Madness and Genetic Determinism: Is Mental Illness in Our Genes? [1st ed.] 978-3-030-21865-2;978-3-030-21866-9

Table of contents :
Front Matter ....Pages i-x
The Beginning (Patrick D. Hahn)....Pages 1-8
Ernst Rüdin and Family Studies (Patrick D. Hahn)....Pages 9-20
Franz Kallmann and Twin Studies (Patrick D. Hahn)....Pages 21-33
The Story of the Genain Sisters (Patrick D. Hahn)....Pages 35-46
Adoption Studies (Patrick D. Hahn)....Pages 47-56
The Mass-Marketing of Mental Illness (Patrick D. Hahn)....Pages 57-67
The Human Genome Project Era (Patrick D. Hahn)....Pages 69-82
The Story of January Schofield (Patrick D. Hahn)....Pages 83-97
Trauma and Psychosis (Patrick D. Hahn)....Pages 99-118
The Asylum Era and Moral Therapy (Patrick D. Hahn)....Pages 119-129
Frieda Fromm-Reichmann and Chestnut Lodge (Patrick D. Hahn)....Pages 131-139
Ronald Laing and Kingsley Hall (Patrick D. Hahn)....Pages 141-148
Soteria House and Open Dialogue Therapy (Patrick D. Hahn)....Pages 149-154
The Ghosts of Rüdin and Kallmann (Patrick D. Hahn)....Pages 155-170
Back Matter ....Pages 171-193

Citation preview

Madness and Genetic Determinism Is Mental Illness in Our Genes? Patrick D. Hahn

Madness and Genetic Determinism

Patrick D. Hahn

Madness and Genetic Determinism Is Mental Illness in Our Genes?

Patrick D. Hahn Biology Loyola University Maryland Baltimore, MD, USA

ISBN 978-3-030-21865-2    ISBN 978-3-030-21866-9 (eBook) https://doi.org/10.1007/978-3-030-21866-9 © The Editor(s) (if applicable) and The Author(s), under exclusive licence to Springer Nature Switzerland AG 2019 This work is subject to copyright. All rights are solely and exclusively licensed by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the ­publisher nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and ­institutional affiliations. This Palgrave Macmillan imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

Preface

On the morning of Saturday 28 March 2016, Karina Morales-Rodriguez and Marta Martinez were shot dead outside the MoneyTree retail financial services provider at the corner of South First and East Walnut Streets of Yakima, Washington, where they both worked.1 Later that day agents of the Pacific Northwest Violent Offender Task Force arrested Manuel Enrique Verduzco without incident at the home of his parents. He was charged with aggravated first-degree murder and pleaded not guilty. On 19 December 2017, the Yakima Herald reported that Verduzco’s lawyers requested that experts be allowed to testify that their client inherited a tendency toward schizophrenia from his father’s side of the family.2 Are people suffering from schizophrenia or any other mental illness really “born that way”? What does it even mean to say that mental illness is caused by genes? These are the questions we will be considering here. How we view these conditions—as problems with living, or as brain disorders, probably inherited—determines how society deals with persons suffering from them. For the single year 2013, total spending on mental health interventions in the United States exceeded $200 billion.3 There are literally trillions of dollars at stake here. The way we view these conditions also touches on some of the most profound questions, such as what kind of society we would like to live in, and what it means to be a human being. As I researched this book, I came to realize that there actually were two separate stories that needed telling. One was the story of biological psychiatry, with its emphasis on bio-genetic explanations for mental illness and somatic remedies, and the other was the story of humanistic ­psychiatry, v

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with its emphasis on personal and social causes and remedies. During the past forty or so years humanistic approaches to mental illness have been almost completely eclipsed by bio-genetic ones, but the humanistic approach has never gone away. I have not attempted to write a comprehensive account of these parallel stories—that would be an effort requiring many volumes—but I have attempted to tell each of these stories as a more-or-less continuous account, summarizing the work of the main players. At all times I have striven to highlight the human cost of scientific and medical hubris. One hundred years have elapsed since the establishment of the German Institute for Psychiatric Research, with Ernst Rüdin as the Director of Psychiatric and Genealogical Studies. The work of Rüdin and his colleagues served as part of the intellectual justification for the T4 Program for the elimination of “life unworthy of life,” which in turn served as the springboard for the Holocaust. Of course, nobody is talking about breeding a “master race” anymore. But as the field of psychiatric genetics enters its second century, with headlines proclaiming on a regular basis that scientists have found the genetic basis of mental illness, it is time to take stock of what we have learned. This is a story of compassionate healers and self-promoting hucksters, of Nazis and monks, of brilliant science and naked corporate greed. It’s a story that is now more relevant than ever. Baltimore, MD, USA

Patrick D. Hahn

Notes 1. Meyers, Donald W, “Witness: Man Accused in Two Yakima Killings Was at Store Day Before,” Yakima Herald, March 28, 2016, https://www. yakimaherald.com/news/crime_and_courts/witness-man-accused-in-twoyakima-killings-was-at-store/ar ticle_f3a525b8-f579-11e5-9a00dfb710d1ccba.html 2. Meyers, Donald W. “Judge Will Rule Whether Suspect in MoneyTree Double Murder Can Use Genetic Evidence of Mental Illness.” Yakima Herald, December 19, 2017, https://www.yakimaherald.com/news/ crime_and_courts/judge-will-rule-whether-suspect-in-moneytree-doublemurder-can/article_77c21c8e-e54c-11e7-8759-8f470977c163.html 3. Roehrig, Charles, “Mental Disorders Top the List of the Most Costly Conditions in the United States: $201 Billion,” Health Affairs, 35, no. 6 (June 2016): 1130.

Acknowledgments

Grateful acknowledgment is made to each of the following for their assistance in preparing this book: To the experts who gave so generously of their time to explain their work to me: Peter Breggin, David Healy, Richard Huganir, Jay Joseph, John Read, Jaako Seikkula, and Daniel Weinberger. To Vickie and Miriam, who courageously shared their stories of iatrogenic harm. And to my wife and daughter, for their unwavering support.

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Contents

1 The Beginning   1 2 Ernst Rüdin and Family Studies   9 3 Franz Kallmann and Twin Studies  21 4 The Story of the Genain Sisters  35 5 Adoption Studies  47 6 The Mass-Marketing of Mental Illness  57 7 The Human Genome Project Era  69 8 The Story of January Schofield  83 9 Trauma and Psychosis  99 10 The Asylum Era and Moral Therapy

119

11 Frieda Fromm-Reichmann and Chestnut Lodge

131

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Contents

12 Ronald Laing and Kingsley Hall

141

13 Soteria House and Open Dialogue Therapy

149

14 The Ghosts of Rüdin and Kallmann

155

References

171

Index 191

CHAPTER 1

The Beginning

L’Enfant Plaza, Washington DC, mid-January, two weeks after the polar vortex brought record-breaking low temperatures to the area. It’s a bright clear day, but a bitterly cold wind is stinging my face. Accompanied by my daughter and her friend, I open the door and we enter the United States Holocaust Memorial Museum. After passing through the metal detectors we enter the cavernous lobby, which is jam-packed with students. A guard passes by, holding a black Labrador retriever at the end of a leash. We take the elevator to the fourth floor and step out to find ourselves facing an image of skeletons, bits of dried flesh clinging to the bones, all stacked like cordwood outside one of the Nazi death camps. Everyone else around us appears to be of high school age, but the natural exuberance and boisterousness of youth has been put on pause. People speak in hushed tones, or not at all. We pass exhibits chronicling Hitler’s rise to power, then pause in front of a bed frame, its coat of white paint peeling away to reveal the bare metal underneath. It’s from the Sachsenberg Clinic, where children were killed by starvation, lethal injections, or overdoses of medication. Behind it is a photomural of the Hadamar Psychiatric Institute, black smoke roiling forth from the chimney. In 1941, the staff of Hadamar held a gathering to celebrate the murder of the 10,000th patient.1 Psychiatrists, nurses, secretaries, and staff all participated. The naked body of a murdered patient lay on a stretcher, © The Author(s) 2019 P. D. Hahn, Madness and Genetic Determinism, https://doi.org/10.1007/978-3-030-21866-9_1

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c­ overed with flowers, and a staff member dressed as a priest performed a mock ceremony. The hospital supervisor gave a speech, and then the beer and wine flowed freely. A local polka band provided entertainment.2 All this was part of the Nazi program of “racial hygiene,” set in motion by some of Germany’s most prominent scientists and medical doctors. The Nazi campaign to eradicate the mentally ill was a dress rehearsal for the Holocaust, but the idea that mental illness is a matter of faulty inheritance goes back much farther than that.

The Roots of the Problem Bethlem Hospital of London (from which we get the term “Bedlam,” a synonym for madness) was founded in 1247 to raise funds for the Church of the Nativity of Bethlehem in the Holy Land.3 An audit conducted in 1403 revealed that the place served as refuge for six inmates judged mente capti, or “mentally ill” in today’s parlance—making it Europe’s oldest psychiatric institution, having functioned in this capacity for at least 600 years.4 Over the years, similar institutions were established across continental Europe and the United States,5 and every such institution required its own medical superintendent. Colloquially these men were known as “madhouse doctors.” In 1808 Johann Christian Reil, Professor of Medicine at the University of Halle in Lower Saxony, coined the term “psychiatrie” for this specialty, from the ancient Greek roots psyche, or soul, and iatreia, or healing.6 It had been known for a long time that madness tended to run in families. John Haslam, an apothecary at Bethlem Hospital, published in 1809 his work Observations on Insanity, in which he discussed the causes of these conditions: The causes which I have been enabled most certainly to ascertain, may be divided into physical and moral. Under the first are comprehended repeated intoxications; blows to the head; fever, particularly when accompanied by delirium; mercury largely or injudiciously administered; the suppression of periodical or occasional discharges and secretions; hereditary disposition; and paralytic affections.7

Haslam’s eclectic approach, with hereditary factors being only one cause of insanity working in conjunction with a multiplicity of others,

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showed more sophistication than that of many of his twentieth-century successors—who had access to far more information about the process of heredity than Haslam did. Many of these early medical superintendents at hospitals for the insane reported great success with what was called “moral therapy8”: cleanliness, fresh air, sunlight, exercise, order, structure, discipline, kindness. (A number of them, Reil included, also stressed the importance of keeping the patients’ families away from them.) But then these hospitals became dumping grounds for those with syphilitic dementia, senile dementia, mental retardation, criminals, vagrants, orphans—the whole spectrum of the downtrodden and the despised. Hence these institutions, which by then were known as “asylums,” morphed into the crowded, filthy “snake pits” of popular imagination.9 As the asylums became more crowded, psychiatrists became more desperate, and their remedies for mental illness more drastic—the spinning chair, ice baths, fever therapy, chemically-induced convulsions, insulin coma, electroshock, lobotomy, and perhaps most egregious of all, Henry Cotton’s wholesale program of literal disembowelment of patients at Trenton State Hospital.10 The swelling of the asylum population was fueled by the industrial revolution, with the migration of a large portion of the rural population to the cities, and the concomitant decline of multi-generation households which once cared for those unable to care for themselves.11 But it is not too hard to understand how these asylum doctors, faced with what must have looked like a growing flood tide of the dregs of humanity, began to suspect they were witnessing the degeneration of the entire human race. Guided by Lamarckian views of inheritance, most nineteenth-century medical professionals viewed hereditary insanity as a kind of snowballing process—dissolution led to madness, and the germs of madness were passed on to the next generation, which led to even more dissolute behavior, and so on. Benedict Augustin Morel, director of the mental asylum at Saint-Yon in the North of France, wrote in 1857 “The degenerate human being, if he is abandoned to himself, falls into a progressive degradation.”12 This was a time when French psychiatry was facing a crisis of identity that seemed to threaten its very existence as a medical specialty. Other branches of medicine were making great strides in elucidating the causes of disease, but psychiatry had come up empty-handed; no credible evidence had been found for any organic lesion underlying any of the

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c­ onditions commonly treated by psychiatrists.13 Moreover, psychiatry was the subject of relentless attacks in the press, and magistrates were deriding psychiatrists’ claims to expertise in legal matters.14 By attributing mental illness to hereditary factors causing some kind of unspecified lesion in the nervous system, one that was too subtle to be measured, psychiatrists were able to reaffirm their identity as real doctors treating real diseases, without having to demonstrate any evidence of any kind of disease process in their patients.15 Morel’s ideas enjoyed wide currency throughout Europe. In 1895, two French psychiatrists, Valentin Magnan and Maurice Paul Legrain, authored The Degenerates, in which they threw down the gauntlet: Degeneracy is more than an individual disease, it is a social menace: It is important to combat it with a rigorous form of social hygiene. One must not forget that the degenerate is often a dangerous individual against whom society should and must reserve the right to defend itself.

Their opus ended with the grim admonition that society must “cut off the problem at the roots.”16 But the efforts of nineteenth-century psychiatrists to understand the hereditary basis of madness came to naught, for a simple reason: researchers lacked a basic understanding of the mechanisms of heredity itself.17

A Call to Arms On 8 March 1865, a monk named Gregor Mendel18 gave a talk at the meeting of the Natural History Society of Brünn, then under the dominion of the Austrian Empire, now a part of the Czech Republic. The brother (who had already given up on a career as a secondary school science teacher, after receiving failing marks in his biology examination) described experiments he had performed in hybridizing pea plants. He noted that when he crossed plants of two different varieties, the progeny always resembled one particular parent—not the other. When the progeny of these unions were crossed with each other, the next generation always displayed the characters of both parents, in a specific ratio. The talk was indifferently received, although Mendel’s findings were published in the Proceedings of the Natural History of the Society of Brünn— and then immediately forgotten. It was not until 1900 that three different teams of European researchers—in Vienna, Tübingen, and Amsterdam—

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rediscovered Mendel’s paper and belatedly credited him with formulating the laws of heredity. At last researchers had the conceptual tools to tackle the thorny problem of the inheritance of mental illness. We shall see how these tools have been applied, and misapplied, beginning in the early twentieth century right up to the present day. We will focus on schizophrenia, as this condition generally is regarded as the most severe and intractable mental illness, and the one most likely to have a biological or genetic basis. If schizophrenia is found to have a genetic basis, that would bolster the case for looking for genetic bases for other mental illnesses. On the other hand, if genetic determinist theories for schizophrenia fail, they are likely to do so for other mental illnesses as well. Schizophrenia is a condition characterized by disorganized thinking, along with delusions and hallucinations. This condition was virtually unknown until the nineteenth century. In fact, the aforementioned John Haslam is credited with the first clinical account of a patient with schizophrenia, and indeed the first complete study of a single psychiatric patient, James Tilly Matthews, whose story is told in Haslam’s book Illustrations of Madness,19 published in 1810. Matthews’s fantastically detailed account of a gang of evildoers controlling his mind with the aid of a diabolical contraption he called the “air loom” is eerily reminiscent of the online rants of modern-day “targeted individuals.” Why was this condition unknown before then? A variety of explanations have been proposed, none of them entirely convincing, but perhaps the reason is simply because no medical professional had taken the time to listen to the ravings of any so-called madman before then. Emil Kraepelin was a German psychiatrist and author of the book widely regarded as the foundation of modern-day psychiatric nosology.20 Originally published in 1883 as Compendium of Psychiatry: For the Use of Students and Physicians, the book was expanded in subsequent multivolume editions as A Textbook: Foundations of Psychiatry and Neuroscience. Kraepelin divided mental illness into two broad categories: “manic-­ depressive psychosis” (corresponding to the modern-day category of affective disorders) and “dementia praecox” (corresponding to the modern-­day notion of schizophrenia, along with syphilitic dementia, or “general paresis of the insane,” thrown in). Others before him had used the term “dementia praecox,” but Kraepelin generally is credited with popularizing it.21 Kraepelin’s concept of schizophrenia comprised three very different conditions: catatonia, or stupor; hebephrenia, a term seldom used a­ nymore but which corresponds more or less to emotional immaturity or silliness;

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and vesania typica, or hallucinations and delusions. Kraepelin did not demonstrate that there was a common cellular or biochemical substrate that united these conditions. Rather, he assumed there was one, and that medical science, by and by, would find evidence for its existence.22 In 1908, the Swiss psychiatrist Paul Eugen Bleuler coined the term “schizophrenia” for this condition, from the ancient Greek roots skhizein, “to split,” and phren, which depending on the context, could mean diaphragm, lungs, heart, brain, or mind. In a lecture to the German Psychiatric Association in Berlin, Bleuler noted: I wish to emphasize that in Kraepelin’s dementia praecox it is neither a question of an essential dementia nor of a necessary precociousness. For this reason, and because from the expression dementia praecox one cannot form further adjectives nor substantives, I am taking the liberty of employing the word schizophrenia for the Kraepelinian concept. In my opinion the breaking up or splitting of psychic functioning is an excellent symptom of the whole group.23

And what about the prognosis for sufferers of this disease? Bleuler rejected Kraepelin’s notion that the condition always ended in dementia, noting “It is impossible to describe all the various courses of schizophrenia.”24 In short, Bleuler had created a diagnostic label for a “disease” with no consistent symptoms, no known cause, and no consistent outcome. In his Textbook of Psychiatry, published in 1924, Bleuler scoffed at Morel’s ideas of degeneration. But he did not scoff at the idea that mental illness is an inherited condition: The most severely burdened should not propagate themselves. … If we do nothing but make mental and physical cripples capable of propagating themselves, and the healthy stocks have to limit the number of children because so much has to be done for the maintenance of others, if natural selection is generally suppressed, then unless we will get new measures our race must rapidly deteriorate.25

A Swiss-born German psychiatrist named Ernst Rüdin heeded this call to arms and made it his life’s work.

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Notes 1. Hugh Gregory Gallagher, By Trust Betrayed: Patients, Physicians, and the License to Kill in the Third Reich (New York: Henry Holt and Company, 1990), 20–21. 2. Ibid., 21. 3. Nicholas Vincent, “Goffredo de Prefettii and the Church of Bethlehem in England,” Journal of Ecclesiastical History 49 no. 2 (April 1998):213–235. 4. Basil Clarke, Mental Disorder in Earlier Britain: Exploratory Studies (Cardiff: University of Wales Press, 1975), 79. 5. Edward Shorter, A History of Psychiatry (New York: John Wiley & Sons, 1997), 5–8. 6. Devin Binder, Karl Schaller, and Hans Clusmann, “The Seminal Contributions of Johann Christian Reil to Anatomy, Physiology, and Psychiatry,” Neurosurgery, 61, no. 5 (November 2007): 1092, https:// doi.org/10.1227/01.neu.0000303205.15489.23; Andreas Marneros, “Psychiatry’s 200th Birthday,” British Journal of Psychiatry, 193, no. 1 (July 2008): 1, https://doi.org/10.1192/bjp.bp.108.051367 7. John Haslam, Observations on Insanity (London: F. and C.  Rivington, 1809), 99. 8. For an account of the era of moral therapy, see Chap. 10 of this volume. 9. Shorter, History, 46–68. 10. For a vivid description of the somatic therapies of the nineteenth and twentieth centuries, see Elliot S. Valenstein, Great and Desperate Cures: The Rise and Decline of Psychosurgery and Other Radical Treatment for Mental Illness (New York: Basic Books, 1986). A detailed and often shocking account of the career of Henry Cotton can be found in Andrew Scull, Madhouse: A Tragic Tale of Megalomania and Modern Medicine (Cambridge: Cambridge University Press, 2005). 11. Shorter, History, 49–52. 12. Ibid., 94. 13. Ian Dowbiggin, “Degeneration and Hereditarianism in French Mental Medicine 1840–90: Psychiatric Theory as Ideological Adaptation,” in The Anatomy of Madness: Essays in the History of Psychiatry, ed. W.F. Bynum, R. Porter, and M. Sheperd (London: Tavistock, 1985), 208. 14. Ibid., 189. 15. Ibid., 208–210. 16. Shorter, History, 96–97. 17. Some nineteenth-century researchers imagined that idiocy, epilepsy, albinism, and deaf-mutism all were manifestations of the same ill-defined hereditary factor. See Theodore M. Porter, Genetics in the Madhouse: The Unknown History of Human Heredity (Princeton: Princeton University Press, 2018), 138.

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18. For an account of Gregor Mendel’s life and works, see Herbert Wendt, In Search of Adam (Boston: Houghton Mifflin, 1956), 309–314. 19. John Haslam, Illustrations of Madness (London: F. and C.  Rivington, 1810). 20. Shorter, History, 103. 21. Ibid., 105–107. 22. Thomas Szasz, Schizophrenia: The Sacred Symbol of Psychiatry (New York: Basic Books, 1976), 10. 23. Paolo Fusar-Poli and Pierluigi Politi, “Paul Eugen Bleuler and the Birth of Schizophrenia (1908),” American Journal of Psychiatry, 165, no. 11 (November 2008): 1407. 24. Paul Eugen Bleuler, Textbook of Psychiatry, trans. A. A. Brill (New York: Macmillan Press, 1924) 434. 25. Ibid., 214.

CHAPTER 2

Ernst Rüdin and Family Studies

Ernst Rüdin completed his medical degree in 1898 and subsequently did post-doctoral research under the tutelage of Emil Kraepelin.1 In 1903, at the Ninth International Congress to Combat Alcoholism, Rüdin advocated the sterilization of chronic alcoholics, a proposal that was soundly rejected.2 Two years later, along with his brother-in-law Alfred Ploetz, he helped found the Society for Racial Hygiene and was named editor of the society’s journal, Archives of Racial and Social Biology.3 Four years after that he succeeded Alois Alzheimer as senior physician at Kraepelin’s Munich Hospital, and that same year he became a German citizen.4 Armed with an understanding of Mendel’s Laws, modern statistical methods of analysis, and Kraepelin’s nosology of psychiatric illnesses, Rüdin went to work. Rüdin studied 701 families in which there was a case of “dementia praecox.”5 His subjects were recruited from the university hospital of psychiatry in Munich as well as the district insane asylum. He also gathered information about the families of victims from doctors, hospitals, schools, offices of vital statistics, government offices, and police reports. Working from this pastiche of second-hand sources, much of it gathered by individuals who were not medical professionals, Rüdin felt able to render psychiatric diagnoses of individuals he had never examined, many of whom were long dead. When he analyzed this information, he concluded that the data best fit a two-locus model in which the schizophrenia allele was recessive at both loci.6 © The Author(s) 2019 P. D. Hahn, Madness and Genetic Determinism, https://doi.org/10.1007/978-3-030-21866-9_2

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In fairness to Rüdin, he maintained that these findings were only preliminary, that the two-locus model of schizophrenia was no more than a working hypothesis.7 But this did not prevent his findings from being used to support an agenda of compulsory sterilization and “mercy killing,” with far-reaching consequences. In 1918, Rüdin’s mentor Kraepelin established the German Institute for Psychiatric Research (later the Kaiser Wilhelm Institute [KWI]) with Rüdin as Director of Genealogical and Demographic Studies.8 Five years after that, Rüdin completed a study on bipolar disorder, or “manic-­ depressive psychosis,” as it was then known. He failed to find convincing evidence for a genetic basis for this condition, and the study was never published.9 In 1925, Rüdin left the institute to become Professor of Psychology at the University of Basel in Switzerland.10 Three years later he returned to the Institute with an expanded budget and a brand-new building made possible by generous funding from the Rockefeller Foundation.11

Task Force 2 On 30 January of 1933, Hitler became Chancellor of the Reich. On 3 June of that same year, Rüdin was appointed to the newly established Standing Committee for Racial Hygiene.12 Rüdin headed “Task Force 2” which was charged with drafting the new law requiring compulsory sterilization of the “unfit.” The Law for the Prevention of Genetically Diseased Offspring (modeled after similar laws in the United States) was passed by the Reichstag on 14 July. This law provided for the compulsory sterilization of those with “congenital mental defects, schizophrenia, manic-depressive psychosis, hereditary epilepsy, hereditary chorea, hereditary blindness, hereditary deafness, severe physical deformity, and severe alcoholism.”13 Up to that time, sterilization was illegal in Germany.14 Under the new law, hundreds of genetic health courts and appellate genetic health courts were established. Each court was presided over by two medical doctors and a lawyer.15 Doctors were required to report every case of genetic disease known to them (with exceptions made for women past the age of forty-five). The patient recommended for sterilization had no right to legal representation or even to see the evidence presented against him, and all cases were decided by a majority vote of the panel.16 The proceedings were

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nothing more than an expensive parody of the legal process. Not surprisingly, the courts decided for sterilization in over 90 percent of cases.17 Between 300,000 and 400,000 patients were sterilized.18 Perioperative mortality was on the order of 1  in 200, meaning that something like 1500–2000 patients died.19 Some of the patients were sterilized by X-rays administered without their knowledge, as they were seated behind desks or standing in front of counters filling out forms. This clandestine procedure sometimes resulted in massive burns.20 In March of 1935, Rüdin called for “widening the spectrum of diseases necessitating sterilization” to include “socially inferior psychopaths on account of moral confusion or severe ethical defects,” as well as “the great mass of serious and incorrigible criminals.”21 Later that year, Franz Kallmann, a visiting scientist at the KWI and a protégé of Rüdin’s, went even further.22 At the International Congress on Population Problems in Berlin, Kallmann argued that schizophrenia was caused by a single recessive gene and demanded compulsory sterilization not just of schizophrenics but of all their first-degree relatives who were carriers of the schizophrenia trait and whom, he averred, could be identified by subtle physical deformities. Fritz Lenz, Professor of Genetics at the University of Göttingen (and himself an ardent Nazi and eugenicist) rose to point out the absurdity of Kallmann’s proposal. Given that 1 percent of the population is schizophrenic, Kallmann’s single-gene model predicted that 18 percent of the population, or nearly one person out of five, would be heterozygous carriers of the schizophrenia allele and therefore candidates for compulsory sterilization. The proposal was shelved, but Rüdin’s obsession with sterilization was not. In 1937, along with Lenz, he oversaw the sterilization of 385 “Rheinlandbastarde,” or the offspring of German women and African troops serving in the French Army which occupied that part of Germany after the First World War.23

The Killing Program But then Hitler decided that sterilization of the “undesirables” was not enough. Sometime in the summer of 1939, he directed Phillipp Bouhler, his Chief of the Chancellery, and Karl Brandt, his personal physician and the Reich Commissioner for Health, to initiate a program to kill handicapped adults. Bouhler convened a secret meeting at the Chancellery with

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a number of prominent physicians, all of whom pledged their cooperation.24 Most of these experts were psychiatrists, including: • Max de Crinis, Director of the Psychiatric University Clinic at Cologne • Valentin Falthauser, Director of the Kaufbeuren District Hospital • Berthold Kihn, Director of the Psychiatric University Hospital at Jena • Werner Heyde, Director of the Psychiatric Hospital at Würzburg • Paul Nitsche, Deputy Director of the Sonnenstein Clinic • Carl Schneider, Chair of Psychiatry at Heidelberg • Wilhelm Bender, Director of the Psychiatric Clinic at Berlin-Buch State Hospital In October of 1939, Hitler signed a decree (backdated to 1 September, the day the Nazis invaded Poland) known as Action T4, which stated: Reichleader Bouhler and Dr. Med. Brandt are responsibly commissioned to extend the authority of physicians, to be designated by name, so that a mercy death may be granted to patients who according to human judgement are incurably ill according to the most critical evaluation of the state of their disease.25

Henceforth the organizational and medical resources which had gone into sterilizing the “undesirables” now would be applied to murdering them. The roster of those eligible for “mercy killing” was eventually extended to include persons suffering from schizophrenia, depression, epilepsy, senile dementia, encephalitis, Huntington’s chorea, mental retardation, arteriosclerosis, blindness, deaf-mutism, tuberculosis, dwarfism, severe malformations, paralysis, and alcoholism.26 Even handicapped veterans of the First World War were targeted (although some of them were granted reprieves at the killing centers), and even some shell-shocked soldiers returning from the Russian front were put to death.27 The T4 Medical Office was established to oversee the evaluation of patients and their selection for “mercy killing.” The office was headed first by Werner Heyde, who later was to step down in December 1941, possibly due to accusations of homosexuality. He was replaced by his deputy, psychiatrist Hermann Paul Nitsche, the former Director of the Sonnenstein Clinic.28

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On 15 August 1940, Heyde convened a meeting with a number of prominent psychiatrists to enlist support for the T4 Program. One of these men, Gottfried Ewald, a one-armed combat veteran of the First World War, voiced his objection to the program. He noted that schizophrenic patients, who constituted the largest group patients targeted for extermination, were not as hopeless as had been claimed, and that new forms of therapy being developed held great promise for these patients. Two other psychiatrists present voiced guarded support for Ewald’s concerns. At this point Dr. Nitsche spoke at length of the pain his schizophrenic brother-in-law had inflicted on the family. The two other psychiatrists recanted, but Ewald held his ground. Heyde dismissed Ewald from the meeting in a polite and collegial fashion, even thanking him for his input,29 and the T4 Program continued apace. Six “euthanasia centers” were established,30 each equipped with undressing rooms, along with a gas chamber disguised as a shower room as well as a crematorium. The decision of who was to live and who was to die was made on the basis of a one-page form distributed to hospitals, sanatoria, and asylums. Each form was filled out by a junior doctor and supposedly reviewed by a senior doctor, who might approve one hundred or more such documents in a single day.31 These senior administrators were paid 10 pfennig for each form if they reviewed fewer than 500 per month, and 5 pfennig per form if they reviewed more than 3500.32 The Charitable Foundation for the Transport of Patients (or “Gekrat”— an acronym for “Gemeinnütziger Krankentransportgeselleschaft”) was established to convey these unfortunates to “observation centers” and from there to the killing centers.33 The buses were painted gray, with the windows blacked out, and the Gekrat logo was printed clearly on the side.34 “There goes the murder box again!” children would shout, as the Gekrat buses rolled past.35 At the killing centers, patients might be greeted by nurses offering coffee and sweet rolls.36 Doctors would conduct a cursory physical examination of each patient. Afterward patients would be herded into undressing rooms and then to a “shower room,” with the promise of getting their clothes back after showering.37 The “shower rooms” were in fact gas chambers where patients were put to death by carbon monoxide gas supplied by I.G. Farben.38 Hitler personally approved this mode of execution after being assured by Dr. Brandt that it was the most humane means available.39

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Doctors watched the demise of their charges through peepholes.40 Afterward, the bodies were disposed of by cremation. The whole process was a model of efficiency, with as little as four hours elapsing between the arrival of the patients and their departure up the chimney.41 The ashes of all the patients were shoveled up and indiscriminately deposited into urns. The family of each patient was sent an urn and told it was the ashes of their loved one, who had to be cremated immediately to avoid the spread of disease.42 Many of the patients transported to these centers knew perfectly well what lay in store for them. The adult victims sometimes shouted abuse at their captors, and often found themselves forcibly sedated.43 On one occasion, four women patients arriving at the killing center at Hartheim Castle were found to have typhus. Rather than send them to the gas chamber, the supervisor, SS officer Christian Wirth, shot the women dead on the spot.44 Hospital bookkeepers meticulously filled out death certificates for each patient murdered. Part of the reason for the physical examination at the killing center was to provide a plausible cause of death45—“carbon monoxide poisoning” obviously would not do. Neither would it have done to have “appendicitis” listed as the cause of death for a patient who had already had his appendix out. Families received falsified death notices and were billed for per diem charges incurred after their loved ones had been murdered.46 Gold dental work was removed from the corpses of the victims and sold to help finance the program,47 while the brains of the victims were sent to Carl Schneider’s Laboratory in Heidelberg, and to Hans Heinze’s laboratory Brandenburg-­ Görden for further study.48 It perhaps does not quite go without saying that all the scientists’ embedding, sectioning, and staining of brain tissue and all the hours they spent peering down the barrels of microscopes brought mankind not one bit closer to discovering the etiology of schizophrenia or devising a cure. The staff who worked at the killing centers received extra alcohol rations, and many of them went about their day’s tasks in a state of intoxication. Drunken hookups and drunken brawls were common.49 A report to the Ministry of Justice claimed the local townsfolk wanted nothing to do with the staff members, who spent their evenings getting hammered at the nearby taverns.50

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As German psychiatry became increasingly preoccupied with killing, the prestige of that medical specialty plummeted. German medical students began staying away from psychiatry in droves.51 A parallel program for the killing of defective infants was established under the aegis of the Reich Committee for Scientific Research of Serious Illness of Heredity and Protonic Origin, which comprised Dr. Brandt, pediatricians Werner Catel and Ernst Wentzler, ophthalmologist Helmut Unger, and psychiatrist Hans Heinze. On 18 August 1939 the committee issued a decree requiring doctors, nurses, midwives, and hospitals to report all cases of serious hereditary disease for patients under the age of three.52 The category “serious hereditary disease” included deformed limbs, head, and spine; paralysis and palsy; dwarfism; blindness; deafness; idiocy; Down’s syndrome; and various brain abnormalities. Each questionnaire was reviewed by a committee of three physicians: Drs. Catel, Wentzler, and Heinze. If all three doctors approved, a certificate was issued authorizing the killing of the infant patient.53 Twenty-eight centers for the killing of infants (officially known as “Children’s wards for expert care”) were established, most of them at major hospitals. Parents were told their children were seriously ill but, fortunately, eligible for advanced therapy. Some of these infants were murdered by lethal injection, while others died slow miserable deaths by starvation, often drawn out over a period of months to avoid arousing suspicion.54 Originally only patients under the age of three were marked for killing, but then the age limit was extended to five years, and then beyond, even to patients in their teens. The selection process was turned over to nurses and orderlies, and children were put to death for pimples, swarthy complexions, or simply annoying the staff. As with the adult killing program, parents continued to be billed for per diem charges even after their children were murdered.55 One of the infant killing centers was located at the Elging-Haar hospital complex located near Munich, headed by psychiatrist Hermann Pfannmüller, who (like Rüdin) had trained under Kraepelin. Dr. Pfannmüller used to conduct tours of the children’s killing ward to educate the public about the biological inferiority of his charges. Ludwig Lehner, a psychologist and German prisoner of war, gave an account of one of these excursions to British investigators after the war. He recalls Dr. Pfannmüller explaining “For me as a National Socialist

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these creatures represent only a burden for our healthy national body. We do not kill with poisons, injections, etc. because that would only provide slanderous new campaign material for the foreign press and certain gentlemen in Switzerland. No, our method is, as you can see, much simpler and far more natural.”56 With these words, he pulled a starving tot from a crib. Holding up the child like a dead rabbit, Dr. Pfannmüller proclaimed, with the air of a true connoisseur, “With this one, for example, it will still take two or three days.”57 In total, over 400,000 mental patients, disabled persons, and others classified as “life unworthy of life” were murdered.58 We will never know the exact number, due to the elaborate deceptions that allowed the German people to deny what was going on. This death toll is, of course, dwarfed by that of the Holocaust. But it should always be kept in mind that they all occurred in places that were known officially as “hospitals”—and that the often protracted, agonizing deaths were designated “mercy killings.” At the Nuremberg Trials, Bouhler’s Deputy Viktor Brack, along with Dr. Brandt and a host of other Nazi doctors, testified that Jewish patients had been excluded from the “mercy killing” program. They lied. Jewish patients were included in the killing program from the beginning.59 Sometime in 1940, the T4 administrators apparently decided that the standard bureaucratic procedures were working too slowly in the case of Jewish patients, and chose to target all Jewish hospital patients for death, regardless of actual prognosis—presaging the Final Solution of the total elimination of the Jewish people. Jewish patients were transported to assembly centers and from there to the killing centers. Families received postdated death notices from “Mental Asylum Chelm” (sometimes misspelled “Cholm”) in Poland, after their loved ones were murdered, and were billed for months of expenses supposedly incurred. (In fact there had been a mental hospital in Chelm, but Nazi troops had murdered all the patients on 12 January 1940, and the place was closed until after the war.60) On 24 August 1941, faced with rising opposition, Hitler secretly ordered a halt to the T4 program.61 The killing of mental patients and other handicapped persons, including children, by means of starvation and lethal injection, continued even after the end of the war. Meanwhile, at least ninety doctors, nurses, technicians, and supervisors from the T4 program were transferred to the newly established killing centers at Belzec, Sobibor, and Treblinka, including the aforementioned

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SS Officer Christian Wirth.62 Thus we see a direct path from the killing of mental patients to the Holocaust. The T4 program had demonstrated the feasibility of the assembly line murder of large numbers of human beings, and that ordinary working men and women were willing to participate in such an enterprise. Once this machinery had been set in motion, it was easy to keep going. It must always be kept in mind that Action T4 did not require German psychiatrists to kill anyone. Rather, it authorized them to do so,63 an authority they exercised with unbridled enthusiasm. It was psychiatrists who wrote the rules stipulating who was to live and who was to die, it was psychiatrists who interpreted those rules, and it was psychiatrists who created and operated the administrative apparatus for the transport, confinement, killing, and cremation of mental patients. It must also be kept in mind that Rüdin and the other German psychiatrists who played key roles in the killing were not cranks or fringe figures. Rather, these men were leaders in their chosen field, with national and sometimes international reputations.64 They published in the same journals, reviewed each other’s papers, and contributed to each other’s festschrifts.65 To this day, Rüdin’s work continues to be cited in the literature of psychiatric genetics as evidence for the hereditary basis of mental illness. In his lifetime, Rüdin was the recipient of titles and professional honors too numerous to list here. In 1939 Hitler awarded Rüdin the Goethe Medal for Arts and Science,66 and the following year he served as President of the Fourth International Congress on Eugenics in Vienna.67 In 1944 he was awarded the Eagle Shield of the German Reich.68 In 1942, after the Holocaust was well underway, Rüdin wrote in the 1942 edition of the Archives of Racial and Social Biology: The results of our science had earlier attracted much attention (both support and opposition) in national and international circles. Nevertheless, it will always remain the undying historic achievement of Adolph Hitler and his followers that they dared take the first trail-blazing and decisive steps towards such brilliant race-hygienic achievement in and for the German people. In so doing, they went beyond the boundaries of purely scientific knowledge. He and his followers were concerned with putting into practice the theories and advances of Nordic race-conceptions … the fight against parasitic alien races such as the Jews and the Gypsies … and p ­ reventing the breeding of those with hereditary diseases and those of inferior stock.69

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Edith Zerbin-Rüdin, a psychiatrist at the Max Planck Institute for Psychiatry (the successor to the KWI) as well as the daughter of Ernst Rüdin, defended her father in an interview in the early 1980s. When asked about Rüdin’s 1942 Archives article, she replied: “It was like that in those days. What should he have done? He would have sold himself to the devil, to obtain money for his institute and his research.”70 After the war, Dr. Brandt defended his role in the killing of mental patients, arguing before the US military tribunal that “Were not the regular professor of the universities with the program? Who could there be who was better qualified than they?”71 Brandt was convicted of crimes against humanity, as was Phillipp Bouhler and Viktor Brack. All three men were hanged. Rüdin’s former protégé Kallmann had already fled Germany years before this, to avoid persecution as an “undesirable” himself due to his Jewish ancestry.

Notes 1. Gundula Kösters et  al., “Ernst Rüdin’s Unpublished 1922–1925 Study ‘Inheritance of Manic Depression Insanity’: Genetic Research Findings Subordinated to Eugenic Ideology,” PLoS Genetics, 11, no. 1 (November 6, 2015): https://doi.org/10.1371/journal.pgen.1005524 2. Robert Proctor, Racial Hygiene (Cambridge: Harvard University Press, 1988), 96–97. 3. Kösters et al., Ernst Rüdin’s “Unpublished Study.” 4. Ibid. 5. Ibid. 6. Ibid. 7. Ibid. 8. Ibid. 9. Ibid. 10. Ibid. 11. Matthias M. Weber, “Ernst Rüdin 1874–1952: A German Psychiatrist and Geneticist,” American Journal of Medical Genetics, 67, no. 4 (July 26, 1996): 327, https://doi.org/10.1002/(SICI)1096-8628(19960726)67: 43.0.CO;2-N 12. Proctor, Racial Hygiene; 40. 13. Benno Müller-Hill, Murderous Science (Oxford: Oxford University Press, 1988), 28. 14. Proctor, Racial Hygiene, 101.

