Preface

We are approaching a period of crisis in the social and behavioral sciences, as decades of attempts to discover “genes for behavior” have, with possible rare exceptions, failed to produce confirmed discoveries. Schizophrenia is the most studied psychiatric disorder, yet in an official 2013 press release the American Psychiatric Association admitted that psychiatry is “still waiting” for the identification of “biological and genetic markers” for its disorders. Although some gene discovery claims have appeared since then, psychiatry continues to “wait.”

I am a clinical psychologist practicing in the San Francisco Bay Area. I have been interested in the “genetics of schizophrenia” topic since the 1990s, beginning with my 1998 doctoral dissertation A Critical Analysis of the Genetic Theory of Schizophrenia. It was around that time that I became interested in the works of critics of the mental health system and the medical model, such as Peter Breggin, David Cohen, David Cooper, Erving Goffman, David Hill, R. D. Laing, Thomas Szasz, and others. This led me to authors who had critically analyzed genetic research in psychiatry and psychology, which include Mary Boyle, Stephan Jay Gould, Don Jackson, Leon Kamin, Richard Lewontin, Theodore Lidz, Alvin Pam, Ken Richardson, and Steven Rose. My first article on schizophrenia and genetics was published in 1999, and between 2003 and 2015 I published three books critically examining genetic research in the social and behavioral sciences. For 20 years, I have looked closely at the methodological shortcomings and controversial assumptions in twin research, including studies of reared-together and reared-apart twin pairs.

Although according to authoritative mainstream authors and researchers “we know” that schizophrenia has an important hereditary basis, there is another side to this story that is largely ignored by psychiatry and the media. My desire to help tell this side of the story led me to choose my dissertation topic 20 years ago. Continuing the work of the pioneering researchers and commentators mentioned above, and drawing from my previous analyses, here I focus on the massive flaws of schizophrenia genetic research in the context of gene discovery failure.

In Chapter 1, I discuss the schizophrenia concept from several different perspectives, and I review several problems with genetic explanations. Chapter 2 describes the ongoing failure to make confirmed discoveries of genes shown to cause schizophrenia and psychosis, and contains a brief critique of the heritability concept. In Chapter 3, I discuss schizophrenia family studies. I show in Chapter 4 that schizophrenia twin studies are based on a critical theoretical assumption that is clearly false, and therefore provide no evidence in favor of genetics. In Chapter 5, which comprises over half of the book, I examine in detail the major problem areas in the most frequently cited adoption studies. These studies played an important role in turning the tide in favor of genetics, yet serve as an example of how entire scientific fields can overlook massively flawed and biased research performed by leading researchers. In Chapter 6, I join calls for a shift in the study of the causes, treatment, and prevention of schizophrenia and psychosis from currently dominant biological and genetic approaches, to non-medical and environmental approaches. My analysis applies to most other “nature-nurture” areas of behavior as well, because similar methods are used. The implications, therefore, are enormous.

I have attempted to cover the main topics and controversies in a way that people outside of the mental health field can understand, and I have therefore kept data reporting to a minimum. For additional information, I have included numerous links to currently available relevant websites, publications, and videos. In contrast to most of what is written in social and behavioral science textbooks, in this e-book I challenge claims made by many of the world’s leading researchers, and show that genetic explanations of schizophrenia rest on false foundations. I am confident that readers will find my analysis refreshingly different from the predicable, sometimes inaccurate, and usually uncritical academic and journalistic accounts of the “genetics of schizophrenia” topic.

Jay Joseph, Psy.D.

August, 2017

Chapter 1

Introduction

“Data don’t tell stories, scientists tell stories.”

