jack London a Nervous Wreck [110] Pearson, J. (1807). Observations on the effects of various articles of the materia medica, in the cure of lues venerea, illustrated with cases. Second edition, with additions. London: printed for J. Callow ... by J. and W Smith. [111] Ibid., pp. 40-41, 168, [112] The Treatment of Swift's Disease (Erythrœdema), Sweet GB. Arch Dis Child. 1930 Dec;5(30):405-10. Although Swift is routinely given priority in identification of acrodynia, German physician Selter gave an account of 8 cases observed in 1903 which he called trophodermatosis. Selter P (1903) Verhandl Ges Kinderheilk, Cassel, 20, 45; Acrodynia (?) A Report of Three Cases in Rural Practice, A. F. McKenzie, Can Med Assoc J. 1923 January; 13(1): 43–47; Acrodynia, A. J. Scott, Jr, Cal West Med. 1926 July; 25(1): 47–50 [113] The term acrodynia had been used before to describe an epidemic affliction appearing in France in the years 1828-1829, “a painful affection of the wrists and ankles especially with an erythematous eruption” attended with disorders of the nervous system. Acrodynia (?) A Report of Three Cases in Rural Practice, A. F. McKenzie, Can Med Assoc J. 1923 January; 13(1), p. 43, citing Dunglinson’s Medical Dictionary published in the mid to late 1800’s. [114] A review of infantile acrodynia ('pink disease'), LEYS D. Arch Dis Child. 1950 Sep;25(123):302-10. [115] Acrodynia (?) A Report of Three Cases in Rural Practice, A. F. McKenzie, Can Med Assoc J. 1923 January; 13(1): 43–47, “peculiar frowning expression”; A review of infantile acrodynia ('pink disease'), LEYS D. Arch Dis Child. 1950 Sep;25(123):302-10, p 307, citing the work of Spitz and Wolf--Anaclitic depression; an inquiry into the genesis of psychiatric conditions in early childhood., SPITZ RA, Psychoanal Study Child. 1946;2:31342. [116] Pink Disease, Allen FM, Ulster Med J, 1945 May;14(1):34-6, “a general mortality of about twenty per cent.”; The Treatment of Swift's Disease (Erythrœdema), Sweet GB. Arch Dis Child. 1930 Dec;5(30):405-10; p 405 “a death rate of 24.5 per cent”; A review of infantile acrodynia ('pink disease'), LEYS D. Arch Dis Child. 1950 Sep;25(123):302-10, death rates of up to 30% have been reported.” [117]Pink Disease: its Morbid Anatomy, with a Note on Treatment, Wyllie WG, Stern RO, Arch Dis Child, 1931 Jun;6(33):137-56, p149” [118] The composition of certain secret remedies—XV.—Soothing Powders for Infants, Br

Med J. 1908 October 3; 2(2492): 1022; San Francisco Call, Volume 77, Number 132, 21 April 1895 — Page 11 Advertisements Column 1 [119] The puzzle of pink disease, J Black J R Soc Med. 1999 September; 92(9): 478–481; A review of infantile acrodynia ('pink disease'), LEYS D. Arch Dis Child. 1950 Sep;25(123):302-10, p 306 “The source of mercury was thought to be teething powder, but mercury ointment and corrosive sublimate had been used locally in other cases.” [120] Acrodynia and Excessive Intake of Mercury, J. G. Dathan Br Med J. 1954 January 30; 1(4856): 247–249; The puzzle of pink disease, J Black J R Soc Med. 1999 September; 92(9): 478–481. [121] London, The Cruise of the Snark p. 339 [122] The Effects of Tropical Light on White Men, Charles Edward Woodruff, New York Rebman Co 1905, pp192-203 [123] Disease and medicine in the armies of British India, 1750-1830: the treatment of fevers and the emergence of tropical therapeutics, Harrison M. Clio Med. 2007;81:87-119, “the favored treatment was purgation via mercury.”; On the Mercurial Treatment of Dysentery, with observation on the same practice in Fevers William Ferguson Med Chir Trans. 1811; 2: 181–200; Cases of Hepatitis, Dysentery, and Diarrhœa, W. T. Black, Prov Med Surg J. 1852 December 8; 16(25): 635–639; An Efficient Intestinal Antiseptic, The Perchlorides of Mercury and Iron in Combination, T. Stacey Wilson Br Med J. 1924 February 16; 1(3294): 270–271. [124] The Effects of Tropical Light on White Men, Charles Edward Woodruff, New York Rebman Co 1905, p 193. [125] London, J. (1914). John Barleycorn, or, Alcoholic memoirs. London: Mills & Boon. pp 258-260; Strangely, Colonel Woodruff had also noted the salutatory effect of alcohol, having run a statistical analysis which showed that men who drank more alcohol were more likely to survive their sojourn in the tropics. Woodruff found that 11% of abstainers died in the tropics, but only 2% of excessive drinkers did. The Effects of Tropical Light on White Men, Charles Edward Woodruff, New York Rebman Co 1905, p 193 [126] London, J. (1914). John Barleycorn, or, Alcoholic memoirs. London: Mills & Boon. pp 266-275 [127] California Digital Newspaper Collection—Wheatley’s Shires, Pacific Rural Press Vol 85 No 10, 8 Mar 193 [128] California Digital Newspaper Collection—Pacific Rural Press, Vol 34, No 14, 1 Oct 1887, Equine Cerebro-Spinal Meningitis [129] A Pathology for Forage Poisoning, or the So-Called Epizootic Cerebro-Spinal Meningitis of Horses (A preliminary report), McCarthy DJ, Ravenel MP, J Med Res. 1903 Oct;10(2):243-9. [130] Ibid., p 243. It’s worth noting here that the spoiled grain theory had also been proposed by German and French writers as a possible cause of acrodynia. Weston, William. Acrodynia, Chapter XXXIV of ABT's Pediatrics Vol II. Philadelphia: W.B. Saunders Company, 1923. P 990 [131] The Book of Jack London, A Biography, by Charmian London, New York The Century Co 1921, p277; California Digital Newspaper Collection—Jack London’s Ideal Hog Yard, Pacific Rural Press, Vol 94, No 20, 17 Nov 1917 [132] California Digital Newspaper Collection—Sheep Questions, Pacific Rural Press, Vol 92, No 14, 30 September 1916