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15. Ibid., 102–103. 16. Müller-Hill, Murderous Science, 29. 17. Proctor, Racial Hygiene, 106. 18. Proctor, Racial Hygiene, 108; Müller-Hill, Murderous Science, 32. 19. Proctor, Racial Hygiene, 109. 20. Ibid., 110. 21. Müller-Hill, Murderous Science, 31. 22. Ibid., 28–29. 23. Ibid., 30. 24. Henry Friedlander, The Origins of Nazi Genocide (Chapel Hill: University of North Carolina Press, 1995), 62–66. 25. Frederic Wertham, A Sign for Cain: An Exploration of Human Violence (New York: Paperback Library, 1966), 162. 26. Wertham, Sign for Cain, 155–156; Robert Jay Lifton, The Nazi Doctors: Medical Killing and the Psychology of Genocide (New York: Basic Books, 1986): 67; Meyer, Joachim-Ernst, “The Fate of the Mentally Ill During the Third Reich,” Psychological Medicine, 18, 3 (August 1988): 575–576; Gallagher, By Trust Betrayed 70–71; Friedlander, Origins, 80–81; Michael Dudley and Fran Gale 2002, “Psychiatrists as a Moral Community? Psychiatry Under the Nazis and Its Contemporary Relevance,” Australian and New Zealand Journal of Psychiatry, 36, no. 5 (October 2002): 586, https://doi.org/10.1046/j.1440-1614.2002.01072.x 27. Gallagher, Betrayed, 70–71. 28. Friedlander, Origins, 70–71. 29. Lifton, Nazi Doctors, 82–83. 30. Friedlander, Origins, 89. 31. Ibid., 76–80. 32. Proctor, Racial Hygiene, 189. 33. Friedlander, Origins, 73. 34. Gallagher, Betrayed, 11–12. 35. Raymond Daniell, “Goering Accused Reds Baselessly: Admission on Reichstag Fire Charge Read Into Nuremberg Trial: Frisk Held Mass Killer: Former Refugee Links Him to ‘Mercy’ Deaths of Unfit Under Secret Law,” New York Times, January 17, 1946, 14. 36. Gallagher, Betrayed, 13. 37. Friedlander, Origins, 94. 38. Ibid., 96. 39. Ibid., 86. 40. Gallagher, Betrayed, 14–15. 41. Wertham, Sign for Cain, 167. 42. Friedlander, Origins, 98. 43. Ibid., 170–171.

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44. Ibid., 96. 45. Ibid., 101–102. 46. Ibid., 105–106. 47. Ibid., 97–98. 48. Ibid., 127. 49. Friedlander, Origins, 109–110; Gallagher, Betrayed, 185. 50. Gallagher, Betrayed, 185. 51. Friedlander, Origins, 156. 52. Gallagher, Betrayed, 128. 53. Ibid., 128–129. 54. Ibid., 131–136. 55. Ibid., 135. 56. Ibid., 127. 57. Ibid., 127. 58. “An Association With a Long Tradition,” German Association for Psychiatry, Psychotherapy, and Psychosomatics, accessed July 24, 2018, https://www.dgppn.de/en/the-dgppn/history.html 59. Friedlander, Origins, 263. 60. Ibid., 271–277. 61. Ibid., 111. 62. Ibid., 296–298. 63. Wertham, Sign for Cain, 162. 64. Ibid., 167. 65. Friedlander, Origins, 155. 66. Robert S.  Wistricht, Who’s Who in Nazi Germany (New York: Bonanza Books, 1982), 261. 67. Müller-Hill, Murderous Science, 12–13. 68. Weber, “Ernst Rüdin.” 329. 69. Müller-Hill, Murderous Science, 61. 70. Ibid., 121. 71. Wertham, Sign for Cain, 157.

CHAPTER 3

Franz Kallmann and Twin Studies

Franz Kallmann had to flee Germany to avoid the wrath of the Nazis, but he doesn’t seem to have felt any malice toward Rüdin, and indeed testified as a character witness for his old boss during the latter’s “denazification” hearing in 1947.1 Moreover, being on the wrong end of eugenics policies doesn’t seem to have dampened Kallmann’s enthusiasm for the subject. With some help from the Emergency Committee in Aid of Displaced Foreign Physicians, he was able to secure a position at the New York State Psychiatric Institute and Hospital, part of the Columbia University Medical Center. In 1938 he published The Genetics of Schizophrenia, the first English-language account of his work on the subject. In the foreword he lays down the gauntlet: Despite various advances in recent years, psychiatric research is still battling on many fronts, in America as elsewhere, for general recognition of genetic concepts and for practical realization of biological principles. The key position in this battle seems to be held by the disease group of schizophrenia, which continues to crowd mental hospitals all over the world and affords an unceasing source of maladjusted cranks, asocial eccentrics, and the lowest type of criminal offenders.2

He then circumspectly notes that “political developments in Germany closed to me the possibility to complete my research there,”3 and thanks his former mentor Rüdin for his help and advice.

© The Author(s) 2019 P. D. Hahn, Madness and Genetic Determinism, https://doi.org/10.1007/978-3-030-21866-9_3

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Therein follows 272 pages of dense, turgid, almost impenetrable prose. On page 2 Kallmann notes: In order to rationalize objectively the difficult etiologic problems of the origin of schizophrenia, the temptation must resisted to take some unfavorable factor in the personal environment of a psychotic individual as a basic causative element for the psychopathological behavior in the course of a possibly endogenous psychosis.4

He means, I take it, something like this: Family dysfunction does not cause schizophrenia—schizophrenics cause family dysfunction. No evidence is adduced in support of this assertion. He then holds out the promise that an understanding of the hereditary etiology of schizophrenia will put us on the path to a cure, by allowing us to identify specific processes in the brain which are disrupted in schizophrenic individuals, to develop biological tests for these abnormalities, and to devise a cure.5 Eighty years later, these promises remain entirely unfulfilled.

An Arduous Task Kallmann and his co-workers studied a group of 1087 schizophrenic probands constituting all of the definite cases of schizophrenia among patients admitted to the Herzberg Hospital in Berlin during the first ten years of its existence, from 1893 through 1902. They prepared a booklet for each proband containing personal information, clinical history, police reports, and the genetic status of the family of the proband.6 Next, they tracked down as many of the probands as they could (over 70 percent were already dead) as well as their relatives, and conducted personal interviews with them. In all, they compiled information on 1087 probands along with 3279 husbands, wives, and parents, 3384 descendants, 3920 siblings and half-siblings, and 2194 nephews and nieces.7 Kallmann describes the arduousness of the task: “Endless negotiations had to be conducted before the persons in questions were convinced that a genetic investigation of the family was both important and harmless. … Quite a few were bad-humored, unpleasant, and obstinate.”8 What any of the interview subjects may have thought of strangers showing up on their doorsteps asking intrusive questions is not recorded.

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Like Rüdin before him, Kallmann also collated data from clinical histories, police reports, school reports, and consulates, and like Rüdin he felt qualified to render diagnoses of individuals he had never met, most of whom were long dead. Kallmann tallied the number of relatives who were judged to belong to the class of “schizoform abnormalities,” which he judged to be “carriers of the schizophrenic trait.” He divided the subjects into the following categories9: I. Schizophrenics

(a) Definite cases (b) Doubtful cases II. Schizoid personalities



(a) Schizoid eccentrics and borderline cases (b) Schizoid psychopaths

Kallmann’s category of “schizoid borderline cases” included “the cranks and eccentrics suggesting schizophrenia and all psychopathic types with schizoid personality—that is, stubborn and perverse recalcitrants, malicious and cold-hearted despots, superstitious and pietistic religio-­ maniacs, secretive reclusives, sectarian dreamers out of touch with reality, and the over-pedantic, avaricious and literal-minded people.”10 His “schizoid psychopaths” included “the unsociable, cold-hearted, indecisive and fanatic types regarded by Schneider as prototypes of the catanoid, heboid, schizoid and paranoid cases respectively, as well as Hoffman’s bullheaded oafs, malicious tyrants, queer cranks, over-pedantic schemers, prudish ‘model children’ and daydreamers out of all touch with reality.”11 Is this the language of science? Or is this the language of a man consumed with anger and hatred toward his fellow human beings, and who has set himself on a quest to rid the world of what he sees as the source of that anger? Moreover, this grab-bag of ill-defined categories seems to intergrade imperceptibly into normality, and Kallmann himself seems to admit as much when he notes: “It was astonishing to see how many eccentric borderline cases were living more or less peaceably outside institutions and how many of them were fairly well-adjusted socially.”12

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Can this vast spectrum of human woes and eccentricities really be the work of a single gene? Kallmann thought so, and indeed he found a correlation between relatedness to schizophrenic probands and the presence of “schizoform abnormalities,” and concluded that schizophrenia was a single-locus trait controlled by a recessive gene, with schizophrenics possessing two copies of the schizophrenia gene, and those with “schizoid personalities” having only one.13 Nevertheless, the correlation was a good deal smaller than would be expected if the penetrance of the “schizophrenia taint” was 100 percent. Kallmann was forced to postulate that what was being inherited was a predisposition to schizoform abnormalities, which was expressed only in the presence of environmental stressors.14 What might those stressors be? Kallmann had already ruled out the home environment, with his proclamation that dysfunctional families do not cause schizophrenia, and so was forced to invoke some vaguely defined “heredito-constitutional factors.”15 The conceptual tools for measuring the heritability of polygenic traits had been elucidated by the geneticists R.A. Fisher and Sewall Wright some twenty years earlier, so it is not clear why Kallmann insisted on clinging to a single-gene model of inheritance. Nevertheless, having satisfied himself that schizophrenia and related conditions were caused by a single gene, Kallmann then turned his attention to the matter to what society ought to do about it. He noted correctly that the fertility rate for schizophrenics was already far below that of the general population, and so decided that the problem would not be solved merely by preventing the “homozygotes” from reproducing. Instead, Kallmann turned his attention to the “heterozygous” carriers of the schizophrenic trait, recommending that parents, siblings, and even half-brothers and half-sisters of schizophrenics be dissuaded from reproducing. Even asymptomatic relatives were under suspicion of being “latent carriers of the schizophrenia trait.”16 In The Genetics of Schizophrenia, Kallmann made it clear that he did not endorse the kind of forcible mass sterilization program that was taking place in his native Germany at the time. Rather, he recommended education and genetic counseling for prospective married couples, with mandatory sterilization being reserved only for those “incorrigibles” who would not accept voluntary sterilization.17

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The Founding Father of Psychiatric Genetics in America Kallmann continued his studies on the inheritance of schizophrenia in America, focusing on twin studies. Such studies have long held a special allure for researchers who hoped to control environmental confounders by comparing monozygotic twin pairs (who share 100 percent of their genes identical by descent) with dizygotic twin pairs (who share only 50 percent). Twin researchers assume that the environment shared by MZ twins is no more alike than that shared by DZ twins. This assumption, called the equal environment assumption, is the foundation of twin studies. The proportion of twin pairs in which both members exhibit the trait, divided by the total number of twin pairs in which at least one member exhibits the trait, is called the concordance rate. In order to estimate the heritability of a trait, or the proportion of variability in a population that is due to genetic variability, researchers take the MZ twin concordance rate, subtract the DZ twin concordance rate, and multiply the result by two. In a 1942 paper in the American Journal of Psychiatry, Kallmann and his co-author S. Eugene Barrera reported some preliminary results of pairs of twins, in which at least one member was schizophrenic: By tracing the constitutional development of these co-twins from childhood until disease onset photographically and by the aid of carefully obtained histories, we found in the great majority of twin pairs with only one schizophrenic member that the non-diseased twin had been physically stronger, taller, and heavier, and far more resistant to infections and other ailments than the twin who did develop schizophrenia.18

In conclusion, they noted: As soon as we shall be able to duplicate or sufficiently reinforce the heredoconstitutional mechanisms responsible for a satisfactory resistance to the disintegrating effects of a schizophrenic process, the therapeutic problem of schizophrenia will be nearer its final solution.19

In a 1946 paper in the same journal,20 Kallmann described the results of his twin studies in more detail. He examined 794 twin index cases culled from resident populations and new admissions to all mental hospitals under the supervision of the New York State Department of Mental

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Hygiene, for which the co-twin was available for examination at the age of fifteen years. From these, 691 twin pairs were selected for analysis (he never explained why the remainder were omitted). These 691 twin pairs included 517 DZ pairs and 174 MZ pairs. Kallmann provides almost no detail on how the data on the co-twins was collected. As one of his defenders later noted, “The abbreviated manner in which Kallmann reported his data left him more open than he would otherwise have been to criticism.”21 Indeed. Nevertheless, let’s take a look at what the data says. Kallmann reports that for the DZ twins, the percentage of concordant twin pairs was 14.7 percent, while for the MZ pairs the percentage was a staggering 85.8 percent.22 He considered these findings as overwhelming evidence of an inherited basis for schizophrenia, which was manifest in most but not all cases. What are we to make of Kallmann’s results? Jay Joseph is a clinical psychologist, the author of Schizophrenia and Genetics: The End of an Illusion, and a long-standing critic of twin studies in particular and genetic determinist views of human behavior in general. In a 2013 book chapter,23 he reviewed the results of the twin studies of schizophrenia. He divided these studies into two categories: “classical” studies (including Kallmann’s) published before 1962, and “contemporary” studies published thereafter. When we examine the data Joseph has collated, one point is immediately apparent: no study has ever come close to replicating the 85.8 percent concordance rate reported by Kallmann. The second point is that reported concordance rates vary wildly, from Kallmann’s 85.8 percent to 11 percent reported in a 1984 study by Koskenvuo and his colleagues.24 The third is that the concordance rate has been steadily dropping over the years. The average concordance rate for the classical studies is 61 percent, as opposed to 23 percent for the contemporary studies. Joseph concludes “in the more methodologically sound [contemporary] studies, when one member of an MZ pair is diagnosed with schizophrenia, nearly 80% of the time his genetically identical co-twin is not diagnosed”25 [Italics in the original]. Supporters of the twin study method have attempted to explain the wildly divergent concordance rates in terms of differences in diagnostic criteria and completeness of assessment on the parts of the different researchers.26 But how can these researchers claim to be measuring the

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hereditary basis of schizophrenia if they cannot even agree among themselves as to what schizophrenia is? All this makes it clear that while we do not have a precise estimate of the concordance rate, we do know that even for genetically identical MZ twins, environmental factors must be of tremendous importance in the genesis of schizophrenia. There is no such thing as a gene for schizophrenia. At most there might be a genetic predisposition to schizophrenia, with environmental influences playing the deciding role. Even the 11 percent concordance rate reported by Koskenvuo et  al. might exaggerate the importance of genetic factors. The concordance rate factors in not just genetic variability but also any confounding environmental factors the researchers have failed to control for. What might those confounding factors be? The same year the paper by Koskenvuo and his colleagues appeared, three prominent scientists— geneticist R.C. Lewontin, neurobiologist Steven Rose, and psychologist Leon Kamin—published Not in Our Genes: Biology, Ideology, and Human Nature.27 The book was a withering broadside directed against genetic determinist views of human nature, and in Chap. 8 the authors direct their attention toward twin studies of schizophrenia. They point out several obvious confounders inherent in such studies. One of these confounding factors is that co-twins of index cases often are not available for examination, and so researchers must make educated guesses regarding both a given twin is schizophrenic or not, and whether or not a given twin pair is MZ or DZ. Such judgments typically are made by the same person, allowing investigator bias to contaminate the diagnosis.28 As we have already seen, Kallmann explicitly stated that he used the diagnostic status (i.e. schizophrenic or non-schizophrenic) of one twin to help determine whether the other one was schizophrenic or not, and used the inflated concordance rate as evidence of the genetic basis of schizophrenia. This sort of blatantly circular argument has been employed by other twin researchers as well.29 Even determining whether or not a given twin pair is mono- or dizygotic is no simple matter, as demonstrated by a 1970 study of American war veteran twins.30 The researchers did not examine any of the twins in person, instead relying on questionnaires to determine whether a given pair was MZ or DZ. The forms asked twins whether they looked as alike as two peas in a pod, whether they were often mistaken for one another, and so on.

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A startling finding appeared from all this. When one twin of a pair of twins diagnosed as schizophrenic returned the questionnaire, 31.3 percent indicated they were MZ. When the non-affected member of a pair returned the questionnaire, only 17.2 percent said they were MZ.31 What could be the reason for this discrepancy? Healthy twins of persons diagnosed with schizophrenia have an obvious vested interest in not being identified as MZ, even if they are, thereby escaping the stigma of possessing the hereditary taint of this condition—especially when this stigma could cause one to be considered unsuitable as a marriage partner, or even a candidate for sterilization.32 All of these factors would tend to exaggerate the concordance rates for MZ twin pairs as opposed to DZ ones. But there is an even more important point to be made here. Any theoretical model is only as strong as its underlying assumptions. The fundamental assumption underlying twin studies, the equal environment assumption, is that MZ and DZ twin pairs share the same amount of environmental similarity. This assumption, which forms the bedrock of the entire field of twin studies, is demonstrably false, a point made at least as far back as 1960 by psychiatrist Don Jackson in his review paper “A critique of the literature on the genetics of schizophrenia.”33 Since then a mountain of empirical studies have confirmed this point.34 Probably anyone with experience of life as it is lived could have guessed as much. Jackson summarized three lines of evidence35 indicating that higher concordance rates among MZ twins are due to greater environmental similarity: (1) Concordance rates for female DZ twin pairs are greater than those of male pairs (presumably due to girls being kept under closer parental supervision than boys—a cultural artifact that was even more true in the era in which most of the subjects of these studies grew up), (2) DZ twin pairs are more concordant than pairs of full siblings born apart, and (3) same-sex DZ twin pairs are more concordant than opposite-sex pairs. All these comparisons support the common-sense view that concordance rates are increased by closer identification and greater environmental similarity of sibling pairs—as are found in MZ twins in comparison to DZ pairs.36 But rather than acknowledge this and close up shop, twin researchers have advanced two arguments in order to salvage the theoretical basis of their field. These arguments have been dissected in a series of writings by the aforementioned Dr. Joseph.37

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Twin researchers have defended the theoretical basis of twin studies with what has been dubbed the “twins create their own environment” argument. In a 1972 paper, psychiatrist Edith Zerbin-Rüdin of the Max Planck Institute for Psychiatry (the successor to the KWI) provided an example: The large difference between the concordance figures for MZ and DZ twins cannot be explained exclusively by the more similar environment of the MZ twins. If MZ twins create a similar environment through their greater similarity, they do so because of the greater inherited similarity in their appearance and response modes. Thus, in a roundabout way, we still come back to the importance of heredity.38

This line of reasoning has been used by numerous other researchers in this field. But, as Joseph39 points out, it is a circular argument. Zerbin-­ Rüdin is telling us, in effect, that the greater phenotypic similarity between MZ twins compared to their DZ counterparts is caused by their greater genetic similarity—and we know this, because identical twins are genetically more similar than DZ twins! Indeed, with her use of the phrase “In a roundabout way,” Zerbin-­ Rüdin herself seems to be acknowledging the circularity of her argument. And it’s all a moot point anyway. As Joseph observes, the fact that MZ twins are genetically more similar to one another than DZ twins may explain why their environments are more similar as well, but it does not alter the fact that they are more similar.40 Supporters of the twin method have made one last attempt to salvage the theoretical basis of twin studies by asserting that the environments are assumed to be similar in respect to the environmental factors that contribute to the etiology of schizophrenia. But since these same researchers admit they do not know what those factors are,41 this argument falls flat. Indeed, the argument is a violation of one of the most basic tenets of science, which is that the burden of proof always rests on the person making a claim, not on the skeptic or doubter. At this point, as another critic of twin studies notes, the equal environment assumption might as well be called the “unequal-environments-­ don’t-matter assumption.”42 Joseph argues that the assumptions behind twin studies can lead only to the obsolescence of that method.43 The problem with family studies is that environmental influences are correlated with relatedness, making it ­difficult

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to separate the influences of heredity from those of environment. If that objection can be waived for the case of MZ twins, there is no reason for it not to be waived for any other kind of family relationship. Or, if we assume that unequal environments don’t matter in the case of MZ twins, there is no reason not to make that assumption with every other kind of family relationship as well. Either way, twin studies, seen in this light, become just a subset of family studies, subject to all the same limitations and with nothing special to recommend them.44 This is more than a matter of mere academic interest, as Joseph makes clear: The conclusions of twin studies have influenced decisions resulting in the allocation of millions of dollars of research money in the direction of genetic research and away from environmental causes of human problems. Pseudoscientific theories of racial and class inequality have been based, in part, on the study of twins. In other words, there is a lot at stake. If the principal defender of the twin method and the equal environment assumption cannot adequately define what he is defending, then this alone raises questions about the assumption.45

Lewontin and his co-authors summed up matters thusly: The Kallmann data still are presented, unblushingly, in purportedly serious reviews of research, but they are now counterbalanced by more recent and more modest results. Perhaps the chief harm brought about by Kallmann’s deluge of incredible and poorly documented data was to create a climate in which the findings of subsequent workers seemed so reasonable and moderate that they escaped serious scrutiny.46

Indeed. To this day the results of Kallmann and his successors continue to be cited as proof of the genetic basis of schizophrenia.47 As for Kallmann himself: he never lost his enthusiasm for his chosen mission of improving the human gene pool. In January of 1945, as the Holocaust continued to operate at full speed, he authored a review article for the American Journal of Psychiatry in which he proclaimed “Psychiatric eugenics appears to be safely on the march.”48 Kallmann continued to write an annual review on the subject for the next nineteen years. When he died in 1965, his obituary49 in Eugenics Quarterly noted:

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The distinguished career of Dr. Franz J. Kallmann as a researcher and teacher came to a close with his death on May 12. His contributions to the field of human genetics were established with his classic work on the genetics of schizophrenia. By 1936 his opposition to Nazi laws requiring compulsory sterilization of mentally ill patients had made his position in his native Germany scientifically untenable. Coming to the United States, he almost single-handedly founded the discipline of psychiatric genetics in this country.

Notes 1. Benno Müller-Hill, Murderous Science (Oxford: Oxford University Press, 1988), 122. 2. Franz J. Kallmann, The Genetics of Schizophrenia (New York: J.J. Augustin, 1938), xiii. 3. Ibid., xiv. 4. Ibid., 2. 5. Ibid., 2. 6. Ibid., 7–16. 7. Ibid., 18. 8. Ibid., 16. 9. Ibid., 101. 10. Ibid., 37. 11. Ibid., 102. 12. Ibid., 104. 13. Ibid., 117. 14. Ibid., 117. 15. Ibid., 153–154. 16. Ibid., 131. 17. Ibid., 267. 18. Franz J.  Kallmann and S.  Eugene Barrera, “The Heredoconstitutional Mechanisms of Predisposition and Resistance to Schizophrenia,” American Journal of Psychiatry, 98, no. 4 (January 1, 1942): 547. 19. Kallmann and Barrera, “Heredoconstitutional Mechanisms,” 550. 20. Franz J. Kallmann, “The Genetic Theory of Schizophrenia: An Analysis of 691 Schizophrenic Twin Families,” American Journal of Psychiatry, 103, no. 3 (November 1946): 309–322. 21. James Shields, Irving I.  Gottesman, and Eliot Slater, “Kallmann’s 1946 Schizophrenic Twin Study in the Light of New Information,” Acta Psychiatrica Scandinavica, 43, no. 4 (December 1967): 385, https://doi. org/10.1111/j.1600-0447.1967.tb05776.x 22. Kallmann, “Genetic Theory of Schizophrenia,” 313.

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23. Joseph, “‘Schizophrenia’ and Heredity: Why the Emperor (Still) Has No Genes,” in Models of Madness: Psychological, Social, and Biological Approaches to Psychosis, ed. John Read and Jaqui Dillon (Abingdon: Routledge, 2013), 72–89. 24. M.  Koskenvuo et  al., “Psychiatric Hospitalization in Twins,” Acta Geneticae Medicae et Gemellologiae, 33, no. 2 (1984): 321. 25. Joseph, “Schizophrenia and Heredity,” 73. 26. Kenneth Kendler, “Overview: A Current Perspective on Twin Studies in Schizophrenia,” American Journal of Psychiatry, 140, no. 11 (November 1983): 1419, https://doi.org/10.1176/ajp.140.11.1413 27. R.C.  Lewontin, Steven Rose, and Leon J.  Kamin, Not In Our Genes: Biology, Ideology, and Human Nature (New York: Random House, 1984). 28. Ibid., 214. 29. Ibid., 214–216. 30. Axel Hoffer and William Pollin, “Schizophrenia in the NAS-NRC Panel of 15,909 Veteran Twin Pairs,” Archives of General Psychiatry, 23, no. 5 (May 1976): 472. 31. Hoffer and Pollin, “Schizophrenia,” 472. 32. Lewontin, Rose, and Kamin, Not In Our Genes, 219. 33. Donald D.  Jackson, “A Critique of the Literature on the Genetics of Schizophrenia,” in The Etiology of Schizophrenia, ed. Donald D. Jackson, (New York: Basic Books, 1960) 63–64. 34. Jay Joseph, “The Equal Environment Assumption of the Classical Twin Method: A Critical Analysis,” Journal of Mind and Behavior, 19, no. 3 (Summer 1998): 323–358; Joseph, “‘Schizophrenia’ and Heredity,” 72–89; Jay Joseph, Schizophrenia and Genetics, (Pennsauken: BookBaby, 2017), chapter 4, Kindle. 35. Jackson, “A Critique of the Literature,” 67–68. 36. Ibid. 37. Joseph, “Equal Environment Assumption,” 330–334, 338–342; Joseph, “‘Schizophrenia’ and Heredity,” 72–89; Joseph, Schizophrenia and Genetics, (Pennsauken: BookBaby, 2017), chapter 4, Kindle. 38. Edith Zerbin-Rüdin, “Genetic Research and the Theory of Schizophrenia,” International Journal of Mental Health, 1 (1972): 48. 39. Joseph, “‘Schizophrenia’ and Heredity,” 76; Joseph, Schizophrenia and Genetics, (Pennsauken: BookBaby, 2017), chapter 4, Kindle. 40. Joseph, Schizophrenia and Genetics, (Pennsauken: BookBaby, 2017), chapter 4, Kindle. 41. Kenneth Kendler, “The Genetics of Schizophrenia: An Overview,” in Nosology, Epidemiology, and Genetics of Schizophrenia, ed. Ming T. Tsaung and John C.  Simpson, (Amsterdam and New  York: Elsevier Science Publishers, 1988), 454.

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42. A. Pam, S.S. Kemker, C.A. Ross, and R. Golden, “The ‘Equal Environments Assumption’ in MZ-DZ Twin Comparisons: An Untenable Premise of Psychiatric Genetics?” Acta Geneticae Medicae et Gemellologiae, 45, no. 3 (1996): 354. 43. Jay Joseph, “Twin Studies in Psychiatry and Psychology: Science or Pseudoscience?” Psychiatric Quarterly, 73, no. 1 (Spring 2002): 76–77. 44. Ibid., 77. 45. Joseph “Equal Environment Assumption,” 334. 46. Lewontin, Rose, and Kamin, Not in Our Genes, 212. 47. Irving I.  Gottesman “Psychopathology Through a Life Span Genetic Prism,” American Psychologist, 56, no. 11 (November 2001): 870, Kathleen Ries Merikangas and Neil Risch, “Will the Genomics Revolution Revolutionize Psychiatry?” American Journal of Psychiatry, 160, no. 4 (April 2003): 625, https://doi.org/10.1176/appi.ajp.160.4.625 48. Franz J.  Kallmann “Heredity and Eugenics,” American Journal of Psychiatry, 101, no. 4 (January 1, 1945): 536. 49. L. Erlenmeyer-Kimling et al. “Franz J. Kallmann, 1897–1965,” Eugenics Quarterly, 12, (1965): 123.

CHAPTER 4

The Story of the Genain Sisters

No account of the era of twin studies would be complete without a discussion of the Genain Quadruplets. Like the story of the Kallikak family,1 the sad sordid tale of the Genain sisters was intended to be an object lesson on the primacy of heredity, but in fact it revealed more about its chroniclers than it did about the role of genes in the etiology of mental illness. The Genain sisters were identical quadruplets, born in 1930, all of whom were diagnosed with schizophrenia as young adults, and who were studied intensively for three years at the National Institutes of Health (NIH) in Bethesda, Maryland. Their story is told in The Genain Quadruplets: A Case Study and Theoretical Analysis of Heredity and Environment in Schizophrenia,2 edited by David Rosenthal, a research psychologist at the National Institute of Mental Health (NIMH). A total of twenty-five different authors contributed to the volume: psychologists, psychiatrists, social workers, a geneticist, a sociologist, a statistician, a social science analyst, a physiologist, and a handwriting analyst.3 It’s a massive tome, over 600 pages in length. The name “Genain” is a pseudonym, derived from the Greek words genos and ainos and literally means “dire birth.” The individual sisters were identified by the pseudonyms Nora, Iris, Myra, and Hester (note that the first initials of their names spell out the abbreviation for the National Institute of Mental Health).4 Their parents were identified by the pseudonyms Henry and Gertrude, and all of their acquaintances and relatives are identified by pseudonyms as well. © The Author(s) 2019 P. D. Hahn, Madness and Genetic Determinism, https://doi.org/10.1007/978-3-030-21866-9_4

35

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In the introduction, Rosenthal states: When one first learns that the quadruplets are both monozygotic and schizophrenic, one can hardly help but wonder what further proof of a genetic etiology of schizophrenia anyone would want to have. As one delves into the family history, however, the matter seems hardly so apparent or simple.5

This is followed by a 125-page account of that history6—a tale of abuse that began literally when the girls were in the cradle, and continued right up until they were taken to the NIH for study.

A Horror Show of a Childhood Both Henry and Gertrude were born into large farming families. Henry left school after the eleventh grade and worked as a farmhand and at a variety of other blue-collar jobs, none of which he stayed at for very long.7 Gertrude’s father didn’t believe girls needed to be educated, and she did not enter school until she was seven. At the age of fourteen, tired of being the family workhorse, she left home to go live with her grandmother. Her father showed up with a shotgun and demanded that she return, and when she refused, he told her never to enter his house again.8 Gertrude managed to complete high school, staying with various friends and relatives and supporting herself by working as a telephone operator, a maid, and a waitress. After flunking out of nursing school, she went to work as a practical nurse for a Dr. Arlington.9 When she met Henry, he was in his mid-30s, and spending his discretionary time hanging out with a gaggle of young men a dozen or so years his junior, drinking and shooting pool.10 He also was having an affair with his brother’s wife, and Dr. Arlington had already treated Henry’s brother and sister-in-law for venereal disease.11 (There is a bizarre twist to this story. Years later, Henry’s sister-in-law left Henry’s brother and married another man, who was subsequently murdered. There were hints that Henry and his brother were responsible, and detectives even stopped by the home to question Henry, although no charges were ever filed.12) Henry asked Gertrude to marry him. She refused, and first he threatened to kill her, then he threatened to kill himself, and then he took to his sickbed. Henry’s family told Gertrude that if she didn’t marry him, he would die of a broken heart.13

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Dr. Arlington counseled Gertrude that she was being unfair to Henry, and at last she relented and agreed to get married. At the time, Gertrude had $8000 in the bank, while Henry had a total of $80 to his name.14 Gertrude was not happy in her new life with Henry, and after three years of marriage decided to have a baby in order to find an outlet for her love. When she told her doctor she suspected she was carrying quadruplets, he was incredulous and asked “Aren’t you a white woman?”15 At the time, Henry was working two and a half days a week as a shipping clerk. When Gertrude gave birth to quadruplet girls, his reaction was “What will they think my wife is—a bitch dog?” Two months later, Henry was laid off from his job and didn’t work for two years.16 Still, they had some help. The city gave them use of a large house, rent-­ free for a year. A dairy provided free milk for all the girls, and other companies provided baby products free of charge. Henry’s former employer sent a check for $100.17 The family became local celebrities. A newspaper headline proclaimed “Daddy Genain quadruply glad.”18 But daily life in the Genain home stood in stark contrast to the rosy picture presented in the headlines. Henry’s octogenarian mother came to live with them, but she was no help at all. A family friend, Mrs. Wheeler, volunteered to help, but the portrait that emerges from the girls’ preschool years is one of a young mother nearly overwhelmed with the task of caring for four babies in assembly-line fashion, feeding them, changing them, bathing them, and putting them down for naps, all according to a rigid schedule.19 Desperate for her husband to find a job, Gertrude convinced him to run for constable. Cashing in on his new-found fame, he was elected by a wide margin. He held this job for twenty-three years, even though, in the words of a colleague, “he had no qualifications whatsoever.”20 Henry would come home drunk, throw things, shove Gertrude, and threaten and verbally abuse her and the children. Once he banged Nora’s and Myra’s heads together “to stop them from crying.” The girls were eight or nine months old at the time.21 Another night he fired a gun at Gertrude, later explaining he had thought she was a burglar. The bullet missed her, although it did leave a hole in her nightgown.22 Henry engaged in extramarital affairs, and impregnated at least two other women. He also contracted a venereal disease, which took six months to treat and cure. During this time Gertrude slept on a pad on the floor next to her husband’s bed. When her mother-in-law found out Gertrude was no longer sleeping with her husband, she told her daughter-­ in-­law she was a bad wife.23

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At the age of five the girls began school, although they were never allowed to visit the homes of other children, or to have other children visit them. The girls grew up socially isolated, with no real friends. People described the quads as passive, timid, and unusually quiet, with little spontaneity or initiative, and the home atmosphere as “fear-ridden,” devoid of fun and humor, and very restrictive.24 During the girl’s sixth year, Mrs. Genain decided to leave and saw a lawyer about a divorce. After talking with the lawyer, Henry promised to mend his ways. Later he told Gertrude, “If you leave me, I will find you wherever you go and I’ll kill you.”25 Henry behaved toward his wife in a suspicious and controlling manner. When she corresponded with her family, he insisted on reading what she wrote. When Gertrude’s mother came to visit, he behaved so nastily toward her she never returned. When she later died, Henry ordered Gertrude not to go to the funeral, and later forbade her to attend the funeral of her father as well.26 Like Gertrude’s father, Henry did not see any value in educating girls, and often sent the girls to bed before they had completed their homework. “He was always angry and hateful and mean,” Myra recalled. “He didn’t actually hurt us, but he banged us around a little bit.”27 Years later, Hester claimed that she had been molested by the school janitor on a regular basis, from the age of seven to the age of eleven. The janitor denied these allegations, and no charges were ever filed.28 Around the same time the molestation was said to have taken place, Hester began masturbating compulsively. Her parents were shocked, and Henry would punish her severely for this behavior: whippings, holding her head underwater, even pouring carbolic acid on the child’s vulva.29 Hester continued masturbating, even engaging in mutual masturbation with her sister Iris, with whom she shared a bed. Gertrude took her daughter to a Dr. Booth, who lectured her on the evils of masturbation and told her she must stop. The same doctor later told NIMH investigators that he found Hester “homely and coarse, not feminine like her sisters,” and probably an early schizophrenic.30 Dr. Booth ordered surgical mutilations for both Hester and Iris, to stop them from masturbating. When Hester broke her stitches while in the hospital, Dr. Booth promised to “fix her now” and threatened to “cut all the flesh out.” He also prescribed sedatives, and ordered Gertrude to tie the girls’ hands at night.31

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Hester and Iris continued masturbating and engaging in sex acts with one another. In front of both girls, Dr. Booth told Gertrude “I can tell you right now, they are institution cases.”32 Later the girls entered junior high school, where they were tormented by boys who knocked their books out of their hands, threw food at them, and pushed them down stairs. Hester began engaging in sex acts with a boy in an empty room after school.33 When Myra began developing breasts, her mother inquired if she had fallen and asked, “What did you do at school that made you start getting these bumps?” and applied a salve to make the “swellings” go down.34 Henry, for his part, never allowed the girls to have any privacy at home, barging into their rooms when they were undressing and even standing in the bathroom doorway watching them change their sanitary pads.35 All four of the girls continued to wet their beds throughout childhood, Nora and Myra until they were sixteen, Iris and Hester until they were eighteen.36 During all this time local newspapers were running puff pieces portraying the Genains as the ideal American family. When the girls turned fourteen, one headline referred to the family patriarch as “Jolly Henry, daddy of 4-of-a-kind.”37 In the eleventh grade, Hester began doing poorly in school and acting out at home, attacking her mother and her sister Nora. Henry reacted to these outbursts by holding Hester’s head under water. During this time, Hester began staying after school, telling her parents that she was doing schoolwork. She later claimed that one of her teachers had been molesting her while she supposedly had been in the library studying.38 That summer a married couple who knew Gertrude offered to take in Hester but her parents refused, and the following year Hester dropped out of school. Her condition continued to deteriorate: she would throw temper tantrums, jump up and down, slap herself, pull her own hair, and kick and strike out with her hands.39 Hester remained at home with her mother and became the family workhorse: dusting, doing the housework, and washing the dishes. Meanwhile all three of her sisters graduated from high school and found full-time clerical work. They continued to live at home, and their father continued to restrict their movements, and forbade them to go on dates.40 If one of the girls went out somewhere, Henry would show up in his car, honking the horn until she came out. He also insisted on driving Nora to work and home each day (they both worked in the same building), and also taking her home every day for lunch.41

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Henry continued his practice of watching the girls getting dressed in the morning, and changing their sanitary pads. He also would pat the girls on the buttocks and grab their breasts. When his wife objected, he told her he was testing them to see how they would react when they went on dates—the dates they were forbidden ever to go on.42 One day at work the elevator operator tried to rape Nora, pulling down her panties and pressing his penis against her crotch. Nora fought back and ran away. She told her father who dismissed the incident, sneering “Just shut your mouth and go on to work.”43 Shortly after that, Nora became ill, suffering from nausea and fatigue. She quit her job and took to her sick bed for the next three months. Iris developed similar symptoms.44 Henry, who by then was suffering from obesity and adult-onset diabetes, told Nora “I’m physically ill, you’re mentally ill. I have guns and I may use them, and I’ll not leave your mother out.” Nora began having crying spells and threatening suicide.45 Meanwhile Iris was sexually assaulted at work. A man entered the washroom she was using, pulled up her dress and tried to pull down her panties. Iris screamed and her attacker fled when someone else entered the room.46 Iris told her supervisor, who informed her that her attacker was an important man who could not be fired, but he assured her he would speak to him about the incident. Iris began experiencing vomiting spells and confusion. Her mother attributed her daughter’s problems to excessive masturbation.47 Nora began pulling her hair and hallucinating, believing people were talking about her and trampling on her. She was admitted to the state hospital, and a report on her noted “Her eyes are staring, she moans, groans, and trembles, she chews her fingers in her mouth or she runs them through her hair.” She was treated with electroshock and Metrazol and discharged as “moderately improved.”48 Nora’s condition subsequently got worse. She suffered from ataxia, blurred vision, dizziness, and inability to bear noise. She said she felt as if she were dreaming all the time, and developed muscle contractions and severe vomiting. Dr. Grant, the family physician, attributed her problems to menstrual difficulties. Once again she was hospitalized and diagnosed with acute schizophrenia.49 Meanwhile at home, Henry began displaying great anger toward Hester. Once he kicked a frying pan out of her hands, sending the pan flying into her face and chipping a tooth.50

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Iris also continued to deteriorate. She began experiencing nausea and restlessness, then finally had a breakdown, screaming “Someone is bothering me. I am pinned down. I am bothered by someone, and they want to fight, and I don’t want to fight.” She began hearing voices and attacked her mother. Like her sister Nora, she was hospitalized and diagnosed with acute schizophrenia. Iris underwent a course of sixteen electroshock treatments and reported that she felt “much better.”51 After Iris returned home, their mother informed Dr. Grant that Iris was back to her usual self again. She reported that Henry was “pleasant and kind” to Iris and Nora, and often took the girls riding.52 Iris received two more shock treatments as an outpatient, and then her condition became markedly worse as she would repeatedly lapse into a catatonic stupor. She was given nine more shock treatments as an outpatient, and then was re-hospitalized and subjected to eight more.53 Meanwhile, Hester continued her role as the family workhorse: taking out the garbage, hanging out the laundry, and cutting the grass. She began experiencing migraine headaches, and started acting out: destroying her sisters’ clothes, smashing light bulbs, and ripping the buttons off her coat. Once she and her mother went to visit a neighbor, who noticed Hester’s body was covered with bruises. Gertrude told the neighbor Hester had fallen down a flight of stairs. Another neighbor noticed that Hester seemed “mad at the whole world.”54 By now Henry was downing twelve to sixteen bottles of beer a day, and experiencing recurring nightmares of murder. He would wake up, demand his gun, and search the house for intruders. Nora wrote to Dr. Grant, suggesting her father was the one who really needed help. Later that year Nora attempted suicide, was re-hospitalized, and given more shock treatments.55 One day at work Myra was sexually assaulted by a client, but when he heard a loud noise he zipped up his trousers and fled. Myra told her boss, who instructed her not to report the incident to the police.56 Myra did as she was told, but that night she woke up screaming, experiencing severe stomach pains and uncontrollable vomiting. She developed a fever and a rash. Myra reported to work the next morning but went home at noon, suffering from more stomach pains, chills, nausea, vomiting, dizziness, and blurred vision.57 Myra took to bed for three weeks. Gertrude decided her daughter was overreacting to the incident, and took her to Dr. Grant, who recommended hospitalization. Myra refused, fearing she would be subjected to

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electroshock, as her sisters had been. Dr. Grant told her he would not have her hospitalized if she promised to do better, and she agreed.58 Meanwhile her sister Iris was hospitalized yet again and subjected to more electroshock treatments, making sixty-seven in all.59 Soon after, Hester had a psychotic breakdown. She kept saying it was getting dark, even when the sun was shining. She complained of being paralyzed, and then began screaming about a fire that threatened to engulf the whole family.60 Gertrude had enough. She was recovering from a bladder operation, and she felt that she was on the verge of a breakdown herself. The entire family met with Dr. Grant, and he convinced them to go to the National Institutes of Health.61

Aftermath The family remained at the NIH for the next three years, undergoing a battery of tests—electroencephalograms, galvanic skin response tests, fingerprint ridge counts, handwriting analysis, and so on. Each of the sisters was assigned a separate therapist, and Henry and Gertrude each were assigned his or her own social worker. They both went back to their hometown, although they returned to Bethesda from time to time to visit their daughters. During the third year of their daughters’ stay at the NIH, Henry died from cirrhosis of the liver.62 A newspaper account eulogized him as a “conscientious public official of splendid reputation.”63 Eventually Myra got well enough to move into a halfway house, and procured full-time clerical work. She married an active-duty serviceman and, while their marriage was not without problems, she seemed to be making a reasonable adjustment to the wider world.64 The other sisters did not fare as well. All three were remanded to another mental institution in their home state. At the time the book was written, Nora had gotten well enough to go home and live with her mother, and was also working full time. She had few friends and never dated, although she had purchased a chord organ and was trying to learn to read music.65 Iris and Hester still were confined to the state hospital at the time of writing. Iris’s prognosis was considered “guarded,” while Hester’s was “poor.”66 In 1981, the sisters were brought back to the NIH for more testing,67 and fifteen years later, some of Rosenthal’s colleagues from the NIH visited the Genain sisters in their hometown for still more testing.68 Rosenthal himself was long retired by then, and he died later that year.69

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As for the Genain sisters themselves, Myra was the only one to marry and have a career, although her marriage ended in divorce. She and her husband had two sons, the older one of whom died in 1996 due to AIDS contracted from a blood transfusion. Her surviving son by then was married with a son of his own.70 Myra’s son reluctantly allowed the NIH scientists to take a sample of his blood, but he refused to participate in neuropsychological testing or to allow investigators any access to his own son at all. Researchers characterized him as “generally suspicious and mistrustful,” and he stated he did not believe any good would come to either his mother or his aunts from participation in the study.71 Myra is the only one of the sisters still living. She has even published a book, under her real name,72 telling her story of what it was like growing up as a member of a famous set of quadruplets. In the book, she acknowledges that her father was abusive and controlling. Every evening when their father arrived at home, the girls had to scramble to pick up their toys, then sit in the rocking chairs in absolute silence. They were not allowed to learn to swim or ice skate, to play with other children (even their own cousins), go to the library, talk on the telephone, work summer jobs, drink alcohol, drive, or go to movies, sporting events, parties, picnics, or dances. They were forbidden ever to date or marry. She skips over the most gory details of the abuse, although she does mention that her sister Hester was made to wash out their father’s smelly spittoon every day, as well as to clean up the sink every time their father vomited in it in the course of his many drunken binges. She also remembers a time at the NIH when their father tried to strangle their mother, and was restrained by the staff and placed in a straitjacket. And what is the lesson to be learned here? None of the relentless testing performed by scientists on the Genain sisters has brought mankind an inch closer to understanding the etiology of schizophrenia, or devising a cure. In the last part of the Genain Quadruplets, Rosenthal reviews the evidence for genetic and environmental theories of the etiology of schizophrenia, and in the final chapter he writes: I have not read or talked to any serious investigator of the heredity-­ environment problem in schizophrenia who has not in some way or other indicated that, in his opinion, both contributed to the disorder.73

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That is fair enough, and indeed Rosenthal provides a more balanced view of the subject than many of his contemporaries and successors, but the very name “Genain” prejudges the matter. It’s not as if there was a control group of four more genetically identical sisters who were not subject to severe abuse for years and years. More to the point, neither Rosenthal nor any of his co-authors ever ask the obvious question: who wouldn’t be crazy after surviving that horror show of a childhood?