—An academic supervisor, quoted in Chris Chambers’ 2017 book The Seven Deadly Sins of Psychology¹

“The substantial hereditary component in schizophrenia,” a pair of researchers wrote in 1993 on the basis of family, twin, and adoption research, “is surely one of the two or three best-established facts in psychiatry.”² After nearly two decades of subsequent well-funded yet failed attempts to identify causative genes at the molecular level, in a 2011 edition of the American Journal of Psychiatry genetic researcher David Goldman asked, “Why is it that the molecular genetics of schizophrenia has seemingly been forever poised on the brink of great breakthroughs?”³

In this e-book I will attempt to answer Goldman’s question in a way that differs greatly from the explanations found in cookie-cutter academic and journalistic accounts of the “genetics of schizophrenia” topic. Rather than focus on better ways to uncover presumed genes, as these publications often do, I will focus on the methodological flaws and controversial assumptions of previous schizophrenia family, twin, and adoptions studies. Genetic interpretations of this body of research led to attempts to discover predisposing genes (“gene variants”) for schizophrenia at the molecular genetic level. Here I provide an updated presentation of the main themes and ideas I have written about over the past 20 years, while reviewing several new and important areas relevant to the critique. Contrary to most of what has been written on this topic, I will attempt to show that there is little if any scientifically acceptable evidence that disordered genes cause schizophrenia. Although my analysis focuses on schizophrenia genetic research, it applies to most other psychiatric conditions because similar methods are used in these areas as well. As Jonathan Leo, a critic of biological psychiatry wrote in 2016, “Schizophrenia holds a unique spot in the annals of mental health research because of its perceived anatomical underpinnings, and is often cited as evidence in favor of a genetic predisposition to other conditions.”⁴

Before turning to my primary objective, which is a critical reappraisal of schizophrenia family, twin, and adoption research, in this chapter and the next I examine problems with genetic theories of schizophrenia in the context of the ongoing failure to make confirmed discoveries of predisposing genes. These problems include low reproduction rates, the fact that the majority of people diagnosed with schizophrenia have no family history of the condition, the questionable reliability and validity of a “schizophrenia” diagnosis, and faulty brain disease theories.

Differing Concepts of “Schizophrenia”

The diagnosis/term dementia praecox (dementia of early life) was developed by the German psychiatrist Emil Kraepelin in the late 19th century. Kraepelin created this diagnosis by combining three previously reported conditions into one syndrome, which he viewed as a progressively deteriorating disease.⁵ In 1911, the Swiss psychiatrist Eugen Bleuler published Dementia Praecox or the Group of Schizophrenias. He coined the term schizophrenia, meaning “split mind.” Although Bleuler based his conception of schizophrenia on Kraepelin’s work, he saw the condition as being characterized by “primary symptoms” such as autism (turning inward), blocking of thoughts, and loose associations (vague connections between thoughts).⁶ Bleuler believed that hallucinations and delusions were “secondary symptoms” resulting from the primary thought disturbance.

Kraepelin and Bleuler believed that the condition each described was caused by a disease process triggered by an inherited predisposition (Anlage). However, psychiatry critic Thomas Szasz (1920-2012) pointed out in 1976 that instead of focusing on what Kraepelin and Bleuler believed, contemporary commentators should instead focus on these investigators’ “utter inability to support their beliefs with a shred of relevant evidence” (italics in original). What Kraepelin and Bleuler helped to accomplish, in Szasz’s view, was to “subtly…redefine the criterion of disease, from histopathology [pathology of tissues] to psychopathology–that is, from abnormal bodily structure to abnormal personal behavior.” ⁷ This lies at the core of modern psychiatric “medical model” approaches, where dysfunctional or socially disapproved personal behaviors are transformed into discrete diseases or disorders devoid of social context. This position is often accompanied by the claim that these disorders are caused by underlying brain pathology or a “chemical imbalance.” Szasz repeatedly pointed out, however, that when a “mental disorder” is shown to be caused by a brain disease, it leaves the realm of psychiatry and becomes the concern of other branches of medicine, such as neurology. In cases where brain pathology is proven—and not just claimed—medical science recognizes that the patient has a brain disease, not a mental disorder.⁸ “Mental illness does not exist not because no one has yet found such a disease,” Szasz wrote, “but because no one can find such a disease: the only kind of disease medical researchers can find is literal, bodily disease” (italics in original).⁹