[133] London, J. (1910). Burning Daylight. New York,: Grosset & Dunlap, p 132 [134] The Book of Jack London, A Biography, by Charmian London, New York The Century Co 1921, p213 [135] London, J. (1916). The turtles of Tasman. New York: Macmillan, p 245 [136] California Digital Newspaper Collection—Agricultural Intelligence, Miscellaneous, Sacramento Daily Union, Vol 44, No 6747, 16 Nov 1872 [137] California Digital Newspaper Collection— Agricultural Intelligence, Lousy Horses, Sacramento Daily Union, Vol 44 No 6866, 5 Apr 1873 [138] California Digital Newspaper Collection—Prevent Spread of Hog Cholera, Pacific Rural Press, Vol 65 No 15, 11 Apr 1903 [139] California Digital Newspaper Collection—The Disinfection of Stables, Pacific Rural Press, Vol 71, No 21, 26 May 1906 [140] California Digital Newspaper Collection – Late Atlantic Intelligence, Sacramento Daily Union, Volume 29, Number 4497, 21 August 186; Abraham Lincoln's blue pills. Did our 16th president suffer from mercury poisoning? Hirschhorn N, Feldman RG, Greaves IA. Perspect Biol Med. 2001 Summer;44(3):315-32. [141] Eden’s Outcasts, the story of Louisa May Alcott and her father, John Matteson, 2007, WW Norton & Company, Inc. New York, paperback ed, pp 281-290 [142] Howard Hughes: The Untold Story, Peter Harry Brown, Pat H. Broeske, 1996 Dutton Adult, Ch 1 [143] London, J. (1914). John Barleycorn, or, Alcoholic memoirs. London: Mills & Boon. p 277John Barleycorn, Jack London 1913, Ch 36 [144] London, J. (1914). John Barleycorn, or, Alcoholic memoirs. London: Mills & Boon, p. 269 [145] London, C. Kittredge. (1921). The book of Jack London. New York: The Century co.. “There were moments, during the preparation for the copyright fight, when Jack became so enraged that I was alarmed about him. But one morning, after an untoward outbreak of "catastrophic red wrath" the preceding night, he came to me with a face of humility.” p 254 “Jack's health was fairly good that summer, though he seemed to be on tension, and prone to argue overlong and over-intensely. Indeed, as time went on, he battled with p314 this and that opponent, or provoked skirmishes, with an increasing fervor and violence that illbetokened a peaceful old age. Oh, well, I'd rather wear out than rust out!" was his verdict on the matter.” pp. 313-314 “Again, over-intense, on hair-trigger to snap up any word as a pretext to start an argument, if he caught me trying to placate or turn him into smoother channels he flew into a mental fury, at times hot, at others deadly cool.” p371 [146] California Digital Newspaper Collection—Pacific Rural Press, Vol 34, No 14, 1 Oct 1887, Equine Cerebro-Spinal Meningitis [147] A review of infantile acrodynia ('pink disease'), Leys D, Arch Dis Child. 1950 Sep;25(123): p 303 [148] The Book of Jack London, A Biography, by Charmian London, New York The Century Co 1921, p 371-372 [149] Ibid, p 372, “One day his master charged: "If anything should happen to me, and Prince's case become hopeless, don't ever let him go off the ranch." So the "Love-Horse" came to sleep with Neuadd, Sonoma Maid and Hilda, in a wooded ravine on the "Beauty Ranch."; Analysis of mercury levels in historical bone material from syphilitic subjects--

pilot studies (short report), Kepa M, Kozłowski T, Szostek K, Drozd A, Walas S, Mrowiec H, Stepańczak B, Głab H, Grupa M, Anthropol Anz. 2012 Jul;69(3):367-77. [150] The Book of Jack London, A Biography, by Charmian London, New York The Century Co 1921, p 382 [151] Five hundred years of mercury exposure and adaptation, Lombardi G, Lanzirotti A, Qualls C, Socola F, Ali AM, Appenzeller O. J Biomed Biotechnol. 2012. [152] Idrija mercury mine, 1689 engraving by Johann Weikhard von Valvasor. (This image is in the public domain because its copyright has expired.) [153] Personality Traits in Miners with Past Occupational Elemental Mercury Exposure, Grum DK, Kobal AB, Arnerič N, Horvat M, Ženko B, Džeroski S, Osredkar J, Environ Health Perspect. 2006 February; 114(2): 290–296, citing Scopoli JA. 1771. De Hydrorgyro Idriensi Tentamina Physico-Chymico-Medica. 2nd ed. Janae et Lipsiae, DEU:Joann. Guil. Hartung. [154] Buck., Albert H. Cyclopaedia of the Practice of Medicine Vol. XIV Diseases of the Nervous System. New York: William Wood and Company, 1877. 612. Print. [155] Kussmaul, Adolph, Untersuchungen uber den Consitutionellen Mercurialismus. Wurzberg: Druck und Verlag der Stahel’schen Buch- und Kunsthandlung, 1861. Print. [156] Hamilton, Alice, Industrial Poisons in the United States. New York: The Macmillan Company, 1925, pp. 254-255 [157] January–June 1829 issue of Blackwood's Edinburgh Magazine, headed Noctes Ambrocianæ. No. XL1V (three fictional characters in conversation refer to a man as “raving”, “dementit” and “mad as a hatter.”); The Clockmaker, 1835, Thomas Chandler Haliburton "And with that he turned right round, and sat down to his map and never said another word, lookin' as mad as a hatter the whole blessed time" and "Father he larfed out like any thing; I thought he would never stop - and sister Sall got right up and walked out of the room, as mad as a hatter." [158] Bates, Josephine W. Mercury Poisoning In the Industries of New York City And Vicinity. [New York]: National civic federation, New York and New Jersey section, 1912. [159] Ibid, p. 80. [160] Ibid., p 6 [161] Ibid., p 7 [162] Ibid., p 17 [163] Ibid., pp. 23, 34, 99, 112, 118, 119, 126 [164] Ibid., pp 19, 22, 91, 109, 117, 121, 126 [165] Ibid., p. 8 [166] Ibid., p 33 [167] Ibid., pp 34, 113 [168] Ibid., p 34. Unfortunately, the medical establishment did not follow up on this line of reasoning, a fact apparent in Hamilton’s later assertions restating the status quo belief that alcohol was a significant causative factor. “It is the universal testimony of hatters and of mercury miners that alcoholism greatly favors the development of mercurial tremor. Indeed, some say that no total abstainer ever has a very severe case of the shakes.” Hamilton, Alice, Industrial Poisons in the United States. New York: The Macmillan Company, 1925, p 241