Notes 1. J. David Smith and Michael L. Wehmeyer, “Who Was Deborah Kallikak?” Intellectual and Developmental Disabilities, 50, no. 2 (April 2012): 169– 178, https://doi.org/10.1352/1934-9556-50.2.169 2. David Rosenthal et  al., The Genain Quadruplets: A Case Study and Theoretical Analysis of Heredity and Environment in Schizophrenia (New York: Basic Books, 1963). 3. Ibid., xiii–xiv. 4. Ibid., 9. 5. Ibid., 7. 6. Ibid., 22–149. 7. Ibid., 22–25. 8. Ibid., 26–29. 9. Ibid., 28–29. 10. Ibid., 24. 11. Ibid., 29–30. 12. Ibid., 70. 13. Ibid., 30. 14. Ibid., 30–34. 15. Ibid., 36. 16. Ibid., 42–43. 17. Ibid., 43–44. 18. Ibid., 366. 19. Ibid., 44–47. 20. Ibid., 53. 21. Ibid., 47. 22. Ibid., 56. 23. Ibid., 56. 24. Ibid., 57–68. 25. Ibid., 69. 26. Ibid., 70–71.

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27. Ibid., 76. 28. Ibid., 78–81. 29. Ibid., 78–82. 30. Ibid., 83–84. 31. Ibid., 84. 32. Ibid., 85. 33. Ibid., 85–93. 34. Ibid., 94. 35. Ibid., 102 36. Ibid., 51. 37. Ibid., 368. 38. Ibid., 104–105. 39. Ibid., 105–108. 40. Ibid., 108–116. 41. Ibid., 111–115. 42. Ibid., 116–117. 43. Ibid., 118. 44. Ibid., 118–119. 45. Ibid., 120–121. 46. Ibid., 121. 47. Ibid., 121. 48. Ibid., 123–125 49. Ibid., 125–126. 50. Ibid., 126. 51. Ibid., 127–132. 52. Ibid., 132. 53. Ibid., 133. 54. Ibid., 134. 55. Ibid., 135–137. 56. Ibid., 140–141. 57. Ibid., 141–142. 58. Ibid., 143–146. 59. Ibid., 146. 60. Ibid., 148–149. 61. Ibid., 149. 62. Ibid., 150–152. 63. Ibid., 368. 64. Ibid., 161–170. 65. Ibid., 170–172. 66. Ibid., 172–175. 67. Lynn DeLisi, Allan F.  Mirsky, Monte S.  Buchsbaum, Daniel P. van Kammen, Karen F.  Berman, Carol Caton, Marian S.  Kafka, et  al., “The

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Genain Quadruplets 25  Years Later: A Diagnostic and Biochemical Followup,” Psychiatry Research, 13, no. 1 (September 1984): 59–76, https://doi.org/10.1016/0165-1781(84)90119-7; Allan F.  Mirsky, Lynn E. DeLisi, Monte S. Buchsbaum, Olive W. Quinn, Pamela Schwerdt, Larry J. Siever, Lee Mann, et al., “The Genain Quadruplets: Psychological Studies,” Psychiatry Research, 13, no. 1 (September 1984): 77–93. 68. Allan F.  Mirsky, Linas A.  Bielauskas, Louis M.  French, Daniel P. van Kammen, Erik Jönsson, and Göran Sedvall, “A 39-Year Followup of the Genain Quadruplets,” Schizophrenia Bulletin, 26, no. 3 (2000): 699–708. 69. Anonymous, “David Rosenthal, 77, Genetics Researcher” New York Times, March 1, 1996, https://www.nytimes.com/1996/03/01/us/davidrosenthal-77-genetics-researcher.html 70. Mirsky et al., “39-year followup,” 699–701. 71. Ibid., 701. 72. Out of respect for her privacy I have chosen not to reveal her true identity. 73. David Rosenthal et al., Genain Quadruplets, 575.

CHAPTER 5

Adoption Studies

The problem with family studies, twin studies included, is that families share an enormous amount of environmental variability in common, making it virtually impossible to disentangle the effects of heredity and of environment. Adoption studies, in theory anyway, hold out the promise of separating these two strands. The Danish Adoption Study1 is the best-known and most influential of these studies, and so it is worth examining in detail. The study was conceived and performed by David Rosenthal and Seymour Kety and their colleagues at the National Institute of Mental Health, in collaboration with their colleagues at the Kommunehospitalet of Copenhagen. Denmark was chosen as the locus for the study because of its small size, homogenous population, and meticulous record-keeping, all of which made it possible to track the biological and adoptive relatives of both the adoptees and the controls throughout their lives. In his mammoth tome A History of Psychiatry, Edward Shorter called it “one of the meatiest research projects in the history of psychiatry.”2 The probands and the controls were selected from some 5500 persons who had been adopted by nonbiological relatives during the years 1924 through 1947, inclusive. The index adoptees consisted of 76 persons who (1) had a biological parent who had been diagnosed as a certain or probably acute, borderline, or chronic schizophrenic, and (2) had been adopted at an early age by nonbiological relatives. The control group consisted of 67 adoptees whose biological parents had no recorded psychiatric © The Author(s) 2019 P. D. Hahn, Madness and Genetic Determinism, https://doi.org/10.1007/978-3-030-21866-9_5

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­ iagnosis, matched to the index subjects in terms of sex, age, socioecod nomic class of the adoptive parents, time spent with the biological family, and preadoption history.3 In addition, they looked at a third group, the “crossfostered” adoptees, 28 subjects who had been born to parents with no psychiatric diagnosis and adopted out to parents who had a diagnosis of schizophrenia or some milder disorder judged to belong to the “schizophrenic spectrum.”4 The researchers took scrupulous care to avoid contaminated diagnosis. Subjects were contacted and asked to come in for an extensive three- to five-hour interview with a psychiatrist who was unaware of the status of his subject. In most cases the subjects themselves knew nothing about their biological parents.5 Not all of the potential study subjects were happy to be contacted by the researchers. Over 20 percent of them refused to participate, sometimes vehemently so. When one psychiatrist arrived at the home of a would-be interviewee for an unannounced visit, her husband sicced his dog on the researcher.6 Nevertheless, let’s take a look at what the researchers found. When we look at the 76 index children, we find that only one of them had ever been hospitalized for schizophrenia7—a rate not significantly different from that of the general population. The Danish Adoption Study found no correlation between a diagnosis of schizophrenia and having a schizophrenic birth mother. At this point, the authors of the Danish Adoption Study could have concluded that there is no strong genetic component to schizophrenia. Indeed, this revelation could have been treated as good news. If genes do not play an overwhelming role in the etiology of schizophrenia, then something in the environment must be the deciding factor—and that is something that could be changed. But the authors did not do this. Instead, rather than limiting their analysis to index and control cases hospitalized for schizophrenia, they extended their analysis to include cases with “schizophreniform disorders,” including “schizophrenic-like border cases,” “borderline schizophrenia,” “paranoid borderline,” “psychotic borderline,” “close to borderline psychotic,” “conceivably paranoid borderline,” “schizophrenic diathesis (with some doubt),” “pronounced prepsychotic features; suspicion of organic brain syndrome,” “schizoid: beginning schizophrenia?,” and “moderately schizoid.”8

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What was the authors’ justification in expanding their analysis to include this grab-bag of ill-defined conditions? Rosenthal answered this question in a 1972 paper, noting that “If we had relied only on hard-core, process cases, we would have found no significant difference between our index and control cases.”9 The authors found that 18.8 percent of the index subjects fell into the top quartile of psychopathology for “schizophreniform disorders,” meaning they were borderline schizophrenic or more seriously impaired—as opposed to 10.7 percent of the crossfostered subjects and 10.1 percent of the controls.10 This last figure is perhaps the most astonishing finding of the study, and one which has gone almost completely ignored. There was no control group of children who had not been adopted, but clearly being adopted is, in and of itself, a major risk factor for “schizophreniform disorders”— perhaps greater than the risk conferred by having a schizophrenic birth mother. The authors themselves ask rhetorically “Is approximately 10% of the Danish population borderline schizophrenic or more severely ill?”11 but they never follow up on the implications of that question. Now let’s look more closely at the differences between the treatment groups. The difference between the index subjects and both the controls and the crossfostered group in fact was not significant at the customary level of p = 0.05, although it was significant at the p = 0.1 level. There was no significant difference between the controls and the crossfostered group.12 Does this mean that bad parenting has nothing to do with the etiology of schizophrenia? The authors themselves reached no such conclusion. With proper scientific caution, they wrote: Does this study, therefore, document the fact that environmental factors play no role in the genetics of schizophrenia? No. … It might still be maintained logically that certain extraordinary forms of family perniciousness will produce schizophrenia in the offspring and that such perniciousness is not correlated completely with a parental status of being schizophrenic.13

In a 1978 paper, Rosenthal and his colleagues tested the reliability of their methods by assembling a panel of three psychiatrists to evaluate a detailed summary of the interviews for 64 index cases and 64 matched controls. This panel of judges discussed each case at length until finally

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coming to a consensus diagnosis. This time there was no significant difference in the rate of “schizophrenia spectrum disorders” between index cases and controls.14 This is an astonishing admission. Rosenthal and his co-authors were in effect saying that their previous diagnoses of spectrum disorders—the very foundation of the study—were not reliable. The paper went on to note that when the consensus diagnoses were combined with the Minnesota Multiphasic Personality Inventory (MMPI) test, the difference between the control and index groups was restored. The authors concluded: Combining two different types of criteria, the divergent MMPI and the consensus diagnosis, illustrates one way to reduce some of the looseness inherent in making psychiatric diagnoses. … The MMPI itself, however, does not provide fully the objective clarification of results that we had hoped to find.15 [Italics added]

This is another astonishing admission. The authors seemed to be saying that their job was to discover a method of data analysis which fit the results they had “hoped to find.” These astounding revelations were buried in a five-page paper with the unpromising title “MMPI assessment of psychopathology in the adopted-­ away offspring of schizophrenics.” Other authors have pointed out more gaping holes in the Danish Adoption Study. Theodore Lidz, Sterling Professor of Psychiatry at Yale University, and his colleagues examined the data and pointed out that the index group included 24 probands either whose parents were manic depressive or else whose diagnosis could not be agreed upon by the original authors. What’s more, when these probands were omitted from the analysis, there was no difference between the index cases and the controls.16 This is odd, especially since elsewhere Rosenthal and Kety and their co-­ authors state “Manic depressive illness was never thought to be in the schizophrenia spectrum by us.”17 Lidz and his colleagues concluded “The investigators in this study … seem to consider the existence of a genetic factor in the etiology of schizophrenic disorders an axiom rather than a hypothesis.”18 The aforementioned work Not in Our Genes discusses the Danish Adoption Study at some length. Lewontin and his co-authors corresponded with the psychiatrist who conducted the interviews for the study,

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who revealed a startling admission: some of these interviews never took place.19 Some of these patients were unavailable or even long dead at the time of the study, and in those cases the psychiatrist would prepare a “pseudo interview” on behalf of the patient, basing his answers to the interview questions on whatever hints he might glean from that patient’s hospital records. The fact that some of the interviews were fabricated was never mentioned in any of the published papers. In other instances, researchers rendered their diagnosis on the basis of a five-minute doorstep conversation.20 Lewontin and his colleagues also state that one of the authors of the Danish Adoption Study informed them that one out of the four adoptive families of index cases had at least one parent who was hospitalized for a mental disorder, whereas none of the control families did.21 This is a blatant violation of the principles of a matched case-control study, which stipulate that there be no significant differences between the case and control families besides the variable under investigation. In his 1972 paper, Rosenthal did admit that there was a significant excess of “moderate psychopathology”22 in the adoptive families of the index cases, although he gave no indication of how large this excess was. He also attempted to explain away this excess by arguing that “moderate psychopathology in adoptive parents of schizophrenics could well reflect the stresses associated with rearing and living with a schizophrenic child”23—echoing Kallmann’s argument that schizophrenic children cause family disturbance, not the other way around. Like Kallmann before him, Rosenthal offered no evidence in support of this assertion. In reading the papers of Rosenthal and Kety and their colleagues, it is hard to avoid the impression that they saw their job as finding a way to analyze their data in order to fit their preconceived notion that schizophrenia is a hereditary condition. The authors themselves say almost as much. This practice, known as Hypothesizing After Results are Known (HARK),24 has been likened to shooting an arrow and then drawing a target around wherever it lands. Today, researchers are encouraged to publish their study protocol in advance to avoid this sort of thing. Of course, there was no concept of doing so back when that the Danish Adoption Study was performed. And yet, in the final analysis (literally), the authors came up empty-handed. The results of the Danish Adoption Study were negative.

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Another much less known study, the Finnish Adoption Study, did produce some intriguing results. Researchers at the University of Oulu compared the adopted-away offspring of schizophrenic mothers with a series of matched controls. They found that 6 out of 91 index cases were psychotic, as opposed to only 1 out of 91 controls. In absolute terms, this works out to a little over 5 percent absolute increase in risk for the index cases, as compared to the controls.25 The researchers also visited the homes of the adoptive families, and when they evaluated family interactions they came up with a startling finding: none of the cases of psychosis occurred in families which were rated as healthy or even mildly disturbed. All seven cases of psychosis occurred in families which were rated as “neurotic” or even more disturbed.26 Moreover, the adoptive families of schizophrenics were no more likely to be disturbed than those of the controls, indicating that the disturbed family environment causes schizophrenia27—not the other way around, as Kallmann and others have maintained. If anything is being passed on here, it is not a “gene for” schizophrenia but rather a small but significant predisposition to schizophrenia and related conditions, and one which is expressed only in a disturbed family environment. A long-term follow-up study with a larger sample size confirmed these results. Adopted families were rated along three separate axes: “critical/ conflictual,” “constricted,” and “boundary problems.” None of these subtypes of family dysfunction appeared more or less harmful than any other. Rather, all three appeared to be equally toxic.28 There does not appear to be a specifically “schizophrenogenic” style of parenting, but rather a generalized vulnerability to any sort of family trauma. Or, put another way, we see that a healthy family environment seems to have a protective effect on vulnerable individuals.29 As a more general point, all adoption studies are based on the premise that adoption serves to randomize environmental variation. Jay Joseph, a clinical psychologist and the author of Schizophrenia and Genetics: The End of an Illusion,30 has argued that such studies are subject to major confounding factors including: • Shared birthmother-child prenatal environment • Late separation from birth parents • Late placement with the adoptive family

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• Selective placement of children with adoptive families of similar socioeconomic status and ethnic and religious backgrounds. Moreover, children judged to be more desirable tend to be placed with families judged to more desirable, and children judged to be less desirable tend to be placed with families so judged. That last point is of particular interest. We have already seen how the Danish Adoption Study blatantly violated the principle that case and control families be comparable. All these factors would tend to overestimate the contribution of hereditary factors over environmental ones. Adoption agencies were created to find homes for children whose birth parents are not able to care for them. They were never designed to carry out controlled experiments for psychiatrists and psychologists. The fundamental premise underlying adoption studies—that adoption serves to randomize environmental variation—is false. At this point the reader may be wondering: what if we were to combine twin studies and adoption studies? Suppose one were to study identical twin pairs that were separated at birth and adopted out to randomly chosen families? Surely that would disentangle the threads of heredity and environment once and for all. That may sound good in theory, but there’s just one problem— nobody has ever done a study like that. As Lewontin et  al. point out, most of the case studies of “separated” identical twins in fact involved instances in which the father died and one twin remained with the mother, while the other was sent to live with relatives. These “separated” twin pairs may have lived in the same city, the same neighborhood, or even on the same street. One such pair of “separated” twins was described as “never apart.”31 In his book Toxic Psychiatry, psychiatrist Peter Breggin summed up matters thusly: When laypersons think of twin studies proving the genetic basis of schizophrenia, they naturally assume that the studies are of twins raised apart. But no such studies of psychiatric disorders exist. The numbers of identical twins raised apart are simply too small to study a problem that affects a tiny fraction of the population. It’s a case of the public filling in the blanks with information that isn’t there.32

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In summary, what have a century of family studies, twin studies, and adoption studies told us about the etiology of schizophrenia and other mental illnesses? They have told us that these conditions tend to run in families, which is not very surprising. They also have told us that individuals vary in the responses to a disturbed family environment, and that some of that variability may be heritable. That’s also not very surprising. Probably anyone with experience of life as it is lived could have guessed as much. “Most people believe that genetic studies are performed by disinterested researchers who are simply trying to find out whether there’s a genetic influence on schizophrenia,” Dr. Joseph told me. “In reality, most psychiatric genetic researchers have strong genetic biases, which make it likely that they will conclude in favor of genetics, even if the results suggest otherwise, or if the assumptions underlying genetic interpretations of the data are highly questionable.” When I ask Dr. Joseph if he thinks people vary in their susceptibility to trauma, he shrugs off the question. “My position is that genetic evidence is not there, and even if it were there, society and science should still focus on improving the social environment and reducing people’s exposure to trauma, regardless of whether some people are more genetically susceptible than others.” In fairness to Rosenthal and Kety and their colleagues, they never ruled out the importance of environmental factors in the genesis of schizophrenia. In a 1976 paper they summed up matters thusly: The evidence that environmental factors are necessary for the development of schizophrenia is equally compelling, and here, too, there is a need for further research to identify the relevant factors among the many psychosocial, physical, chemical, and infectious influences that affect the developing individual, and to examine how they interact with hereditary vulnerabilities to produce or prevent the syndrome we call schizophrenia.33

Unfortunately, these caveats were to be dismissed, forgotten almost completely in the ensuing years of the Prozac Era, with its siren song of “It’s nobody’s fault.”

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Notes 1. Seymour S. Kety, et al., “The Types and Prevalence of Mental Illness in the Biological and Adoptive Families of Adopted Schizophrenics,” Journal of Psychiatric Research, 6, Supplement 1 (November 1968): 345–362, https://doi.org/10.1016/0022-3956(68)90026-5; David Rosenthal et  al., “The Adopted-Away Offspring of Schizophrenics,” American Journal of Psychiatry, 128, no. 3 (September 1971): 307–311, https://doi. org/10.1176/ajp.128.3.307; David Rosenthal, “Three Adoption Studies of Heredity in the Schizophrenic Disorders,” International Journal of Mental Health, 1, no. 1–2 (1972): 63–75, https://doi.org/10.1080/002 07411.1972.11448565; Paul H. Wender et al., “Crossfostering: A Research Strategy for Clarifying the Role of Genetic and Experiential Factors in the Etiology of Schizophrenia,” Archives of General Psychiatry, 30, (1974): 121–128, https://doi.org/10.1001/archpsyc.1974.01760070097016; Henning Paikin et al., “Characteristics of People Who Refused to Participate in a Social and Psychopathological Study,” in Genetics, Environment & Psychopathology, ed. J. Higgins and B. Bell, (New York: American Elsevier Publishing Company, 1974), 293–322; Seymour S. Kety et al., “Studies Based on a Total Sample of Adopted Individuals and Their Relatives: Why They Were Necessary, What They Demonstrated, and What They Failed to Demonstrate,” Schizophrenia Bulletin, 2, no. 3 (1976): 413– 428, https://doi.org/10.1093/schbul/2.3.413; Richard J. Haier, et al., “MMPI Assessment of Psychopathology in the Adopted-Away Offspring of Schizophrenics,” Archives of General Psychiatry, 35, no. 2 (February 1978): 171–175. 2. Shorter, History, 244. 3. Rosenthal et al., “Adopted-Away Offspring,” 307–308. 4. Wender et al., “Crossfostering,” 123. 5. Rosenthal et al., “Adopted-Away Offspring,” 308. 6. Paikin et al., “Characteristics,” 308. 7. Rosenthal et al., “Adopted-Away Offspring,” 310. 8. Ibid., 310. 9. Rosenthal, “Three Adoption Studies,” 73–74. 10. Wender et al., “Crossfostering,” 126. 11. Ibid., 126. 12. Ibid., 125. 13. Ibid., 127. 14. The data can be found in Table 3 of Haier et al., “MMPI Assessment,” 174. The difference between the index and control cases is not significant (chi-square = 0.68, d.f. = 1). 15. Ibid., 175.

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16. Theodore Lidz, Sidney Blatt, and Barry Cook, “Critique of the Danish-­ American Studies of the Adopted-Away Offspring of Schizophrenic Parents,” American Journal of Psychiatry, 138, no. 8 (August 1981): https://doi.org/10.1176/ajp.138.8.1063, 1064–1065. 17. Kety et al., “Studies,” 417. 18. Lidz, Blatt, and Cook, “Critique,” 1067. 19. Lewontin, Rose, and Kamin, Not in Our Genes, 224. 20. Paikin et al., “Characteristics,” 308. 21. Lewontin, Rose, and Kamin, Not in Our Genes, 223. 22. Rosenthal, “Three Adoption Studies,” 73. 23. Ibid., 73–74. 24. Joseph, Schizophrenia and Genetics, chapter 5, Kindle. 25. Pekka Tierni et al., “The Finnish Adoptive Family Study of Schizophrenia,” Yale Journal of Biology and Medicine, 58, no. 3 (May–June 1985): 227–237. 26. Ibid., 232. 27. Ibid., 236–237. 28. Pekka Tierni et al., “Genotype-Environment Interaction in Schizophrenia-­ Spectrum Disorder: Long-Term Follow-Up Study of Finnish Adoptees,” British Journal of Psychiatry, 184, (March 2004): 216–222. 29. Ibid., 236. 30. Joseph, Schizophrenia and Genetics, chapter 5, Kindle. 31. Lewontin, Rose, and Kamin, Not In Our Genes, 106–108. 32. Breggin, Toxic Psychiatry, 96–97. 33. Kety et al., “Studies,” 427.

CHAPTER 6

The Mass-Marketing of Mental Illness

I tried killing myself thirty times.

So says Vickie, a young nurse from Philadelphia who was first prescribed Paxil at the age of ten. Vickie recalls her life before she began taking psychiatric medication. “I had a pretty nice life. I grew up with money, I was never deprived of anything, my parents were very supportive of me. I had a great upbringing.” But she had a tendency toward shyness, and her parents became concerned. “I was just shy,” Vickie remembers. “I had friends but I liked to be home, and I liked to watch TV, and I liked to read, and I actually liked to be alone.” Nevertheless, her mother took her to see a psychiatrist for a forty-five minute consultation, during which her mother did most of the talking. When Vickie’s mother mentioned that she, too, had been shy as a child, the psychiatrist concluded that Vickie’s condition most likely was hereditary in origin. He diagnosed the child with “social anxiety disorder” and prescribed Effexor. After six months, there didn’t seem to be any improvement in her condition, so her mother brought her back to the same psychiatrist, who prescribed Paxil. The effects were devastating, Vickie recalls. “I really just wanted to die. I cried all the time. Almost daily I would sit in my room and cry.” Once more her mother took Vickie to the psychiatrist, who doubled her prescribed dose of Paxil. © The Author(s) 2019 P. D. Hahn, Madness and Genetic Determinism, https://doi.org/10.1007/978-3-030-21866-9_6

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Vickie found her condition worsening. “It was a downward spiral that I got into and couldn’t get out of.” She felt compelled to harm herself— starving herself, binging and vomiting, pulling her own hair out, cutting herself, and obsessively picking at the scabs. She also tried dozens of times to end her own life. “I tried slitting my wrists, overdosing on Tylenol PM, I tried hanging myself, I tried drowning myself. I even considered jumping off a bridge at one point. It wasn’t a cry for help. I just wanted to die.”

The Re-branding of Psychiatry In 1973, a paper appeared in Science with the provocative title “On being sane in insane places.”1 Psychologist David Rosenhan organized an experiment in which eight healthy volunteers, including himself, presented themselves at twelve different mental hospitals, with some of the volunteers presenting at more than one. Each volunteer told the staff that he or she was hearing voices, which seemed to be saying the words “empty,” “hollow,” and “thud.” This complaint was chosen for a reason: then as now, there was no recognized mental illness which can be diagnosed solely on the basis of this particular complaint.2 All of the volunteers were subsequently admitted, in every case but one with a diagnosis of schizophrenia (the remaining one was diagnosed with manic-depressive disorder). Once admitted, the volunteers behaved normally and reported that they no longer heard the voices. They talked openly and honestly about their lives, pre-admission, with the obvious exception that they were there as part of an experiment.3 In no case did any staff member detect the ruse on the part of these “pseudopatients.” Indeed, the most trivial conflicts of their pre-admission lives, accurately described by pseudopatients during therapy sessions, were interpreted as evidence of their “mental illness.”4 Each pseudopatient was discharged with a diagnosis of schizophrenia “in remission,” after an average stay of 19 days. One of these pseudopatients was in for 52 days before being released.5 When Dr. Rosenhan shared his results with the staff of another mental hospital, they claimed such a deception would never go undetected on their watch. Rosenhan offered them a challenge: he would send them one or more pseudopatients over the next three months, to see if they could be detected.6

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Nineteen patients presenting at the hospital during the prescribed period were identified as pseudopatients with “high confidence” by at least one psychiatrist and at least one other staff member. In fact no pseudopatients presented at the hospital during this period. Dr. Rosenhan concluded, with considerable understatement, “Any diagnostic process that lends itself so readily to massive errors of this sort cannot be a very reliable one.”7 The Rosenhan experiment, as it came to be known, was just one of a series of shocks in the 1960s and 1970s which shook psychiatry to its foundations. By the end of that decade, psychiatry was facing a crisis of identity which seemed to threaten its very existence.8 Books such as The Myth of Mental Illness9 by psychiatrist Thomas Szasz and The End of Psychiatry10 by psychiatrist E. Fuller Torrey questioned the central paradigm of biological psychiatry. The minor tranquilizers, such as Valium, had been exposed as the dangerous and highly addictive drugs they were, while the major tranquilizers, such as Thorazine, were widely derided by patients forced to take them as instruments of torture. Other somatic therapies for psychiatric disorders, such as lobotomy, were as discredited as bloodletting.11 An army of nonmedical therapists, such as psychologists and social workers, were competing with psychiatry for customers. Meanwhile, psychiatrists had the lowest salaries of any medical specialty, and medical students began staying away from psychiatry in droves.12 Psychiatry was at crossroads. Practicing psychiatrists could have focused their efforts on talk therapy, and accepted the salary of a psychologist or a social worker. Medical schools could have begun shuttering residency programs in psychiatry, and the American Psychiatric Association could have been merged with that other APA, the American Psychological Association. In short, they could have begun dismantling the profession of psychiatry. Of course they didn’t do that. Instead, they began a vigorous program of re-branding psychiatry, as described by reporter Robert Whitaker in his blockbuster work of nonfiction, Anatomy of an Epidemic.13 The drug companies supplied the financial muscle. The psychiatrists themselves, along with the newly released third version of the Diagnostic and Statistical Manual of Mental Disorders, lent the enterprise the appearance of scientific objectivity. The National Institute of Mental Health (NIMH) provided the official government stamp of approval. The National Alliance on Mental Illness (NAMI) put a human face on the problem.14

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The public was saturated with the message that mental illnesses were caused by “broken brains,” and that “astonishing advances” in the field were leading the way to the “comprehension and cure of all mental illnesses.”15 In fact, every major class of psychiatric drug had been discovered before this re-branding campaign began. The antimanic properties of lithium had been discovered in the 1940s, while the first major tranquilizers, the first minor tranquilizers, and the first antidepressants all had been introduced in the 1950s, but now sales of these drugs skyrocketed. The number of diagnostic categories skyrocketed as well. The third edition of the Diagnostic and Statistical Manual of Mental Disorders listed 265 separate mental illnesses, up from 182 for the second edition and 106 for the first. The boundaries of “mental illness” were stretched to encompass all of everyday unhappiness, and even beyond that (as Vickie’s testimony so vividly illustrates). The twentieth-century successors of the madhouse doctors of yesteryear now were claiming dominion over every significant problem with human thoughts and feelings and behaviors. Those engaged in this re-branding campaign had an obvious vested interest in promoting the belief that psychiatric disorders are genetically based, and they proceeded to do so with alacrity.

Well-Behaved Little Superachievers Stephen Faraone is a clinical psychologist at the Pediatric Psychopharmacology Unit of the Massachusetts General Hospital and the Department of Psychiatry of Harvard Medical School (two institutions which have relentlessly promoted the diagnostic category of pediatric bipolar disorder for children as young as two years of age16). In a 1996 commentary in the Journal of the American Academy of Child and Adolescent Psychiatry (JAACAP),17 Dr. Faraone recommended that clinicians rendering a diagnosis take into account any psychiatric disorders the patient’s parents may have had—employing the same blatantly circular argument Kallmann used decades earlier. In the same piece, he explained that telling parents that psychiatric disorders are genetically based helps ensure medication compliance: Many parents are reluctant for their children to take psychotropic medication and others find it difficult to maintain the prescribed regimen. These problems are mitigated by discussing the genetic etiology of ADHD. Many

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parents hold naïve beliefs about the etiology of their children’s problems; they are quick to attribute them to life circumstances, events in the past, or parental inadequacies. … For many psychiatric disorders, genetic data provide the quickest and most convincing means of showing patients how biology plays a role in their condition.18

Harold S. Koplewicz is a Professor of Clinical Psychiatry and Vice Chairman of the Department of Psychiatry at the New  York University (NYU) School of Medicine. The same year Dr. Faraone published his commentary in JAACAP on the need to convert parents to the view that mental disorders are inherited conditions, Dr. Koplewicz stepped into the breach with his book It’s Nobody’s Fault: New Hope and Help for Difficult Children.19 In the first chapter, Dr. Koplewicz sets his readers straight: Until 20 years ago there was a general belief that early childhood traumas and inadequate parenting were responsible for childhood psychiatric disorders. … The fact is, when a child has a brain disorder, it is not the parents’ fault. … A brain disorder is the result of what I call ‘DNA Roulette.’ In the same way a child comes into the world with large ears, a tendency to go gray in his late twenties, or, like Kenny, beautiful hazel eyes and deep dimples, a child is born with a brain that functions in a particular way because of its chemical composition. … It is brain chemistry that is responsible for brain disorders, not bad parenting.20 [Italics in the original]

Dr. Koplewicz heaps sarcasm on those who attribute mental illness to sexual abuse or other childhood traumas, referring to such explanations as “the fine art of storytelling”21: Sexual abuse is a common phenomenon, and bulimia is a common disorder; it stands to reason, therefore, that there will be a substantial number of women with bulimia who have been sexually abused. That still doesn’t prove a cause-and-effect relationship. … Naturally all children are affected by the events of their lives. But unless he has the brain chemistry that makes him vulnerable to a psychiatric disorder, the child will not end up with a disorder. By the same token, a brain disorder doesn’t miraculously disappear if the unpleasant environmental factors are altered.22

Dr. Koplewicz informs his readers that mental illness is caused by a chemical imbalance in the brain. Fortunately, modern psychopharmacology has developed safe and effective treatments for these chemical imbalances, as he emphasizes repeatedly:

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• “When luck fails and there’s a severe imbalance in the brain, the child will experience emotional or behavioral difficulties.”23 • “Our aim is always the same: to restore chemical balance to the brain.”24 • “Our job is to find the best strategy to restore balance.”25 • “The challenge is to find the right balance for each child.”26 • “If the chemical imbalance is severe and a child’s activities in any of these areas are significantly altered for an extended period of time, we take a closer look.”27 • “We know that children with psychiatric disorders have a chemical imbalance in the brain that is caused by a genetic abnormality, but we don’t know what the specific abnormality is.”28 How does this balancing act work out for children and their parents? Just great, according to Dr. Koplewicz: ‘We got our life back,’ and ‘We finally could think about having another child,’ and ‘It was a miracle’ are the kinds of comments heard every day from parents whose children’s lives have been turned around by medication.29

Dr. Koplewicz goes on to tell the story of Margaret, who at the age of seven was “completely miserable,” whose parents were told that she needed full-day special education, and would “never succeed at anything.” But today, after having her brain chemicals balanced with the aid of Ritalin, Margaret makes straight A’s, plays the French horn in the school band, and has plenty of friends.30 Of course, there never was any convincing evidence for the chemical imbalance theory of mental illness, but that doesn’t seem to faze the author. The book is peppered with breezy little anecdotes like this one, with children suffering tremendous personal problems, whose distraught parents had tried everything and found themselves at the end of their rope until they discovered Dr. Koplewicz, whose pills transformed these boys and girls into well-behaved little superachievers. Apparently none of Koplewicz’s patients ever suffers from worsening depression, dyskinesia, akathisia, self-harm, suicidality, or any of the other devastating and well-­ documented toxic effects of these drugs. In a 1999 article in Salon, Dr. Koplewicz declared “There are 5 or 6 million kids who could potentially benefit from Selective Serotonin Reuptake Inhibitors (SSRIs). I actually think we’re not medicating kids enough.”31

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At the time, none of the SSRIs had been approved for use in children. Dr. Koplewicz also reiterated the central message of It’s Nobody’s Fault: Psychiatric illness is not caused by bad parenting. It is not that your mother got divorced, or that your father didn’t wipe you the right way. It really is DNA roulette: You got blue eyes, blond hair, sometimes a musical ear, but sometimes you get the predisposition for depression.32

In 2001, Dr. Koplewicz’s name appeared as one of 22 notional authors on GlaxoSmithKline (GSK)’s infamous Study 32933 of Paxil (marketed in the United Kingdom as Seroxat), which concluded that the drug was “generally well tolerated and effective for major depression in adolescents,” even though the data demonstrated no advantage over placebo for any of the eight original outcome variables specified by the study planners—and that nearly one out of eight youths given the drug experienced suicidality or self-harm, as opposed to fewer than one out of 40  in the placebo group.34 The next year, the BBC news program Panorama aired the documentary “Secrets of Seroxat,”35 which told of patients who experienced devastating withdrawal symptoms after discontinuing the drug. Panorama, which have never before repeated a topic, went on to air three more episodes about this drug,36 and in so doing began the slow arduous process of unraveling the truth about GSK’s Study 329. The years that followed brought more bad news for the drug companies. In 2004, a Food and Drug Administration (FDA) advisory committee voted 15 to 8 to include a black-box warning for all SSRI antidepressants (including Paxil) on the increased risk of suicidality in children—the strongest sanction available short of removing a drug from the market.37 The warning read, in part, “Antidepressants increased the risk compared to placebo of suicidal thinking and behavior (suicidality) in children, adolescents, and young adults in short-term studies of major depressive disorder and other psychiatric disorders.”38 In 2009, psychologist Irving Kirsch, a lecturer at Harvard University Medical School and Director of the Program in Placebo Studies at Harvard and the Beth Israel Deaconess Medical Center, published The Emperor’s New Drugs 39 in which he and his colleagues analyzed all of the randomized controlled trial data submitted to the FDA for approval of four antidepressants (including Paxil), and found that the benefits of these drugs were virtually indistinguishable from those of placebo. The book was a devastating indictment of the psychopharmaceutical industry.