The psychiatric genetics field was founded in Germany in the early part of the 20th century. German “Munich School” psychiatric geneticists in the interwar period performed family and twin studies in an attempt to establish the genetic basis of psychiatric disorders and socially disapproved behavior (such as criminality). Their primary goal was to promote the eugenic program (called “racial hygiene” in Germany) of curbing the reproduction of people they viewed as carrying the “hereditary taint of mental illness,” by sterilization or other means (see Chapter 3).¹⁰ It is important to note that eugenic theories, laws, and practices, which harmed millions of people, were backed by a false set of claims (premises) based on very bad “science” and on the social prejudices of the economically powerful, who helped fund and support the eugenics movement. Eugenicists claimed that hereditary influences on human behavior are very important, and that environmental influences on human behavior are relatively unimportant. An excellent account of eugenics pseudoscience in the first half of the 20^th century is found in Allan Chase’s 1977 book The Legacy of Malthus: The Social Costs of the New Scientific Racism.¹¹

Modern psychiatric geneticists perform family, twin, adoption, and molecular genetic research. They attempt to assess the influence of genetic factors on mental disorders in order to better understand, treat, and prevent them, while promoting the use of genetic counseling programs.

For contemporary psychiatry and its psychiatric genetics subfield, schizophrenia is “a severe mental disorder with a lifetime risk of about 1%, characterized by hallucinations, delusions and cognitive deficits, with heritability estimated at up to 80%,” or “a heritable brain illness with unknown pathogenic mechanisms.”¹² According to the biologically oriented U.S. National Institute of Mental Health (NIMH), “Schizophrenia is a chronic and severe mental disorder that affects how a person thinks, feels, and behaves. People with schizophrenia may seem like they have lost touch with reality….The symptoms can be very disabling.” Schizophrenia’s “positive symptoms,” according to the NIMH, include “hallucinations,” “delusions,” “thought disorders (unusual or dysfunctional ways of thinking),” and “movement disorders (agitated body movements).” Schizophrenia’s “negative symptoms” include “flat affect (reduced expression of emotions via facial expression or voice tone),” “reduced feelings of pleasure in everyday life,” “difficulty beginning and sustaining activities,” and “reduced speaking.” In recent versions of the American Psychiatric Association’s (APA) Diagnostic and Statistical Manual (commonly known as the “DSM”), which lists psychiatry’s mental disorders and their diagnostic criteria, only some of these symptoms are necessary to diagnose someone with schizophrenia. Mainstream sources usually state that the schizophrenia population prevalence or lifetime risk is roughly 1% or a bit lower. Schizophrenia prevalence is higher in men than in women through most of adulthood, but equalizes by the end of the risk period at age 45.¹³

While recognizing that some people do experience and exhibit the behaviors and “symptoms” listed above, many commentators have challenged the claim that schizophrenia is a genetically based brain disease, and some have challenged the concept of schizophrenia itself. According to psychologist John Read, the word “schizophrenia” is a “scientifically meaningless and socially devastating label.”¹⁴ Szasz saw the schizophrenia concept/label as being “wonderfully vague in its content and terrifyingly awesome in its implications.”¹⁵ Modern commentators such as critical psychiatrists Joanna Moncrieff and Hugh Middleton reject the word “schizophrenia,” and prefer terms “such as ‘psychosis’ or just ‘madness,’ [which] would be preferable because they are less strongly associated with the disease model, and enable the uniqueness of each individual’s situation to be recognized.”¹⁶ The word psychosis is difficult to define, but it generally describes people who have lost touch with reality, sometimes accompanied by hallucinations and delusions, in the absence of an organic cause.

Mainstream researchers long ago abandoned the search for a major causative single gene, and now view schizophrenia and other psychiatric conditions as “multifactorial complex disorders” caused by a complex interaction of multiple genes and multiple environmental risk factors. This idea is based on the earlier predisposition-stress (diathesis-stress) theory of psychiatric disorders. The authors of mainstream publications usually emphasize the position that genetic factors are believed to play a major role, and that environmental factors, while necessary, are not well understood. In his 1999 book Molecules and Mental Illness, genetic researcher and popularizer Samuel Barondes wrote, “There are at present no leads to the environmental factors that cause schizophrenia and no strategy for their identification.”¹⁷ This helps maintain focus and emphasis on the presumed genetic factors. Critics have noted that in psychiatry’s conception of schizophrenia, “life events have been relegated to the role of ‘triggers’ of an underlying genetic time bomb.”¹⁸