[169] Seager, Henry R. American Labor Legislation Review, Industrial Diseases, Proceedings of the Second National Conference on Industrial Diseases. Vol. II No 2. New York: American Association for Labor Legislation, 1912. [170] Diseases of Occupation and Vocational Hygiene, Ch VII Mercury Poisoning, Teleky L (1916) P. Blackiston’s Son & Co., Philadelphia Kindle edition [171] Ibid., location 3561-3578 [172] Ibid., location 3564 [173] Ibid., location 3568 [174] Probably from the work of Rene Martial, the author of Travail et folie; influences professionnelles sur l'étiologie psychopathiqu (Paris, Bloud, 1909) and other writings on the effects of industry on the mental condition of French workers including Le nitrate acide de mercure dans l’operation de secretage, Revue. d’Hygiene 1911 33, 234, and Sur l’emploi du nitrate acide de mercure dans l’industrie de la couperie de poils, Rev. d’hyg 1911, 463 [175] Hamilton, Alice, Industrial Poisons in the United States. New York: The Macmillan Company, 1925, pp 242-243 [176] Diseases of Occupation and Vocational Hygiene, Ch VII Mercury Poisoning, Teleky L (1916) P. Blackiston’s Son & Co., Philadelphia Kindle edition, location 3593 [177] Hamilton, Alice, Industrial Poisons in the United States. New York: The Macmillan Company, 1925, p 239 [178] Flu Shot Disabled Beautiful Cheerleader (Dystonia Disorder) http://youtu.be/oGT0rudstQ [179]Diseases of Occupation and Vocational Hygiene, Ch VII Mercury Poisoning, Teleky L (1916) P. Blackiston’s Son & Co., Philadelphia Kindle edition, location 3724 (“Oberlander found mercury in the urine 190 days after giving the substance in a mercury cure. The elimination in this 190 days’ period, however, was not continuous for there were often spaces of time, 10 days, in which no mercury would be noted in the urine.”) [180] Was Paganini poisoned with mercury? O'Shea JG. J R Soc Med. 1988 Oct;81(10):594-7, citing Benati. [181] Isaac Newton: mercury poisoning or manic depression?, Lieb J, Hershman D, Lancet. 1983 Dec 24-31;2(8365-66):1479-80; Sir Isaac Newton: mad as a hatter., Broad WJ, Science. 1981 Sep 18;213(4514):1341-2, 1344; Sir Isaac Newton and his madness of 169293., Keynes M, Lancet. 1980 Mar 8;1(8167):529-30; Mercury poisoning: a probable cause of Isaac Newton's physical and mental ills., Johnson LW, Wolbarsht ML, Notes Rec R Soc Lond. 1979 Jul;34(1):1-9; [Pascal's disease in 1647] [Article in French], Hist Sci Med. Le Guern M, 2010 Jan-Mar;44(1):11-5. (“Blaise Pascal's serious physiological disorders could be the consequence of a long exposition to mercury fumes as he was studying the first device of vacuum. Weakness headache, paralysis of the lower limbs were described by his sisters. Probably such were the causes of his bad health and of the disorders which hit him until his death”.) [182] Pearson, J. (1807). Observations on the effects of various articles of the materia medica, in the cure of lues venerea, illustrated with cases. Second edition, with additions. London: printed for J. Callow ... by J. and W Smith; [183] Globus is an uncomfortable sensation of a mass in the esophagus or airway making swallowing difficult. It is still considered a hysterical conversion disorder. Globus hystericus: a brief review, Finkenbine R, Miele VJ. Gen Hosp Psychiatry. 2004 JanFeb;26(1):78-82.

[184] Notes of a case of Mercurial Erethism, Bateman T, Med Chir Trans. 1818;9(Pt 1):220-33. [185] Ibid p 233 [186] Short Notes of the Opinions and Practice of the Late John Pearson, Esq., F.R.S., on Syphilitic Disease, Oke WS, Prov Med Surg J. (1848) May 17;12(10):257-60, fn p258 “Erethismus Mercurialis, “a morbid state of the system, named and described first by Mr. Pearson in his ‘Principles of Surgery.’ Chap.I.” [187] Unusual Symptoms Following the Use of Unguentum Hydrargyri Ammoniati, Green WE, Br Med J, 1884 May 3;1(1218):853-4 [188] Diseases of Occupation and Vocational Hygiene, Ch VII Mercury Poisoning, Teleky L (1916) P. Blackiston’s Son & Co., Philadelphia Kindle edition, location Teleky location 3659 [189] Ibid., location 3668 [190] Hamilton, Alice, Industrial Poisons in the United States. New York: The Macmillan Company, 1925 p 235 [191] Diseases of Occupation and Vocational Hygiene, Ch VII Mercury Poisoning, Teleky L (1916) P. Blackiston’s Son & Co., Philadelphia Kindle edition, location 3736 [192] Chronic occupational metallic mercurialism, Faria Mde A. Rev Saude Publica. 2003 Feb;37(1):116-27, abstract [193] Perils of mercury, Sunderman FW. Ann Clin Lab Sci. 1988 Mar-Apr;18(2):89-101 [194] Mercury Poisoning from an Unsuspected Source, M. Tamir, B. Bornstein, M. Behar, and M. Chwat, Br J Ind Med. 1964 October; 21(4): 299–303. [195] Psychiatric manifestations of mercury poisoning, Fagala GE, Wigg CL. J Am Acad Child Adolesc Psychiatry. 1992 Mar;31(2):306-11, abstract [196] Mercury chronic toxicity might be associated to some cases of hydrocephalus in adult humans? Silva Sieger FA, Díaz Silva GA, Ardila GP, García RG. Med Hypotheses. 2012 Jul;79(1):13-6, abstract. [197] Cutaneous mercury granuloma: a case report, Altmeyer MD, Burgdorf MR, Newsome RE, Wang AR. Cutis. 2011 Oct;88(4):189-93, abstract. [198] Long-term exposure to methylmercury and psychiatric symptoms in residents of Minamata, Japan, Yorifuji T, Tsuda T, Inoue S, Takao S, Harada M. Environ Int. 2011 Jul;37(5):907-13, abstract [199] Gestational exposure to methylmercury and n-3 fatty acids: effects on high- and lowrate operant behavior in adulthood, Paletz EM, Craig-Schmidt MC, Newland MC. Neurotoxicol Teratol. 2006 Jan-Feb;28(1):59-73, abstract [200] Assessment of chronic neuropsychological effects of mercury vapour poisoning in chloral-alkali plant workers, Pranjić N, Sinanović O, Karamehić J, Jakubović R, Bosn J Basic Med Sci. 2002 Dec;2(1-2):29-34, abstract [201] Chronic neurobehavioural effects of mercury poisoning on a group of Zulu chemical workers, Powell TJ. Brain Inj. 2000 Sep;14(9):797-814, abstract [202] Effects of occupational exposure to mercury in workers at a light bulb factory in Santo Amaro, São Paulo, Brazil], Zavariz C, Glina DM. Cad Saude Publica. 1993 AprJun;9(2):117-29, abstract [203] Specificity of psychiatric manifestations in relation to neurotoxic chemicals, Ross