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The following year saw the publication of Robert Whitaker’s aforementioned Anatomy of An Epidemic,40 an even more devastating indictment of the psychopharmaceutical industry. This book showed, by means of official facts and figures easily available on the internet, that the proportion of Americans disabled by psychiatric conditions has skyrocketed since the beginning of the modern psychopharmaceutical era. That makes no sense if you believe these drugs are curing mental illness. It makes perfect sense if you believe these drugs are causing mental illness. In 2012, GSK agreed to pay out $3 billion to the United States Department of Justice to settle claims of illegal marketing of its products, including Paxil. In a press release, Deputy Attorney General James M. Cole declared “This historic action is a clear warning to any company that chooses to break the law.”41 The day the settlement was announced, GSK’s stock price went up.42 None of this seems to have slowed Dr. Koplewicz down. In 2009 he left NYU to found the Child Mind Institute,43 an “independent national nonprofit dedicated to transforming the lives of children struggling with mental health and learning disorders.”44 At least 13 of his erstwhile colleagues from NYU came over to join him.45 On 3 June 2011 the New York Times featured a profile of Dr. Koplewicz46 which, oddly enough, ran not in the Health section but in Fashion and Style. The piece was pure hagiography, portraying Koplewicz as a saintly figure dedicated to the healing of sick children. One of Koplewicz’s colleagues is quoted as saying “Harold really wants to do something meaningful for children, which is kind of an amazing thing.” Another tells us “I see Harold as an entirely decent, honorable, honest human being. The guy’s a force of nature.” Garber Neidich, chairwoman of the board of the Child Mind Institute, adds “Harold could make so much more money in private practice. He does this because he believes in it.” Dr. Koplewicz certainly is not lacking friends in high places. According to the article, his friends include “former New Jersey governor Jon S. Corzine and Secretary of State Hillary Rodham Clinton.” Moreover, with the help of the aforementioned Ms. Neidich, he has raised $142 million for the Child Mind Institute. These fundraising efforts include the inaugural gala, which raked in $5.5 million. “Guests included Mr. Corzine, Dr. Ruth Westheimer, the Goldman Sachs president Gary Cohn, Robert DeNiro, Grace Hightower, and the billionaire J.  Christopher Flowers,” the article breathlessly adds.

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Dr. Koplewicz’s role in Study 329 is not explored. And while the piece prominently identifies Koplewicz as the son of a Holocaust survivor, no mention is made of the similarity of his views and those of Ernst Rüdin. * * * As for Vickie, she has managed, against all odds, to regain a semblance of normalcy. By the time she reached her early 20s, her condition stabilized somewhat, although she remains dependent on Paxil. She has attempted many times to taper off the drug, but every time she tries she experiences uncontrollable sweating, nausea, vomiting, crushing migraine headaches, horrible vivid nightmares, and terrifying rage. She now works as a nurse and is raising three children, although her marriage crumbled under the strain of her condition. “I can’t really have a relationship with anybody. As soon as anybody finds out that I have these issues, their views on me change.” Her liver has sustained significant damage, and she believes a transplant is in her future. “It’s a horrible medication,” she says of GlaxoSmithKline’s blockbuster drug. “Paxil turned me into a monster.”

Notes 1. D.L.  Rosenhan, “On Being Sane in Insane Places,” Science, 179, no. 4070 (January 19, 1973): 250–258, https://doi.org/10.1126/ science.179.4070.250 2. Ibid., 251. 3. Ibid., 251. 4. Ibid., 253. 5. Ibid., 252. 6. Ibid., 252. 7. Ibid., 252. 8. This crisis is documented by author Robert Whitaker, Anatomy of an Epidemic: Magic Bullets, Psychiatric Drugs, and the Astonishing Rise of Mental Illness in America (New York: Broadway Books, 2010), 263–268. For a contemporary view of the crisis, see Anonymous, “Psychiatry On The Couch: To Shake The Blues, Freud’s Disciples Seek New Directions,” Time, April 2, 1979, http://content.time.com/time/magazine/article/0,9171,916740,00.html 9. Thomas S.  Szasz, The Myth of Mental Illness: Foundations of a Theory of Personal Conduct (New York: Harper & Brothers, 1961).

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10. E. Fuller Torrey, The End of Psychiatry (Radnor: Chilton, 1974). 11. Whitaker, Anatomy of an Epidemic, 267–268. 12. Ibid., 265–266. 13. Whitaker, Anatomy of an Epidemic, 268–282. 14. Ibid., 276–280. 15. Ibid., 274–275. 16. Patrick D Hahn, “A Mania for Drugging Children,” Nine-part series in the Canada Free Press, July 25–August 2, 2016, https://canadafreepress. com/article/he-was-a-beautiful-child 17. Steven Faraone, “Discussion of ‘Genetic Influence on Parent-Reported Attention Related Problems in a Norwegian General Population Twin Sample,’” Journal of the American Academy of Child and Adolescent Psychiatry, 35, no. 5 (1996): 598. 18. Ibid., 598. 19. Harold S. Koplewicz, It’s Nobody’s Fault: New Hope and Help for Difficult Children (New York: Random House, 1996). 20. Ibid., 5–6. 21. Ibid., 7. 22. Ibid., 7–8. 23. Ibid., 47. 24. Ibid., 51. 25. Ibid., 51. 26. Ibid., 52. 27. Ibid., 53. 28. Ibid., 55. 29. Ibid., 67. 30. Ibid., 67. 31. Rob Waters, “Johnny Get Your Pills,” Salon, June 17, 1999, https:// www.salon.com/1999/06/17/antidepressants/ 32. Ibid. 33. Martin B. Keller et al., “Efficacy of Paroxetine in the Treatment of Adolescent Major Depression: a Randomized, Controlled Trial,” Journal of the American Academy of Child and Adolescent Psychiatry, 40, no. 7 (July 2001): 762–772, https://doi.org/10.1097/00004583-200107000-00010. 34. Joanna LeNoury et  al., “Restoring Study 329: Efficacy and Harms of Paroxetine and Imipramine in Treatment of Major Depression in Adolescence,” BMJ 2015; 351:h4320 https://doi.org/10.1136/bmj. h4320; Peter Doshi, “No Correction, No Retraction, No Apology, No Comment: Paroxetine Trial Reanalysis Raises Questions About Institutional Responsibility,” BMJ, 351, (2015), https://doi.org/10.1136/bmj.h4629.

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35. Panorama, “Secrets of Seroxat,” Narr. Shelley Jofre, BBC, October 13, 2002. 36. Panorama, “Seroxat: Emails From the Edge,” Narr. Shelley Jofre, BBC, May 11, 2003; Panorama, “Taken on Trust,” Narr. Shelley Jofre, BBC, September 21, 2004; Panorama, “Secrets of the Drug Trials,” Narr. Shelley Jofre, BBC, January 29, 2007. 37. Gardiner Harris, “FDA Panel Urges Stronger Warning on Antidepressants,” New York Times, September 15, 2004, https://www.nytimes. com/2004/09/15/health/fda-panel-urges-stronger-warning-on-antidepressants.html 38. Gardiner Harris, “FDA Toughens Warning on Antidepressant Drugs,” New York Times, October 16, 2004, https://www.nytimes.com/2004/10/16/ politics/fda-toughens-warning-on-antidepressant-drugs.html 39. Irving Kirsch, The Emperor’s New Drugs: Exploding the Antidepressant Myth (London: Bodley Head, 2009). 40. Whitaker, Anatomy of an Epidemic. 41. “GlaxoSmithKline to plead guilty and pay $3 billion to resolve fraud allegations and failure to report safety data,” United States Department of Justice, accessed September 6, 2017, https://www.justice.gov/opa/pr/ glaxosmithkline-plead-guilty-and-pay-3-billion-resolve-fraud-allegationsand-failure-report 42. Charles Riley and Emily Jane Fox, “GlaxoSmithKline in $3 Billion Fraud Settlement,” CNN, July 2, 2012, https://money.cnn.com/2012/07/02/ news/companies/GlaxoSmithKline-settlement/index.htm 43. Don Kaplan, “NYU Squeezes Kiddie Shrinks,” New York Post, January 312,011, https://nypost.com/2011/01/31/nyu-squeezes-kiddie-shrinks/ 44. “About Us,” Child Mind Institute, accessed July 10, 2018, https://childmind.org/about-us/ 45. Kaplan, “NYU squeezes kiddie shrinks.” 46. Abby Ellin, “When a Child’s Anxieties Need Sorting,” New York Times, June 3, 2011, https://www.nytimes.com/2011/06/05/fashion/whena-childs-anxieties-need-sorting.html

CHAPTER 7

The Human Genome Project Era

The scene: Hunterian Building, on the campus of Johns Hopkins Medical Institutions (JHMI) in downtown Baltimore, afternoon, mid-April. It rained this morning, and the gray storm clouds looming overhead outside promise more of the same, but here inside it’s warm and dry. I’m standing in the laboratory of Richard Huganir, Director of both the Department of Neuroscience and the Kavli Neuroscience Discovery Institute at JHMI. Dr. Huganir is not a psychiatrist or a medical doctor of any kind. Rather, he is a biochemist whose work on the development of the normal brain has led him to work on genetic variants implicated in the etiology of schizophrenia and other mental illnesses. We walk past the lab benches, almost every square inch of which is covered with reagent jars, squirt bottles, test tubes, Tygon tubing, glass dishes, syringes, cardboard boxes, centrifuges, and God knows what else. His assistants smile shyly as we pass, all of them young, clean-cut, and good looking. Everyone is serious, focused, and intent. Dr. Huganir opens the door to a side room and shows me his electron microscopes—one worth $400,000, and the other priced at half a million. Another door leads us to the electrophysiology lab. His graduate student Elena shows me the apparatus used to restrain a mouse, while a computer screen allows researchers to view its neural networks. A fluorescent dye which binds calcium shows the firing of the synapses in real time. The mouse can even trot on a horizontally rotating plastic

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disk while a virtual reality system fools the mouse into believing it is running a maze as the innermost workings of its brain are being probed. Another room holds the 2-photon microscope (worth $2 million) which is used to generate rotatable three-dimensional images of neural networks. Dr. Huganir mentions that the device can image a million synapses all at once. He tells me they are collaborating with Hopkins scientists who have experience working with the Hubble Space Telescope, to find ways of processing all these data. Imagine that—the same computing power used to understand the entire physical universe studied by astronomers is now being applied to comprehending the working of a single brain. And not even the brain of a human being, but that of a mouse. My head spinning, I accompany Dr. Huganir back to his office.

Promises Made On 14 April 2003, the International Human Genome Sequencing Consortium, led in the United States by the National Human Genome Research Institute (NHGRI) and the Department of Energy, announced the successful completion of the Human Genome Project, two years ahead of schedule.1 That same year, Francis Collins, Director of the NHGRI, authored an article in NAMI Advocate, a publication of the National Alliance on Mental Illness (an organization that receives massive funding from the drug companies2): The human genetic blueprint will speed researchers’ efforts to understand the biological pathways involved in mental illness and to develop better methods of diagnosis and treatment. … Genomic research will help to ease the societal stigma many people face by providing more precise methods of diagnosing mental illness and by furnishing conclusive evidence of the biological roots of such conditions.3

Fifteen years on, how have those promises held up? What have we learned about the “biological roots” of schizophrenia and other “mental illnesses?” In fact, the search for specific genes for mental illness started years before this. The case of the 22q11.2 deletion is instructive. This mutation is associated with a whole host of physical abnormalities and somatic illnesses which in turn gave rise to a variety of diagnostic labels, such as

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DiGeorge Syndrome, Shprintzen’s Syndrome, Velocardiofacial Syndrome, and Conotruncal Anomaly Face Syndrome. In 1981, Finnish scientists first made the connection between DiGeorge Syndrome and a deletion of some thirty to fifty genes on the long arm of chromosome 22.4 Other researchers soon determined that these other aforementioned syndromes were manifestations of the same underlying genetic condition.5 Today all of them have been subsumed under the same diagnostic label: 22q11.2 Deletion Syndrome.6 Something like 20–30 percent of individuals with this syndrome suffer from psychotic symptoms.7 Fortunately, this genetic variant is rare, on the order of 1 in 4000 births. What’s more, the vast majority of individuals with schizophrenia—about 99 percent of them—do not have this mutation.8 The 22q deletion was discovered by chance. Doctors found a family in which four children had been born with DiGeorge Syndrome, and in which the father was found to have a translocation between chromosomes 20 and 22. All the children with DiGeorge Syndrome were found to have inherited from their father a copy of chromosome 22 missing the same segment of DNA.9 The new technique of linkage analysis promised to put the search for genes for mental illness on a more systematic basis. Linkage analysis examines individuals in the same family with the same, presumably genetically based condition, and looks for the co-occurrence of that trait with another one with a known location in the genome. On 26 February 1987, a paper in Nature reported the discovery of a marker on chromosome 11 linked to the incidence of bipolar disorder in the Old Order Amish.10 The following year, another paper in the same journal described the discovery of a marker on chromosome 5 linked to the incidence of schizophrenia in five Icelandic and two British families.11 An accompanying commentary hailed the discovery as a major milestone in the history of medicine: Schizophrenia is arguably the worst disease affecting mankind, even AIDS not excepted. Indeed schizophrenia is the more daunting because so little is known of its causation. While arguments may persist that infection by the virus HIV (human immunodeficiency virus) is not a sufficient explanation of the transmission of AIDS, at least enough is known for rational avoidance strategies to be possible. The occurrence of schizophrenia, by contrast, seems mostly

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a bolt from the blue for those affected. Even the diligent practice of what has been painfully learned in half a century about the proper bringing-up of children gives no assurance that schizophrenia will not strike.12

The commentary went on to blast the “relativistic” view of madness espoused by critics of psychiatry such as Thomas Szasz, and expressed hope that the new findings would improve medication compliance: This view has for years provided too many opportunities for confusion in the treatment of patients with schizophrenia, not to mention opportunities for patients to decline whatever treatments have been on offer. Even the demonstration that there is a handful of patients (in Iceland) differing in measurable ways from the other members of their families should help banish this source of confusion.13

The commenter’s enthusiasm was premature, however. Subsequent studies with larger sample sizes failed to find evidence for either the postulated gene for bipolar disorder on chromosome 11,14 or the postulated gene for schizophrenia on chromosome 5.15 This was the beginning of a soon-to-be familiar pattern, with scientists announcing the discovery of the locus of a gene for schizophrenia or some other mental illness, only to have their hopes dashed when further studies by other researchers (or sometimes even the same researchers) failed to corroborate their initial findings. The retractions of these findings never got anywhere near as much publicity as the initial announcement. A 1987 article on page one of the New York Times announced that “scientists have discovered the first proof that some cases of manic-­ depressive illness are linked to a specific genetic defect.”16 The retraction, published six years later, ran on page twelve.17 A 1988 article on page one of the NYT heralded the discovery of “the first concrete evidence for a genetic basis to schizophrenia,” noting that the discovery “provides solid evidence of a biological cause of some forms of schizophrenia that cannot be explained away as a feature of destructive upbringing or other bad social experience.”18 The retraction, published a year later, ran on page three.19 In his History of Psychiatry, Edward Shorter informed readers that “[b]y 1995, the gene or genes for schizophrenia had been tentatively placed on Chromosome 6.”20 Like many other such discoveries, this one, too, has long since sunk beneath the waves.

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What went wrong? Strictly speaking, linkage analysis does not test the hypothesis that a given condition is genetically based. Rather, it tells us the likeliest location in the genome for a gene associated with that condition—assuming that the gene exists at all. This works well enough for conditions with well-defined diagnostic boundaries, in which the mode of transmission and the frequency of the gene are already known. This is not the case for schizophrenia and other mental illnesses. When the authors of these models begin playing with the frequency and penetrance of these hypothesized “schizophrenia genes,” and postulating the existence of phenocopies that lack the schizophrenia gene, the evidence for the existence of those genes becomes a lot less robust than it appears, and customary levels of statistical significance cannot be applied. A 1992 editorial in Psychological Medicine, with the provocative title “Will schizophrenia become a graveyard for molecular geneticists?,” argued that those authors had employed assumptions which led them to a systematic overestimation of the evidence for linkage and a systematic production of false positives.21 Around the time those words were written, the focus shifted from linkage studies to candidate-gene studies. These studies ask whether variation in a particular gene, already known to play a role in the development of the nervous system, is associated with an increase or a decrease in the risk of schizophrenia. More than 1400 candidate-gene studies were performed, over half of them on 18 specific genes.22 Such studies often were reported as having produced positive results whenever the level of significance reached the customary (but wholly arbitrary) value of p = 0.05. But given that hundreds of such studies were performed, and thousands of hypotheses were tested, it was inevitable that a certain number would attain the preset level of significance purely by chance. Moreover, there is a well-known and overwhelming bias23 in favor of publishing positive results (journals are usually loath to publish negative results), resulting in a flood of papers purporting to have discovered a gene or genes for schizophrenia. In fact, the actual results of these studies, considered as a whole, appear random, with no consistent agreement on which genes have an effect on the risk of schizophrenia, or whether those effects are positive or negative.24

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Since that time, the new discipline of genome-wide association studies has given scientists tools for probing the human genome with a previously undreamed-of level of precision. In these studies, researchers compare the DNA of those who have the condition of interest (case subjects) with those who do not (control subjects). The DNA of both types of subjects is scanned for the presence of single-nucleotide polymorphisms, or SNPs. A typical study looks at thousands of case subjects and thousands of control subjects, and as many as a million or more SNPs, in order to find alleles correlated with the condition of interest. In an effort to eliminate false positives, levels of significance are customarily set at 5 × 10−8 (corresponding to the customary level of p = 0.05 divided by one million25). These techniques have enabled researchers to go over the human genome with a fine-tooth comb. And what have the researchers found?

Promises Unfulfilled In the year 2000, researchers Robert Plomin and John Crabbe predicted “Within a few years, psychology will be awash in genes associated with behavioral disorders.”26 Has this promise been fulfilled? In 2007, scientists from all over the world joined to form the Psychiatric Genomics Consortium (PGC).27 The Schizophrenia Working Group of the PGC was formed with 302 researchers working in 35 countries on 4 continents.28 These researchers reported their findings in the 24 July 2014 issue of Nature.29 They had examined the genomes of 36,989 cases and 113,075 controls, and found 108 loci associated with schizophrenia. The long-­ term drought had turned into a flood. However, to the consternation of many of these researchers, the effects of these genes were tiny. The newly discovered “schizophrenia genes” had odds ratios on the order of 1.2 or even smaller. Assuming that 1 percent of the population has schizophrenia, this works out to an absolute increase in risk of about one in 500—or less. Many of these genes are also (weakly) correlated with bipolar disorder and other “mental illnesses” as well,30 which seems counter to the idea that these conditions are properly regarded as discrete disease states. Kenneth Kendler is the Rachel Brown Banks Distinguished Professor of Psychiatry at Virginia Commonwealth University. In a 2005 paper31 he

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discussed the validity of the concept of genes “for” mental illnesses. In order to determine whether “X is a gene for Y,” he proposed the following criteria: 1. Strength of association: Using the example of Mendel’s pea plants, he noted that if a plant has two copies of the gene for wrinkled seeds, the plant will produce wrinkled seeds, whereas if it has one or two copies of the gene for round seeds, it will not produce wrinkled seeds. The “odds ratio” for wrinkled seeds is infinite, or at least astronomically large. Kendler proposed an odds ratio of 100 or more as a lower threshold limit for deciding that “X is the gene for Y.” 2. Specificity of association: Kendler noted that the hereditary elements Mendel studied were quite specific in their action: one gene influenced pea color but not shape or stem length, while another influenced pea shape but not color or stem length. 3. Noncontingency of association: A pea plant with two copies of the gene for wrinkled seeds will produce wrinkled seeds under a wide variety of environmental conditions—provided conditions permit the formation of seeds at all. 4. Causal proximity: There should be a direct and immediate association between the gene and the trait. For example, the gene for the purple flower color in pea plants codes for an enzyme which synthesizes the purple pigment. 5. Appropriate level of explanation: does the label “a gene for” address the phenomenon at the most appropriate level? Kendler gives a hypothetical example of a gene which confers perfect pitch. Such a gene might increase the likelihood that its bearer would enjoy the music of Mozart. Would it be appropriate to describe the gene as a “gene for liking Mozart?” Such a gene might well increase the likelihood of enjoying the music not just of Mozart, but also of Hayden, Beethoven, or Brahms. Calling it a gene for perfect pitch is more parsimonious and has greater predictive power. Genes “for” commonly known human diseases, such as cystic fibrosis, TaySachs disease, and sickle-cell anemia, pass all five of these tests with flying colors. However, not one of the genes “for” schizophrenia or any other mental illness can pass even one of them. Even if we consider the 22q deletion of a “gene” (strictly speaking, it is not, although it is a genetic variant inherited in a Mendelian fashion), that mutation cannot meet any of these criteria.

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Moreover, even the cumulative effect of all these “schizophrenia genes” put together was modest. Those in the top decile in terms of genetic risk scores had between a 5 and 20 percent risk of schizophrenia (as opposed to an estimated 1 percent lifetime risk in the general population). In other words, even the great majority of those with the highest genetic risk for schizophrenia never received a diagnosis of schizophrenia. In aggregate, these “schizophrenia genes” accounted for no more than a small portion of the postulated liability to schizophrenia.32 Years of research by some of the best minds in the world, using state-­ of-­the-art methods, had failed to find any gene correlated with anything more than a tiny increase in the risk of schizophrenia. And yet a long line of psychiatric genetic researchers, stretching all the way back to Kallmann and Rüdin, had been saying that schizophrenia was mainly an inherited condition. What happened to the “missing heritability” of schizophrenia?33 Of course, the obvious explanation is that there wasn’t any, and that the critics of psychiatric genetic studies had been right all along. Or, some of the missing heritability could be accounted for in the form of gene-environment interactions. Traditional population genetics methods (i.e. family studies, twin studies, and adoption studies) assume that phenotypic variation can be partitioned neatly into a genetic component and a component due to the environment, with a negligible amount of variation due to gene-­environment interactions, but that assumption is untenable. For complex traits such as mental illness, gene-environment interactions are probably the rule, not the exception. We saw a possible example of just such an interaction in Chap. 4, when we noted that the Finnish Adoption Study showed an excess of schizophrenia in adopted-away children of schizophrenic mothers—but all these cases occurred in adoptive families which were seriously disturbed. Of course, it could be that there are still more genes correlated with schizophrenia that could be detected with larger sample sizes. But if such genes are out there, their effect sizes must be even tinier than those of the ones already detected. At this point, the proposed existence of these genes seems more like an article of faith than a testable hypothesis. And does it even matter? What difference does it make if there are dozens of genes with tiny effects, or hundreds or even thousands of genes with even tinier effects? At some point the effects of these hypothesized genes are going to become indistinguishable from that of random environmental variation. The fact that we have already found so many genes

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that are (weakly) correlated with schizophrenia enormously complicates the task of using these findings for the discovery of new drug targets. Perhaps it is time, as psychologist Jay Joseph has argued,34 to question the utility of calculating heritability scores for schizophrenia and other complex human traits. To this day there are no diagnostic biomarkers for schizophrenia or any other mental illness. Moreover, the boundaries between schizophrenia and “schizophreniform disorders” are not well defined, much less so those between the latter category and everyday human eccentricities. How meaningful is it to talk about the “heritability” of a disorder whose diagnostic boundaries seemingly can be contracted or expanded at will, for the convenience of investigators? Heritability is not a “nature-nurture ratio.” It does not tell you anything about the relative contributions of heredity and environment to any specific trait for any specific individual. Heritability is a property of a population, not of an individual. Scientists can measure the amount of variation in a trait in a population, and decompose this variation into a component attributed to genes and a component attributed to environment, but these values have no “true” value independent of a given population in a given environment. Heritability values are not constants, like the atomic weight of carbon or the speed of light. The concept of heritability was invented to enable agricultural scientists to predict the results of controlled breeding experiments of plants and animals on factory farms, where the range of environmental variation is severely restricted, and where genotype-environment interactions can therefore be assumed to be negligible. The very concept of heritability is of dubious value when applied to human beings, who experience a vastly greater range of environmental variation and who can make conscious decisions to change their own environments. Why have these genes been conserved by natural selection, anyway? A 1966 paper by psychiatrist Leonard Heston of the University of Minnesota gives us a hint.35 The study compared forty-seven individuals, born to schizophrenic mothers and put up for adoption within two weeks of birth, with a set of fifty matched controls. Five cases of schizophrenia were found in the experimental subjects, with none in the controls. An additional thirty-one experimental subjects were judged to exhibit “significant psycho-social impairment” (including eight said to correspond to Kallmann’s category of “schizoid psychopaths”) as opposed to nine of the controls.

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But the real surprise came when Heston looked at the twenty-one experimental subjects who had no serious psychosocial impairment. In the words of the authors, these individuals “were not only successful adults but in comparison to the control group were more spontaneous when interviewed and had more colorful life histories. They held the more creative jobs: musician, teacher, home-designer; and they followed the more imaginative hobbies: oil painting, music, antique aircraft. Within the experimental group there was much more variability of personality and behavior in all social dimensions.” Perhaps those same genes which, in the wrong environment, predispose an individual to schizophrenia or other mental illness, foster greater imagination and creativity in a supportive and nurturing environment. Rather than regarding these alleles as “schizophrenia genes,” perhaps we ought to regard them as gifts which require proper stewardship by the family and society at large. * * * Back at Dr. Huganir’s office, we sit down and I ask him about his work on candidate genes for schizophrenia, from over a decade ago. “As you probably know, candidate genes are sort of out of favor now,” he explains. “In fact I was part of a genetics working group at NIH that recommended that people don’t study candidate genes any more. To get funding from the NIH to study schizophrenia your work really has to be tightly linked to the new genetics.” Dr. Huganir notes that many of the same genes correlated with schizophrenia are also implicated in autism and intellectual disability, but the character of the mutations is not the same. “In intellectual disability cases,” he notes, “The mutations are really severe. There’s a total loss of function, they just knock out the protein. Whereas the mutations linked to autism and schizophrenia are so much more subtle.” They don’t truncate the protein or delete the protein. These are missense mutations that more subtly affect the function of the protein.

Dr. Huganir mentions that some of these schizophrenia-associated mutations are very old, and have been part of the human gene pool for a very long time. When I ask him if he has any idea why these mutations have been conserved by natural selection, he tells me that some of the same genes have been found to be correlated with increased creativity.

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Given that there are so many genes associated with schizophrenia, and that most of these mutations are quite rare, what does this tell us about the chances of using genetic research to lead to pharmacological remedies for this condition? Dr. Huganir states that the best bet is to focus on those genes with the largest effect size, and try to discern their normal function in cellular processes. “If we find the nodal points, or the place of commonality between the various genes, and develop therapeutics that will target those and shift the balance back toward the normal function of that pathway, I think that’s the way to go forward.” Is all this emphasis on genes a distraction from addressing the environmental causes of schizophrenia? Dr. Huganir asserts that this is not an either/or situation. “There’s an interest at the NIH on identifying kids who by their behavior have a risk for schizophrenia.” Such children, he says, could be targeted early for behavioral therapy or other kinds of assistance. I note the effect sizes for the schizophrenia-associated genes that have been found through genome-wide association studies are tiny—on the order of 1 in 500, or even less. I ask him a question: Suppose you took a genetic test and found you had a gene that gave you a one in 500 increase in your risk of developing schizophrenia. What would you do differently? “Probably nothing,” he replies, but then adds “In the long run, genetics will give us the knowledge to identify people at risk so they can either change their behavior or change their environment to decrease their risk, or hopefully to develop therapeutics or a cure.” It’s time to go. Dr. Huganir wishes me good luck with getting my book published. Accompanied by our media contact person, Vanessa Wasta, I take the elevator to the ground floor and we exit the building. Just as we take our leave of one another, the rain starts falling once more.

Notes 1. “International Consortium Completes Human Genome Project,” National Human Genome Research Institute, accessed July 25, 2018. https:// www.genome.gov/11006929/2003-release-international-consortiumcompletes-hgp/ 2. “Grassley probes financing of advocacy group for mental health,” Mind Freedom, accessed September 1, 2018, http://www.mindfreedom.org/ kb/psych-drug-corp/nami/grassley-nami

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3. Francis S. Collins “The Genome Era and Mental Illness,” NAMI Advocate, (Summer/Fall 2003): 29–30, https://www.genome.gov/pages/news/ documents/genomemental.pdf, 29. 4. Albert De La Chapelle et al., “A Deletion in Chromosome 22 Can Cause DiGeorge Syndrome,” Human Genetics, 57, no. 3 (1981): 253–256. 5. Deborah A. Driscoll et al., “Deletions and Microdeletions of 22q11.2 in Velo-Cardio-Facial Syndrome,” American Journal of Medical Genetics, 44, no. 2 (September 15, 1992): 262–268, https://doi.org.10.1002/ ajmg.1320440237; J. Burn et al., “Conotruncal Anomaly Face Syndrome Is Associated With a Deletion Within Chromosome 22q11,” Journal of Medical Genetics 30, no. 10 (October 1993): 822–824. 6. Donna M.  McDonald-McGinn and Kathleen Sullivan, “Chromosome 22q11.2 Deletion Syndrome (DiGeorge Syndrome/Velocardiofacial Syndrome),” Medicine, 90, no. 1 (January 2011): 1–18 7. Ibid., 9. 8. Anat Horowitz et  al., “A Survey of the 22q11 Microdeletion in a Large Cohort of Schizophrenia Patients,” Schizophrenia Research, 73, no. 2–3 (March 1, 2005): 263–267, https://doi.org/10.1016/j. schres.2004.02.008, 263. 9. De La Chapelle et al., “A Deletion in Chromosome 22,” 253–256. 10. Janice A.  Egeland et  al., “Bipolar Affective Disorders Linked to DNA Markers on Chromosome 11,” Nature, 325, no. 6107 (February 26  – March 4, 1987): 783–787, https://doi.org/10.1038/325783a0 11. Robin Sherrington et  al., “Localization of a Susceptibility Locus for Schizophrenia on Chromosome 5,” Nature, 336, no. 6195 (November 10, 1988): 164–167, https://doi.org/10.1038/336164a0 12. Anonymous, “Where Next With Psychiatric Illness?” Nature, 336, no. 6195 (November 10, 1988), 95, https://doi.org/10.1038/336095a0 13. Ibid., 96. 14. John R. Kelsoe et al., “Re-Evaluation of the Linkage Relationship Between Chromosome 11p Loci and the Gene for Bipolar Affective Disorder in the Old Order Amish,” Nature, 342, no. 6247 (November 16, 1989): 238– 243, https://doi.org/10.1038/342238a0; Michele C. LaBuda et al., “A Follow-Up Report of a Genome Search for Affective Disorder Predisposition Loci in Old Order Amish,” American Journal of Human Genetics, 59, no. 6 (1996): 1343–1362, https://www.ncbi.nlm.nih.gov/pmc/articles/ PMC1914888/ 15. James L.  Kennedy et  al., “Evidence Against Linkage of Schizophrenia to Markers on Chromosome 5  in a Northern Swedish Pedigree,” Nature, 336, no. 6195 (November 10, 1988): 167–170, https://doi. org/10.1038/336167a0; Peter McGuffin et al. “Exclusion of a Schizophrenia Susceptibility Gene From the Chromosome 5q11-q13 Region: New Data and a Reanalysis of Previous Reports,” American Journal of Human Genetics,

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47, no. 3 (September 1990): 524–535; Michael J. Owen, David Crauford, and David St. Clair, “Localisation of a Susceptibility Locus for Schizophrenia on Chromosome 5,” British Journal of Psychiatry, 157, no. 1 (July 1990): 123–127, https://doi.org/10.1192/bjp.157.1.123; G.  Kalsi et  al. “New DNA Markers With Increased Informativeness Show Diminished Support for a Chromosome 5q11-13 Schizophrenia Susceptibility Locus and Exclude Linkage in Two New Cohorts of British and Icelandic Families,” Annals of Human Genetics, 63, (May 1999): 235–247. 16. Harold M. Schmeck, Jr., “Defective gene tied to form of manic-­depressive illness.” New York Times, February 26, 1987, https://www.nytimes. com/1987/02/26/us/defective-gene-tied-to-form-of-manic-depressiveillness.html 17. Natalie Angier, “Scientists Now Say They Can’t Find a Gene For Manic Depressive Illness.” New York Times, January 13, 1993, https://www. nytimes.com/1993/01/13/health/scientists-now-say-they-can-t-find-agene-for-manic-depressive-illness.html 18. Harold M.  Schmeck, Jr., “Schizophrenia Study Finds Strong Signs of Hereditary Cause.” New York Times, November 10, 1988, https://www. nytimes.com/1988/11/10/us/schizophrenia-study-finds-strong-signsof-hereditary-cause.html 19. Harold M. Schmeck, Jr., “Scientists Now Doubt They Found Faulty Gene Linked to Mental Illness.” New York Times, November 7, 1989, https:// www.nytimes.com/1989/11/07/science/scientists-now-doubt-theyfound-faulty-gene-linked-to-mental-illness.html 20. Shorter, History, 246. 21. Michael J. Owen, “Will Schizophrenia Become a Graveyard for Molecular Geneticists?” Psychological Medicine, 22, no. 2 (May 1992): 289–293. 22. Steven A. McCarroll, Goping Feng, and Steven Hyman, “Genome-Scale Neurogenetics: Methodology and Meaning,” Nature Neuroscience, 17, no. 6 (June 2014): 759, https://doi.org/10.1038/nm.3716 23. John P.A.  Ioannidis, “Why Most Published Research Findings Are False,” PLoS Medicine, 2, no. 8 (August 2005): 696–701, https://doi. org/10.1371/journal.pmed.0020124 24. Steven A. McCarroll, Goping Feng, and Steven Hyman, “Genome-Scale Neurogenetics,” 759, https://doi.org/10.1038/nm.3716 25. Patrick F.  Sullivan, “The Psychiatric GWAS Consortium: Big Science Comes to Psychiatry,” Neuron, 68, no. 2 (October 21, 2010): 183, https://doi.org/10.1016/j.neuron.2010.10.003 26. Robert Plomin and John Crabbe, “DNA,” Psychological Bulletin, 126, no. 6 (November 2000): 806. 27. Patrick F. Sullivan, “Psychiatric GWAS Consortium,” 183. 28. Katherine E.  Tansey, Michael J.  Owen, and Michael C.  O’Donovan, “Schizophrenia Genetics: Building the Foundations of the Future,”

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Schizophrenia Bulletin, 41, no. 1 (2015): 15, https://doi.org/10.1093/ schbul/sbu162 29. Schizophrenia Working Group of the Psychiatric Genetics Consortium, “Biological Insights From 108 Schizophrenia-Associated Genetic Loci,” Nature, 511, no. 7510 (July 24, 2014): 421–427, https://doi. org/10.1038/nature13595 30. International Schizophrenia Consortium, “Common Polygenic Variation Contributes to the Risk of Schizophrenia That Overlaps With Bipolar Disorder,” Nature, 460, no. 7256 (August 6, 2009): 748–752, https://doi. org/10.1038/nature08185; Huang et al., “Cross-Disorder Genomewide Analysis of Schizophrenia, Bipolar Disorder, and Depression,” American Journal of Psychiatry, 167, no. 10 (October 2010): 1254–1263, https:// doi.org/10.1176/appi.ajp.2010.09091335; Cross-Disorder Group of the Psychiatric Genetics Consortium, “Identification of Risk Loci With Shared Effects on Five Major Psychiatric Disorders: a Genome-Wide Analysis,” Lancet, 381, no. 9875 (April 20, 2013): 1371–1379, https:// doi.org/10.1016/S0140-6736(12)62129-1; Lee et  al., “Genetic Relationship Between Five Psychiatric Disorders Estimated From Genome-­ Wide SNPs,” Nature Genetics, 45, no. 9 (August 11, 2013): 984–994, https://doi.org/10.1038/ng.2711; Steven A. McCarroll, Goping Feng, and Steven Hyman, “Genome-Scale Neurogenetics,” 757; Henriksen et  al., “Genetics of Schizophrenia: Overview of Methods, Findings and Limitations,” Frontiers in Human Neuroscience, 11, (2017): 326, https:// doi.org/10.3389/fnhum.2017.00322; Brainstorm Consortium, “Analysis of Shared Heritability in Common Disorders of the Brain,” Science, 360, no. 6395 (June 22, 2018): https://doi.org/10.1126/science.aap8757 31. Kenneth Kendler, “‘A Gene For…:’ The Nature of Gene Action in Psychiatric Disorders,” American Journal of Psychiatry, 162, no. 7 (July 2005): 1243–1252, https://doi.org/10.1176/appi.ajp.162.7.1243 32. Daniel Weinberger informed me the “significant genes”—the ones that reached the p = 10−8 level of significance—account for 2 or 3 percent of the liability to schizophrenia in the general population. Dr. Weinberger is Director and CEO of the Lieber Institute for Brain Development and the Maltz Laboratories as well as Professor of Psychiatry, Neurology, Neuroscience, and Human Genetics at JHMI. See Chap. 14 of this volume for my conversation with him. 33. Jay Joseph, “The ‘Missing Heritability’ of Psychiatric Disorders: Elusive Genes or Non-Existent Genes?” Applied Developmental Science, 16, no. 2 (April 2012): 65–83, https://doi.org/10.1080/10888691.2012.667343 34. Ibid., 75–76. 35. L.L. Heston, “Psychiatric Disorders in Foster Home Reared Children of Schizophrenic Mothers,” British Journal of Psychiatry, 112, no. 489 (August 1966): 819–825.

CHAPTER 8

The Story of January Schofield

Just as the story of the Genain sisters was emblematic of the era of twin studies, the story of Jani and Bodhi Schofield is emblematic of the era of genome-wide association studies and the modern psychopharmaceutical era with its rallying cry of “It’s nobody’s fault.” January Schofield was one of the youngest persons ever to be diagnosed with schizophrenia. Her story was told in a series of five television documentary programs produced between 2010 and 2017 by Homerun Entertainment for Discovery Communications (now known as Discovery, Inc.).