The predisposition-stress/multifactorial complex disorder position has been very successful in supporting the idea that psychiatric disorders have an important genetic basis. Critical psychologist Mary Boyle (video) observed that the model seems inclusive and reasonable in the sense that “who could deny that biological and psychological or social factors interact?” At the same time, the model “firmly maintains the primacy of biology, not least through word order, and potentially de-emphasizes the environment by making it look as if the ‘stress’ part of the vulnerability-stress model consists of ordinary stresses which most of us would cope with, but which overwhelm only ‘vulnerable’ people.”¹⁹ Boyle noted that by “inserting an unspecified innate vulnerability between the person and their environment, the claimed vulnerability and not the environment becomes the focus of concern.”²⁰ The question centers on how science and society should approach schizophrenia and psychosis, and whether the causes are mainly located inside of the human body, as mainstream psychiatry claims, or outside of the body, as many critics argue.

A leading group of psychiatric genetic researchers wrote in 2015 that, apart from genetics, the “underlying causes and pathogenesis of the disorder remains unknown.”²¹ However, evidence pointing to specific environmental influences has been accumulating in recent years.

Evidence in Support of Environmental Causes

As superbly reviewed by John Read (video) in several chapters in the 2013 second edition of Models of Madness: Psychological, Social and Biological Approaches to Psychosis, since the turn of the 21^st century many studies have linked schizophrenia and other psychotic conditions to childhood adversities such as having experienced bullying, emotional abuse, incest, neglect, parental loss, physical abuse, and sexual abuse—findings that are known to clinicians who work with people diagnosed with psychotic disorders.²² Read also reviewed the evidence linking schizophrenia and other psychotic disorders to social factors such as poverty, racism, migratory stress, and urbanicity. He concluded, “There is ample evidence that inequality, deprivation and discrimination, filtered through their social and personal meanings, are key causal factors in psychosis.”²³

In support of the 2001 “Traumagenic Neurodevelopmental” (TN) model, in 2014 Read, Roar Fosse and their colleagues summarized research findings pointing to significant risk factors for psychosis, which include “mother’s health, nutrition and stress during pregnancy, being the product of an unwanted pregnancy, early loss of parents via death or abandonment, separation of parents, witnessing interparental violence, dysfunctional parenting (often intergenerational), war trauma, rape or physical assaults as an adult, racial or other forms of discrimination, heavy marijuana use in early adolescence, and poverty.”²⁴ They described psychological processes through which childhood adversities may lead to symptoms of psychosis later in life as consisting of attachment, dissociation, dysfunctional cognitive processes, psychodynamic defenses, problematic coping responses, impaired access to social support, behavioral sensitization, and revictimization.²⁵ Read commented that “the idea that bad things happening in childhood can drive you crazy is not…controversial in the real world beyond biological psychiatry.”²⁶

Supporters of genetic theories often point to older psychoanalytic ideas that “schizophrenogenic mothers” cause schizophrenia as an example of unsupported, and even harmful, environmental theories. There are, however, many psychologically damaging influences in the wider social and political environment. Dysfunctional and abusive family conditions are just one component of the larger picture of non-genetic factors that can lead to psychosis and a schizophrenia diagnosis.

If trauma and psychologically unhealthy family, social, and political arrangements are indeed the main factors underlying emotional problems and psychiatric disorders such as schizophrenia, depression, and many others, then focusing on genetics and the brain are monumental diversions, in much the same way as the tobacco industry cited an alleged genetic predisposition to develop lung cancer in an attempt to divert attention from the carcinogenic effects of smoking tobacco. While mainstream psychiatric researchers and others worry about the “societal burden of mental disorders,”²⁷ from another perspective, much human psychological distress and dysfunction could be characterized as the mental burden of societal disorders. As the evolutionary biologist (and behavioral genetics critic) Richard Lewontin once put it, “Problems of health and disease have been located within the individual so that the individual becomes a problem for society to cope with rather than society becoming a problem for the individual.”²⁸

Problems with Genetic Explanations of Schizophrenia

Most Diagnosed People Have No Family History of Psychosis

Psychiatry claims that schizophrenia is a “highly heritable disorder” even though, as reported in the 2013 Fifth Edition of the DSM (DSM-5), “most individuals who have been diagnosed with it have no family history of psychosis.”²⁹ In a 2006 Swedish study based on a population-based cohort of 7,739,202 individuals of known parentage, Paul Lichtenstein and colleagues found that in families in which one member was diagnosed with schizophrenia, in more than 96% of these families there were no other similarly diagnosed family members.³⁰