WD, Sholiton MC. Acta Psychiatr Scand Suppl. 1983;303:100-4 In contrast to nonexposed controls, abstract [204] Psychiatric aspects of methylmercury poisoning, Maghazaji HI. ,J Neurol Neurosurg Psychiatry. 1974 Aug;37(8):954-8, abstract [205] Health effects associated with long-term occupational exposure of employees of a chlor-alkali plant to mercury,Neghab M, Norouzi MA, Choobineh A, Kardaniyan MR, Zadeh JH, Int J Occup Saf Ergon. 2012;18(1):97-106, abstract [206] Occupational and environmental toxicology of mercury and its compounds, Satoh H. Ind Health. 2000 Apr;38(2):153-64, abstract [207] Personality traits in miners with past occupational elemental mercury exposure, Kobal Grum D, Kobal AB, Arneric N, Horvat M, Zenko B, Dzeroski S, Osredkar J. Environ Health Perspect. 2006 Feb;114(2):290-6, abstract [208] Chronic psychological effects of exposure to mercury vapour among chlorine-alkali plant workers, Pranjić N, Sinanović O, Jakubović R. Med Lav, 2003 Nov-Dec;94(6):53141, abstract [209] Chronic elemental mercury intoxication: neuropsychological follow-up case study, Hua MS, Huang CC, Yang YJ. Brain Inj. 1996, May;10(5):377-84, abstract [210] Chronic low-level mercury exposure and neuropsychological functioning, Uzzell BP, Oler J, J Clin Exp Neuropsychol. 1986 Oct;8(5):581-93, abstract [211] Mercury-induced toxicity of rat cortical neurons is mediated through N-methyl-DAspartate receptors, Xu F, Farkas S, Kortbeek S, Zhang FX, Chen L, Zamponi GW, Syed NI, Mol Brain. 2012 Sep 14;5:30. doi: 10.1186/1756-6606-5-30, abstract. [212] http://www.epa.gov/ttn/atw/hlthef/mercury.html, Technology Transfer Network Air Toxics Web Site, Mercury CompoundsHazard Summary-Created in April 1992; Revised in January 2000; http://www.who.int/foodsafety/publications/chem/mercuryexposure.pdf World Health Organization, Guideance for identifying populations at risk from mercury exposure, August 2008 (Symptoms of mercury exposure include “emotional lability (often referred to as “erethism” and characterized by irritability, excitation, excessive shyness, confidence loss, and nervousness)”) [213] In 1966 it was discovered that farmers in Brazil had been spraying a mercury compound licensed only for use as a fungicide for seed dressing directly onto tomato and other vegetable crops. Misuse of organomercury fungicides in Brazil., Almeida WF, Pregnolatto W, Pigati P, Bull World Health Organ. 1976;53 Suppl:133-8. [214] Rice is a significant source of methylmercury: research in china assesses exposures, Barrett JR. Environ Health Perspect. 2010 Sep;118(9):a398; Human exposure to methylmercury through rice intake in mercury mining areas, Guizhou province, China, Feng X, Li P, Qiu G, Wang S, Li G, Shang L, Meng B, Jiang H, Bai W, Li Z, Fu X. Environ Sci Technol. 2008 Jan 1;42(1):326-32 [215] California Digital Newspaper Collection – Visalia Weekly Delta, Volume 1, No 18, 22 Oct 1859– Pacific Rural Press, Vol 28, No 13, 27 Sept 1884, A New Remedy for Phylloxera [216] California Digital Newspaper Collection – San Francisco Call, Volume 81, Number 173, 22 May 1897 [217] The mercury-cell process for producing chlorine and lye was developed in 1892. O’Brien, TF, Bommaraju TV, Hine F, Handbook of Chlor-Alkali Technology, Springer Science + Business Media, Inc. New York, 2005

[218] Smith WE, Smith AM, Minamata, Holt, Rinehart and Winston, New York 1975 p 178 [219] Organicmercurials were first used as an antifungal seed treatment in 1913, with use becoming worldwide by the 1930s. 552 F.2d 370 First National Bank in Albuquerque v. United States of America [220] Organomercury poisoning in Iraq: history prior to the 1971-72 outbreak, Al-Damluji SF. Bull World Health Organ. 1976;53 Suppl:11-3. [221] Tragically, the poisoning would recur on a much greater scale, years later, when the seed grain arrived too late for planting and the Iraqi villagers washed off the pink dye, assuming that doing so would remove the poison. Thousands were hospitalized and hundreds, mostly children, died. Poisoning with alkylmercury compounds, Br Med J. 1978 March 11; 1(6113): 599–60; Clinical and epidemiological aspects of methylmercury poisoning.Bakir F, Rustam H, Tikriti S, Al-Damluji SF, Shihristani H. Postgrad Med J. 1980 Jan;56(651):1-10. [222] Smith WE, Smith AM, Minamata, Holt, Rinehart and Winston, New York 1975 pp 26-28 [223] Ibid., p 182 [224] Shinobu would suffer lifelong disability. She learned why in third grade, “I remember I thought, ‘Why do we special class kids have to sit in the back of the bus? After all, we are the same human beings.’ That is the trip when I found out how I got sick. I overheard my teachers talking. One of them said about me, ‘Oh, she’s a congenital patient, one of the children who were born sick because their mothers ate the poisoned fish.’ I got a big shock. I got my answer. I knew for the first time.” Smith WE, Smith AM, Minamata, Holt, Rinehart and Winston, New York 1975 p 155 [225]Smith WE, Smith AM, Minamata, Holt, Rinehart and Winston, New York 1975 p 78 [226] Ibid., p 80 [227] Ibid., pp 28-33. [228] Reappraisal of the historic 1959 cat experiment in Minamata by the Chisso Factory, Eto K, Yasutake A, Nakano A, Akagi H, Tokunaga H, Kojima T. Tohoku J Exp Med. 2001 Aug;194(4):197-203. [229] Methyl mercury poisoning in Canada, Shephard DA, Can Med Assoc J. 1976 Mar 6;114(5):463-72; An excellent documentary on the tragedy Grassy Narrows mercury poisoning can be viewed at www.intercontinentalcry.org/the-scars-of-mercury. [230] Smith WE, Smith AM, Minamata, Holt, Rinehart and Winston, New York 1975 p 142 [231] Jensen S, Jernolöv A, 1967, Biocidinformation, Nordforsk, Stockholm; Biological methylation of mercury in aquatic organisms, Jensen S, Jernelöv A. Nature. 1969 Aug 16;223(5207):753-4. [232] Mercury in food, Tolan A, Elton GA. Biochem J. 1972 Nov;130(2):69-70 [233] Dr. Berglund of the Swedish National Institute of Public Health stated, “I feel personally that the problem exists [in the United States] as it does in other parts of the world, but it is not recognized.” Environmental negligence: the mercury problem., Joselow MM, Am J Public Health. 1971 Sep;61(9):1745-7 [234] First Tuesday: The Perfect Pesticide ... For Man (Mercury Poisoning) 10/6/70 NBC News Clip 5112448188_s02 [235] Mercury residues in chicken eggs and tissues from a flock exposed to methylmercury dicyandiamide.