A Portent of Things to Come The first episode, Born Schizophrenic: January’s Story1 which premiered on 4 May 2010, chronicles her life from birth to the age of seven years. January Schofield was born on 8 August 2002, the first child of Michael and Susan Schofield. She seems to have been a precocious baby, quite bright for her tender age—something the producers try to cast as evidence for her being born with mental illness. A title card ominously informs us “But from the moment she cast eyes on her newborn daughter, Susan can tell something is not quite right.” A video recorded the day January was born shows Susan holding her new baby and asking a nurse, “Her eyesight looks pretty good. She’s focused. Is that normal?” © The Author(s) 2019 P. D. Hahn, Madness and Genetic Determinism, https://doi.org/10.1007/978-3-030-21866-9_8

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The nurse replies “They don’t usually do that. They don’t focus.” It seems like an innocuous enough exchange, but clearly the audience is supposed to interpret this as a portent of bad things to come. Another title card states “By the end of the twelfth week, Susan and Michael begin to notice something else, something the doctors can’t explain.” “She knew things she wasn’t supposed to know,” Susan explains. “I mean, she was pointing to your nose, your eyes, your mouth, she knew all this stuff. Things that babies just don’t know, she was doing.” Again, the implication is obvious: something is wrong with this child. Another video recorded around that time shows little Jani looking around the room—behavior her parents interpret as proof their daughter was hallucinating. Susan asks “Are her eyes still following?” “Yeah, she seems to be following from there over to there again,” Michael replies, before turning to his infant daughter and inquiring “You see things Mommy and Daddy can’t see, huh?” Just before Jani turned three, she invented an imaginary friend, a dog she named Lo, and then a whole stable of imaginary friends, as well as a whole slate of new names for herself, such as “Jani Firefly” and “Blue-­ Eyed Tree Frog.” The next title card tells us, “Over the next several years, the Schofields do their best to manage Jani’s idiosyncrasies.” Why a three-­ year old’s games of make-believe needed “managing” is never explained. When January was four years old, her parents had a second child, a son they named Bodhi. Around this time little Jani’s behavior really does seem to have taken a turn for the worse. She threatened to throw herself out the window, and then began kicking, hitting, and biting her mother and father. These are behaviors that would try the patience of any parents. But rather go to family counseling or attend parenting classes, Michael and Susan took their young daughter to a psychiatrist who prescribed the powerful antipsychotic drug Risperdal. “The Risperdal didn’t work,” Michael states flatly. At various times Jani was diagnosed with anxiety disorder, bipolar disorder, and attention-deficit/hyperactivity disorder (ADHD). Her condition continued to deteriorate. When she was six years old she ran out of her classroom at school and tried to throw herself through doors and windows. The teachers locked Jani in the assistant principal’s office (we are never told who thought that was a good idea), and she proceeded to destroy the place. The school authorities called Jani’s parents, who

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assented to having the police come and take her daughter to the UCLA Medical Center. “I’d reached the point where I was willing to let Jani go into the care of the state if it meant that she’d get the help that she needed,” Michael recalls. Jani was diagnosed with schizophrenia, one of the youngest patients ever to receive such a label. No one seems to have considered the possibility that her outburst could have been a drug effect, even though akathisia, or uncontrollable restlessness, is a well-known toxic effect of antipsychotic medications. The ethics of giving a new psychiatric diagnostic label to a patient already under the influence of a powerful psychotropic drug is never discussed. Jani reported seeing visions, mainly rats, cats, dogs, and numbers. Her doctors believed she was hallucinating almost all the time, and she was prescribed another antipsychotic drug, Clozaril. Michael and Susan were concerned, understandably so, about Jani hurting her baby brother, so they made a decision to protect Bodhi from his sister’s rages while keeping the family together, after a fashion. They rented two separate apartments in the same complex, one for Jani and one for Bodhi. Each night the parents switch apartments, enabling both of them to spend some time with each of their children. A scene shows Jani taking her medication—lithium (commonly prescribed for bipolar disorder) and Clozaril. Susan brandishes a bottle of Thorazine, yet another antipsychotic drug, which she says is for those occasions when Jani’s behavior becomes unmanageable. The toxic effects of lithium include malignant hypertension, irreversible kidney damage, and sudden cardiac death, while the toxic effects of so-called antipsychotic drugs include uncontrollable muscle movements (tardive dyskinesia) which may become permanent, worsening of psychotic symptoms (tardive psychosis), pancreatitis, shrinkage of the frontal lobes of the brain, ventricular arrhythmia, and sudden cardiac death. No mention is made of any of this. For the past year, we are told, Jani has been in and out of the psychiatric hospital. Her IQ has been measured at 146, but she is judged unable to attend regular classes. Instead, she goes to school for one hour every day, after all the other kids are gone. In another scene, Marc DeAntonio, Head of Pediatric Psychiatry at UCLA, tells us:

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There is some part of the chromosome that is expressing genes incorrectly. People who have more severe forms of schizophrenia, they have more of these abnormal genes and that’s what causes the early expression. And because they have more of these abnormal genes, it’s also why it’s more resistant to treatment. Whatever unfortunate reason, Jani was born with a number of abnormal genes that express this schizophrenic tendency, and it came out very early.

Not a shred of evidence is adduced in support of these assertions. Certainly no mention is made of whether anyone has performed a gene scan and found Jani has an excess of “abnormal genes.” We see Jani meeting with her psychiatrist. “I still see the numbers, especially Five,” Jani explains. “What does Five want to do?” her psychiatrist asks. “It wants to eat the baby,” Jani answers solemnly—then bursts out laughing, seemingly enjoying this process of toying with gullible grownups. At the end of the documentary, we see Jani and her father riding around a park on scooters. “If I knew then what I know now, I’d still do it all over again,” Michael explains in voice-over as the background music wells up emotionally. “Because Jani was meant to be here.” The second episode, Jani’s Next Chapter,2 premiered on 3 June 2012. Jani still is reporting hallucinations, but nevertheless her condition seems to be improving. She now goes to school two hours a day and is shown taking cooking classes and horseback riding lessons. The family has re-­ united under a single roof. But, ominously, it is Jani’s little brother Bodhi who now is beginning to have serious problems. He has been diagnosed with autism and prescribed Risperdal—the same drug Jani was prescribed at that age. His mother suspects he may have schizophrenia. In one scene, we see little Bodhi riding in a car, screaming at something that isn’t there, and in another scene, he keeps repeating “Twenty-nine is brown!” “He has schizophrenia!” Jani exclaims. No one considers the possibility that Bodhi is imitating the behaviors that garner his older sister so much attention. The third episode, Jani at 10,3 premiered on 27 May 2013, and consisted primarily of outtakes from the first two episodes, although with a few updates. Jani’s conditions seems to have stabilized—she is making friends and has not needed to be re-hospitalized—but Bodhi’s has taken a turn for the worst. Still in diapers at the age of five, his tantrums have gone from ten a day to twenty-five a day to becoming more or less continuous.

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The fourth episode, Jani and Bodhi’s Journey,4 first aired on 26 May 2014. Bodhi’s condition continues to deteriorate—at the age of six, he still is in diapers, and still throws tantrums and bites himself. His doctors have prescribed the antipsychotic drugs Seroquel and olanzapine. But Jani, against all expectations, seems to be thriving. Her obsession with her imaginary friends is fading, and she now attends regular classes full time and has plenty of real-life friends her age. Perhaps this is because of the effects of the drugs, or perhaps Jani has just decided to grow up, as most of us eventually do. The series doesn’t say. The fifth episode, Big Changes,5 first aired on 30 May 2017. The episode consisted almost entirely of outtakes from previous episodes, although in the last few minutes we get an update. Michael and Susan have gotten divorced. Michael has moved out of state, although he still talks on the telephone to Jani and Bodhi every night. Susan has found a new partner, and they have set a date for their wedding. Not once in five episodes did the producers give any consideration to alternatives to bio-genetic explanations for schizophrenia, or acknowledge that alternative viewpoints even exist. When Jani was three months old, her looking around the room was interpreted as evidence of mental illness. When she was three years old, her games of make-believe were interpreted as evidence of mental illness. When she was four years old, her temper tantrums were interpreted as evidence of mental illness. Is anything other than being a perfectly behaved little robot now evidence of mental illness? Raising children can be a frustrating business. There is no doubt about that. But generations of parents were able to discipline their children (and had the backing of society in doing so), and found ways to cope with their four-year-olds’ tantrums without resort to neuroleptic drugs. The mendacity of the producers is stunning. Animated rats, cats, and dogs are frequently superimposed on the screen, with the obvious implication that this is what Jani is seeing. How the producers could possibly know what is going on inside Jani’s head is never explained. No one considers the possibility that Jani reported hallucinations because that is what the grownups around her clearly expected her to be doing. Nor do the producers ever mention that hallucinations are far more common than previously realized, and that they are not necessarily a sign of serious problems. Literally millions of people experience auditory or visual hallucinations but are not bothered by them, and do not seek help for them.6

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No consideration is given to the long-term effects of powerful antipsychotic drugs and lithium on Jani’s developing young brain. No one ever asks why neuroleptic drugs were given to a four-year-old, not as a desperate last resort but apparently before behavioral interventions had even been given a serious try. Nor is any consideration given to the possibility that any of Jani’s problems may be drug effects. And other than the unsupported proclamations of Dr. DeAntonio, not a shred of evidence is adduced that Jani or any other human being was ever “born schizophrenic.”

An Ugly Incident Both Michael and Susan have written books describing their experiences. Michael’s book, January First: A Child’s Descent into Madness and Her Father’s Struggle to Save Her, was published in 2012.7 The book is written in diary form, and chronicles the period from June 2006 (when Bodhi was born) through July 2011. The portrait of January that emerges in these pages is one of a domestic tyrant who acts as if her every whim must be obeyed, because that is how those around her treat her. The portrait of her father is that of a man who not only is utterly ineffective at disciplining his child but sees no reason to. “I will not shut any aspect of Jani down,” he vows. “I will not restrict anything because I worry once she shuts down in order to conform, her full potential might be lost.”8 At the age of four, January’s IQ was measured at 146. Michael writes that he was disappointed it wasn’t a lot higher “I want to be able to say, when Jani does something antisocial, ‘Well, she has an IQ of 280.’”9 Apparently putting a stop to the antisocial behavior is not an option. When he tries to enroll his four-year-old daughter in a school for gifted children and is rebuffed on the perfectly reasonable grounds that Jani still is not toilet trained, he grumbles that “stupid rules that prevent her from reaching her potential.”10 In an astonishing admission, he reveals that he and Susan had a second child for no other reason than because Jani wanted them to.11 In the entry for 22 December 2007, soon after Bodhi was born, Michael describes a particularly ugly incident, which led to Jani being prescribed Risperdal:

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We cannot let Bodhi make a sound. In the three days since we brought him home, we have come to fear the slightest peep out of him. As soon as he begins to stir, even before he opens his eyes, we put a pacifier or bottle into his mouth.12

Jani turns up the volume on the television full blast, ignoring her father’s command to turn it down, waking the newborn baby from his sleep. Bodhi begins crying, and Jani ignores her father’s commands to leave the room, then hurls the television remote at her little brother (fortunately, she misses).13 Susan picks up the baby, to shield him from Jani’s wrath. Jani attacks her mother, who twists away from Jani and falls on the couch. Michael intercedes and Jani launches herself at him, hitting and kicking.14 Michael picks up Jani to restrain her, and she sinks her teeth into his chin. “This is the most physical pain I have felt in my life,”15 he notes. She rakes her nails over his face, and he holds her until she is finished struggling, at which point she asks brightly “Do we have any mac ‘n’ cheese?”16 Shortly after that incident, Michael and Susan took Jani to a child psychologist, who after one meeting (during which Jani hit the psychologist) referred her to the psychiatrist who prescribed Risperdal.17 Within a period of less than a month Jani was hospitalized at three different psychiatric facilities—Alhambra BHC, UCLA Medical Center, and Loma Linda University Hospital.18 Each time doctors could find nothing seriously wrong with Jani and she was quickly released. A doctor at Loma Linda asks them “You know what this is teaching her? It’s teaching her that when life gets too hard, run away.”19 He points out that Jani is perfectly capable of following rules while in hospital, and gently advises them to let their daughter know her behavior at home is unacceptable. When Susan angrily retorts that they have already tried that, Michael speaks the single most self-revealing sentence in the entire book: “No, we haven’t. As soon as the violence started, we ran straight to a shrink. We never stood up to her.”20 We also find out that Jani has been given a number of other medications besides the ones mentioned in the documentary series: Seroquel, Depakote, Ritalin, Haldol, and Lexapro. Michael himself has been taking Lexapro for years, and near the end of the book he downs the entire bottle in a half-hearted attempt at suicide.21 No mention is made of the fact the Lexapro and all the other drugs in its class have been linked to both suicidality and completed suicides.

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On 5 June 2013, a year after Michael’s book came out, the Dr. Phil show aired an episode about the Schofield family, titled “Edge of Insanity: My Schizophrenic Child.”22 Dr. Phil visited Jani in her home and they made cookies together, and then the good doctor proceeded to pepper her with earnest questions about her imaginary friends. Jani tolerated this interrogation politely enough, appearing anything but insane, although perhaps a bit bored by the whole enterprise. Susan’s book, Born Schizophrenic: A Mother’s Search for Her Family’s Sanity,23 was released on 5 May 2017. In one memorable scene, Susan takes four-year-old Jani with her to the doctor’s office. Jani screams at the receptionist for addressing her as “January” instead of Jani, breaks the doctor’s ultrasound machine, and then pulls down a box of papers, scattering them all over the office. After the visit, the doctor instructs Susan never to bring her daughter to her office again, and in the car Susan actually apologizes to Jani, telling her “You’re extremely smart and people just don’t appreciate it.”24 In another scene, shortly after Jani has been started on Risperdal, Susan is taking Jani and Bodhi to the zoo when Jani unfastens her seat belt, climbs over the car seat, and proceeds to grab the gear shift while her mother is driving on the freeway. Susan shoves Jani into the back seat and Jani proceeds to throw a shoe at her mother.25 Again, no one considers the possibility that this is a drug effect, even though uncontrollable agitation is an acknowledged toxic effect of Risperdal. Susan also details her efforts to get her doctors to prescribe Clozaril for Bodhi, as they did for Jani. Elsewhere she informs her readers that “the latest research” demonstrates that Clozaril “repairs damaged brain tissue.”26 The book chronicles Susan’s relationship with Michael, from their first meeting all the way through to the breakup of their marriage. It’s hard not to feel sympathy—whose marriage would not have cracked under that much strain? The book ends with a plea to make psychiatric medications more accessible and affordable.27 The pain experienced by Michael and Susan Schofield, and their children, is not to be belittled. Michael and Susan obviously are smart, educated people—she is a former radio and television reporter with a degree in communications, and he was a lecturer in the Department of English at Cal State Northridge—and yet it never seems to occur to either of them to put their reporting and research skills into investigating the claims of the psychiatric profession and the psychopharmaceutical industry about biogenetic explanations and drug-centered treatments for mental illnesses.

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“The overriding factor is love for the child” After I finished reading Michael’s and Susan’s books, I called Peter Breggin to get his take on matters. Dr. Breggin is a psychiatrist with half a century’s experience and the author of Toxic Psychiatry28 and Medication Madness.29 He indicated to me that he was not familiar with the story of January Schofield and so could not comment directly on her case, but he had plenty to say about the advisability of giving antipsychotic drugs to pre-­ adolescent children: All the antipsychotic drugs are extreme neurotoxins. They are poisonous to brain cells. That’s their signature biochemical effect. They don’t correct a biochemical imbalance—that’s just a talking point from the drug companies. Probably the most salient characteristic of children who get labeled schizophrenic is that they have difficulty in relating to people, and they stay by themselves, and they’re not engaged in a trusting manner with adults. They’re fearful about people. They have the wrong ideas about them. Any neurotoxins will worsen their difficulties relating to people. There is simply no reason to give children, who are having trouble with their relationships, drugs that will impair their frontal lobes, making it even harder or impossible to make meaningful, caring relationships with the people around them.

Next I ask Dr. Breggin about the ethics of giving new psychiatric diagnoses to patients who are already under the influence of psychotropic drugs such as Risperdal: One of the problems that Risperdal in particular produces is akathisia, which is an inner agitation that can make people feel crazy and suicidal and violent. Akathisia feels like you are been tortured from the inside out. People often can’t find the words to describe how it feels. Once you put somebody on a psychiatric drug that gives them neurotoxicity, you cannot and should not make a separate diagnosis of a new psychiatric disorder, especially when it’s known that the drug can produce the disorder you are diagnosing. So you really have to stop all the drugs and give the child the kind of therapy the child needs. Unless the family is totally dysfunctional, you want to do family therapy with the child. When I see a disturbed child, in addition to taking him off his psychiatric drugs, carefully and slowly, with the knowledge and the cooperation of the family, I offer them family therapy.

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You help the child re-enter human society by helping the adults and the older children in how they relate to the child. And usually I don’t end up working a great deal with the child. Instead, I tell the parents ‘If you change what you’re doing, if you learn to give consistent and kindly discipline, if you take the time to build a trusting relationship with your child, if you learn not to explode when your child makes you upset and angry, if you teach mutual respect, and if you learn unconditional love, you will make the most powerful contribution to your child’s recovery.

Dr. Breggin added, “Not some mental health professional, not me, certainly not some drug or mental hospital. The child is going to respond best to improvements in how the parents approach the child.” I have had children with the most severe diagnoses, I’ve had young people coming straight out of mental hospitals, who have had wonderful recoveries when their parents are cooperative. They learn to be more loving, they learn to be more disciplined, they spend more time with the child. The whole secret to helping the children is helping the parents.

If a child is reporting auditory or visual hallucinations, is that a reason to press the panic button? First of all, it’s common for children to produce what the parents or what the authorities expect, including seemingly bizarre behaviors. That’s not unusual. And the other thing is, that children have all kinds of experiences which we shouldn’t panic over. If a child is waking from nightmares, or going to sleep and having unusual experiences in the twilight zone, if a child has bizarre ideas, don’t rush to diagnosing the child! You do whatever is necessary to create a more disciplined and loving relationship with your child, while learning what is so disturbing in your child’s world.

If a child is a terror at home, but is perfectly capable of following rules while in hospital, what does that tell you? One of the first things that I look for when the parents come in is: Where is the child having these negative interactions with other people? They may tell me that it’s at school but not at home. I say well, that’s good news, and so we have to find out what is going on at school. If they say the child is doing well at school, but really is just a horror at home, I say well, you just have to look at what goes on at home. So let’s talk about how you discipline at home.

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Many parents are at a loss as to how to discipline children. Good discipline requires a good, loving relationship so that your child wants to please you. If you and your child are both getting out of control, clearly you must rebuild your relationship by doing things together with the child while you learn how to remain calm, and even kind when requiring discipline. You need to regain moral authority through a solid parental relationship.

Does Clozaril repair damaged brain tissue? The idea that neurotoxins repair brain tissue indicates the extreme to which the drug companies and their minions will go to justify poisoning people. One of the things that they like to say is that these drugs are somehow protective of brain cells. And where do they get that from? From some bizarre petri dish experiments on isolated nerve cells. Or they may say that these drugs cause neurogenesis, the growth of new brain cells, and that’s a good thing. That’s a very popular selling point now. The fact is the neurogenesis is a response to brain injury! Use common sense. The idea that neurotoxins somehow protect a child or an adult, improving their mental functioning, is beyond reason.

The conversation shifts to the topic of the Genain sisters. I remind Dr. Breggin that I first learned about the sisters through his book Toxic Psychiatry,30 and this brings me to the most important question of the day. “I have to admit I’m feeling a little disheartened,” I tell him. “Is there any middle ground between parents abusing their children, and children abusing their parents?” Dr. Breggin chuckles softly, and I get an inkling of the warmth and reassurance generations of patients must have felt in his presence. He begins: Of course there’s a middle ground which parents have sought, I’m sure, for thousands of years. And that middle ground has to do with having a loving and caring attitude toward your child, so that you use discipline in moderate fashion. The goal is a responsible, loving human being, able to take care of himself or herself, and to take care of others, someone who has the depth to love others, and to love nature, and in my opinion, to have a spiritual relationship with something greater than themselves. The overriding factor is love for the child, along with accepting the fact that at times they are going to be angry at you because you’re providing them with discipline. And when you have a loving relationship, discipline

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can be provided without violence. It’s provided by an interpersonal relationship where you spend so much time with your child, you have such a good relationship with your child, your child doesn’t want to disappoint you.

A Case of Munchausen’s Syndrome by Proxy? On 25 and 26 February 2019, Michael and Susan Schofield had a reunion of sorts on two consecutive episodes of the Dr. Phil show, nearly seven years after their first appearance. By this time Michael had moved on, quite literally: he was married to another woman and living in Minnesota, 1800 miles away from Jani and Bodhi. In terms of his fatherly duties he was (again, literally) phoning in most of the time. Susan had also remarried, and had achieved a measure of notoriety through her YouTube channel, on which she and her new husband, Cory Cabana, had posted more than 180 videos of Bodhi.31 Viewers were shown clips from these videos. At the age of eleven, Bodhi already has the lanky body of an adolescent boy, but he drools (a well-­ known toxic effect of so-called antipsychotic medication), his eyes appear glazed, and he seems barely able to speak, communicating mainly in oneor two-word sentences.32 “I believe Bodhi will suffer permanent brain damage from the medication he is on,” Michael told viewers. “Susan is punishing me for the divorce and the way things ended.” He noted that Susan has recorded videos of Bodhi in the shower, and on the toilet, and had them posted on her channel. He also notes that their son has been hospitalized at least twenty times.33 Susan, for her part, acknowledged that Bodhi has been on over twenty different medications, and, astonishingly, that she had consulted fifty different doctors in her quest to find one willing to prescribe Clozaril for him.34 The following day, viewers were introduced to Charles Sophy, psychiatrist and Medical Director for Child and Family Services for the City of Los Angeles. Speaking in a calm, level voice, without rancor, Dr. Sophy laid it on the line for Susan and her new husband: “It’s not about your child. It’s about the two of you being selfish. Both of your kids are drowning in all this crazy drama that you do. Why is [Bodhi] on the toilet and you are videotaping him? It’s exploiting him.”35

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“I’m exploiting the mental healthcare industry,” Susan retorted, to which Dr. Sophy replied “You’re exploiting your son. Your son. Your son. Who was on the toilet? The mental healthcare industry, or your son?”36 Michael opined that his ex-wife was afflicted with Munchhausen’s Syndrome by Proxy, while Cory acknowledged that they had finally found a doctor willing to prescribe Clozaril for Bodhi, but the boy had to be taken off the drug after suffering from neutropenia,37 a deficiency of white blood cells that can leave the body vulnerable to serious infection. Dr. Phil offered to assemble a team of experts to evaluate Bodhi and get him the care he needs, on one condition: that Susan and Cory take down their YouTube channel. When Susan refused, Dr. Phil abruptly dismissed them, but a few minutes later they came back on to the set and agreed to his terms.38 On 2 April 2019, the Verge reported that the authorities had removed Bodhi and Jani from their parent’s custody, and that the Los Angeles County Children’s Court had placed a gag order on all parties while the case was being investigated.39 At the time of writing this, the case still was wending its way through the legal system. How it will play out is anyone’s guess. And while Dr. Sophy is to be applauded for his no-nonsense candor, neither he nor anyone else involved seems to be questioning the fundamental premise of biological psychiatry, that these conditions called “mental illnesses” are properly regarded as biologically-based brain diseases, probably genetic in origin. The underlying assumption behind bio-genetic explanations for so-­ called mental illnesses seems to be that society is basically healthy, and that these conditions are the product of defective brains or defective genes, thereby absolving the rest of us from addressing the social and familial factors that form a major—and changeable—component of these conditions. It is to these factors that we now turn.

Notes 1. Homerun Entertainment 2010. 2. Homerun Entertainment 2012. 3. Homerun Entertainment 2013. 4. Homerun Entertainment 2014. 5. Homerun Entertainment 2017.

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6. Adrian Honig et  al., “Auditory Hallucinations: A Comparison Between Patients and Nonpatients,” Journal of Nervous and Mental Disease, 186, no. 10 (October 1998): 646–651; van Os et al., “Strauss 1969 Revisited: A Psychosis Continuum in the General Population?” Schizophrenia Research, 45, no. 1–2 (September 29, 2000): 11–20, https://doi. org/10.1016/S0920-9964(99)00224-8; Anthony P.  Morrison, Sarah Nothard, Samantha E. Bowe, and Adrian Wells, “Interpretations of Voices in Patients With Hallucinations and Non Patient Controls: A Comparison and Predictors of Distress in Patients,” Behavior Research and Therapy, 42, no. 11 (November 2004): 1315–1323, https://doi.org/10.1016/j. brat.2003.08.009; Vanessa Beavan, Sarah Nothard, Samantha E.  Bowe, and Adrian Wells, “Interpretations of Voices in Patients With Hallucinations and Non Patient Controls: A Comparison and Predictors of Distress in Patients,” Behavior Research and Therapy, 42, no. 11 (November 2004): 1315–1323, https://doi.org/10.1016/j.brat.2003.08.009 7. Michael Schofield, January First: A Child’s Descent Into Madness and Her Father’s Struggle to Save Her (New York: Crown, 2012). 8. Ibid., 12. 9. Ibid., 16 10. Ibid., 19. 11. Ibid., 29. 12. Ibid., 33. 13. Ibid., 33–35. 14. Ibid., 36. 15. Ibid., 39. 16. Ibid., 40. 17. Ibid., 43–53. 18. Ibid., 78–133. 19. Ibid., 141. 20. Ibid., 143. 21. Ibid., 272–274. 22. Dr. Phil, “Edge of Insanity: My Schizophrenic Child,” Peteski Productions, June 5, 2013. 23. Susan Schofield, Born Schizophrenic: A Mother’s Search For Her Family’s Sanity (CreateSpace Independent Publishing Platform, 2017). 24. Ibid., 46. 25. Ibid., 65. 26. Ibid., 121–122. 27. Ibid., 317–318. 28. Breggin, Toxic Psychiatry. 29. Peter Roger Breggin, Medication Madness: The Role of Psychiatric Drugs in Cases of Violence, Suicide, and Crime (New York: Saint Martin’s, 2008).

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30. Breggin, Toxic Psychiatry, 105–107. 31. Dr. Phil, “Edge of Insanity: I Believe I Have a Second Schizophrenic Child,” Peteski Productions, February 25, 2019. 32. Ibid. 33. Ibid. 34. Ibid. 35. Dr. Phil, “A Second Schizophrenic Child or a Misdiagnosing Mom: Can Bodhi Be Helped?” Peteski Productions, February 26, 2019. 36. Ibid. 37. Ibid. 38. Ibid. 39. Makena Kelly, “How a YouTube Channel Unraveled a Medical Nightmare,” Verge, April 2, 2019, https://www.theverge.com/2019/4/2/18290555/ youtube-children-parents-susan-schofield-lie-schizophrenia-exploitationprivacy

CHAPTER 9

Trauma and Psychosis

When my brother was forcing me to have oral sex with him, I did not understand what was going on. I did not understand why he wanted to pee in my mouth.

So says Miriam, who was diagnosed with schizoaffective disorder at the age of fourteen. The abuse at the hands of her older brother began when Miriam was six years old, or perhaps even before that. She says she doesn’t remember anything at all about her life before that age. “We were latchkey kids before the term was even invented,” Miriam explains. Her father worked two jobs and was almost never around, and her mother worked full time as well. “My mother was all about the shopping, and the decorated home, and the jewelry, and the hair and all that,” Miriam recalls. “She would go to the mall and leave my brother and I in the car where he would make me have oral sex with him while she was in there shopping, and that’s how I lived.” For a long time Miriam suffered in silence, terrified to tell anyone what was going on. “My brother was the golden child, she remembers. My mother worshipped the ground he walked on.” When she finally dared to tell her mother about the abuse, it did not go well. “I didn’t even get two words out and my mother slapped me across the face and said ‘I never want to hear you talk about that again.’”

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The abuse escalated. When Miriam was home alone with her older brother, he would invite his friends over to assist in tormenting her. They would make her strip naked, tie her to a chair, and poke her with sticks as if she were a captive animal. They would gather snails from a tree in the yard and cook them in a pan on the stove and force them down her throat. Miriam began having night terrors, horrible visions of loved ones being mutilated and dismembered. She would arise and go downstairs and walk around the kitchen table in circles, mumbling incoherently to herself. At the age of fourteen, her parents finally took her to a psychiatrist. She did not volunteer any information about being abused, and the psychiatrists did not ask. The psychiatrist diagnosed Miriam with schizoaffective disorder, a label that was gladly received by her parents. “It was a real relief for them to hear ‘Oh, gee, she’s mentally ill, so anything she says probably doesn’t have much validity,’” Miriam notes. Miriam’s psychiatrist indicated that her condition could be hereditary, and asked if there was any history of mental illness on either side of her family, but neither of her parents knew—or was willing to say—much about their family medical histories. The psychiatrist prescribed amitriptyline and Valium, and Miriam was committed to a mental hospital. This was the beginning of a tale of iatrogenic harm that beggars belief. “People in there, they’re so bored out of their minds they’re looking for anything to do,” she explains. “Stealing, having sex with each other, anything they could do.” You see girls burning themselves with cigarettes, trying to hang themselves in the bathroom, selling their medication.

During her stay in the mental hospital, Miriam was sexually assaulted, both by fellow patients and by multiple staff members. She also learned from the other girls about cutting herself, and she says she experienced a strange sense of relief by doing so. Miriam’s first stay in the mental hospital lasted eight months. When she returned home, her parents took her to a pastor for counseling, and the pastor raped her. In the years that followed, Miriam was hospitalized ten times. She received a variety of diagnoses in addition to the initial one of Schizoaffective Disorder—Schizotypal Personality Disorder, Anxiety Disorder, Major Depressive Disorder, Borderline Personality Disorder, Major Depressive Disorder, Major Depressive Disorder with Psychotic Features, PTSD,

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Dissociative Identity Disorder (Multiple Personality Disorder), Depersonalization Disorder, Treatment Resistant Depression, and Epilepsy. When she balked at receiving a diagnosis of bipolar disorder, her doctor exclaimed “All the cool, fun, artistic people are bipolar! Don’t you want to be that?” She was prescribed a dizzying variety of different medications, literally dozens of different ones from every major class of psychiatric drug—antidepressants, antipsychotics, anticonvulsants, anxiolytics, hypnotics, stimulants. She also experienced a dizzying variety of toxic effects, including sedation, massive weight gain, headaches, stomach problems, bradycardia, wild fluctuations in blood pressure, pericarditis, akathisia (uncontrollable restlessness), dyskinesia (uncontrollable movements), and multiple suicide attempts. In addition, she began having seizures, as many as twenty-­ five a day. “The only benefit I found on the drugs was the sedation factor,” she explains. “When you’re depressed, sometimes you just have to stop thinking. That’s the only benefit of any of those drugs. It numbs you down so you don’t have to feel your pain. And guess what? When you come off the drugs, the pain is still there.” During this time Miriam also lived through three failed marriages. The last one was to a man she describes as a sex addict. She says he had liaisons with hundreds of different women whom he met in at work, in bars, online, anywhere he could meet them. Miriam decided to forego the psych meds once and for all. Her third husband was not supportive. He would hold her down and literally force the pills down her throat. But when he made sexual advances toward her daughter, who was twelve years old at the time, she decided she had had enough and left him. At that time Miriam was taking seven different drugs—Cymbalta, Abilify, Vyvanse, Keppra, Xanax, Lamictal, and Clonazepam. She went from doctor to doctor, trying to find one who would assist her to kick the drugs that had caused her so much misery. Not one would help. She obtained a copy of the book Psychiatric Drug Withdrawal1 by psychiatrist Peter Breggin and tapered off the drugs, one by one, without anyone else’s assistance. She has been drug-free for the past three and a half years. The seizures have stopped, all the excess weight came off, and at last she is able to think clearly.

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A Message That Went Unheard The young mother presented to the doctor with classic symptoms of schizophrenia. She had become reclusive and suspicious, avoiding family gatherings and complaining that the neighbors were behaving toward her in a rude and hostile manner. She believed she was under constant surveillance, and that people were reading her thoughts.2 Her condition took an ominous turn, as she began experiencing visual, auditory, and tactile hallucinations. She saw visions of male and female genitalia, heard voices threatening and reproaching her, and felt sensations in her own genitalia, as if a heavy hand lay upon her lap. Her cognitive abilities remained intact, and upon questioning she revealed that she had been sexually assaulted by her older brother from the age of six to the age of ten.3 The time was the winter of 1895, and the doctor was a Viennese neurologist named Sigmund Freud. This was not an isolated case. One after another, Freud’s patients related memories of sexual assaults that occurred in early childhood. Freud concluded that childhood sexual abuse was a causative factor in “hysteria,” at the time a catch-all term for a wide variety of mental problems. He laid out his thesis in a series of three papers, all published in 1896.4 But, barely a year later, he changed his mind, and decided these tales of long-ago violations were nothing but “infantile fantasies” produced by the subconscious minds of his patients. Freud walked up the edge of the cliff, looked down—and then turned away. This was a message the world was not ready to hear. Almost twenty years later, Freud explained in his book On the History of the Psycho-Analytical Movement: If hysterics refer their symptoms to imaginary traumas, then this new fact signifies that they create such scenes in their phantasies, and hence psychic reality deserves to be given a place next to actual reality. This was soon followed by the conviction that these phantasies serve to hide the autoerotic activities of the early years of childhood, to idealize them and place them on a higher level, and now the whole sexual life of the child made its appearance behind these phantasies.5

This was a bizarre turn in Freud’s thinking. He had always maintained that conditions such as “hysteria” were actual brain diseases. Now he was saying, in effect, that these actual brain diseases were caused by events that had never happened.

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This story is told by psychoanalyst and author Jeffrey Moussaieff Masson in his book The Assault on Truth: Freud’s Suppression of the Seduction Theory.6 In the course of researching his book, Dr. Masson shared his findings with Freud’s daughter Anna, who wrote to him in reply: Keeping up the seduction theory would mean to abandon the Oedipus complex, and with it the whole importance of phantasy life, conscious or unconscious phantasy. In fact, I think there would have been no psychoanalysis afterwards.7

Perhaps she was right. Perhaps there would have been no psychoanalysis, at least as it exists today. Perhaps instead of inventing “complexes” and “drives” out of thin air (similar to the way modern-day psychiatry invents “chemical imbalances” out of thin air8), Freud and his successors would have turned their attention to helping patients with problems that are perfectly understandable responses to overwhelming stress and trauma. Who knows how the world might have become a different place today as a result? Almost forty years after Freud published his findings on child sexual abuse, another psychiatrist, Sándor Ferenczi, gave a talk at the International Psycho-Analytic Congress in Wiesbaden, in September 1932.9 Ferenczi was one of Freud’s star pupils as well as his former analysand, and was often addressed by the great man as “Dear Son.” Freud by then was too sick to attend the congress, but most of the other great names in psychoanalysis were there to witness Ferenczi take on the most taboo subject in the field.10 Like Freud, Ferenczi had patient after patient come into his office and tell stories of violations that began long ago, always before the age of eight. Unlike Freud, he had a ready answer to those who would dismiss these stories of early childhood sexual abuse as mere “infantile fantasies”— because he’d also had patient after patient come into his office and confess to having done these things to small children.11 Ernest Jones, President of the International Psychoanalytical Association, had Ferenczi’s paper translated into English and promised to publish the translation in the International Journal of Psycho-Analysis, where it would have received a much wider audience. But the following year Ferenczi died at the age of fifty-nine from pernicious anemia. Jones, under pressure from his professional colleagues, reneged on his promise and had the proofs of Ferenczi’s last paper destroyed.12

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In the years that followed, the overweening emphasis was on bio-­ genetic explanations of schizophrenia, with environmental stressors—if they were mentioned at all—usually confined to the role of “triggers,” immediately precipitating an episode of psychosis. A minority of psychoanalytically-­oriented psychiatrists did continue to explore the role of environmental factors in the genesis of schizophrenia, offering theories about “disordered communication,” “overprotective mothers,” “double binds,” and so forth. The history of all this arid theorizing will not be recounted here. Suffice it to say that severe child abuse seems to have been off their radar. Psychiatrist Don Jackson was an early critic of genetic theories of the origin of schizophrenia, and a pioneer in the use of psychotherapy to treat psychotic symptoms. But even he tip-toed around the subject of out-and-­ out abuse. In his 1960 book chapter “A critique of the literature on the genesis of schizophrenia,” he said of the cause of schizophrenia, “Assuredly it is nothing as obvious as beatings, rape, poverty, or the overgeneralized notion of rejection.”13 In that same chapter, Jackson mentioned two cases of male twins concordant for schizophrenia, both of whom suffered from the fear of choking on a banana, and two cases of concordant female twins, both of whom suffered from the fear of being poisoned by semen.14 He never considered the possibility that these fears may have stemmed from reallife experience. Another chapter by two other authors in the same volume15 describes children as young as five hospitalized for psychotic symptoms, behaving in a sexually seductive or aggressive manner toward the staff, and engaging in open genital or anal masturbation. The possibility that these behaviors are reactions to early childhood sexual abuse is never explored. We have already seen, in examining the story of the Genain Quadruplets, how adroit mid-twentieth-century psychiatrists were in ignoring the evidence that was, literally, right before their eyes. As recently as 1975, a popular American textbook of psychiatry estimated the frequency of incest to be one in a million.16 A 1979 article in Time quoted psychologist Steven Matthysse, who had this to say about the genesis of schizophrenia: “I’d be surprised if the family environment made the slightest bit of difference.”17 The first systematic attempts to investigate the relationship between childhood trauma and schizophrenia did not take place until the 1980s.