Twin researcher and authoritative schizophrenia author Irving Gottesman (1930-2016) wrote in his 1991 book Schizophrenia Genesis: The Origins of Madness,

“The vast majority of schizophrenics will have neither parent who is overtly schizophrenic—some 89 percent—and will have neither parents nor siblings who are affected—some 81 percent. Furthermore, a sizable majority—about 63 percent—will have negative family histories—that is, ‘clean pedigrees’—even allowing for such first-degree relatives as children and such second-degree relatives as nieces and nephews” (italics in original).³¹

Although Gottesman was a leading supporter of genetic theories of schizophrenia for five decades, it is difficult to imagine schizophrenia as a genetically based disorder when most people carrying the diagnosis have no family history of it.

Low Reproduction Rates

People diagnosed or labelled with schizophrenia often do not have children. The persistence of a “hereditary disorder” in which the gene carriers reproduce at low rates does not seem possible. As biological psychiatrist E. Fuller Torrey once put it, “It is…difficult to explain why [schizophrenia] has not died out since people with schizophrenia reproduce at an extremely low rate.”³² Biological psychiatrist Nancy Andreasen, former Editor-in-Chief of The American Journal of Psychiatry, could only note that it is “fascinating” that “schizophrenia persists in the human population despite the fact that the majority of people who develop it do not marry or procreate.”³³ Although most people labeled “schizophrenic” in Nazi Germany tragically and criminally were either sterilized or killed by the regime and its willing accomplices in science and medicine (see Chapter 3), studies show, contrary to genetic predictions, a high incidence rate of new schizophrenia cases in Germany.³⁴ As a pair of commentators noted, “this atrocity provided proof against the very reasoning used to instigate it.”³⁵

In support of genetic theories and the idea that schizophrenia is a medical illness, psychiatry has claimed that schizophrenia rates are similar throughout the world. In Schizophrenia Genesis, for example, Gottesman felt “safe to conclude that the incidence of schizophrenia in most human populations around the world today is rather similar.”³⁶ John Read has shown, however, that schizophrenia prevalence and incidence studies do not support this claim. He noted that recent psychiatry textbooks have finally abandoned this “uniform prevalence myth.”³⁷

Is “Schizophrenia” a Valid Disorder that Can Be Reliably Identified?

Another key issue is whether “schizophrenia” is a valid disorder that can be reliably identified (diagnosed) by psychiatrists, and there is plenty of evidence that it isn’t, even more so in the era when several frequently cited genetic studies were performed. Establishing the reliability and validity of a psychiatric disorder is a prerequisite for any attempt to search for genetic influences or genes. Reliability in psychiatry refers to the ability of psychiatrists to consistently agree on a diagnosis.

Although a disorder must be valid in addition to being reliable, reliability must be established before determining whether a diagnosis is valid. “If researchers can’t agree on who has ‘schizophrenia,’” Read pointed out, “then the supposed properties of ‘schizophrenia’ cannot be evaluated.”³⁸ Validity refers to whether a diagnosis is a discrete biological entity, with natural boundaries that separate it from other diagnoses. In their 2013 book Mad Science: Psychiatric Coercion, Diagnosis, and Drugs, professors of social work Stuart Kirk, Tomi Gomory, and David Cohen questioned the validity of psychiatric disorders. “To state that a mental illness is a valid concept (that it truly identifies a phenomenon of nature),” they wrote, “means that some body of evidence has been amassed according to the guidelines of a specific biomedical theory, and then has survived rigorous tests devised upon the notion that the specific theory might be false” (italics in original). They emphasized that simply “describing a set of behaviors and labeling them as pathological symptoms never establishes the validity of an illness,” because “the criteria merely describe what is claimed a priori to be an illness.”³⁹ Genetic research is often cited in support of the position that schizophrenia is a valid medical disorder.