J Howell Can Vet J. 1969 August; 10(8): 212–213. [236] Methylmercury poisoning, Clinical follow-up and sensory nerve conduction studies, Snyder RD, Seelinger DF. J Neurol Neurosurg Psychiatry, 1976 Jul;39(7):701-4. [237] A nearly identical case occurred in Romania in 1974 when a mother and her three children ate the meat of a hog which had been feed with mercury treated seed grain. The mother and a daughter survived the ordeal with lingering constriction of the visual field, but the two sons, aged 10 and 15 died. Accidental ethyl mercury poisoning with nervous system, skeletal muscle, and myocardium injury, Cinca, Dumitrescu, Onaca, Serbänescu, Nestorescu, J Neurol Neurosurg Psychiatry. 1980 February; 43(2): 143–149. [238]United States Court of Appeals, Tenth Circuit. - 552 F.2d 370, First National Bank in Albuquerque, As Guardian for and On behalf of Dorothy Jean Huckleby, et al.,plaintiffsappellants, v. United States of America, Defendant-appellee [239] Berton Roueche, Annals of Medicine, “Insufficient Evidence.,” The New Yorker, August 22, 1970, p. 64; That use was still ongoing at least 10 years later as evidenced by the experience of a Yakima, Washington family whose home flock of chickens was contaminated through feeding of seed grain treated with a mercurial fungicide. Organic mercury exposure from fungicide-contaminated eggs, Englender SJ, Atwood RG, Landrigan PJ, Clarkson TW, Greenwood MR, Smith JC, Arch Environ Health. 1980 JulAug;35(4):224-8. [240] David Brinkley reported the Huckleby’s story on the NBC Evening News on Tuesday, February 17, 1970. A more general story appeared on First Tuesday, October 6, 1970, in which the panelists discussed “the perfect pesticide.” [241] www.glsc.usgs.gov [242] Methylmercury Poisoning—An Assessment of the Sportfish Hazard in California, Dales L, Kahn E, Wei E, Calif Med. 1971 March; 114(3): 13–15 [243] Investigation of a Pacific pilot whale stranding on San Clemente Island, Hall JD, Gilmartin WG, Mattsson JL. J Wildl Dis. 1971 Oct;7(4):324-7. [244]Dietary recommendations regarding pilot whale meat and blubber in the Faroe Islands, Weihe P, Joensen HD. Int J Circumpolar Health. 2012 Jul 10;71:18594, “From the latest research results, the authors consider that the conclusion from a human health perspective must be to recommend that pilot whale is no longer used for human consumption.” [245] Poisoning with alkylmercury compounds, Br Med J. 1978 March 11; 1(6113): 599– 60; Clinical and epidemiological aspects of methylmercury poisoning.Bakir F, Rustam H, Tikriti S, Al-Damluji SF, Shihristani H. Postgrad Med J. 1980 Jan;56(651):1-10. [246] In a personal remark to the author of Tempest in a teapot, Eyl TB. Am J Clin Nutr. 1971 Oct;24(10):1199-203. [247]Fredrick John Stare (1910–2002), Hegsted DM, J. Nutr. May 1, 2004 vol. 134 no. 5 1007-1009 [248] The New York Times, Mercury in Tuna, Nick Fox, Jan. 21, 2008 [249] In 1970, a Welch physician reported that he had seen a number of adult patients with pink disease, characterized by polyneuropathy and facial redness, a diffuse erythema due to capillary dilation noticeable in those parts of the skin exposed to light. "Adult pink disease", Harrop-Griffiths H. Br Med J. 1970 May 2;2(5704):298. [250] Agency for Toxic Substances and Disease Registry (1999) Toxicological profile for mercury (update) Atlanta, GA: Department of Health and Human Services, pp 235-262,

410-476 [251] Too much of a good thing (fish): methylmercury case study, Risher JF, J Environ Health. 2004 Jul-Aug;67(1):9-14. [252] 1 microg/L divided by 1,000 = 1 ppm. Using a conversion factor addressing that concentration of mercury in hair is 300 times the concentration of mercury in blood the first test revealed concentrations of 67.8ppm or 226microg/L (67.8 divided by 300, multiplied by 1,000) and the second test revealed a concentration of 125microg/L or 37.5ppm (125 divided by 1,000, multiplied by 300). Interrelationships of blood and hair mercury concentrations in a North American population exposed to methylmercury, Phelps RW, Clarkson TW, Kershaw TG, Wheatley B. Arch Environ Health. 1980 May-Jun;35(3):161168. (“Mercury levels in newly formed hair were found to reflect those in blood with the concentration in hair being approximately 300 times that in blood.”) [253] Too much of a good thing (fish): methylmercury case study, Risher JF, J Environ Health. 2004 Jul-Aug;67(1):9-14 [254] Blood organic mercury and dietary mercury intake: National Health and Nutrition Examination Survey, 1999 and 2000, Mahaffey KR, Clickner RP, Bodurow CC, Environ Health Perspect. 2004 Apr;112(5):562-70 [255] Methylmercury: a new look at the risks.Mahaffey KR, Public Health Rep. 1999 SepOct; 114(5): 396-9, 402-13 [256] Human Biomonitoring to Optimize Fish Consumption Advice: Reducing Uncertainty When Evaluating Benefits and Risks, Scott M. Arnold, Tracey V. Lynn, Lori A. Verbrugge, John P. Middaugh, Am J Public Health. 