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Heartbreaking Realities In 1991, psychiatrist Peter Breggin wrote the following passage about patients with acute schizophrenia, which he interpreted as a psychospiritual crisis: People undergoing psychospiritual crises express the most intense degree of shame and humiliation I have ever witnessed. Some of my patients’ faces have seemed on the verge of bursting with shame when reliving severe humiliations from the past. At the core is a feeling of being utterly worthless, humiliated, or meaningless. At the same time they often feel enormous anger or hate, because when blame is shifted outward, so is rage.18

These words were written in the heyday of the Prozac era, a time in which the public was saturated with the message that “mental illnesses” were caused by chemical imbalances in the brain, and that the psychopharmaceutical industry had safe and effective medications to correct these imbalances. At that moment in history, Dr. Breggin was like a voice crying in the wilderness. A paper by John Read, Professor of Clinical Psychology at the University of East London, confirms this.19 Dr. Read and his colleagues searched the database PsychINFO from 1872 through February 2008 and found 75,063 entries for the term for “schizophrenia.” Of those entries, 15,481, or 20.6 percent, concerned biological causes (as evidenced by the use of the terms “neurotransmitters,” “brain,” or genetics”) while only 262, or 0.3 percent, dealt with child abuse or neglect.20 What could be the reason for the imbalance? Read and his co-authors note that an announcement for the first Congress of the Schizophrenia International Research Society in 2008 listed over 200 presentations, predominantly about genes, brains, and drugs, with none of them mentioning child abuse, neglect, or poverty. The society is funded by eight different drug companies.21 Nevertheless, the evidence is there, for those willing to look. Dr. Read and his colleagues have noted that the concept of “schizophrenia” intergrades imperceptibly into normalcy as well as into other psychiatric diagnostic categories. Moreover, clinicians sometimes will render a diagnosis other than schizophrenia upon learning that a patient has suffered child abuse in the past, using a form of circular logic as justification: since schizophrenia is bio-genetic in origin, rather than environmental, the patient must not be suffering from schizophrenia!22

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Moreover, the experiences of those labeled “schizophrenic” intergrade imperceptibly into normalcy.23 The label itself is disjunctive (meaning two patients can have a diagnosis of schizophrenia and have no symptoms in common), and lacks reliability and validity.24 For these reasons, Read and his colleagues have concentrated on psychotic symptoms (hallucinations, delusions, paranoia) rather than specific diagnostic categories. In a series of papers, they reviewed the literature on the relationship between childhood maltreatment and psychosis,25 including eleven large-­ scale population studies in five different countries (the United Kingdom, the Netherlands, Australia, the United States, and Germany). The studies covered numerous forms of childhood maltreatment, including sexual abuse, physical abuse, emotional abuse, violence in the home, running away from home, childhood institutionalization, serious neglect, and bullying. Ten of the eleven studies found a significant correlation between childhood maltreatment and psychotic symptoms, including visual hallucinations, auditory hallucinations, tactile hallucinations, delusions, and full-blown schizophrenia, with odds ratios ranging from 1.5 (i.e. a 50 percent increase in risk) on up.26 One study found that women with psychotic symptoms were fifteen times more likely to have suffered sexual abuse than those with no mental disorder. What about the study that did not find a significant correlation? That one, by Josie Spataro and her colleagues,27 found that childhood sexual abuse was correlated with a 20 percent increase in the likelihood of schizophrenic disorders, although the correlation did not rise to customarily accepted levels of significance. This study raises some interesting questions. The authors themselves mention several sources of systematic bias in their study that would cause them to underestimate the correlation between child sexual abuse and schizophrenia.28 But, as Read and his colleagues pointed out in an earlier paper,29 perhaps the biggest source of bias was that the case subjects were drawn not from a population-wide survey but from official records of cases of abuse identified by the authorities. In such cases the child victims most likely would have been removed from their homes and offered some kind of support or therapy. Perhaps the lesson here is not that childhood sexual abuse has no aggravating effect on psychotic symptoms, but that reporting the abuse, being believed, and receiving help and support has a mitigating effect.30

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There’s more. Nine of the eleven studies reviewed by Read and his colleagues looked for a dose-dependent relationship between childhood maltreatment and psychotic symptoms. All nine found it.31 One study found that those who had experienced five or more different types of childhood maltreatment were 200 times more likely to be diagnosed as psychotic than those who had not experienced any.32 These studies also show that childhood abuse is related to the content of hallucinations and delusions. It is here that we get a glimpse of the heartbreaking realities behind the cold clinical language of psychiatric diagnostic labels. Here are a few examples: • A woman whose mother had physically and emotionally abused her as a child heard her mother’s voice commanding her to kill herself.33 • A woman who had been sexually abused as a child believed her body was covered in semen.34 • A fifteen-year-old boy, who at the age of seven had been raped repeatedly by his uncle, heard voices telling him he was “sleazy” and should kill himself.35 • A man, who in boyhood had been abused over many years by means of forced anal penetration, heard the perpetrator’s voice telling him to touch children.36 • Another man, who had suffered sexual abuse from an early age and had been raped several times by strangers and violent partners, suffered anal bleeding after inserting hose into himself in an attempt to wash “aliens” from his body.37 Hallucinations may stem from problems with source monitoring,38 in which internal thoughts or emotional states are attributed to external agents. This source monitoring may actually serve a protective function, sparing the subject from the terror and humiliation of childhood trauma by experiencing it as an event in the present. Paranoia and delusions may also have their roots in childhood trauma. Paranoia stems from a state of hypervigilant awareness, which may well be essential to surviving an abusive situation, in which violence may be unleashed on the child at any moment.39 Delusions are a cognitive attempt to make sense out of the paranoid emotional state. These patterns learned in childhood may be the source of boundless misery once their usefulness has been outlived.40

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Such patterns might leave their mark on a developing brain, in the form of dysregulation of the hypothalamus-pituitary-adrenal (HPA) axis and increased activity of dopaminergic neurons, in effect keeping the brain and body in a permanent state of high alert. Can these changes be regarded as the “cause” of schizophrenia? Read and his co-authors refute this notion: “This is akin to assuming that because the brain operates differently when we are grieving, it is the brain that caused our sadness.”41 These changes are not the mark of a defective brain. Rather, they are the mark of a normal brain responding to overwhelming stress and trauma. Traumatic experiences early in childhood may adversely impact a child’s ability to form lasting friendships with age peers, leaving the child without this source of support and resilience during the tumultuous years of adolescence. A British study looked at subjects who had experienced repeated or severe physical or sexual abuse and found that normal peer relationships during adolescence had a protective effect against the development of psychopathology later in life.42 The trauma experienced by these unfortunates often continues long past childhood. The majority of adult female mental patients experience sexual assault, along with about a quarter of the males.43 Some of these assaults take place within an institutional setting.44 Physical assaults by intimate partners or other family members also are common.45 The studies reviewed by Read and his colleagues also show there is no specifically “schizophrenogenic” style of parenting. Rather, any of a wide variety of traumas and other adverse childhood experiences may predispose an individual to the development of schizophrenia or psychotic symptoms—or any of a wide variety of other conditions, including depression and anxiety. Since Read and his co-authors published their findings, at least thirteen narratives or systematic reviews (including eight meta-analyses) have been published on the correlation between adverse child experiences and psychosis.46 Most forms of adverse childhood experiences that have been looked at are correlated with anywhere from a two- to four-fold increase in the risk of psychosis. An Irish study not only found a dose-response between bullying and physical abuse and psychotic symptoms but also found that when the abuse stopped, the occurrence of psychotic symptoms dropped sharply.47 Yet another meta-analysis published in January 2018 in the Schizophrenia Bulletin found that childhood trauma and sexual abuse were correlated not just with the presence of hallucinations and delusions but also with their severity.48

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There is no longer any doubt: the correlation of schizophrenia and related disorders with trauma and other adverse childhood experiences is robust, reliable, and dose-dependent. It cuts across national boundaries, income brackets, and ethnic identities. It has been verified again and again in prospective cohort studies, population-based cross-sectional studies, and case-control studies. As if all this were not enough, the link between schizophrenia and trauma has been confirmed in a macabre way. A 1998 study of elderly patients in an Israeli mental hospital found a disproportionately large number of Holocaust survivors among them, with half suffering from schizophrenia.49 This is more than a bit ironic, given that the Holocaust was an outgrowth of the T4 Program, which in turn was an attempt by German psychiatrists to stamp out mental illness. Seen in the light of these findings, the unwillingness of some researchers to look at the evidence that was literally right before their eyes seems particularly egregious. A 2001 paper by a team that included Stephen Faraone of Massachusetts General Hospital examined the relationship between traumatic brain injury and schizophrenia. The researchers found that subjects diagnosed with schizophrenia had three times the rate of traumatic brain injury than did their never-mentally-ill relatives.50 Despite having interviewed each subject as to the nature of the head injury, the researchers never mention whether any of these injuries were deliberately inflicted, and if so by whom. Instead, they attribute the higher rate of traumatic brain injuries to an interaction between these injuries and a hypothesized “schizophrenia gene.”51

“Not just triggers” A few biogenetically-oriented psychiatrists have long given a perfunctory nod to the role of psychological and social factors as “triggers” in the etiology of mental illness. But in a telephone interview, Dr. Read blasted the “triggering” metaphor: “Triggering implies that there is something underlying to be triggered, and the usual thing that’s assumed to be triggered is some sort of genetic disposition. So ‘triggering’ is minimizing child abuse and neglect and rape and war. Traumas are direct causes of mental health problems including psychosis, not just triggers.” Dr. Read told me that the bio-genetic view of mental illness results in a lot of miscommunication between psychiatrists and their clients. “The clients come in with one view, that they have a life history to tell, and that

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their problems are caused by the bad things that have happened in their lives, and they meet a psychiatrist who isn’t interested or—to be fair—who just wants to listen long enough to count some symptoms and pick a diagnostic label and then pick a color pill. Their compassion to listen to people’s life stories gets trained out of them in medical school.” We need to abandon the biological model of mental illness. We need to abandon that simplistic model. It’s not evidence-based. We have no evidence. We have never found the biochemical imbalance for depression or the dopamine overactivity for psychosis. These are just drug-company-­ invented myths. So we need to just abandon it. We have a situation where some people actually put in writing in scientific journals that the reason there’s a high rate of abuse of children who eventually go on to become schizophrenic is because these children are genetically predisposed to schizophrenia, and they are displaying the early signs of schizophrenia and are therefore more prone to be abused, which I find to be a horrendous example of blaming the victim.

The Myth of the Schizophrenogenic Mother There is one more point that needs to be addressed. No account of the history of twentieth-century psychiatry is complete without a discussion of the “schizophrenogenic mother”—a sinister figment of the imagination of misogynist psychiatrists who, we are told, was held solely and completely responsible for the genesis of schizophrenia in her children—at least, in those bad old days before the advent of modern psychopharmaceutical drugs and direct-to-consumer advertising. In The Feminine Mystique, author Betty Friedan proclaimed: It was suddenly discovered that the mother could be blamed for almost everything. In every case history of a troubled child; alcoholic, suicidal, schizophrenic, psychopathic, neurotic adult; impotent, homosexual male; frigid, promiscuous female; ulcerous, asthmatic, and otherwise disturbed American, could be found a mother. … Clearly something was ‘wrong’ with American women.52

This theme recurs frequently in the psychiatric literature: The standard procedure is to assume that the child’s problem is reactive to maternal handling in a one-on-one relationship. … Single bits of data fitting in with these speculations are quoted as typical of the child’s feelings and the

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mother’s attitudes and are taken as proof of the thesis of noxious maternal attitudes as universal causation.53 All the prevailing psychodynamic theories added up to maternal culpability in the causation of child behavior problems.54 It became standard practice to believe that mothers were the cause of their children’s psychosis.55 Generations of American mothers had to suffer unwarranted reproaches as schizophrenogenic mothers.56 This approach was typified by such hurtful and destructive concepts as the schizophrenogenic mother.57

So, did psychiatrists really “blame the mother” to the exclusion of all other causes? Where did this notion come from? As with most myths, the myth of the schizophrenogenic mother has a grain of truth behind it. In a 1948 article, psychiatrist Frieda Fromm-­ Reichmann wrote: The schizophrenic is painfully distrustful and resentful of other people, due to the severe early warp and rejection he encountered in important people of his infancy and early childhood, as a rule, mainly in a schizophrenogenic mother.58

(BTW, the word “schizophrenogenic” is a God-awfully clumsy term; “schizogenic” would have been preferable, but it’s probably too late now to change.) Dr. Fromm-Reichmann was a psychoanalyst famed for her compassion and skill in reaching even the most seemingly intractable cases of schizophrenia.59 The above remarks were a passing aside in a paper devoted almost exclusively to the dynamics of the therapist-patient relationship in schizophrenia. Examination of the writings of Dr. Fromm-Reichmann’s psychoanalytically-oriented colleagues in the 1950s and 1960s reveals that from the beginning they understood perfectly well that the concept of the schizophrenogenic mother was not sufficient to explain the genesis of schizophrenia, that this condition was the product of disturbed families, not just disturbed mothers: Very little is known about the fathers of schizophrenic children. No systematic exploration of fathers was undertaken in connection with the present

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study; however, eight fathers were interviewed and the impression was that they, too, had great personality difficulties. They seemed to be perfectionistic and obsessive people, as sick as their wives.60 In our data, it is apparent that the paternal influences are noxious as frequently as the maternal.61 There was a history of rejection by the mother in three cases; by the father in four cases; and by both parents in eight cases.62 A small point that seems to emerge from the above figures is that rejection by the mother does not appear to any greater degree in either group. … If a psychogenic theory of schizophrenia is to be persisted with, it would seem necessary to study more complex factors than pure maternal attitudes. I am wondering whether the total pattern of parental attitudes may not be a worthwhile object [of research].63 Eleven percent of the males and 11% of the females had rejecting fathers. Ten percent of the males and 8% of the females had rejecting mothers. This might prompt us to re-examine our theories of personality development which accredit to the mother a very great significance in the family and the father a position of relative unimportance.64 We do not assume that the double bind is inflicted by the mother alone, but that it may be done by either the mother alone or some combination of mother, father, and siblings.65 Perhaps the next phase will include a study of schizophrenia (or schizophrenias) as a family-borne disease involving a complicated host-vector-recipient cycle that includes much more than can be connoted by the term “schizophrenogenic mother.66 As our studies were uncovering serious difficulties in all areas of transactions in these families, we preferred to bring balance to the topic by directing attention to the total situation before focusing on the mother.67

On the other hand, the mother-child relationship is the most important human relationship there is. Is it really such a stretch to suggest that bad consequences may follow when this relationship goes awry? The above-cited paper by Trude Tietze68 discusses the case history of a young woman with schizophrenia whose mother was obsessed with preventing her daughter from masturbating. This woman had two surgical mutilations performed on her infant daughter’s clitoris—one when the child was two years old, and one when she was one year old. This same woman would inspect her daughter’s vulva every night, and beat her if she judged the child’s labia were “irritated.”

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Could it be that this woman’s actions had something to do with her daughter’s problems later in life? And does just posing the question make one anti-motherhood—or anti-womanhood? Is all this just a tempest in a teapot? Actually no. In his 2012 book Shrinks: The Untold Story of Psychiatry, former APA President Jeffrey Lieberman ridicules those benighted psychiatrists of yesteryear who were foolish enough to believe that mental illness could have its roots in childhood trauma and abuse,69 and then sings unqualified praise for the modern psychopharmaceutical industry—ignoring the fact that as consumption of psychiatric medications has skyrocketed, so has the suicide rate70 and the proportion of Americans disabled by psychiatric illnesses.71 The real myth of the schizophrenogenic mother is the idea that psychiatrists ever seriously promoted the idea that mothers are solely responsible for schizophrenia in their children. And this myth has for too long been used as a straw woman to divert attention from serious discussion of the role of abuse and trauma in the genesis of schizophrenia and other mental illnesses, and to promote biological explanations and pharmacological interventions for these conditions instead. It’s time to lay this myth to rest for good. * * * As for Miriam, today she is living on disability payments. “The mental health system traps you into a path of poverty and despair that you just can’t climb out of,” she avers. “You depend on the medical insurance, you depend on the money coming in, and they penalize you if you try to work.” She also had her driver’s license revoked because of the seizures she says were drug-induced, and even though she has been seizure-free for three years she still has not gotten her license back. After her brother died, Miriam moved across the country to be closer to her mother and try to rebuild her relationship with her, but it didn’t work. “She was still in denial, still claiming it was all my fault.” Miriam’s abusive childhood left her determined not to make the same mistakes with her own daughter. “She was not going to feel the pain I felt when growing up, and she was going to know that I loved her and would do anything for her to protect her.” Today her daughter is a local television celebrity and, in her spare time, a record-setter in her chosen avocation.

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I ask Miriam what she wishes those around her had done differently when she was a child. She doesn’t hesitate a moment before answering: There’s a really simple solution called Love. Love those children, okay? Watch out for them. Know the signs. Abuse happens behind closed doors, and it happens more than people know.

Indeed. The fact that these conditions called “mental illnesses” have their roots in personal and social factors suggests they might best be addressed on a personal and social level. That is a matter we shall turn to next.

Notes 1. Breggin, Toxic Psychiatry. 2. Sigmund Freud, “Further Remarks on the Neuropsychosis of Defense,” in Selected Papers on Hysteria and Other Psychoneuroses, Second Enlarged Edition, trans. A.A.  Brill (New York: Journal of Nervous and Mental Disease Publishing Company, 1912), 166. 3. Ibid., 166–174. 4. Sigmund Freud, Heredity and the Aetiology of the Neuroses (Plano: Read Books Ltd., 2013), Kindle; Freud, “Further Remarks”; Sigmund Freud, “The Aetiology of Hysteria,” trans. James Strachey, Appendix B in Jeffrey Masson, The Assault on Truth, Freud’s Suppression of the Seduction Theory (New York: Farrar, Straus, & Giroux, 1984), 251–282. 5. Sigmund Freud, On the History of the Psycho-Analytical Movement, trans. A.A. Brill (New York: Journal of Nervous and Mental Disease Publishing Company, 1917), 11, https://babel.hathitrust.org/cgi/pt?id=hvd. hc4nan;view=1up;seq=7 6. Jeffrey Moussaieff Masson, The Assault on Truth: Freud’s Suppression of the Seduction Theory (New York: Farrar, Straus, & Giroux, 1984). 7. Ibid., 113. 8. Terry Lynch, The Depression Delusion: The Myth of the Chemical Imbalance (Limerick: Mental Health Publishing, 2015). 9. Sándor Ferenczi, “Confusion of Tongues Between Adults and the Child,” trans. Jeffrey M. Masson and Marianne Loring in Masson, The Assault on Truth, Freud’s Suppression of the Seduction Theory (New York: Farrar, Straus, & Giroux, 1984), 289. 10. Masson, Assault on Truth, 145–153. 11. Ferenczi, “Confusion,” 288–289. 12. Masson, Assault on Truth, 151–153.

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13. Jackson, “Critique,” 38. 14. Ibid., 69–70. 15. Maleta J.  Boatman and S.A.  Szurek, “A Clinical Study of Childhood Schizophrenia,” in The Etiology of Schizophrenia, ed. Donald D. Jackson, (New York: Basic Books, 1960) 396–399. 16. John Read and Richard P. Bentall, “Negative Childhood Experiences and Mental Health: Theoretical, Clinical, and Primary Prevention Implications,” British Journal of Psychiatry, 200, no. 2 (February 2012): 89, https://doi. org/10.1192/bjp.bp.111.096727 17. Anonymous, “Psychiatry on the Couch.” 18. Breggin, Toxic Psychiatry, 39. 19. John Read et  al., “Child Maltreatment and Psychosis: A Return to a Genuinely Integrated Bio-Psycho-Social Model,” Clinical Schizophrenia and Related Psychoses, 2, no. 3 (October 2008): 235–254, https://doi. org/10.3371/CSRP.2.3.5 20. Ibid., 236. 21. Ibid., 236. 22. John Read, et  al., “Childhood Trauma, Psychosis and Schizophrenia: A Literature Review With Theoretical and Clinical Implication,” Acta Psychiatric Scandinavica, 112, no. 5 (October 2005): 333, https://doi. org/10.1111/j.1600-0447.2005.00634.x 23. Ibid., 340. 24. John Read, Richard P.  Bentall, and Roar Fosse, “Time to Abandon the Bio-Bio-Bio Model of Psychosis: Exploring the Epigenetic and Psychological Mechanisms by Which Adverse Life Events Lead to Psychotic Symptoms,” Epidemiologia e Psychiatria Sociale, 18, 4 (2009): 299. 25. John Read and Nick Argyle, “Hallucinations, Delusions, and Thought Disorder Among Adult Psychiatric Inpatients With a History of Child Abuse,” Psychiatric Services, 50, no. 11 (November 1999): 1467–1472, https://doi.org/10.1176/ps.50.11.1467; Read et  al., “Childhood Trauma,” 330–350; Read et al., “Child Maltreatment,” 235–254; Read, Bentall, and Fosse, “Bio-Bio-Bio Model,” 299–310. 26. Read, Bentall, and Fosse, “Bio-Bio-Bio Model,” 301–303. 27. Josie Spataro et al., “Impact of Child Sexual Abuse on Mental Health,” British Journal of Psychiatry, 184, no. 5 (May 2004): 416–412, https:// doi.org/10.1192/bjp.184.5.416 28. Ibid., 418–419. 29. Read et al., “Childhood Trauma,” 338. 30. Ibid., 338. 31. Read, Bentall, and Fosse, “Bio-Bio-Bio Model,” 301. 32. Read et al., “Childhood maltreatment,” 243. 33. Read and Argyle, “Hallucinations, Delusions, and Thought Disorders,” 1469.

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34. Read et al., “Childhood Maltreatment,” 241. 35. Ibid., 241. 36. Ibid., 241. 37. Ibid., 241. 38. Read, Bentall, and Fosse, “Bio-Bio-Bio Model,” 305. 39. Ibid., 305. 40. Richard P.  Bentall, “Understanding Psychotic Symptoms.” In Models of Madness: Psychological, Social, and Biological Approaches, edited by John Read and Jaqui Dillon, (Abingdon: Routledge, 2013) 226–227. 41. Read et al., “Child Maltreatment,” 246. 42. Stephan Collishaw et al., “Resilience to Adult Psychopathology Following Childhood Maltreatment: Evidence From a Community Sample,” Child Abuse & Neglect, 31, no. 3 (March 2007): 211–229, https://doi. org/10.1016/j.chiabu.2007.02.004 43. Lisa A. Goodman, Mary-Ann Dutton, and Maxine Harris 2001. “Recent Victimization in Women and Men With Severe Mental Illness: Prevalence and Correlates,” Journal of Traumatic Stress, 14, no. 4 (October 1995): 615–632. 44. Anouk L. Grubaugh et al., “Patients’ Perception of Care and Safety Within Psychiatric Settings,” Psychological Services, 4, no. 3 (August 2007): 193– 201, https://doi.org/10.1037/1541-1559.4.3.193; Bruno Biancosino et  al., “Violent Behavior in Acute Psychiatric Inpatient Facilities: A National Survey in Italy,” Journal of Nervous and Mental Disease, 197, no. 10 (October 2009): 772–782, https://doi.org/10.1097/ NMD.0b013e3181bb0d6b 45. M. Cascardi et al., “Physical Aggression Against Psychiatric Inpatients By Family Members and Partners,” Psychiatric Services, 47, no. 5 (May 1996): 531–533, https://doi.org/10.1176/ps.47.5.531 46. Craig Morgan and Charlotte Gayer-Anderson, “Childhood Adversities and Psychosis: Evidence, Challenges, Implications,” World Psychiatry, 15, no. 2 (June 2016): 93–102, https://doi.org/10.1002/wps.20330 47. Ian Kelleher et  al.,, “Childhood Trauma and Psychosis in a Prospective Cohort Study: Cause, Effect, and Directionality,” American Journal of Psychiatry, 170, no. 7 (July 2013): 734–740, https://doi.org/10.1176/ appi.ajp.2012.12091169 48. Thomas Bailey et al., “Childhood Trauma is Associated With Severity of Hallucinations and Delusions in Psychotic Disorders: A Systematic Review and Meta-Analysis,” Schizophrenia Bulletin, January 2, 2018, https://doi. org/10.1093/schbul/sbx161 [Epub ahead of print]. 49. Primo Terno et al., “Holocaust Survivors Hospitalized for Life: The Israeli Experience,” Comprehensive Psychiatry, 39, no. 6 (November/December 1998): 364–367, https://doi.org/10.1016/S0010-440X(98)90049-9.

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50. Dolores Malaspina et  al., “Traumatic Brain Injury and Schizophrenia in Members of Schizophrenia and Bipolar Disorder Pedigrees,” American Journal of Psychiatry, 158, no. 3 (March 2001): 440–446, https://doi. org/10.1176/appi.ajp.158.3.440 51. Ibid., 444. 52. Betty Friedan, The Feminine Mystique (New York: W.W.  Norton and Company, 1963) 189. 53. Stella Chess, “Mal de Mére,” American Journal of Orthopsychiatry, 34, (1960): 613. 54. Stella Chess, “The ‘Blame the Mother’ Ideology,” International Journal of Mental Health, 11, no. 1–2 (1982): 95, https://doi.org/10.1080/0020 7411.1982.11448908 55. John Neill, “Whatever Became of the Schizophrenogenic Mother?” American Journal of Psychotherapy, 64, no. 4 (October 1990): 502. 56. Shorter, History, 177. 57. Garfinkel, Paul E., “The Changing Culture in Relation to the Practice of Psychiatry,” Psychotherapy and Psychosomatics 70, No. 5 (September– October 2001): 229, https://doi.org/10.1159/000056259 58. Frieda Fromm-Reichmann “Notes On the Development of Treatment of Schizophrenics by Psychoanalytic Psychotherapy,” Psychiatry, 11, no. 3 (August 1948): 265, https://doi.org/10.1080/00332747.1948.110 22688 59. For a discussion of the life and works of Fromm-Reichmann, see Chap. 11 of this volume. 60. Trude Tietze, “A Study of the Mothers of Schizophrenic Patients,” Psychiatry, 12, no. 1 (1949): 64. 61. Ruth Wilmans Lidz and Theodore Lidz, “The Family Environment of Schizophrenic Patients,” American Journal of Psychiatry, 106, no. 5 (1949): 344. 62. E.R. Clardy, “A Study on the Development and Course of Schizophrenia in Children,” Psychiatric Quarterly, 25, no. 1 (January 1951): 86. 63. E.J.A. Nuffield, “The Schizogenic Mother,” Medical Journal of Australia, 2, no. 8 (August 1951): 285. 64. C.W.  Wahl, “Some Antecedent Factors in the Family History of Schizophrenics,” American Journal of Psychiatry, 110, (1954): 670–671, https://doi.org/10.1176/ajp.110.9.668 65. Gregory Bateson et al., “Towards a Theory of Schizophrenia,” Behavioral Science, 1, no. 4 (1956): 253, https://doi.org/10.1002/bs.3830010402 66. Donald D. Jackson, “A Note on the Importance of Trauma in the Genesis of Schizophrenia,” Psychiatry, 20, no. 2 (May 1957): 184. 67. Theodore Lidz et  al. “The Mothers of Schizophrenic Patients,” in Schizophrenia and the Family, ed. Theodore Lidz, Stephen Fleck, and Alice R. Cornelison (New York: International Universities Press, 1965), 290.

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68. Tietze, “Study of the Mothers,” 62–63. 69. Jeffrey Lieberman and Ogi Ogas, Shrinks: The Untold Story of Psychiatry (New York: Little, Brown, and Company, 2015): 79–86. 70. “Increase in Suicide in the United States, 1999–2014,” CDC, accessed July 31, 2018, https://www.cdc.gov/nchs/products/databriefs/db241. htm 71. Whitaker, Anatomy of an Epidemic.

CHAPTER 10

The Asylum Era and Moral Therapy

We should take great care not to do any harm where it is not in our power to do any good.1

These words were penned by William Battie in his Treatise on Madness, published in 1758. Battie was a medical doctor with an impeccable academic pedigree. Born in 1703, educated at Eton and King’s College, Cambridge, he later became a Fellow of the Royal Society and President of the Royal College of Physicians.2 In 1742 he became Governor of Bethlem Hospital, the only major home for the insane in England at the time. As Governor, he abolished sightseeing at Bethlem and also created the post of resident Apothecary, the position occupied by John Haslam some years later. In 1751 he opened his own institution, Saint Luke’s Hospital for Lunatics.3 Saint Luke’s was organized as what today we would call a teaching hospital. For the first time anywhere in the world, medical students were allowed to walk the wards of a hospital for the insane and to receive clinical instruction there.4 In his treatise, Battie distinguished between anxiety (overreaction to stimuli present in the real world), “insensibility,” or mental retardation as we now would say (underreaction to those same stimuli), and madness, which consists of perception of objects and events not really existing in the

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world.5 Battie conceived of madness as arising to a disturbance in the fibers that constitute the nervous system, and postulated a variety of causes— head injury, internal exostoses of the cranium, induration of the sinuses and the dura mater, inflammation, tumors, toxins (including alcohol and opium), gluttony, idleness, debauchery, and hereditary factors.6 Battie was skeptical of many of the remedies for illness common in his day—bleeding, cathartics, emetics, blistering, cold baths, errhines, diaphoretics, and so forth (although he did employ them). He recommended cleanliness, fresh air, rest, quiet, plain food, and exercise. Interestingly, Battie also stressed the importance of keeping the patient’s family and friends away during the recovery period.7 This was the first suggestion that madness was curable—or at least a condition that could be managed until the body healed itself. By the time Battie died in 1776, over 1000 patients had passed through his hospital, and half of them were discharged as “cured.” In the early nineteenth century, when Bethlem was investigated by Parliament for abuses, Saint Luke’s was held up as an example of what a hospital for the insane should be.8

Moral Therapy Saint Luke’s was an early experiment in what came to be known as “moral therapy,” a term coined by Phillipe Pinel, who is regarded as the father of French psychiatry. Born in the province of Toulouse, the son of a village doctor, Pinel earned his doctoral degree from the Faculty of Medicine in Toulouse, an institution considered a rural backwater by the bigwigs at the University of Paris.9 Twice the young man applied for the prestigious Prix de Diest to study at the Paris Faculty of Medicine and qualify for practice in that great city. Twice the bigwigs denied his application, the second time excoriating the “painful mediocrity” of his medical knowledge. Pinel eked out a living as the editor of the Gazette de Santé, and as the doctor in a private home for the insane—in fact practicing medicine without a license, since his degree was not recognized in Paris.10 But the French revolution swept away much of the old order, and opened opportunities for Pinel and his friends. At the same time, beliefs in the inherent worth and dignity of every human being led to calls for the curing of the insane, as opposed to mere warehousing.11

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Pinel was appointed to a Chair in Hygiene at the School of Medicine in Paris (he was later moved to Internal Medicine), and was also made medical superintendent of the Pitie-Salpetriere University Hospital for women12 (the institution was located in a former gunpowder factory, hence the name; saltpeter is an essential ingredient for the manufacture of that commodity). Perhaps because of his long-term status as an outsider looking in, Pinel was suspicious of dogma and medical authority. He believed the true authorities were not the doctors, whose knowledge of the insane was limited to transitory visits, but to the attendants (or “concierges”), who lived with the patients night and day.13 Like Battie in England, Pinel was skeptical of the somatic therapies of the day—bleeding, purgatives, cold baths, and so on. His “moral therapy” stressed the human qualities of the attending physician—kindness, empathy, and an authoritative yet reassuring manner.14 Cadaver studies led Pinel to conclude that madness was not necessarily associated with any kind of visible abnormality of the brain. He also regarded cases that were as beyond the reach of moral therapy, or any kind of medical intervention. Custodial care was the best that could be hoped for in such cases.15 Pinel was not above a bit of theatricality to get his point across. A young man who refused to eat was confronted by Pinel and a group of hospital attendants, all armed and carrying chains. Pinel addressed the young man in a thundering voice, threatening him with the cruelest of punishments if he did not eat the soup they had brought him; the young man complied and subsequently recovered. A tailor was terrified that he was going to be beheaded for treason, and Pinel arranged a mock trial in which young doctors dressed in black robes interrogated the man and finally acquitted him of all charges. The man’s condition improved, although he subsequently relapsed.16 Pinel also stressed the importance of accurate record-keeping, noting what worked and—just as important—what didn’t work.17 How did all this work out for the patients? Pinel compiled the results of a four-year study of all first-time admissions to Salpetriere for mania and melancholy and concluded that 93 percent were cured.18 Pinel’s “moral therapy” helped inspire another early experiment in helping patients with severe mental illness—The Retreat at York.

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“The most grievous of human diseases” The Retreat opened on 11 May 1796 under the aegis of William Tuke, a wealthy Quaker merchant, after a female member of the York Society of Friends congregation died while in the custody of the York Asylum.19 Built to hold thirty patients at a time, the Retreat was constructed on twenty acres of land just half a mile outside the city walls. The rooms were well lit and airy, the windows without bars, with only a hedge delineating the grounds from the surrounding countryside.20 The grounds were used to graze dairy cows, providing milk and butter for the patients and staff. On the north side of the house was a one-acre garden which supplied fruits and vegetables, as well as affording patients opportunities both for occupational therapy and for relaxation and contemplation. The garden was divided by gravel walkways and interspersed with trees and shrubs, and shielded from the prying eyes of passersby by a hedge.21 On the south side of the house were separate courtyards for male and female patients to enjoy the fresh air and sunshine. For the patients’ amusement, these courtyards were furnished with animal companions— hawks, seagulls, rabbits, and poultry.22 Patients were provided with a wholesome, nourishing diet,23 and patients and the superintendent ate together.24 William Tuke’s son Samuel wrote an account of the early days of the institution, titled Description of the Retreat, in which he explained the philosophy behind the Retreat: Many errors in the construction, as well as the management of insane asylums, appear to arise from excessive attention to safety [Italics in the original]. People in general, have the most erroneous notions of the constantly outrageous behavior, or malicious dispositions, of deranged persons; and it has, in too many instances, been found convenient to encourage these false sentiments, to apologize for the treatment of the unhappy sufferers, or admit the vicious neglect of the attendants. In the construction of such places, cure and comfort ought to be as much considered, as security; and I have no hesitation in declaring, that a system which, by limiting the power of the attendant obliges him not to neglect his duty, and makes it his interest to obtain the good opinion of those under his care, provides more effectually for the safety of the keeper, as well as of the patient, than all of the apparatus of chains, darkness, and anodynes.25

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Thomas Fowler, the medical superintendent of the Retreat, initially employed the usual remedies of the day—bleeding, blisters, evacuants, and so on, but quickly became disillusioned with them, leading him to conclude, in the words of Samuel Tuke, “that medicine, as yet, possesses very inadequate means to relieve the most grievous of human diseases.” Instead, the Retreat emphasized a healthy diet, fresh air, exercise, and warm baths.26 Most importantly, the Retreat relied on moral treatment. Again, in the words of Tuke: “If we adopt the opinion that the disease originates in the mind, applications made immediately to it are obviously the most natural and the most likely to be attended with success.”27 Corporal punishment was strictly forbidden, as were chains,28 although straitjackets were occasionally employed to restrain patients who presented a danger to themselves or others. For the most violently deranged patients, a special apparatus was designed to keep the patient tied down to the bed while still enabling him to turn over and change positions.29 The staff found that violent and vociferous patients tended to respond best to a kind and somewhat low tone of voice. No attempt was made to reason with them regarding their hallucinations and delusions.30 Female patients exercised their creative abilities in sewing and knitting,31 and both men and women were encouraged to read, write, and play ball, chess, and drafts,32 as well as attending religious services.33 According to the younger Tuke, “What ever tends to promote the happiness of the patient is found to increase his desire to restrain himself by exciting the wish not to forfeit his enjoyments.”34 The administrators of the Retreat understood the importance of early intervention, even offering discounts to families who had relatives admitted within six months of the onset of symptoms.35 Again, how did this work out for the patients? Tuke summarizes outcomes for 149 patients admitted from 1796 through the end of 1811. Of particular interest are the chronic cases, a group that included 61 cases of mania, 21 of melancholia, and 6 of dementia. Of these, 19 had died, 39 remained at the Retreat, 6 were removed from the Retreat by friends as “improved,” 4 were discharged so much improved as not to need further confinement, and 16 were discharged as “perfectly recovered.”36 In addition two of the cases of dementia were discharged as not suitable objects. None of the six cases of dementia exhibited even a partial recovery.37

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Keep in mind these were patients deemed “incurable” who had been suffering from severe mental illness for fifteen or twenty years or even more and sometimes had been brought to the Retreat in chains.38 Every single case of recovery must have seemed little short of miraculous.

Order and Discipline In reading the stories of these early nineteenth-century psychiatrists, the general impression is one of men who sincerely wanted to help their charges but who were hampered at every turn both by lack of knowledge and by lack of resources. Consider Ernst Horn, a contemporary of Pinel, who was appointed Second Director of the Psychiatric Section of Charité Hospital in Berlin in 1806.39 At the time, Charité was the largest institution of its kind in the Kingdom of Prussia. Horn immediately ordered a clean-up operation, removing the excrement that caked the halls, replacing wooden chamber pots with tin ones, requiring patients to take warm baths, replacing the old straw in bed ­mattresses with fresh, and ordering laundresses to clean patients’ gowns thoroughly.40 Horn asked for more money to pay for training and higher salaries for the hospital staff, most of whom were drawn from the lowest socioeconomic sectors of society (many of the female attendants were former sex workers who had grown too old and haggard to ply their former trade). His request was denied. He also asked that patients be provided with a healthier diet, asserting that food was at least as important as medicine in promoting recovery. The bureaucrats in charge of appropriations replied that the kitchen was not a drugstore.41 As the ward’s population swelled, Horn attempted, whenever possible, to return the harmless but incurable cases to their families, and to remand the dangerous ones to other, smaller institutions. He separated female patients from male, young girls from scabrous old whores, and also tried to separate patients according to habits such as cleanliness and loudness.42 Believing idleness was a major cause of his patients’ problems, Horn instituted a policy of strict order and discipline. Patients awoke and had breakfast in their rooms at 5:00 AM. From 6:00 AM to 7:00 AM, they attended religious services or were read aloud to from newspapers or books. For the next hour, both men and women cut firewood, and for the next hour, some of them pulled a heavy wagon for exercise, while others were allowed to rest.43

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From 9:00 AM to 10:00 AM, patients (again, both men and women) participated in military drill, with knapsacks strapped to their backs and carrying heavy wooden toy rifles. The hour between 10:00  AM and 11:00 AM was devoted to hydrotherapy, followed by an hour of instruction in drawing or painting. Lunch hour began at noon, followed by an hour of rest and relaxation.44 This was followed by hours devoted to woodwork, geography classes, and more hours devoted to recreation and relaxation. From 8:30 PM to 9:00 PM, patients received more religious instruction, with bedtime following immediately afterward.45 Like many of his predecessors, Horn stressed the importance of keeping the patients’ family members away from them during the recovery period.46 He was also a believer in the somatic therapies of the day, including “hydrotherapy,” which often involved dousing patients with icy water or directing a forcible stream of water at their genitals. Other procedures employed included hunger, bleeding, blistering, emetics, scalding, the rotating swing, and restraining patients in giant burlap bags.47 Horn was charged by the authorities when a twenty-one-year-old female patient died suddenly while imprisoned in one of these bags. Reill testified on his behalf, and Horn was acquitted.48 How did his patients fare? Horn published a report (in part an effort to clear his name after a sensational trial), detailing outcomes for 2190 patients that were treated at Charité between 1806 and 1818. These years coincided with two major epidemics, so it is not too surprising to learn that 512 of these patients died. Of the remainder, 936 were discharged as recovered, 517 were discharged unrecovered, 219 were transferred to other institutions, and 6 escaped.49 How did the nineteenth-century asylum doctors compare to their modern-day counterparts, with their armamentarium of modern-day psychotropic drugs? The answer may come as a surprise.

Astonishing Findings David Healy is a Professor of Psychiatry at Bangor University in Wales and the author of Mania: A Short History of Bipolar Disorder.50 Dr. Healy and his colleagues examined mental health service utilization patterns in North West Wales for the years 1894–1896 and compared the data to that from 1996.51

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North West Wales was almost ideal for comparisons of this kind. Between 1896 and 1996, the population of this area changed almost not at all in terms of size, age composition, ethnic composition, poverty, or rurality. Moreover, for both periods, there was effectively only one point of access to mental health service users in Wales: Denbigh Asylum for 1894–1896, and the North West Wales District General Hospital Psychiatric Unit for 1996. This is about as close to a controlled experiment as it is possible to get for this sort of thing.52 Dr. Healy and his colleagues found that for the period 1894–1896, first admissions for the condition we now call schizophrenia averaged eight per year, whereas for the year 1996 the number was thirteen, or an increase of 60 percent. But the real surprise came when they looked at total admissions, which averaged ten per year for 1894–1896. By 1996 this figure had risen to 82—a 720 percent increase, due mainly to the elevated rate of re-admission for schizophrenia.53 For the period 1894–1896, the lifetime admission rate for schizophrenia was 1.4 per patient, which means that most patients were admitted only once in their lives, with an average length of stay of about 2.2 years. After that, most of them went home and got on with their lives. By 1996, the rate had risen to 6.9 readmissions per patient. Hospital stays had gotten shorter, but total time spent in hospital had increased.54 The picture for patients in the 1894–1896 cohort was not all rosy. Thirty percent of these patients died within five years of admission, many of them due to pneumonia or tuberculosis they contracted in hospital. Most of these deaths could be easily prevented today with the use of modern antibiotics. The five-year death rate for patients admitted in 1996 was 14 percent, or less than half of the 1894–1896 rate. On the other hand, for patients in the 1996 cohort between the ages of 15 and 55, most of the deaths were due to suicide or drug overdose.55 There were no suicides in the 1894–1896 cohort. In summary, compared to the period 1894–1896, in 1996 there were more admissions for schizophrenia, outcomes had gotten worse, and patients were more likely to die as a direct result of their mental illness. In an expanded analysis,56 Dr. Healy and his colleagues compared mortality rates for first-time admissions for schizophrenia in North West Wales for the periods 1875–1924 and 1994–2010. Their findings were nothing short of astounding. In comparison with the general population, patients

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with schizophrenia in the contemporary cohort were ten times more likely to be dead at the end of their first year of treatment than their counterparts from a century before. Elsewhere Dr. Healy noted “There is no other illness in medicine where such a statement could be made.”57 All the deaths (7 out of a total of 227 patients) in the contemporary cohort were due to suicide. In the first year of treatment, patients hospitalized for schizophrenia now are hundred times more likely to commit suicide than the rest of us. By contrast, only one patient out of 655 in the historical cohort committed suicide.58 What is the reason for this change? It was not that those in the historical cohort lacked the means to kill themselves. Asylum patients in Wales in the nineteenth and early twentieth centuries spent almost all their waking hours at liberty in asylum farms, kitchens, and sewing rooms, with plenty of sharp objects within reach and ample opportunities to commit suicide.59 Dr. Healy and his co-authors argue that the likeliest explanation for the excess of suicides in the modern-day cohort is due to antipsychotic drugs, which did not become available until the 1950s. In a previous paper,60 Healy analyzed RCT data for the antipsychotics Risperdal, Zyprexa, Seroquel, Serdolect, and Geodon. He found the rate of suicidal acts in the treatment arm was almost four times that of the placebo arm. There were no suicides out of 1351 patients given placebo, whereas the 12,817 patients in the treatment arm included 33 completed suicides. Or as Dr. Healy put it, graphically and succinctly, “When it comes to dead bodies in current psychotropic trials, there are a greater number of them in the active treatment groups than in the placebo groups. This is quite different from what happens in penicillin trials or trials of drugs that really work.”61 Dr. Healy told me “If you look at asylum records both in North Wales and elsewhere, up to about 1950, people with schizophrenia didn’t commit suicide. They just didn’t.” This was not an illness that led to people actually going on to kill themselves. It’s the combination of the illness and its treatment that results in people actually committing suicide.