Biological psychiatrist Robin Murray wrote in 2017 that one of the “mistakes” he made in his long research career was to “follow…the fashion of the herd” by thinking of “schizophrenia” as a discrete disorder. “I expect to see the end of the concept of schizophrenia soon,” Murray wrote, “already the evidence that it is a discrete entity rather than just the severe end of psychosis has been fatally undermined.”⁴⁰ Many critics of psychiatry have argued that psychiatric disorders are not reliable or valid discrete illnesses, but instead describe people’s varying psychological responses to having experienced adverse events and environments, or are socially disapproved behaviors or responses to oppression that psychiatry labels as mental (medical) disorders.⁴¹

The prominent genetic researcher Lionel Penrose wrote in 1968, “The study of the genetics of schizophrenia is unsatisfactory from almost every point of view,” with the first reason being that “there is no certainty that the condition can be defined or even recognized.”⁴² This position found support in the “Cross-National Project for the Study of the Diagnosis of Mental Disorders in the United States and the United Kingdom” in the late-1960s, which assessed the diagnostic practices of New York and London psychiatrists. Comparing psychiatrists’ diagnoses of the same people, the study found “that the American psychiatrists, in general, applied the diagnosis of schizophrenia to a much wider variety of clinical conditions than did their British colleagues.”⁴³ The researchers concluded, “The evidence presented from this series of studies strongly indicates that the diagnoses routinely made in clinical practice should not be relied upon in epidemiological studies.”⁴⁴ Later, we will see that the famous Danish-American schizophrenia adoption studies were based on such diagnoses.

In 1973, an experiment (video) by Stanford University psychologist David Rosenhan was published in the prestigious journal Science under the title “On Being Sane in Insane Places.”⁴⁵ The first part of the study involved the use of eight healthy associates or “pseudopatients,” who simulated auditory hallucinations in order to gain admission to a psychiatric hospital. Asked by the hospital staff what the voices said, the pseudopatients replied that they were often unclear, but as far as they could tell they said “empty,” “hollow,” and “thud.” Although for the remainder of their hospital stay/confinement (ranging from 7 to 52 days) the pseudopatients acted normally, most were diagnosed with schizophrenia and were discharged with a diagnosis of “schizophrenia in remission.” In the second part of the study, psychiatric staff members at one hospital were asked to identify one or more future pseudopatients who, they were told, would arrive during the next three months. The staff suspected many individuals as being pseudopatients, but in fact none had been sent. Rosenhan concluded that “it is clear that we cannot distinguish the sane from the insane in psychiatric hospitals.” Without going into more detail about this fascinating and controversial study, the results supported the views of psychiatry’s critics, who argued that schizophrenia is a label for deviant behavior that cannot be easily recognized by psychiatric professionals, and has little if any validity.

Although psychiatry claims to have subsequently solved the reliability and validity problems of its disorders with the development of better diagnostic criteria, much doubt remains.⁴⁶ The criteria for diagnosing schizophrenia are still so vague that, as Read showed, there are 15 ways that two people can meet the DSM criteria for schizophrenia without sharing any symptoms in common.⁴⁷ “The people studied by one researcher,” as Read put it, “may have little in common with those being studied by another researcher.”⁴⁸ Allen Frances, former Chair of the 1994 DSM-IV Task Force, wrote in 2011 that “schizophrenia is admittedly a flawed construct with limited descriptive and explanatory power. It is…wildly heterogeneous with dozens of different presentations and probably hundreds of different causes (none of them known)….There is no available biological test available for its diagnosis and none is on the horizon.”⁴⁹ We will see in Chapter 5 that the definition of schizophrenia used in the earlier schizophrenia adoption studies was very different from the definition used by contemporary molecular genetic researchers, even though these adoption studies played an important role in justifying the search for genes.