2005 March; 95(3): 393–397 [257] Mercury and Tuna: U.S. Advice Leaves Lots of Questions, A Schoolboy's Sudden Setback, The Wall Street Journal, August 1, 2005, Peter Waldman [258] Mercury levels in high-end consumers of fish, Hightower JM, Moore D, Environ Health Perspect. 2003 Apr;111(4):604-8. [259] Rubin, Courtney. "Go Fish: The Diet Trend of the Moment." Details Magazine. Feb 2013: 72. Print. [260] The quote “It's okay to eat fish because they don't have any feelings.” is attributed to Kurt Cobain, the notoriously tormented musician and suicide. [261] Fish faddism causing low-level mercury poisoning in the Caribbean: two case reports, Pinto Pereira LM, Teelucksingh S, Cases J. 2009 Apr 29;2:7009 [262] “With a half-life of 70 days, at least five half-lives would need to be completed for the steady state levels of organic mercury to drop and with a return of a sense of comparative well being.” Fish faddism causing low-level mercury poisoning in the Caribbean: two case reports, Pinto Pereira LM, Teelucksingh S, Cases J. 2009 Apr 29;2:7009 [263] Some Of The Effects Of Excessive Smoking., Mann JD, Br Med J. 1908 Dec 5;2(2501):1673-5 (“Most men, if they choose to smoke, can do so within certain limits without injuring their health.”) [264] Wootton, David. Bad Medicine, Doctors Doing Harm Since Hippocrates. Paperback edition. New York: Oxford University Press, Inc., 2007, p.263. Print. [265] Excessive cigarette smoking, Leroy E. Burney Public Health Rep. 1957 September; 72(9): 786. Statement [266] In 2011 an article was published in the Journal of Toxicology by a group of physicians urging their colleagues to “ask patients if they eat fish: how often, how much, and what kinds,” and advising that methylmercury poisoning is difficult to detect and easily

mistaken for other conditions, “unless one considers this specific diagnosis.” Recognizing and Preventing Overexposure to Methylmercury from Fish and Seafood Consumption: Information for Physicians, Susan M. Silbernagel, David O. Carpenter, Steven G. Gilbert, Michael Gochfeld, Edward Groth, III, Jane M. Hightower, Frederick M. Schiavone J, Toxicol. 2011; 2011: 983072. Published online 2011 July 13. [267] A methylmercury level of 8 ppm, for example, would reduce by halves to 4 ppm, 2 ppm, 1 ppm, 0.5 ppm and 0.25 ppm in 5 half lives. [268] A review of infantile acrodynia ('pink disease'), Leys D, Arch Dis Child. 1950, Sep;25 (123):302-10 [269] Acute Mercury Poisoning : A Parallel Histological and Chemical Study of the Renal and Hepatic Tissue changes as compared with the Rapidity of Absorption and the Amount of Mercury Present in the circulating Blood at the Time such changes Occur, Burmeister WH, McNally WD, J Med Res. 1917 Mar;36(1):87-98.1 [270] Bioremediation and tolerance of humans to heavy metals through microbial processes: a potential role for probiotics?Monachese M, Burton JP, Reid G. Appl Environ Microbiol. 2012 Sep;78(18):6397-404. [271] Effects of diet on mercury metabolism and excretion in mice given methylmercury: role of gut flora. Rowland IR, Robinson RD, Doherty RA. Arch Environ Health. 1984 NovDec;39(6):401-8. [272] Methylmercury poisoning: long-term clinical, radiological, toxicological, and pathological studies of an affected family, Davis LE, Kornfeld M, Mooney HS, Fiedler KJ, Haaland KY, Orrison WW, Cernichiari E, Clarkson TW. Ann Neurol. 1994 Jun;35(6):6808. [273] Long term persistence of mercury in the brain, Cavanagh JB, Br J Ind Med. 1988 Oct;45(10):649-51 [274] Persistent mercury in nerve cells 16 years after metallic mercury poisoning, Hargreaves RJ, Evans JG, Janota I, Magos L, Cavanagh JB, Neuropathol Appl Neurobiol. 1988 Nov-Dec;14(6):443-52. [275] Demonstration of mercury in the human brain and other organs 17 years after metallic mercury exposure, Opitz H, Schweinsberg F, Grossmann T, Wendt-Gallitelli MF, Meyermann R, Clin Neuropathol. 1996 May-Jun;15(3):139-44. [276] Mercury in human brain, blood, muscle and toenails in relation to exposure: an autopsy study, Björkman L, Lundekvam BF, Laegreid T, Bertelsen BI, Morild I, Lilleng P, Lind B, Palm B, Vahter M. Environ Health. 2007 Oct 11;6:30; Dental amalgam and mercury levels in autopsy tissues: food for thought.Guzzi G, Grandi M, Cattaneo C, Calza S, Minoia C, Ronchi A, Gatti A, Severi G, Am J Forensic Med Pathol. 2006 Mar;27(1):425. [277]People with high mercury uptake from their own dental amalgam fillings. Barregård L, Sällsten G, Järvholm B, Occup Environ Med. 1995 Feb;52(2):124-8; Factors influencing mercury evaporation rate from dental amalgam fillings, Björkman L, Lind B, Scand J Dent Res. 1992 Dec;100(6):354-60. [278] Psychometric evidence that mercury from silver dental fillings may be an etiological factor in depression, excessive anger, and anxiety, Siblerud RL, Motl J, Kienholz E, Psychol Rep. 1994 Feb;74(1):67-80. [279] Mercury from maternal "silver" tooth fillings in sheep and human breast milk. A source of neonatal exposure, Vimy MJ, Hooper DE, King WW, Lorscheider FL, Biol Trace Elem Res. 1997 Feb;56(2):143-52.