These are astonishing findings. In what other branch of medicine have outcomes gotten worse since the nineteenth century?

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Notes 1. William Battie, A Treatise on Madness (London: J. Whiston and B. White, 1758), 98. 2. Richard Hunter and Ida McAlpine, “Introduction,” in A Treatise on Madness by William Battie, M.D., and Remarks on Dr. Battie’s Treatise on Madness by John Monro, M.D.: A Psychiatric Controversy of the Eighteenth Century, introduced and annotated by Richard Hunter and Ida McAlpine, (London: Dawsons, 1962), 9–10. 3. Ibid., 10. 4. Ibid., 11. 5. Battie, Treatise, 4–6. 6. Ibid., 50–67. 7. Ibid., 68–99. 8. Hunter and McAlpine, “Introduction,” 12–13. 9. Jan Goldstein, Console and Classify: The French Psychiatric Profession in the Nineteenth Century (Cambridge: Cambridge University Press, 1987), 65–67. 10. Ibid., 67–69. 11. Ibid., 70. 12. Ibid., 71. 13. Ibid., 72–76. 14. Ibid., 79–89. 15. Ibid., 90. 16. Ibid., 82–83. 17. Ibid., 101–102. 18. Ibid., 102–103. 19. Samuel Tuke, Description of the Retreat: An Institution Near York for Insane Persons of the Society of Friends Containing an Account of Its Origin and Progress, the Modes of treatment, and a Statement of Cases (London: W. Alexander, 1813), 22. 20. Ibid., 93–94. 21. Ibid., 95. 22. Ibid., 96. 23. Ibid., 123–125. 24. Ibid., 99. 25. Ibid., 106–107. 26. Ibid., 110–113. 27. Ibid., 131. 28. Ibid., 141. 29. Ibid., 164–167. 30. Ibid., 150–151. 31. Ibid., 156.

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32. Ibid., 180–181. 33. Ibid., 160–161, 180–181. 34. Ibid., 177. 35. Ibid., 88–89. 36. Ibid., 201–203. 37. Ibid., 203. 38. Ibid., 214. 39. George Windholz, “Psychiatric Treatment and the Condition of the Mentally Disturbed at Berlin’s Charité in the Early Decades of the Nineteenth Century,” History of Psychiatry, 6, 22 Pt. 2 (June 1995), 159. 40. Ibid., 162. 41. Ibid., 163. 42. Ibid., 166. 43. Ibid., 167. 44. Ibid., 167. 45. Ibid., 167–168. 46. Ibid., 166. 47. Ibid., 169–171. 48. Ibid., 159–160. 49. Ibid., 174. 50. David Healy, Mania: A Short History of Bipolar Disorder (Baltimore: Johns Hopkins University Press, 2008). 51. David Healy, et  al., “Psychiatric Bed Utilization: 1896 and 1996 Compared,” Psychological Medicine, 31, no. 5 (July 2001): 779–790, https://doi.org/10.1017/S003329170100396; David Healy, et  al., “Service Utilization in 1896 and 1996: Morbidity and Mortality Data From North Wales,” History of Psychiatry, 16, no. 1 (2005): 27–41. 52. Healy et al., “Psychiatric Bed Utilization,” 780. 53. Healy et al., “Service utilization,” 34. 54. Ibid., 36. 55. Ibid., 35–36. 56. David Healy et  al., “Mortality in Schizophrenia and Related Psychoses: Data From Two Cohorts, 1875–1924 and 1994–2010,” BMJ Open, 2, no. 5 (October 8, 2012): https://doi.org/10.1136/bmjopen-2012-001810 57. David Healy, “The Madness of Psychiatry,” Dr. David Healy, October 29, 2012, https://davidhealy.org/the-madness-of-psychiatry/ 58. Healy et al., “Mortality in Schizophrenia,” 3–4. 59. Healy et al. 2012, 8. 60. David Healy, “Shaping the Intimate: Influences on the Experiences of Everyday Nerves,” Social Studies of Science, 34, no. 2 (April 2004): 219– 245, https://doi.org/10.1177/0306312704042620 61. Healy, Mania, 132.

CHAPTER 11

Frieda Fromm-Reichmann and Chestnut Lodge

The place: Heidelberg, Germany, home of that nation’s oldest university, founded in 1386. The time: 17 May 1933. Joseph Behringer, Director of the Militant League for German Culture, gave a lecture on “The disparagement of German art between 1919 and 1933,” and later that evening a torchlight procession departed from the town hall on Jubilee Square.1 Students, professors, and members of paramilitary groups—the SS, the SA, and the Steel Helmets (Der Stahlhelm)—marched from Neckerstaden to Sofienstrasse, Hauptstrasse, and finally to University Square, where students earlier had built a pyre, supported by scaffolding poles, twelve-feet high, consisting of books slated for burning. Some of these had been confiscated from public libraries and the town’s trade union library, and others the students themselves had voluntarily purged from their own personal collections.2 The leader of the students gave one last speech against “Jewish-­ corrosive, Marxist-Bolshevik, frivolous writing” and then the pile of books was set ablaze. Similar demonstrations took place all over Germany.3 During the period 1933–1944, thousands of Jewish physicians fled Europe to escape the wrath of the Nazis.4 One of them was Frieda Fromm-­ Reichmann, psychoanalyst and the owner of an asylum in Heidelberg. Over one hundred of her relatives who remained behind were murdered in the Holocaust.5 Dr. Fromm-Reichmann’s story is told in the masterful biography To Redeem One Person is to Redeem the World by Gail Hornstein, Professor of Psychology at Mount Holyoke College. © The Author(s) 2019 P. D. Hahn, Madness and Genetic Determinism, https://doi.org/10.1007/978-3-030-21866-9_11

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Fromm-Reichmann’s ex-husband, psychoanalyst Erich Fromm, arranged for her to take a temporary position as an analyst at Chestnut Lodge, a small family owned mental hospital in Rockville, Maryland.6 She remained there for the rest of her life, staying in a small cottage on the asylum grounds. The arrival of Dr. Fromm-Reichmann at Chestnut Lodge proved to be one of the most fortuitous events in the history of psychiatry.

Rose Garden Chestnut Lodge (“For mild nervous and mental diseases,” as the place billed itself ) was sited in a former hotel purchased in 1908 by Ernest Luther Bullard, a physician and former asylum superintendent in Wisconsin. Ernest’s only son, Dexter, graduated from medical school and began his residency in psychiatry, but left after only two months when his father suffered a heart attack and called his son home to help with the family business.7 Initially, Chestnut Lodge catered mainly to the worried well—more of a spa than an insane asylum. But as the Great Depression took its toll, and asylums around the country began closing, Dexter Bullard decided the lodge needed to carve out a unique niche for itself in order to stay in business, and he chose to specialize in the psychoanalytic treatment of chronic schizophrenics. No one had ever before devoted an entire hospital to such an undertaking.8 Such patients were a far cry from the worried well. These were wretches the rest of the psychiatric profession had given up on, patients who would strip off their clothes, urinate or masturbate openly in the ward, smear their feces on the walls, attack the staff, or crawl out onto a window ledge and threaten to jump. Despite never having been certified in psychiatry, Dr. Bullard was uniquely qualified for this task. He had grown up on the grounds of asylums, with mental patients as his playmates and baby-sitters. He never saw them as the “other.”9 Neither did Dr. Fromm-Reichmann. She proved to be an indefatigable therapist, choosing to work with the most seemingly intractable cases. Rejecting insulin coma, electroshock, lobotomy, and all the other somatic therapies that were currently in vogue,10 she based her therapeutic style on two pillars: sheer dogged persistence, and a willingness to try almost anything she thought might help.11

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Dr. Fromm-Reichmann typically would see each of her patients for four to six hours a week,12 sometimes for years, carefully noting even the smallest improvements and reminding the patient of them during the next visit.13 She might sit with a patient for an entire hour in silence, waiting for some kind of meaningful utterance.14 She saw patients late at night, or on weekends, or when they were in restraints or behind locked doors—wherever and whenever they needed her, regardless of circumstances. Patients who appeared too fragile to leave at the end of the allotted hour were allowed to stay for two.15 She took patients for walks around the hospital grounds, or for drives in the country, or even to the symphony.16 She admonished the young therapists-in-training to “make every hour with the patient a memorable experience.”17 She was willing to tolerate any behavior, no matter how disgusting or bizarre, as long as it didn’t threaten the safety of the patients or the staff, and as long as it seemed necessary to protect some vulnerable part of a patient’s psyche. She never shamed patients for such behavior, knowing they were already thoroughly ashamed of themselves. She viewed a mental hospital as a place where patients could be as crazy as they needed to be18—although she didn’t hesitate to confront patients whose behaviors appeared deliberately manipulative.19 One night Dr. Fromm-Reichmann was called to the hospital to assist a patient in crisis. When she arrived, the man was clambering over the furniture, crying out alternately in English, French, German, and Hebrew, claiming his enemies were out to get him. Dr. Fromm-Reichmann began clambering over the furniture with him, answering him in Hebrew, German, French, or English—whichever language he was using at the moment—telling him that she couldn’t see these enemies he was talking about, but that if she ever did see them she would surely protect him from them.20 Dr. Fromm-Reichmann’s conviction that any patient, no matter how impaired, might be helped stemmed not from arrogance but from humility. Her reasoning was as follows: since we know so little about what causes schizophrenia, how can we ever know any patient is beyond reaching?21 Dr. Fromm-Reichmann’s most famous patient, Joanne Greenberg, arrived at Chestnut Lodge in September of 1948. Sixteen years old at the time, Joanne lived most of her life in a fantasy world of her own making that she called Yria, ruled over by the God Antilobia. At times severely disturbed, she saw visions of blood running out of faucets, cut her arms with the jagged lids of tin cans, and crushed lit cigarettes into the open wounds.22

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When Joanna was just three years old, her mother suffered a miscarriage. Joanna’s mother and father went away for an entire month, leaving the little girl to wonder why she had been abandoned.23 Joanne Greenberg had been born with a deformity in her urinary system which made it impossible for her to control her bladder. She was whipped and shamed for wetting herself, behavior that lay absolutely beyond her control. Her father called her a “wet stinker” and other names.24 When she was five years old and doctors finally figured out what her problem was, her parents took her to the hospital twice for surgeries, each time assuring the child that her doll, not she, would be the one to undergo the operation. Joanne would later note: My parents thought first I was so dumb I would believe it the first time, second that I was so dumb I would believe it the second time, the same parents who would say I was so bright and this and that.25

Her father was also in the habit of giving her enemas, apparently with no medical indication.26 Joanne was a precocious child and well-read far beyond her years, but this did not earn her the respect of her classmates, who ostracized her instead. Later she was sent to a summer camp where, as the only Jewish child there, she was subjected to vicious anti-Semitic harassment. When she told her parents what was going on, they refused to believe her.27 Joanne became a compulsive eater, and her weight ballooned up to over 200 pounds. By the age of 14 she had become suicidal and began hallucinating.28 But, after spending two years at Chestnut Lodge and two more years as an outpatient, Joanne got well enough to enroll in university. After graduating and getting married (to a psychiatrist), using the pen name Hannah Green, she published I Never Promised You a Rose Garden, a fictionalized account of her therapeutic relationship with Dr. Fromm-Reichmann, whom she re-named “Dr. Fried.” Sales were slow at first, but eventually the book went on to sell millions of copies and was translated into a dozen different languages.29 The year 1976 saw the release of the cinematic version of Greenberg’s story, albeit with some notable changes. Deborah Blau, the novel’s ­protagonist, was re-named “Deborah Blake.” Her Jewish heritage was entirely written out of the story, as was the history of vicious antiSemitic harassment Deborah had endured at the hands of her age peers.

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The character of “Dr. Fried” was portrayed by Bibi Andersson, a blond Swedish actress who stood nearly seven inches taller than the real-life Frieda Fromm-Reichmann.30 Greenberg herself received stacks of letters from admirers, including many current or former mental patients, although she was savagely attacked by psychiatrists for suggesting that schizophrenia could be cured—as if that were a bad thing. Some of these psychiatrists went so far as to obtain Greenberg’s home telephone number and call her. As Dr. Hornstein points out, that is an astonishing level of intrusiveness, one not usually encountered even in psychotic patients.31 Meanwhile, historian Edward Shorter dismissed Greenberg’s story in a brief endnote: “For details of the supposed trauma, see ‘Frieda Fromm-Reichmann discusses the Rose Garden case.’”32 Joanne Greenberg raised two sons, became certified as a paramedic, taught courses at the Colorado School of Mines, and became a well-known author. In the afterword to the 2009 edition of Rose Garden, she concluded with these words: “Mine is a life of work and love, surrounded by fine, generous, and loving people, wealth beyond measure.”33 Other than Greenberg’s testimony, is there any evidence that Chestnut Lodge did anyone any lasting good? There is. Psychiatrist Clarence Schultz conducted follow-up surveys on 302 admissions to the lodge from the period 31 July 1948 through 30 June 1958, excluding temporary emergency admissions and geriatric custodial cases. Half of those had been admitted to at least one other mental hospital for at least six months previous to coming to Chestnut Lodge. In her biography of Dr. Friedmann, Dr. Hornstein re-analyzed data for the subset of respondents whose diagnosis could be reliably determined.34 She found that three-fourths of these patients had been either psychotic (63 percent) or suffering from severe personality disorder (13 percent). An independent judge rated the responses and determined that 41 percent were “extremely positive” and an additional 17 percent were “positive.” Only 7 percent of responses were “extremely negative.” There was no correlation between initial severity of mental illness and outcome.35 The ministrations of Chestnut Lodge did not come cheaply. One of the ironies of working there was the nurses and attendants knew they could never have afforded the services of the lodge, had they needed them.36 Nevertheless, every person who was rescued from the back wards of mental hospitals and restored to functioning was one more person spared from a lifetime of dependency.

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The Decline and Fall of Chestnut Lodge Dr. Fromm-Reichmann died on 28 April 1958, but the work at Chestnut Lodge continued. In 1969, after ruling the place for over fifty years as a benevolent autocrat, Dexter Bullard relinquished control over the lodge and passed the reins over to his son, psychiatrist Dexter Bullard Junior. The elder Bullard died in 1981.37 Chestnut Lodge subsequently fell on hard times. In the 1980s the institution was sued by a disgruntled former patient, Raphael Osheroff 38—the first in a series of setbacks which eventually led to the place’s undoing. Dr. Osheroff, a nephrologist, had become depressed after a series of personal setbacks, including two divorces and a child custody battle with his second ex-wife. In addition, Osheroff’s partners were pressuring him to sell the practice, and his marriage with his third wife was falling apart.39 Dr. Osheroff retained the services of a psychiatrist, who prescribed antidepressants, but they didn’t help. Osheroff became obsessed with thoughts of suicide, and his psychiatrist recommended hospitalization.40 It is not clear from published accounts whether he became suicidal before or after he began taking antidepressants, although since that time a mountain of evidence has accumulated showing that these drugs cause suicidality in some patients. On 2 January 1979, Dr. Osheroff checked himself into Chestnut Lodge, where his condition continued to decline. He began pacing relentlessly back and forth in the locked ward, until he developed foot ulcers. He lost forty pounds, and stopped shaving and bathing. He refused to cooperate with his therapists, and would later describe his time at the lodge as a “journey deeper and deeper into the depths of an inferno that Dante himself could never have conceived of.”41 After seven months at Chestnut Lodge, Dr. Osheroff checked out and went to another private institution, Silver Hill in Connecticut. There he was prescribed antidepressants, and this time they seemed to work. He was released, but in the meantime his hospital admitting privileges had been suspended, he was forbidden to see his children, his third wife had left him, and his trusted former partner was trying to take over their medical practice. Dr. Osheroff filed suit against Chestnut Hill for failing to prescribe antidepressants.42 Dr. Osheroff never alleged that he was not offered treatment at Chestnut Lodge, or that the treatment was delivered in an incompetent manner. He had tried antidepressants previously, and found they didn’t

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help him. But what is most astonishing about this case is that Dr. Osheroff was at Chestnut Lodge voluntarily. He could have signed himself out any time he had wanted to. Nevertheless, in 1989, Chestnut Lodge settled with Dr. Osheroff for an undisclosed sum.43 Chestnut Lodge began prescribing more psychotropic medications, bringing its practice more into line with that of other institutions. Ironically, they ended up getting sued for that, as well.44 In October 1982, 26-year-old Rachel Giller was admitted to Chestnut Lodge after already being hospitalized six times at other institutions for psychotic episodes. She was assigned to Manuel Ross, the same therapist who had treated Osheroff. She was taken off all of her drugs, and her condition rapidly deteriorated.45 Rachel began screaming, hitting staff members, crawling around naked, and smearing her feces. No one seems to have considered the possibility that her symptoms were related to psychiatric drug withdrawal. She spent most of the next three years in seclusion or in restraints. At one point she refused to eat and was tube-fed. Twice she formally requested a new therapist, but the request was denied.46 In May of 1985, Rachel was given the anticonvulsant drug Tegretol. By December of that year she displayed symptoms of severe anemia: bleeding gums, headaches, and bruises. Later that month, she was prescribed the antibiotic erythromycin and began hemorrhaging—a well-known toxic effect of combining that drug with Tegretol—one that was even listed in the Physician’s Desk Reference.47 Rachel was transferred to Johns Hopkins Hospital, where her parents were told her only chance of surviving was a bone marrow transplant. Although her sister was a perfect match, the doctors refused, saying she was too psychotic to be a candidate for such a procedure. She was transferred to UCLA Medical Center, where she received the transplant that saved her life, although she was left with permanent liver damage.48 She spent the next two years in another private psychiatric hospital, and then went to live with her parents, who said she had regressed so badly she had to re-learn basic skills, such as how to sleep in a bed and how to eat with utensils.49 Rachel and her family filed suit against Chestnut Lodge, retaining the same lawyer who had represented Samuel Osheroff. But this time the legal system ruled in favor of the lodge, and on 7 March 1991 the case was dismissed “with prejudice,” meaning it could not be re-opened.50

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Four years later Dexter Bullard Jr. died,51 and a year after that his children sold the lodge, which was merged with the Community Psychiatric Clinic to form CPC Health, which continued to operate the institution until the year 2000 when the organization declared bankruptcy.52 The main building was purchased by a developer who planned to convert it to condominiums, but on 7 June 2009 the place burned to the ground.53 In June of 2017, the site where Chestnut Lodge had been located was purchased by the town of Rockville and converted into a park.54

Notes 1. Alon Confino, A World Without Jews, The Nazi Imagination From Persecution to Genocide (New Haven: Yale University Press, 2014) 39–40. 2. Ibid., 40–41. 3. Ibid., 41. 4. Eric D. Kohler, “Relicensing Central European Refugee Physicians in the United States, 1933–1945.” Simon Wiesenthal Center Annual, 6, Chapter 1, accessed July 31, 2018, http://motlc.wiesenthal.com/site/pp.asp?c=g vKVLcMVIuG&b=394727 5. Gail A. Hornstein, To Redeem One Person is to Redeem the World: The Life of Frieda Fromm-Reichmann (New York: Free Press, 2000) 118. 6. Ibid., 82. 7. Ibid., 85–93. 8. Ibid., 88–98. 9. Ibid., 92. 10. Ibid., 201. 11. Ibid., xv–xvii. 12. Ibid., 304. 13. Ibid., 212. 14. Ibid., 48. 15. Ibid., xvi. 16. Ibid., xvi. 17. Ibid., 141. 18. Ibid., 170. 19. Ibid., xv. 20. Ibid., 143. 21. Ibid., 140. 22. Ibid., 222–233. 23. Frieda Fromm-Reichmann, “Frieda Fromm-Reichmann discusses the ‘Rose Garden Case,’” Psychiatry, 45, no. 2, (May 1982): 129. 24. Ibid., 128. 25. Ibid., 129. 26. Ibid., 133. 27. Ibid., 129, 131.

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28. Ibid., 129–131. 29. Ibid., 346–348. 30. “Bibi Andersson: Biography,” Internet Movie Database, accessed August 12, 2018, https://www.imdb.com/name/nm0000761/bio?ref_ =nm_ov_bio_sm 31. Hornstein, Redeem the World, 370–371. 32. Shorter, History, 378. 33. Joanne Greenburg, I Never Promised You a Rose Garden (Saint Martins, 1964, 1992, Afterword 2009), 291. 34. Hornstein, Redeem the World, 432. 35. Ibid., 432. 36. Ibid., 198. 37. David McK. Rioch, “Dexter Bullard, Sr., and Chestnut Lodge,” Psychiatry, 47, no. 1 (February 1984):1–8. 38. Boodman, Sandra G., “‘A horrible place, a wonderful place.’” Washington Post, October 8, 1989, https://www.washingtonpost.com/archive/lifestyle/magazine/1989/10/08/a-horrible-place-a-wonderful-place/ ee4d7572-7ac0-4159-baf8-e8112a983e50/?utm_term=.e79f49907296 39. Ibid. 40. Ibid. 41. Ibid. 42. Ibid. 43. Ibid. 44. Ibid. 45. Ibid. 46. Ibid. 47. Ibid. 48. Ibid. 49. Ibid. 50. Ibid. 51. Anonymous, “D.M. Bullard Jr. 66; Led Psychiatric Unit,” New York Times, August 12, 1995, https://www.nytimes.com/1995/08/12/obituaries/ dm-bullard-jr-66-led-psychiatric-unit.html 52. City of Rockville Community Planning & Development Services, Chestnut Lodge Design Guidelines. (2004). Accessed January 7, 2018, https://www. rockvillemd.gov/DocumentCenter/View/6847 53. Nesa Nourmohammadi, “A Year Later, Historic Chestnut Lodge Still Mourned.” Washington Post, June 17, 2010, http://www.washingtonpost.com/wp-dyn/content/article/2010/06/16/AR2010061603175. html 54. Neal Earley, “Rockville Closer to Finalizing Plans for Chestnut Lodge.” Montgomery County Sentinel, May 14, 2018, http://www.thesentinel. com/mont/news/local/item/6799-rockville-closer-to-finalizing-plansfor-chestnut-lodge

CHAPTER 12

Ronald Laing and Kingsley Hall

While Frieda Fromm-Reichmann was making history at Chestnut Lodge, on the other side of the pond a young British army psychiatrist was also bearing witness to the ravings of the seriously mentally ill, and finding something of value therein. Ronald David Laing was born on 7 October 1927 in Glasgow, Scotland, the only child of solidly middle-class parents.1 A gifted student, the young Ronnie Laing taught himself languages by reading Martin Heidegger’s Sein Und Zeit in the original German, and Jean-Paul Sartre’s L’Être et le Neant in the original French.2 At the end of his public school days, his classics teacher told him his knowledge of Latin and Greek was already the equivalent of an M.A. in those subjects.3 He also was a gifted pianist, an enthusiastic if undistinguished rugby player, and an outstanding long- and middle-distance runner.4 In 1945 Laing enrolled in Glasgow University to study medicine. In his spare time he went rock climbing and drinking with his friends in the Mountaineering Club, and also founded the Socratic Club, a philosophical debating society, and somehow got Bertrand Russell to agree to serve as club president.5 In an early incident that would foreshadow his later taste for controversy as well as his sympathy for the downtrodden, Laing and another student walked out during the presentation of X-ray films made by Nazi doctors showing joint movements and peristalsis, noting that the Jewish concentration camp inmates that had served as the unwilling subjects of these films had died from prolonged radiation exposure.6 © The Author(s) 2019 P. D. Hahn, Madness and Genetic Determinism, https://doi.org/10.1007/978-3-030-21866-9_12

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The Land of the Dead Laing failed his medical examinations the first time around and passed them on the second.7 He was drafted and served two years as a psychiatrist in the British Army, back when psychiatrists literally were instructed not to allow schizophrenic patients to speak to them. Permitting schizophrenics to talk was likened to giving laxatives to someone with diarrhea, or allowing a hemophiliac to continue bleeding—it just made the problem worse.8 It was during this time that Laing testified at the courts-martial of attendants who were charged with beating patients. “They thought they would get away with it, of course, because I would never listen to nutcases,” he told writer Bob Mullan many years later. “But I was already listening to nutcases”9 [Italics in the original]. Laing took a position at Gartnavel Royal Mental Hospital in Glasgow, where he was assigned to the refractory ward of the female side of the hospital. This turned out to be a formative experience for the young doctor. He later likened the place to the land of the dead depicted in Homer’s Odyssey. There were more than fifty women there, some of whom had been confined for ten, thirty, or even sixty years. These women had experienced all the treatments the psychiatry of that era had to offer—insulin coma, electric shocks, lobotomy.10 Most sat huddled in chairs, speaking to no one. One lay on the floor, curled up underneath a table. In a daily dehumanizing ritual, the patients were made to line up and each one had to remove her nightdress and to put on her hospital day-gown. The nurses were harassed and overworked.11 Laing ordered the use of neuroleptic drugs on the ward be cut back almost to zero. The number of windows broken by patients soared. He then ordered the doors unlocked. The smashing of windows ceased. Once the patients knew they could leave if they really wanted to, they stopped trying to break out.12 Laing decided to try an experiment. He selected eleven of the most socially withdrawn patients on the ward. These women ranged in age from twenty-two to sixty-three, and all had been in the ward for at least four years. Two nurses were given the sole job of being with these eleven patients.13 A large, brightly lit, newly decorated room was made available for the eleven patients, who were provided with magazines, along with materials for knitting, sewing, rug-making, blanket-making, drawing, and other pastimes. Later they were also given a gas stove and an oven for baking.

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One of the hospital psychiatrists brought some buns these women made to the doctors’ sitting room, and offered them to his colleagues. Most of the psychiatrists refused to touch them.14 But a change came over these supposedly “refractory” patients. They began wearing dresses and stockings, styling their hair and putting on makeup. Within eighteen months all of these women were released from the hospital—and within a year, all of them were back.15 Laing wondered: Had these women found more companionship inside than they could outside?16 After leaving Gartnavel, Laing accepted a position at Southern General Hospital, where the Department of Psychological Medicine at the University of Glasgow was located. One of his patients was a teenage boy named Philip, who staggered into Laing’s office in a dreadful state— incontinent, stinking of feces and urine, trembling, gesticulating strangely, and mumbling incoherently. When he did speak, it was clear he was suffering from paranoia, delusions, and hallucinations.17 When Philip was fourteen years old, he came home to find his mother lying in a pool of blood, dead. She had suffered from tuberculosis and choked to death on her own blood. Philip’s father accused the boy of being responsible, by means of being conceived and then exhausting his mother throughout pregnancy and his whole life. Two months later Philip’s father hanged himself.18 Laing saw Philip in his office for an hour every day for six weeks, listening to him sympathetically, and noticed that during his time in Laing’s office much of the haze the boy was in seemed to clear up, as they discussed philosophy and higher mathematics—although his condition would deteriorate once more as he was returned to the ward.19 The long-term prognosis for Philip was grim. Both of Philip’s parents had been psychotic. He had no close relatives, no one willing to take him in. It seemed as if there was no alternative to consignment to a mental hospital—most likely for the rest of his life.20 Laing saw an alternative. He took Philip into his own home. The incontinence stopped almost immediately. Within a couple of weeks the boy began walking normally, then speaking falteringly but coherently.21 After three months the boy was doing well enough to be placed into foster care. Fifteen years later he came back to visit Laing. By this time Philip was married with two children, working full time, and taking evening classes in psychology.22

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Laing subsequently took a post as a psychiatrist at the Tavistock Clinic in London, and also began training as a psychoanalyst. Later he left Tavistock to open a private practice.23 In terms of his therapeutic style, Laing was a pragmatist, preferring practical solutions in the here-and-now to digging up the roots of childhood trauma. He once likened mental illness to being in prison: getting up and walking out, if you are able to do so, is more important than agonizing over how you got in there in the first place.24 A young woman came to Laing, afflicted with catatonic schizophrenia. After a consultation during which they both sat together in silence for most of the session, she decided to drop out of university and get a job as an artist’s model, which required her to remain stock-still for long periods of time. She plied this trade for a time until she got better, then resumed her studies.25 A young man came to him claiming to be Jesus Christ. Noting that Jesus was a carpenter, Laing asked the man to fix his desk.26 During this time Laing became skeptical of the prevailing paradigm that viewed schizophrenia as a disease process, probably genetic in origin, rather than an interactional communication process that afflicted an entire family. He also felt stymied by the unwillingness of those around him to change the mode of intervention—visiting families on site rather than in the sterile environment of the clinic, and including children in the healing process.27 Laing decided to launch one of the most audacious—and infamous— projects in the history of psychiatry. He conceived of a place where psychiatrists and the seriously mentally ill could live together as equals, and work on their problems together, without forced medication or electroshock or restraints or locked doors.28

A Quixotic Undertaking Laing chose Kingsley Hall as the venue. Kingsley Hall had been built by a Quaker family, the Lesters, and named after a brother who had died in childhood. He spoke to Muriel Lester, the senior member of the family, and outlined his vision to her. “I explained that I felt there was a serious gross violation of primitive human decency in the way we treated people who were mentally out of it as far as other people were concerned,” he explained to Mullan. “There was just a rampage—lobotomies and electric shocks and comas and incarceration and everything, and no one cared.”29

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The Philadelphia Association was formed to administer the project, and in 1965 the trustees of Kingsley Hall leased the building to the association for five years, for the nominal sum of one shilling a year. The place became a kind of a Mecca for anyone who fancied himself a part of the avant-­ garde, and quickly filled up with assorted hangers-on.30 But the project was a quixotic undertaking, doomed from the start. One resident went on a tantrum, trying to smash down walls and doors.31 He also ran up hundreds of pounds worth of phone bills, calling Ethiopia as part of a mad plan to relocate the project to that distant nation. When Laing ordered him not to use the phone anymore, the man ripped the phone out of the wall out of spite.32 There were complaints about noise, slammed doors, and residents wandering around the streets barefoot in the winter. Mary Barnes, a resident of Kingsley Hall and a former nurse, once climbed up to the roof, naked and covered in feces, and performed a sun dance (she did subsequently recover and go on to have a successful career as an artist). Disgruntled neighbors hurled insults and stones, broke windows, and even kicked down doors.33 Kingsley Hall closed after the five-year lease was up. By this time Laing was tired.34 He shuttered his practice and left on a sojourn to Sri Lanka and India, conversing with monks and holy men.35 In the years that followed, he went veering off into directions that might charitably be described as “esoteric”—rebirthing, shamanism, and writing bad poetry.

A Troubled and Troubling Figure Probably no figure in the history of psychiatry has been the subject of more ad hominem attacks than Laing36—and indeed his personal life was hardly beyond reproach. Over the course of his lifetime he fathered ten children by four different women.37 After leaving his first wife, he refused to pay anything more than the legal minimum amount of child support.38 Laing’s ex-wife went back to Glasgow with their five children, to live in penury. Their son Adrian, who was thirteen years old at the time, took after-school jobs to help out.39 Laing’s autumn years brought disappointment. In 1975, his second-­ oldest daughter, Susan, was diagnosed with terminal leukemia. Against the wishes of both her mother and her fiancé, Laing insisted on traveling to Glasgow to tell her she was not expected to live to see her twenty-first birthday, then returned to London, leaving the rest of the family to deal with the resulting upheaval.40

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A year later, Laing’s oldest daughter Fiona had a breakdown. “It was a double bind, you see,” Adrian Laing later told the Guardian. “Either he had nothing to do with it and his theories were shit, or he had everything to do with it and he was shit.”41 Laing was a complex, charismatic, troubled, and troubling figure, as was indifferent toward his own family as he was compassionate toward his patients. He burned the candle at both ends—working endless hours treating patients, transcribing interviews, and writing books, allowing himself only four hours of sleep a night.42 He smoked too much, drank too much, and dropped acid with his patients. In 1984, he pled guilty to possession of a few grams of hashish and received a conditional discharge.43 That following year Laing visited a friend in Vancouver, psychologist Andrew Feldmar, and he continued to return to Vancouver every year until his death. A film crew recorded some of his talks and workshops there, and these recordings became the basis of the documentary Did You Used to be R.D. Laing,44 which was broadcast late at night on Channel 4 shortly after his death. The program reveals occasional flashes of wit and insight from Laing, but clearly this was a man whose best days were behind him. His conduct became more erratic. In 1987 Laing surrendered his medical license after being accused of assaulting a patient (the accusation was later withdrawn).45 He found himself at the age of 61 with no profession or fixed address or income, other than the ever-diminishing royalties from the sales of his books.46 On 23 August 1989, while playing tennis in Saint Tropez, he dropped dead from a heart attack.47 Laing was a popular figure on the lecture circuit, and his books have sold millions of copies and been translated into dozens of different languages. He has been compared to Thomas Szasz, the author of The Myth of Mental Illness, but Laing himself bristled at the comparison, telling Mullan: I’ve never denied the existence of mental distress, mental misery, confusion, suffering, and so on but I’ve tried to show that this was socially more ­intelligible than most people supposed. Having said that, out of—actually maybe sentimentality or of some schmucky compassion for other people—I actually wanted to help.48 [Italics in the original]

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In the end, perhaps Laing’s greatest contribution was the idea of Kingsley Hall, which served as the inspiration for a much more successful project, Soteria House.

Notes 1. Bob Mullan, Mad to be Normal: Conversations With R.D. Laing (London: Free Association Books, 1995), 3. 2. Mullan, Mad to be Normal, 110. 3. Ronald David Laing, Wisdom, Madness, and Folly: The Making of a Psychiatrist (New York: McGraw-Hill, 1985), 87. 4. Mullan, Mad to be Normal, 65; Laing, Wisdom, Madness and Folly, 86–87. 5. Mullan, Mad to be Normal, 70–72. 6. Laing, Wisdom, Madness, and Folly, 91–92. 7. Ibid., 107–108. 8. Ibid., 123. 9. Mullan, Mad to be Normal, 124. 10. Laing, Wisdom, Madness, and Folly, 148–151. 11. Ibid., 150–151. 12. Ibid., 32–33. 13. Ibid., 152. 14. Ibid., 152–154. 15. Ibid., 154–155. 16. Ibid., 155. 17. Ibid., 182–183. 18. Ibid., 181–182. 19. Ibid., 183–184. 20. Ibid., 187. 21. Ibid., 187. 22. Ibid., 187–188. 23. Mullan, Mad to be Normal, 143, 169. 24. Third Mind Productions, Did You Used to be R.D.  Laing? Channel 4, October 3, 1989. 25. Ibid. 26. R.D. Laing, Interview by Gregory Jackson, CBS Cable, 1982. 27. Mullan, Mad to Be Normal, 168–169. 28. Ibid., 172. 29. Ibid., 175. 30. Ibid., 176–178. 31. Ibid., 181.

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32. Ibid., 189. 33. Ibid., 180–181. 34. Ibid., 179. 35. Ibid., 228. 36. In his book Shrinks, former APA President Jeffrey Lieberman states that psychiatrist E. Fuller Torrey told him “People who knew Laing told me that he became a guy asking for money by giving lectures on ideas he no longer believed in.” Not a shred of evidence is adduced to corroborate this third-­hand accusation against a dead man. The same third-hand accusation is leveled against the late Thomas Szasz, again without a shred of corroborating evidence. Lieberman, Shrinks, 113. 37. Elizabeth Day and Graham Keeley, “My Father R.D.  Laing: He Solved Other People’s Problems But Not His Own,” Guardian, May 31, 2008, https://www.theguardian.com/books/2008/jun/01/mentalhealth. society 38. Ibid. 39. Ibid. 40. Ibid. 41. Ibid. 42. Mullan, Mad to be Normal, 276. 43. Russell Miller, “R.D. Laing: The Abominable Family Man,” Sunday Times, April 12, 2009, https://www.thetimes.co.uk/article/rd-laing-the-abominable-family-man-mqkbxw8jj2x 44. Third Mind Productions, Did You Used to be R.D. Laing? 45. Day and Keeley, “My Father R.D. Laing.” 46. Miller, “Abominable Family Man.” 47. Ibid. 48. Mullan, Mad to be Normal, 202.

CHAPTER 13

Soteria House and Open Dialogue Therapy

A Compassionate Alternative The word Soteria is Greek for “salvation” or “deliverance.” The Soteria Project was conceived by psychiatrist Loren Mosher, a psychiatrist at the National Institutes of Health who had visited Laing at Kingsley Hall in the 1960s. Mosher conceived the project as a compassionate alternative to institutionalization for persons suffering from acute schizophrenia.1 The first Soteria House was established in a residential neighborhood in San Francisco in 1971. Another house, Emanon, was created four years later.2 Then, as now, the prevailing model for the etiology and treatment of schizophrenia was the biomedical one.3 Doctors had final authority and decision-making powers. Patients were seen as having a disease to be cured, with neuroleptic medication as the primary mode of treatment. By contrast, at Soteria the emphasis was on growth, development, and learning, with the goal of understanding and sharing a psychotic person’s experience and ultimately integrating it into his or her life story. What psychiatry sees as a “schizophrenic reaction” was re-conceptualized as an altered state of consciousness, experienced by an individual undergoing a crisis of living.4 The staff members were recruited for their empathy and communication skills. Most of them were college-educated. None of them were trained as mental health professionals, although many of them aspired to

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careers as such. None of them had ever had a serious mental illness or drug problem, although, interestingly, most of them had grown up with a family member who did.5 They also were largely apolitical.6 This was not by accident. Mosher went out of his way to avoid unnecessary conflict with the surrounding community. He helped to win acceptance for his project by having the house repainted and the yard replanted. The last thing he wanted was to see his project crash and burn, as Kingsley Hall did.7 All the patients were recruited from two psychiatric emergency rooms in the Bay area. All had been diagnosed with acute, first-onset schizophrenia, all were between the ages of eighteen and thirty, and all were either never-married, separated, widowed, or divorced. These selection criteria were chosen in order to obtain a relatively homogeneous group of acute, first-onset schizophrenics at high risk for long-term hospitalization and/ or chronic disability.8 In order to establish an informal, home-like atmosphere, the number of patients (or “residents,” as they were called at Soteria) was limited to six. Staff members worked rotating 36-or 48-hour shifts, so that two full-time staff members, one man and one woman, were always present. In addition, the house utilized the services of unpaid volunteers and one quarter-­ time psychiatrist. The latter was seen as a stable, reassuring presence in addition to his formal medico-legal responsibilities.9 Decision-making and responsibilities were shared between the staff and the residents. Staff and residents alike shared in shopping, cooking, and housekeeping tasks.10 Suicide, violence, unannounced visitors, illegal drugs, and sexual relations between residents and staff were strictly prohibited, but otherwise rules and structure were kept to the bare minimum needed for adequate function.11 The use of neuroleptic drugs was also kept to a bare minimum. If a resident showed no improvement after six weeks, these drugs might be prescribed, and the resident was asked to monitor his or her response to the drug carefully so that the dosage level could be adjusted as needed. After a trial of two weeks, the resident was usually given the option of continuing or discontinuing the drug. Fewer than 10 percent of subjects were given antipsychotic drugs during their stay at Soteria House.12 The acute phase normally lasted between four to six weeks, after which the staff would work with the resident to develop and work toward realistic long-term goals. The average stay at Soteria House was five months, and 85–90 percent of residents successfully re-integrated into the community.13

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How does this compare to treatment at conventional mental hospitals? Mosher and his colleagues compared and assessed two-year outcomes for residents at Soteria House and Emanon. As a comparator group, they used patients referred to area mental hospitals after being recruited from the same two psychiatric emergency rooms from which the residents of Soteria House and Emanon came. The results were clear. Soteria House alumni were significantly more likely to be employed, to be employed full time, and to be living alone or with peers. They showed significant improvements in composite outcome, social functioning, and psychopathology. They also were less likely to be readmitted to hospital and had fewer days of re-admission, although these differences were not significant. Fifty-seven percent of Soteria House alumni had never taken antipsychotic drugs, whereas 100 percent of the controls had. And, although stays at Soteria House and Emanon tended to be longer, overall cost was the same for both groups.14 None of the variables measured revealed superior outcomes for regular mental hospitals. Soteria House was not a magical cure. But for the majority of sufferers of acute, first-onset schizophrenia, the Soteria Project demonstrated that empathetic care, delivered by nonprofessionals in a residential setting, produced outcomes that were equal to or superior to those in a well-­ staffed mental hospital, with minimal use of neuroleptic medication, and no increase in financial cost. Despite all this, Emanon was closed in 1980, and Soteria House was shut down three years later. No comparable program has been initiated in the United States since then. As Mosher pointed out, no third-party payer in the United States seems willing to underwrite this form of care. The only consistently available mental health benefit has been for inpatient care in hospital settings, with drugs as the first-line treatment, and the psychiatric profession certainly does not seem interested in changing this situation.15 Indeed, as Mosher pointed out, any proposal to replicate the Soteria Project most likely would not make through the process of institutional review, as it would involve withholding a treatment (neuroleptic medication) of supposedly proven efficacy.16 While the Soteria Project has been nearly forgotten in the United States, it has inspired a number of comparable programs in Europe, all aiming to create a warm, home-like atmosphere for sufferers of acute schizophrenia.17 But in Finland, they have gone one step further—treating sufferers in their actual homes.