The genetically oriented child psychiatrist Michael Rutter wrote in 2006 that “critics have had a field day in arguing that if researchers cannot even define the psychiatric categories properly, how can they possibly investigate genetic influences?” Although Rutter disagreed, and believed that future “genetic findings will be very helpful” in validating psychiatric disorders, the critics’ argument remains in full force today.⁵⁰

Genetic and Brain Disease Claims Do Not Cross-Validate Each Other

Andreasen wrote in 1998 that American psychiatry may need “to organize a reverse Marshall Plan so that the Europeans can save American science by helping us figure out who really has schizophrenia or what schizophrenia really is.”⁵¹ This authoritative author’s stunning admission in American psychiatry’s leading journal that her field doesn’t know what schizophrenia is, or who has it and who doesn’t, did not prevent her from claiming in her 2001 book Brave New Brain: Conquering Mental Illness in the Era of the Genome that “schizophrenia” is a “brain/mind disease” caused by an “‘invisible lesion’ that cannot be seen with the naked eye or under a microscope.”⁵²

As Frances noted there are no laboratory tests for schizophrenia (or any other psychiatric disorder), and the condition is diagnosed on the basis of family history, personal history, behavior, self-report, and the reports of others.⁵³ “Schizophrenia,” wrote Moncrieff and Middleton, “remains a condition that is defined by unusual talk and behaviour.”⁵⁴ In the 1995 edition of Surviving Schizophrenia, Torrey wrote that “objective measures for diagnosis, such as laboratory tests of blood and cerebrospinal fluid” are “clearly needed,” and “may be available before many years.”⁵⁵ Like most other aspects of schizophrenia biological and genetic research, Torrey’s hoped-for development of laboratory tests remains unfulfilled.

The evidence that schizophrenia is caused by brain functioning unrelated to social context and personal history is weak.⁵⁶ John Read and colleagues’ Traumagenic Neurodevelopmental model integrates biological and psychological research by highlighting the similarities between the structural and functional abnormalities in the brains of abused children, and adults diagnosed with schizophrenia and psychosis.⁵⁷ In other words, apart from brain tissue reduction caused by the anti-psychotic (neuroleptic) drugs that most people diagnosed with schizophrenia are prescribed,⁵⁸ possible differences in the brain functioning of people diagnosed with schizophrenia and psychosis, and their heightened sensitivity to stress, are likely the result of having experienced childhood trauma, abuse, and neglect. Psychologist Richard Bentall wrote in 2009 that “biological investigators have almost universally failed to consider the possibility that their findings might reflect the tribulations of life, rather than some lesion or genetic scar carried by the victim from birth.”⁵⁹ It is very likely that the brain activity of a child who is chronically sad and scared as the result of being bullied at school will look different in a neuroimaging scan than will the brain of a happy and calm non-bullied child. This does not mean that the bullied child has a brain disease or a “chemical imbalance,” and a similar process may have occurred in people with more serious symptoms that fall into the schizophrenia and psychosis categories. As Read pointed out, most psychiatric brain researchers “ignore the fact that the brain is designed to respond to the environment. What use would a brain be that did not do so?”⁶⁰ Earlier speculation that schizophrenia is caused by a genetically linked deficiency of the neurotransmitter dopamine (the “dopamine hypothesis”) has largely gone by the wayside.⁶¹

Although the technological tools for identifying diseases and genes have been around for decades (including post-mortem brain studies), the claim in psychiatry that schizophrenia is a “heritable brain disease” is apparently based on “missing” genes (see Chapter 2) and Andreasen’s “invisible” inherited brain disease lesions. As Boyle put it, in the absence of direct evidence psychiatry must resort to “smoke and mirrors” tactics to support its brain disease claims.⁶² John Read quoted a passage from the 1913 edition of Kraepelin’s textbook, where Kraepelin wrote that the causes of dementia praecox “are at the present time still wrapped in impenetrable darkness.” Read commented that the key phrase is “at the present time,” which has “been used ever since by researchers forever on the verge of finding the biological cause of schizophrenia.”⁶³

Theoretically, however, schizophrenia could be a brain disease and yet have no genetic basis whatsoever. Nevertheless, the claim that schizophrenia is a brain disease is frequently cited in support of the genetic position, and the claim that schizophrenia is rooted in genetics is frequently cited in support of the brain disease position. As the critical psychiatrist R.D. Laing once observed, “These two theories do not, however, as is claimed, reciprocally validate each other. Rubbing two phantom flints produces only the illusion of fire.”⁶⁴

***

In Chapter 2, I will describe the continuing failure to discover “genes for schizophrenia” and psychosis, a pattern similar to other psychiatric conditions and behavioral characteristics (traits). I will also explore additional problems with the claim that schizophrenia is a “highly heritable” condition.