[280] Ex miners at the Idrija mercury mine who experienced long term intermittent exposure to inorganic mercury have had a higher risk of suicide compared to age-matched controls since the 1960’s. Personality traits in miners with past occupational elemental mercury exposure, Kobal Grum D, Kobal AB, Arneric N, Horvat M, Zenko B, Dzeroski S, Osredkar J. Environ Health Perspect. 2006 Feb;114(2):290-6. [281] The inhibition of mercury absorption by dietary ethanol in humans: cross-sectional and case-control studies, Martin MD, Naleway C. Occup Environ Med. 2004 Feb;61(2):e8. [282] A small dose of ethanol increases the exhalation of mercury in low-level-exposed humans, Sällsten G, Kreku S, Unosson H. J Toxicol Environ Health A. 2000 May 26;60(2):89-100. [283] High-risk occupations for suicide, Roberts SE, Jaremin B, Lloyd K, Psychol Med. 2012 Oct 26:1-10; The suicide mortality of working physicians and dentists, Petersen MR, Burnett CA, Occup Med (Lond). 2008 Jan;58(1):25-9; Metal toxicosis in horses, Casteel SW, Vet Clin North Am Equine Pract. 2001 Dec;17(3):517-27 (“common use of mercurycontaining blistering agents”) [284] In June 2012, an attempt in the Senate to invalidate MATS nearly passed, with 46 votes to overturn against 53 votes to keep MATS in place. Niemark, Jill. "Coal Power Cleans Up Its Act. New regulations could prevent thousands of heart and asthma attacks every year." Discover Magazine. 17 Jan 2013: 32-33. Print. [285] [Mercury emission characteristics from coal-fired power plants based on actual measurement].[Article in Chinese], Wang S, Wang HM, Zhu FH, Chen H, Sun XL, Zuo Y, Liu G. Huan Jing Ke Xue. 2011 Jan;32(1):33-7. [286] Hernández, J. (1755). A philosophical and practical essay on the gold and silver mines of Mexico and Peru: containing the nature of the ore, and the manner of working the mines, the qualities and use of quicksilver, the cleansing and refining these metals : with many useful observations concerning the assay of metals, the manner of conveying them to Europe, and remarks on the gold mines in Hungary, and those of Asia and Africa. London: Printed for J. Scott [287] Mercury levels in lichens from different host trees around a chlor-alkali plant in New Brunswick, Canada, Sensen M, Richardson DH. Sci Total Environ. 2002 Jul 3;293(1-3):3145; Exposure and impact assessment of emissions from mercury recycling using domestic rabbits, Reichrtová E, Bencko V. Cent Eur J Public Health. 1995 Feb;3(1):42-7; Largescale spatial variation in mercury concentrations in cattle in NW Spain, López Alonso M, Benedito JL, Miranda M, Fernández JA, Castillo C, Hernández J, Shore RF. Environ Pollut. 2003;125(2):173-81. [288] Raccoon (Procyon lotor) as a bioindicator of mercury contamination at the U.S. Department of Energy's Savannah River Site, Lord CG, Gaines KF, Boring CS, Brisbin IL Jr, Gochfeld M, Burger J. Arch Environ Contam Toxicol. 2002 Oct;43(3):356-63. [289] In comparison, domestic cats found dead in Minamata had liver mercury concentrations of 37 to 145 ppm. Reproductive impairment in the Florida panther: nature or nurture? Facemire CF, Gross TS, Guillette LJ Jr, Environ Health Perspect. 1995 May;103 Suppl 4:79-86. [290] Retrospective and current risks of mercury to panthers in the Florida Everglades, Barron MG, Duvall SE, Barron KJ, Ecotoxicology. 2004 Apr;13(3):223-9. [291] Altered behavior of neonatal northern watersnakes exposed to maternally transferred mercury, Chin SY, Willson JD, Cristol DA, Drewett DV, Hopkins WA, Environ Pollut. 2013 May;176:144-50; Emergence of delayed behavioral effects in offspring mice exposed to low levels of mercury vapor during the lactation period, Yoshida M, Watanabe C, Honda

A, Satoh M, Yasutake A, J Toxicol Sci. 2013 Feb;38(1):1-6.); Effects of environmental methylmercury on the health of wild birds, mammals, and fish, Scheuhammer AM, Meyer MW, Sandheinrich MB, Murray MW, Ambio. 2007 Feb;36(1):12-8. Review. [292] Effects of methylmercury on approach and avoidance behavior of mallard ducklings, Heinz G. Bull Environ Contam Toxicol. 1975 May;13(5):554-64; Relationship between blood mercury levels and components of male song in Nelson's sparrows (Ammodramus nelsoni), McKay JL, Maher CR. Ecotoxicology. 2012 Nov;21(8):2391-7. [293] Nocera, J.J. and P.D. Taylor. 1998. In situ behavioral response of common loons associated with elevated mercury (Hg) exposure. Conservation Ecology 2. Article no. 10 [294] Chronic metals ingestion by prairie voles produces sex-specific deficits in social behavior: an animal model of autism, Curtis JT, Hood AN, Chen Y, Cobb GP, Wallace DR. Behav Brain Res. 2010 Nov 12;213(1):42-9; Chronic inorganic mercury exposure induces sex-specific changes in central TNFα expression: importance in autism? Thomas Curtis J, Chen Y, Buck DJ, Davis RL. Neurosci Lett. 2011 Oct 17;504(1):40-4. [295] Heavy metals in liquid pig manure in light of bacterial antimicrobial resistance, Hölzel CS, Müller C, Harms KS, Mikolajewski S, Schäfer S, Schwaiger K, Bauer J, Environ Res. 2012 Feb;113:21-7. [296] Toxic element contamination of natural health products and pharmaceutical preparations, Genuis SJ, Schwalfenberg G, Siy AK, Rodushkin I. PLoS One. 2012;7(11):e49676; Beastly beauty products: exposure to inorganic mercury in skinlightening creams, Washam C. Environ Health Perspect. 2011 Feb;119(2):A80. [297] Assessing elemental mercury vapor exposure from cultural and religious practices, Riley DM, Newby CA, Leal-Almeraz TO, Thomas VM. Environ Health Perspect. 2001 Aug;109(8):779-84. [298] UNEP INC5 Press release 19 January, 2013 ‘Minamata’ Convention Agreed by Nations Global Mercury Agreement to Lift Health Threats from Lives of Millions WorldWide [299] Effects of neurotoxicants on synaptic transmission: lessons learned from electrophysiological studies, Atchison WD, Neurotoxicol Teratol. 1988 Sep-Oct;10(5):393416. Review; Biomarkers in environmental medicine: alterations of cell signalling as early indicators of neurotoxicity, Castoldi AF, Coccini T, Rossi A, Nicotera P, Costa LG, Tan XX, Manzo L, Funct Neurol. 1994 Mar-Apr;9(2):101-9. Review. [300] Persistent behavioral impairments and alterations of brain dopamine system after early postnatal administration of thimerosal in rats, Olczak M, Duszczyk M, Mierzejewski P, Meyza K, Majewska MD, Behav Brain Res. 2011 Sep 30;223(1):107-18.. [301] Interactions between D1 and D2 dopamine receptor family agonists and antagonists: the effects of chronic exposure on behavior and receptor binding in rats and their clinical implications, Braun AR, Laruelle M, Mouradian MM, J Neural Transm. 1997;104(45):341-62. [302] Unusual Symptoms Following the Use of Unguentum Hydrargyri Ammoniati, Green WE, Br Med J, 1884 May 3;1(1218):853-4 [303] A Review of Infantile Acrodynia ('Pink Disease'), Leys D, Arch Dis Child. 1950 September; 25(123): 302–310. [304] Ancestry of pink disease (infantile acrodynia) identified as a risk factor for autism spectrum disorders., Shandley K, Austin DW, J Toxicol Environ Health A. 2011;74(18):1185-94 [305] Pink Disease-Ten Years After (The Epilogue), Dathan J, Harvey C,. Br Med J, 1965