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A Cure for Schizophrenia Open Dialogue Therapy was the brainchild of psychiatrist Jukka Aaltonen, psychologist Jaako Seikkula, and their colleagues in western Lapland.18 There, patients with acute psychotic reactions—or any other serious mental illness—are treated by a crisis team, usually consisting of a psychiatrist, a psychologist, and a nurse. The first crisis meeting usually takes place within 24 hours of the first contact with the mental health system.19 Patients, their families and friends, and sometimes even their employers and neighbors are invited in order to mobilize support for the patient. The crisis team may meet with the patient and his support system daily or even more often, for the first ten or twelve days. After that meetings are scheduled according to a joint plan.20 As with the Soteria Project, the use of neuroleptics is kept to a bare minimum. The focus is firstly on promoting dialogue within the family, and secondarily with promoting change in the patient and his family. In the beginning, the patient’s hallucinations and delusions are not challenged. Rather the patient is encouraged to tell more about his experiences.21 How does all this work out with patients? A five-year follow-up study of first-episode nonaffective psychotic patients in western Lapland treated in this manner found that the mean length of hospitalization was seventeen days, and only 26 percent of them had ever been given neuroleptics. Moreover, 82 percent had no residual psychotic symptoms, 86 percent were actively studying, working, or seeking employment, and only 14 percent were living on disability allowance. There was no matched control group, but these are amazingly good results compared to treatment-as-usual.22 Since the first mobile crisis team was organized in 1990, the incidence of new cases of schizophrenia in western Lapland has plummeted, most likely because the prompt and thorough intervention afforded by Open Dialogue Therapy led to an early amelioration of psychotic symptoms, which must persist for six months before a diagnosis of schizophrenia can be rendered.23 Mental healthcare costs in western Lapland had dropped as well, by more than one-third.24 For twenty years now Jaako Seikkula has been a Professor of Psychotherapy at the University of Jyväskylä. He told me that since Open Dialogue Therapy was initiated, the incidence of new cases of schizophrenia in western Lapland had declined by an astonishing 90 percent. He also stated that two-thirds of these patients are treated without any neuroleptic drugs.

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When I asked Dr. Seikkula if Open Dialogue Therapy was a cure for schizophrenia, his answer was short and straight to the point: Yes. Why isn’t this front-page headline news?

Notes 1. Loren R.  Mosher, Ann Reifman, and Alma Menn, “Characteristic of Nonprofessionals Serving as Primary Therapists for Acute Schizophrenics,” Hospital and Community Psychiatry, 24, no. 6 (June 1973): 391–396; Loren R.  Mosher and Alma Menn “Soteria: An Alternative to Hospitalization for Schizophrenics,” Current Psychiatric Therapies, 21, (1982): 287–296; Loren R.  Mosher, “The Soteria Project: the FirstGeneration American Alterative to Psychiatric Hospitalization,” in Alternatives to the Hospital for Acute Psychiatric Treatment, ed. Richard Warner, (Washington DC: American Psychiatric Publications, 1995), 111– 132; and Loren R.  Mosher, “Soteria and Other Alternatives to Acute Psychiatric Hospitalization: a Personal and Professional Review,” Journal of Nervous and Mental Disease, 187, no. 3 (March 1999): 142–149. 2. Mosher, “Soteria Project,” 112. 3. Ibid., 113. 4. Ibid., 113. 5. Mosher et al., “Nonprofessionals,” 393–394. 6. Mosher et al., “Nonprofessionals,” 393. 7. Mosher, “Soteria Project,” 111. 8. Ibid., 116. 9. Mosher and Menn, “Alternative to Hospitalization,” 193. 10. Ibid., 193. 11. Mosher, “Soteria Project,” 111. 12. Ibid., 115. 13. Mosher, “Soteria and Other Alternatives,” 142. 14. Mosher, “Soteria Project,” 120. 15. Ibid., 125. 16. Mosher, “Soteria and Other Alternatives.” 17. Tim Calton et al., “A Systematic Review of the Soteria Paradigm for the Treatment of People Diagnosed With Schizophrenia,” Schizophrenia Bulletin, 34, no. 1 (January 2008): 181–192, https://doi.org/10.1093/ schbul/sbm047 18. Ville Lehinten et  al., “Two-Year Outcome in First Episode Psychosis Treated According to an Integrated Model. Is Immediate Neuroleptisation Always Needed?” European Psychiatry, 15, no. 5 (2000): 312–320; Seikkula, Jaakko, Birgitta Alakare, and Jukka Aaltonen, “Open Dialogue in Psychosis II: A Comparison of Good and Poor Outcome Cases,” Journal

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of Constructivist Psychology, 14, (2001):267–284; Jaako Seikkula et  al. “Open Dialogue Approach: Treatment Principles and Preliminary Results of a Two-Year Follow-Up on First Episode Schizophrenia,” Ethical Human Sciences and Services, 5, no. 3 (Fall/Winter 2003): 164–182; Jaako Seikkula et al. “Five-Year Experience of First-Episode Psychosis in Open-Dialogue Approach: Treatment Principles, Follow-Up Outcomes, and Two Case Studies,” Psychotherapy Research, 16, no. 2 (March 2006): 214–228. 19. Seikkula et al., “Open Dialogue Approach,” 165. 20. Ibid., 166. 21. Ibid., 166. 22. Seikkula et al., “Five-Year Experience,” 220. 23. Jaako Seikkula, email April 25, 2018. 24. Seikkula et al., “Five-Year Experience,” 225.

CHAPTER 14

The Ghosts of Rüdin and Kallmann

The ghosts of Rüdin and Kallmann still loom large over the field of psychiatric genetics, although they are seldom mentioned by name anymore. More often, we are told that a century of family and twin studies have demonstrated a heritability of schizophrenia of “up to 80%,” without mentioning where that upper figure comes from.1 Now that the field of psychiatric genetics is entering its second century, it is time to take stock of what we have learned. For a century, the authors of family studies, twin studies, and adoption studies have been telling us that schizophrenia and other mental illnesses are inherited diseases, while their critics have maintained that these studies are fatally flawed. These two sides have been exchanging intellectual salvos for decades now, but the new science of genome-wide association analysis seems poised to put an end to this controversy once and for all. Psychiatric genetics researchers have not found any gene that causes schizophrenia or any other mental illness and they are not going to find one, for a very simple reason: no such gene exists. And indeed, how could it? We already noted in Chap. 1 that the diagnostic category of “schizophrenia,” as conceived by Bleuler, had no known biological cause, no consistent outcome, and no consistent symptomology. Almost a century later, none of that has changed. The Rosenhan experiment demonstrated that psychiatrists cannot reliably distinguish between those who have schizophrenia and those who do not, and forty years later

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the latest edition of the DSM stipulated twelve different ways two patients could qualify for a diagnosis of “schizophrenia” with no overlap in symptoms between them. How could there be a gene for such a meaningless diagnostic category?2 Perhaps it is time to question whether the construct of “schizophrenia” serves any useful purpose to anyone outside the psychopharmaceutical industry. In a 2013 book chapter, psychologist Richard Bentall detailed the research on the psychogenic roots of hallucinations and delusions (summarized in Chap. 9 of this volume) and concluded: I hope this brief summary of what is known about hallucinations and delusions is sufficient to convince the reader that research on specific complaints constitutes a viable alternative to the Kraepelinian paradigm. … If this program of research is successful, then, once the full range of psychotic complains has been investigated, there will be no ghostly ‘schizophrenia’ left behind requiring an explanation.3

More than forty years ago, psychiatrist Thomas Szasz4 noted that in other branches of medicine, a diagnosis is an explanation for what has happened to a patient. In psychiatry, “schizophrenia” and other diagnostic labels are a justification for doing something to a patient. That, too, has not changed. We have already seen that the claimed effect sizes of the so-called schizophrenia-associated alleles are puny—on the order of a 1  in 500 absolute increase in risk, or even less, and that even the aggregate effect of all of these alleles is quite modest. And in a field that has been replete with false positives, claims for even these tiny effects should be taken with a grain of salt. Moreover, these alleles are not specific in their action, but are also (weakly) correlated with bipolar disorder, depression, and other diagnostic labels as well. All a century of psychiatric genetic research has told us is that individuals vary in their susceptibility to stress and trauma—and that some of that variability may be heritable. That’s not really very surprising. Probably anyone with experience of life as it is lived could have guessed as much. Our genes are not our destiny. At this point we could decide that we have gotten our answer—that genes are not the deciding factor. Indeed this revelation should be greeted as good news—if genes are not the deciding factor, then the environment is, and that is something we can change.

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And yet government funding agencies continue to pour funding into the field of psychiatric genetics. Who benefits? Kallmann promised us that the new field of psychiatric genetics would enable us to devise biological tests and cures for “schizophrenia” and other mental illnesses. His successors have been renewing that promissory note for the last eighty years, and yet it remains entirely unfulfilled. There is still no biological test for any mental illness, and a century of research into psychiatric genetics has not resulted in a single new treatment for these conditions. Is anyone surprised? Consider the great medical discoveries which have been made in the past. Almost anyone’s short list might include smallpox vaccination, quinine for malaria, diphtheria antitoxin, tetanus antitoxin, insulin for diabetes, and antibiotics for bacterial infection. Which of these discoveries was enabled by an understanding of the genetic basis underlying the disease? In fact, none of them were. A number of psychiatric genetics researchers have advanced the argument that gene scans could be used to identify children at high risk for mental illness.5 These children, we are told, could be targeted for medication or other early interventions. And what would be the long-term consequence of telling large number of children and their parents that they have a genetically based predisposition to schizophrenia or some other potentially devastating “brain disease”? Are we going to end up raising a generation of psychic cripples? We don’t know. If these proposals ever are put into practice, this is going to be a gigantic uncontrolled experiment. Moreover, we already have seen that even the great majority of individuals with high genetic risk scores for schizophrenia will never go on to be diagnosed with the condition. Any preventive intervention for these individuals would need to have a very high benefit-to-risk ratio—and if that be the case, we may as well make the intervention available to everyone. Examples of this sort of thing abound. There are stop-smoking interventions of varying degrees of effectiveness. We make these available to anyone who wants them, not just those who have high genetic risk scores for lung cancer or chronic obstructive pulmonary disease. We already know the conditions that are optimal to prevent most cases of severe mental illness. As we have seen, there is overwhelming evidence that “schizophrenia” and other mental illnesses are correlated with physical abuse, sexual abuse, emotional abuse, and a wide variety of other

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adverse childhood experiences. These are indeed terrible problems, but they are also something we can start addressing right now. Two other arguments routinely employed in defense of viewing these conditions as genetic disorders is that this makes patients more likely to take psychotropic drugs, and that it reduces “stigma.” Do either of these arguments hold water? The first argument begs the obvious question: if psychotropic medications really are doing substantial good, why do some psychiatrists feel the need to subterfuge to get people to take them (or to give them to their children)? We have already noted psychologist Irving Kirsch’s devastating 2009 critique of antidepressants,6 and author Robert Whitaker’s even more devastating 2010 critique of psychotropic medications in general.7 In 2016, Whitaker released a white paper8 on the harms and benefits of the so-­ called antipsychotic drugs. Step by step, in workmanlike fashion, Whitaker lays out the evidence against the long-term use of antipsychotic drugs. Once again, the case is devastating: • Long-term outcomes for schizophrenia and other psychotic disorders have worsened since the introduction of antipsychotic drugs. • Patients who took the drugs long term had worse outcomes than those who never took them, or who took them only for brief periods. The long-term outcome was independent on initial illness severity. Indeed, more seriously impaired patients who never took these drugs did better than less seriously impaired patients who did. • Outcomes for patients in less-developed countries, where antipsychotic drugs are seldom used are better than outcomes in developed countries, where such drugs are widely employed. • Antipsychotic drugs have been shown to cause long-term structural changes in the brain, and these changes correlate with severity of psychotic symptoms. In plain English, the so-called antipsychotic drugs cause the very problems they are intended to cure. (At this point, the reader may recall that January Schofield was not diagnosed with schizophrenia until she had been taking the antipsychotic drug Risperdal for months.) Whitaker points out that almost all the data purporting to support the use of these drugs come from relapse studies, which show that, among

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patients who have been taking these drugs for the long term, the relapse rate is higher among those who stop taking them. But this begs the question of whether they would be better off had they never started the drugs in the first place. Indeed, despite widespread use of these drugs, standardized mortality rates for people diagnosed with schizophrenia have been rising steadily for the past four decades or more.9 Would this sort of outcome be considered acceptable in any other branch of medicine? What is left? The claim that telling people that mental illness has a genetic basis reduces stigma? Biologically oriented psychiatrists even have invented a term for belief in bio-genetic explanations for mental illness: “mental health literacy.” But is there evidence that “mental health literacy” leads to reduced stigma for sufferers of mental illness? Psychologist John Read and his colleagues reviewed the literature in search of an answer to that question. Dr. Read and his co-authors found that, in fact, a belief in bio-genetic explanations of mental illnesses leads to increased belief in the dangerousness and unpredictability of the mentally ill, increased pessimism in the chances of their recovery, and a greater desire to avoid contact with persons so labeled. These points have been replicated in study after study, in at least sixteen different countries.10 In addition, the toxic effects of the so-called antipsychotic drugs—obesity, drooling, uncontrollable movements—are themselves stigmatizing, a point the proponents of “mental health literacy” never seem to consider. More recently, the first meta-analysis on the subject,11 by researchers at the University of Melbourne, demonstrated that acceptance of bio-genetic explanations for mental illness was positively correlated with a greater perception of dangerousness and increased pessimism for the chances of recovery for the mentally ill. Moreover, the few studies that have looked at the matter have shown that public attitudes toward the mentally ill have actually gotten worse as acceptance of bio-genetic theories of mental illness has increased. A German study found that between the years 1990 and 2001, the number of respondents who attributed schizophrenia to hereditary factors increased from 41 percent to 60 percent.12 The same study found an increase in the number of respondents who would not want person suffering from schizophrenia as a tenant, co-worker, neighbor, child carer; would not view such a person as a desirable addition to one’s family or social circle; and would not recommend such a person for a job.

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In this country, the General Social Surveys of 1996 and 2006 found increasing acceptance of neurobiological or genetic explanations for mental illness—and also an increase in the number of respondents who were unwilling to accept a mentally ill person as someone to work closely with, have as a neighbor, socialize with, make friends with, or have marry into one’s family.13 Read and his co-authors warn us “We should remain cognizant of the fact that biogenetic explanations for mental health problems have been linked to many harsh policies, including compulsory sterilization and extermination.”14 “Far too much mental health education is based on teaching people that mental illness is an illness like any other,” Dr. Read told me. “Ninety-­five percent of all studies into that approach have shown that it makes attitudes worse. These approaches are not evidence-based. They are ideologically based. It’s not an accident that a lot of them are funded by drug companies.” In a 2004 book chapter titled “Genetics, Eugenics, and Mass Murder,” Dr. Read and his co-author, psychoanalyst Jeffrey Masson, described the role of German psychiatry in the Nazi program to eliminate people labeled “mentally ill” and added: We document these awful events, however, precisely because they so clearly illustrate, again, the three themes present throughout the history of the treatment of people considered mad: (1) Social control in the interest of the powerful, (2) damaging and violent ‘treatments,’ and (3) the ability of experts to generate theories camouflaging what is really happening.15

In conclusion, they state: The engine powering the machine is no longer the racism of the eugenicists, having been largely superseded by the profit-motive of the pharmaceutical industry. The belief in the bio-genetic ideology that has fuelled the engine remains as strong as ever. The function of expert theories has remained constant: the camouflaging of socio-political realities behind a mask of scientific and caring endeavour.16

On 11 May 2017, Wired quoted former National Institute of Mental Health (NIMH) Director Thomas Insel as follows: I spent 13 years at NIMH really pushing on the neuroscience and genetics of mental disorders, and when I look back on that I realize that while I think I succeeded at getting lots of really cool papers published by cool scientists

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at fairly large costs—I think $20 billion—I don’t think we moved the needle in reducing suicide, reducing hospitalizations, improving recovery for the tens of millions of people who have mental illness.17

Indeed. All this genobabble is a preposterous distraction from the task of caring for broken, damaged, hurting human beings. To the extent that we see “mental illnesses” as the product of faulty genes, and not as more extreme versions of the confusion, distraction, rage, anxiety, and despondency we all experience, we evade responsibility for addressing the circumstances which make human beings feel confused, distracted, rageful, anxious, or despondent. Instead of inquiring of the mentally ill “What’s wrong with those people?” perhaps we should ask them directly “Who did what to you?” * * * And what about Manuel Enrique Verduzco, whom we learned about in the Introduction? His attorneys agreed that he killed Karina Morales-­ Rodriguez and Marta Martinez, but argued he could not be held responsible because he was suffering from schizophrenia.18 Geneticist Randall Libby testified that Verduzco was carrying genes that made him 5–10 percent more likely to develop schizophrenia than a person who did not have a family history of the disorder.19 On 13 April 2018, the Yakima Herald reported that after seven hours of deliberation, the jury found Verduzco guilty of aggravated first-degree murder, which carries a mandatory sentence of life in prison without parole.20 On 18 April 2018, the Psychiatric Genetics Consortium published a paper in Nature Genetics announcing the discovery of 44 genetic variants linked to major depressive disorder.21 The odds ratios for these genetic variants ranged from 1.04 on down. Assuming (as the authors did) a lifetime risk of 15 percent for this condition, this means the absolute increase in risk for associated with any of these genetics variants is approximately one in 167, or even less. Once again, the matter of the “missing heritability” reared its head. Together, all of these genetic variants were said to account for 8.7 percent of the population variance for this trait. Noting that this estimate is far below that obtained from twin studies or family studies, the authors attributed this discrepancy to “etiological heterogeneity.” The possibility that the estimates obtained from twin studies or family studies were wildly overinflated was not considered.

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The paper generated a blizzard of laudatory news stories, none of which mentioned the paltriness of the effect sizes of these genetic variants, although the story in Gizmodo22 did feature an impressive multicolored “wiring diagram” of the human brain. The relevance of this diagram to the content of the article was never explained. At the end of the article, the author stated “Major depression affects some 14 percent of the global population, and yet only about half of patients respond well to existing treatments.” No mention was made of the fact that between 35 and 45 percent of patients “respond” to a placebo,23 which means that something like five or more patients must be exposed to the hazards of antidepressants in order to get one additional patient to respond. And even this begs the question of whether “response” in clinical trials bears any workable connection to any kind of meaningful real-life outcome. On 14 May 2018, a paper published in Biological Psychiatry by the ENIGMA Schizophrenia Working Group24 reported that the cerebral cortices of patients diagnosed with schizophrenia who received antipsychotic medication were significantly thinner than those of unmedicated schizophrenics. This difference persisted even after controlling for illness severity. There was no significant difference in cortical thickness between the brains of unmedicated patients and normal controls—this despite the fact that the study did not distinguish between unmedicated patients and never-medicated patients. In conclusion, the authors stated “We caution that the likelihood that antipsychotic medications are associated with thinner cortex in individuals with schizophrenia should by no means be interpreted as a contraindication for their use in treating patients with severe mental illness.”25 Two weeks later, Nature Medicine published a paper by Daniel Weinberger of the Johns Hopkins Medical Institutions (JHMI) and his colleagues titled “Convergence of Placenta Biology and Genetic Risk for Schizophrenia.”26 Dr. Weinberger and his colleagues found an interaction between polygenic risk scores for schizophrenia and gestational complications such as obesity, diabetes, and preeclampsia. The combination of a high polygenic risk score and early life complications significantly increased an individual’s likelihood of being diagnosed with schizophrenia later in life. But once again, the absolute increase in risk was small. The odds ratio for individuals in the top quintile for polygenic risk scores who also suffered early life complications was 8.36, which works out to an absolute

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increase in risk of about 5 percent. In other words, even the vast majority of individuals with high polygenic risk scores and early life complications did not go on to be diagnosed with schizophrenia. None of the laudatory news stories made this clear. And so on a blazing hot day in the first week of July I find myself back on the campus of JHMI, in the Rangos Building, home of the Lieber Institute for Brain Development. With its glass partitions, wall-to-wall carpeting, and ubiquitous computer work stations, the place looks more like a Silicon Valley start-up than a building on a university campus. I’m in a conference room with Daniel Weinberger, Director and CEO of the Institute and the Maltz Laboratories as well as Professor of Psychiatry, Neurology, Neuroscience, and Human Genetics at JHMI. Dr. Weinberger is board-certified in both psychiatry and neurology, and he’s also the corresponding author of the Nature Medicine paper. We’re both seated on ergonomically-designed swivel chairs at the end of an ellipsoid conference table, and I lean forward to listen as he discusses his work. I begin by inquiring whether some pregnancy complications might correlate with psychosocial problems. Diabetes and obesity can be the product of disordered eating. They also can be side effects of antipsychotic medications, which presumably are not prescribed unless there is some serious problem on the part of the mother. Preeclampsia is a well-known side effect of antidepressant medications, which again presumably are not prescribed unless the mother has serious problems. Could these pregnancy complications Dr. Weinberger and his colleagues looked at actually be surrogates for behavioral disturbances on the part of the mother? “We actually looked at a number of features of the mother’s mental state,” he tells me, “And we found no evidence that those predicted complicated pregnancies.” “All the measurable things we could get from the maternal history— like smoking, stress reported during pregnancy, psychiatric diagnoses—we couldn’t find any relationship between those and a complicated p ­ regnancy.” Although, he cautions, “Not finding something doesn’t mean it’s not there.” I ask Dr. Weinberger how these findings might translate into clinical practice. We already have recognized interventions for conditions such as obesity, diabetes, preeclampsia, and so forth, which presumably can be made available to pregnant women who need them. Should the fetal genetic

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risk score make any difference? He suggests that the highest-risk pregnancies might be identified in advance and followed particularly carefully. Since psychiatric medications are known to cause obesity, diabetes, and preeclampsia, does this suggest that doctors should not prescribe these drugs to pregnant women, or women who might become pregnant? “I think there’s always been great caution about prescribing medicines that get through the placenta to the brain of the fetus during pregnancy,” Dr. Weinberger asserts. “Obviously these should be avoided unless there’s absolutely no alternative. Which is worse? The potential risk to the fetus of the mother on a psychotropic drug? Or an untreated psychosis, or severe depression? Which, undoubtedly, because of the changes to cortisol and everything else, are having their own adverse effects on fetal development.” This is when some kind of informed judicious judgement has to be made. But clearly, without any question, caution is the appropriate strategy. You need to be very cautious.

I mention that the combination of a high genetic risk score and complicated pregnancy still accounts for only a small proportion of the total risk for schizophrenia. Where does the rest come from? Dr. Weinberger notes there are many genes that don’t interact with obstetric complications, adding “There are many other environmental factors that we don’t know about.” We talk more about the schizophrenia-associated alleles identified by means of genome-wide association studies. “The ones that we call the ‘significant genes’—ones that achieved this rarified level of statistical significance of ten to the minus eight p value—explained something like two to three percent of the liability to schizophrenia,” he explains. But the other thing to remember is that these studies are a hugely heterogeneous population. Very diverse ancestries. So in any given family, it may be that all of schizophrenia is explained by ten genes. But that one family that was explained by ten genes is diluted out by all the other millions of families. So when you come up with these numbers, they are predicting schizophrenia in the world-wide sample. They’re very misleading for what accounts for genetic risk in an individual. Because we have no way of doing that. These numbers are all based on these huge heterogeneous populations. So they’re telling you about the human species but they’re not helping you much at the individual subject level.

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Since the causes of schizophrenia are so heterogeneous, what does that mean for efforts to find a pharmacological cure for this condition? Dr. Weinberger pauses for a moment to gather his thoughts. He begins: There is no gene for mental illness. There are genes for brain development and function. That’s what the genes are about. They can’t be about mental illness. A gene doesn’t know anything about a hallucination or a panic attack. The only thing genes ‘know’ about is the molecular biology of a cell. So genes are about building brains. So this is a real challenge, to wonder how any of these genetic findings lead to a treatment, given the heterogeneity involved. Having said that, I’ll give you the other side of the coin and give you a sense of how it might work. We have drugs in psychiatry that actually work. They make people better. None of them are curative. Most people who take antidepressants get better. Most people who take antipsychotics are much better on them than off them. Lithium, for some people, is a virtually curative drug as long as you take it. So at least for a significant percentage of people who get these drugs, they are much better when they are on them than when not on them. No treatment in psychiatry—talk treatment, electricity treatment, magnetization treatment, medical treatment—none of these treatments were developed with any knowledge of the causes of any of these conditions. Genes are causes, and having some inkling to causes means there has to be a better strategy than pure accident. It’s the same thing going on in cancer and every field in medicine. So how do you do it?

He likens the cascade of cellular events that produce a dysfunctional brain to a row of falling dominoes. If you can find the key domino at the center of the cascade, you may be able to prevent all the other dominoes from falling. * * * I asked every one of the experts I interviewed for this book the following question: What has the field of psychiatric genetics contributed to mankind? Dr. Seikkula declined to comment. As for the others, here are their answers: Jay Joseph, clinical psychologist and author of Schizophrenia Genetics: The End of an Illusion27:

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The field of psychiatric genetics has produced no findings that help improve the human condition, and its baseless claims have caused great harm in many ways. I’m not only speaking about sterilization and other eugenic measures that the field vigorously promoted in the first half of the 20th century. I’m referring to the false claims made by the psychiatric genetics field about the alleged major importance of genetic factors. These claims have helped obscure the role of trauma and other environmental causes of human distress and psychological dysfunction. For the drug companies, it’s very important that psychiatric disorders are seen as biological and genetic—that something is wrong with the body and the brain—which is why they promote the idea that psychiatric disorders are genetic diseases or ‘chemical imbalances’ in need of medication. They make huge profits through the promotion of such ideas, even though the evidence in favor of genetic causes and chemical imbalances is weak.

Richard Huganir, Director of the Department of Neuroscience and the Kavli Neuroscience Discovery Institute at JHMI: Most of the antipsychotic drugs were developed decades ago and we haven’t progressed very far since then. And a lot of pharmaceutical companies are dropping out of neuroscience in general or schizophrenia research or even Alzheimer’s disease in particular, because it’s such a difficult nut to crack. So I think genetics is one of our only hopes. The genetics so far has been very unsophisticated. It didn’t have the power or the technical approaches to address the question I think we have now. So I personally think the golden age of psychiatric genetics is upon us, and in ten to twenty years we’re going to really see a great progression. So: so far not much, but I’m hopeful.

Peter Breggin, psychiatrist and author of Medication Madness 28 and Guilt, Shame, and Anxiety 29: It helped contribute to the Holocaust. It contributed to the German extermination of its mental health population, in a program that is well-­ documented. And that contributed to the Holocaust. And it has contributed nothing positive to the world. It misleads people still into taking drugs, and to feeling they are incurable. Psychiatric genetics is eugenics. It’s a disaster.

John Read, Professor of Clinical Psychology at the University of East London:

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Absolutely nothing. And there are the negative effects of conveying to the public that human distress can be understood largely or partly in terms of genetics. The worst it has contributed—I know this sounds extreme—but it has been directly responsible for the deaths of a quarter of a million people in the 1930’s and 1940’s when genetic ideas were actually acted on to try and purify gene pools of schizophrenia and some other things. So, that’s the worst it’s contributed. In terms of positive contributions I turn this question back to the person asking the question: Identify to me one person in the mental health services anywhere in the world who has ever benefitted from genetic research, and that’s a struggle to do that.

David Healy, Professor of Psychiatry at Bangor University and author of Mania: A Short History of Bipolar Disorder 30: I don’t know that it’s contributed anything at all. In day-to-day clinical practice, I never have a need to get a gene scan done. Overall, the genetic argument is a political argument. It’s a calling card that we believe these things are biological. There could be a bit more work done to try to explain to people just because a gene is involved doesn’t mean the gene has caused it. There’s hundreds of genes involved, and each contributes a teeny little bit, which means there isn’t ever going to be a genes test for this.

Daniel Weinberger, Director and CEO of the Institute and the Maltz Laboratories and Professor of Psychiatry, Neurology, Neuroscience, and Human Genetics at JHMI: We have now learned more about the basic cell biology of mental illness than we ever knew in all of past history. We know what every cancer gene does. It transforms a normal cell into a cancer cell. We have no idea what a gene for mental illness does. We have no idea what it means to inherit a risk factor for mental illness, at a basic cellular level. And the genes are beginning to be able to help us to answer that question. Those are long-term potential benefits. Here’s the short-term real benefit for mankind: one of the biggest impediments to progress in mental illness is stigma. And science is the solution to stigma. That there are genes for mental illness, I think, has enormous impact on destigmatizing the reality of this. If you walk around this institute, we have these phenomenally bright young scientists, MD-PhD’s from Harvard, Stanford—they never would

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have gone into mental illness research twenty years ago. When I got into this field, this was a backwater. And this has all changed. We now have the people from the backgrounds and the schools that would never have gone into this field, and it’s because the genes make it hard-core science. And this, I think, has a huge de-stigmatization factor. So I think it has a big impact, even though it’s not obviously helping any individual’s medical condition or psychiatric condition. That, it’s not doing.

* * * At the end of the interview, I thank Dr. Weinberger for his time, and he says he hopes he has been of help. He accompanies me to the elevator, and wishes me good luck with my project, a topic he finds fascinating. “Psychiatric genetics” he notes, “Has a checkered history.”

Notes 1. E.g., International Schizophrenia Consortium, “Common Polygenic Variation,” 748; Patrick F.  Sullivan Mark J.  Daly, and Michael C.  O’Donovan, “Genetic Architectures of Psychiatric Disorders: The Emerging Picture and Its Implications,” Nature Reviews Genetics, 13, no. 8 (July 10, 2012): 538, https://doi.org/10.1038/nrg3240; McCarroll et al. 2014; Javier Arnedo et al., “Uncovering the Hidden Risk Architecture of the Schizophrenias: Confirmation in Three Independent Genome-Wide Association Studies,” American Journal of Psychiatry, 172, no. 2 (February 1, 2015): 139, https://doi.org/10.1176/appi.ajp.2014.14040435 2. John Read. “The Invention of ‘Schizophrenia’: Kraepelin and Bleuler,” in Models of Madness: Psychological, Social, and Biological Approaches to Schizophrenia, ed. John Read and Jaqui Dillon, (Abingdon: Routledge, 2013) 20–33. 3. Bentall, “Understanding Psychotic Symptoms,” 231. 4. Szasz, Sacred Symbol, 88. 5. E.g., Steven Hyman, “The NIMH Perspective: Next Steps in Schizophrenia Research,” Biological Psychiatry, 47, no. 1 (January 1, 2000): 6; Plomin and Crabbe, “DNA,” 823; Francis S.  Collins and V.A.  McKusick, “Implications of the Human Genome Project for Medical Science,” JAMA, 285, no. 5 (February 7, 2001): 543; Thomas R. Insel, “Translating Scientific Opportunity Into Public Health Impact,” Archives of General Psychiatry, 66, no. 2 (February 2009): 130, https://doi.org/10.1001/ archgenpsychiatry.2008.540

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6. Kirsch, Emperor’s New Drugs. 7. Whitaker, Anatomy of an Epidemic. 8. Robert Whitaker, “The Case Against Antipsychotics: A Review of Their Long-term Effects,” accessed February 8, 2018, https://www.madinamerica.com/wp-content/uploads/2016/07/The-Case-AgainstAntipsychotics.pdf 9. Sukanta Saha, David Chant, and John McGrath, “A Systematic Review of Mortality in Schizophrenia: is the Differential Mortality Gap Worsening Over Time?” Archives of General Psychiatry, 64, no. 10 (October 2007): 1123–1126, https://doi.org/10.1001/archpsyc.64.10.1123 10. John Read, Nick Haslam, L.  Sayce, and E.  Davies, “Prejudice and Schizophrenia: A Review of the ‘Mental Illness is an Illness Like Any Other’ Approach,” Acta Psychiatrica Scandinavica, 114, no. 5 (November 2006): 303–318, https://doi.org/10.1111/j.1600-0447.2006.00824.x; John Read, Nick Haslam, and Lorenza Magliano, “Prejudice, Stigma, and ‘Schizophrenia’: The Role of Bio-Genetic Ideology,” in Models of Madness: Psychological, Social, and Biological Approaches to Schizophrenia, ed. John Read and Jaqui Dillon (Abingdon: Routledge, 2013), 157–177. 11. Erlend P.  Kvaale, Nick Haslam, and William H.  Gottdeiner, “The ‘Side Effects’ of Medicalization: A Meta-Analytic Review of How Biogenetic Explanations Affect Stigma,” Clinical Psychology Review, 33, no. 6 (August 2013): 782–794, https://doi.org/10.1016/j.cpr.2013.06.002 12. Matthias C.  Angermeyer and Herbert Matschinger, “Causal Beliefs and Attitudes to People With Schizophrenia,” British Journal of Psychiatry, 186, no. 4 (April 2005): 331–334, https://doi.org/10.1192/ bjp.186.4.331 13. Bernice A. Pescosolido, Jack K. Martin, J. Scott Long, Tait R. Medina, Jo C. Phelan, and Bruce G. Link, “A Disease Like Any Other?” A Decade of Change in Public Reactions to Schizophrenia, Depression, and Alcohol Dependence,” American Journal of Psychiatry, 167, no. 11 (November 2010): 1321–1330, https://doi.org/10.1176/appi.ajp.2010.09121743 14. Read et al., “Prejudice and Schizophrenia,” 312. 15. John Read and Jeffrey Moussaieff Masson. “Genetics, Eugenics, and Mass Murder,” in Models of Madness: Psychological, Social, and Biological Approaches to Schizophrenia, ed. John Read and Jaqui Dillon, (Abingdon: Routledge, 2004) 35. 16. Ibid., 40. 17. Adam Rogers, “Star Neuroscientist Tom Insel Leaves the Google-­Spawned Verity for … a Startup?” Wired, May 11, 2017, https://www.wired. com/2017/05/star-neuroscientist-tom-insel-leaves-google-spawned-verily-startup/

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Index1

A Adoption studies, 47–54, 76, 155 B Battie, William, 119–121 Bentall, Richard, 156 Bethlem Hospital, 2, 119 Bleuler, Paul Eugen, 6, 155 Brandt, Karl, 11 Breggin, Peter, vii, 53, 91–93, 101, 105, 166

E Equal environment assumption, 25, 28–30 Ewald, Gottfried, 13

C Candidate-gene studies, 73 Collins, Francis, 70

F Family studies, 9–18, 29, 30, 47, 54, 76, 155, 161 Faraone, Stephen, 60, 61, 109 Ferenczi, Sándor, 103 Finnish Adoption Study, 52, 76 Freud, Anna, 103 Freud, Sigmund, 102, 103 Fromm-Reichmann, Frieda, 111, 131–138, 141

D Danish Adoption Study, 47, 48, 50, 51, 53 Diagnostic and Statistical Manual of Mental Disorders, 59, 60

G Genain Quadruplets, 35, 43, 104 Genome-wide association studies, 74, 83, 155 Greenberg, Joanne, 133–135

 Note: Page numbers followed by ‘n’ refer to notes.

1

© The Author(s) 2019 P. D. Hahn, Madness and Genetic Determinism, https://doi.org/10.1007/978-3-030-21866-9

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192 

INDEX

H Haslam, John, 2, 3, 5, 119 Healy, David, vii, 125–127, 167 Horn, Ernst, 124, 125 Hornstein, Gail, 131, 135 Huganir, Richard, vii, 69, 70, 78, 79, 166 I Insel, Thomas, 160 J Jackson, Don, 28, 104 Johns Hopkins Medical Institutions (JHMI), 69, 82n32, 162, 163, 166, 167 Joseph, Jay, vii, 26, 28–30, 52, 54, 77, 165 K Kallmann, Franz, 11, 18, 21–31, 51, 52, 60, 76, 77, 155–168 Kendler, Kenneth, 74, 75 Kety, Seymour, 47, 50, 51, 54 Kirsch, Irving, 63, 158 Koplewicz, Harold, 61–65 Kraepelin, Emil, 5, 6, 9, 10, 15 L Laing, Adrian, 145, 146 Laing, Ronald David, 141–147, 149 Lenz, Fritz, 11 Lidz, Theodore, 50 Linkage studies, 73

M Masson, Jeffrey Moussaieff, 103, 160 Mendel, Gregor, 4, 5, 9, 75 Morel, Benedict Augustin, 3, 4, 6 Mullan, Bob, 142, 144, 146 N Not in Our Genes: Biology, Ideology, and Human Nature, 27 O Open Dialogue Therapy, 149–153 Osheroff, Samuel, 137 P Paxil, 57, 63–65 Pfannmüller, Hermann, 15, 16 Pinel, Phillipe, 120, 121, 124 R Read, John, vii, 105–109, 159, 160, 166 Reil, Johann Christian, 2, 3, 125 Rosenhan experiment, 59, 155 Rosenthal, David, 35, 36, 42–44, 47, 49–51, 54 Rüdin, Ernst, vi, 6, 9–18, 21, 23, 65, 76, 155–168 S “Schizophrenogenic mother”, 52, 108, 110–114 Schofield, January, 83–95, 158

 INDEX 

Schofield, Michael, 83–91, 94, 95 Schofield, Susan, 83–85, 87–91, 94, 95 Seikkula, Jaako, vii, 152, 153, 165 Shorter, Edward, 47, 72, 135 Soteria House, 147, 149–153 Study 329, 63, 65 Szasz, Thomas, 59, 72, 146, 148n36, 156 T Tuke, Samuel, 122, 123 Tuke, William, 122 22q Syndrome, 71 Twin studies, 21–31, 35, 47, 53, 54, 76, 83, 155, 161

193

U United States Holocaust Memorial Museum, 1 V Verduzco, Manuel Enrique, v, 161 W Weinberger, Daniel, vii, 82n32, 162–165, 167, 168 Whitaker, Robert, 59, 64, 65n8, 158 Wirth, Christian, 14, 17 Z Zerbin-Rüdin, Edith, 18, 29