May 1;1(5443):1181-2. [306] Ancestry of pink disease (infantile acrodynia) identified as a risk factor for autism spectrum disorders., Shandley K, Austin DW, J Toxicol Environ Health A. 2011;74(18):1185-94 [307] Genetic effects on toxic and essential elements in humans: arsenic, cadmium, copper, lead, mercury, selenium, and zinc in erythrocytes, Whitfield JB, Dy V, McQuilty R, Zhu G, Heath AC, Montgomery GW, Martin NG. Environ Health Perspect. 2010 Jun;118(6):77682. [308] Genetic background of lead and mercury metabolism in a group of medical students in Austria, Gundacker C, Wittmann KJ, Kukuckova M, Komarnicki G, Hikkel I, Gencik M, Environ Res. 2009 Aug;109(6):786-96. [309] The influence of nutrition on methyl mercury intoxication, Chapman L, Chan HM. Environ Health Perspect. 2000 Mar;108 Suppl 1:29-56. [310] Unexpected development of artistic talents, Gordon N. Postgrad Med J. 2005 Dec;81(962):753-5. [311] Einstein's brain: gliogenesis in autism? Yuan TF. Med Hypotheses. 2009 Jun;72(6):753; Variability of neuropathologic lesions in experimental methylmercurial encephalopathy in primates. Shaw CM, Mottet NK, Body RL, Luschei ES. Am J Pathol. 1975 Sep;80(3):451-70 (Neuronal degeneration and astroglial proliferation predominated); Changes in the number of astrocytes and microglia in the thalamus of the monkey Macaca fascicularis following long-term subclinical methylmercury exposure, Charleston JS, Body RL, Bolender RP, Mottet NK, Vahter ME, Burbacher TM, Neurotoxicology. 1996 Spring;17(1):127-38. (microglia showed significant increase); Cognitive deficit in 7-yearold children with prenatal exposure to methylmercury, Grandjean P, Weihe P, White RF, Debes F, Araki S, Yokoyama K, Murata K, Sørensen N, Dahl R, Jørgensen PJ, Neurotoxicol Teratol. 1997 Nov-Dec;19(6):417-28. (mercury has the ability to reduce the number of neurons and the cytoarchitecture in individuals with prenatal exposure to mercury). [312] Tortured genius. www.Urbandictionary.com Retrieved April 19, 2013 [313] Relationship between blood mercury concentration and waist-to-hip ratio in elderly Korean individuals living in coastal areas, You CH, Kim BG, Kim JM, Yu SD, Kim YM, Kim RB, Hong YS. J Prev Med Public Health,2011 Sep;44(5):218-25 [314] Gastric stimulation for weight loss, Mizrahi M, Ben Ya'acov A, Ilan Y. World J Gastroenterol. 2012 May 21;18(19):2309-19; Influence of vagal nerve stimulation on food intake and body weight--results of experimental studies, Sobocki J, Królczyk G, Herman RM, Matyja A, Thor PJ, J Physiol Pharmacol. 2005 Dec;56 Suppl 6:27-33. [315] Hair tissue mineral analysis and metabolic syndrome, Park SB, Choi SW, Nam AY. Biol Trace Elem Res. 2009 Sep;130(3):218-28. Epub 2009 Feb 17. [316] Methylmercury exposure and adverse cardiovascular effects in Faroese whaling men, Choi AL, Weihe P, Budtz-Jørgensen E, Jørgensen PJ, Salonen JT, Tuomainen TP, Murata K, Nielsen HP, Petersen MS, Askham J, Grandjean P, Environ Health Perspect. 2009 Mar;117(3):367-72. Epub 2008 Oct 16. [317] Intake of mercury from fish, lipid peroxidation, and the risk of myocardial infarction and coronary, cardiovascular, and any death in eastern Finnish men, Salonen JT, Seppänen K, Nyyssönen K, Korpela H, Kauhanen J, Kantola M, Tuomilehto J, Esterbauer H, Tatzber F, Salonen R. Circulation. 1995 Feb 1;91(3):645-55. [318] Mercury exposure and risk of hypertension in US men and women in 2 prospective

cohorts, Mozaffarian D, Shi P, Morris JS, Grandjean P, Siscovick DS, Spiegelman D, Willett WC, Rimm EB, Curhan GC, Forman JP, Hypertension. 2012 Sep;60(3):645-52. Epub 2012 Aug 6. [319] Here are a few of them dating from the year 2000; Mercury intoxication and arterial hypertension: report of two patients and review of the literature, Torres AD, Rai AN, Hardiek ML. Pediatrics. 2000 Mar;105(3):E34. (In children with severe hypertension and elevated catecholamines, the physician should consider mercury intoxication); Weight loss, hypertension, weakness, and limb pain in an 11-year-old boy, Shih H, Gartner JC Jr, J Pediatr. 2001 Apr;138(4):566-9; Mercury intoxication resulting from school barometers in three unrelated adolescents, Koyun M, Akman S, Güven AG. Eur J Pediatr. 2004 Mar;163(3):131-4. Epub 2004 Jan 13. (Three adolescents with severe hypertension due to mercury intoxication); Mercury intoxication in a 2-year-old girl: a diagnostic challenge for the physician, Michaeli-Yossef Y, Berkovitch M, Goldman M. Pediatr Nephrol. 2007 Jun;22(6):903-6. Epub 2007 Feb 20; A previously healthy 11-year-old girl with behavioural disturbances, desquamation of the skin and loss of teeth, van der Linde AA, Lewiszong-Rutjens CA, Verrips A, Gerrits GP. Eur J Pediatr. 2009 Apr;168(4):509-11. Epub 2008 Nov 29; Acrodynia and hypertension in a young girl secondary to elemental mercury toxicity acquired in the home, Mercer JJ, Bercovitch L, Muglia JJ. Pediatr Dermatol. 2012 Mar-Apr;29(2):199-201; Elemental mercury poisoning presenting as hypertension in a young child, Brannan EH, Su S, Alverson BK. Pediatr Emerg Care. 2012 Aug;28(8):812-4. [320] Role of mercury toxicity in hypertension, cardiovascular disease, and stroke, Houston MC, J Clin Hypertens (Greenwich). 2011 Aug;13(8):621-7. Epub 2011 Jul 11 (mercury toxicity should be evaluated in any patient with hypertension [321] Long-term risk of sustained hypertension in white-coat or masked hypertension, Mancia G, Bombelli M, Facchetti R, Madotto F, Quarti-Trevano F, Polo Friz H, Grassi G, Sega R, Hypertension. 2009 Aug;54(2):226-32, Epub 2009 Jun 29.