Schizophrenia and Genetics: A Closer Look at the Evidence


“The substantial hereditary component in schizophrenia,” a pair of researchers wrote in 1993, “is surely one of the two or three best-established facts in psychiatry.”1 But is it really?

For mainstream psychiatry and psychiatric genetics, 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 “highly heritable neuropsychiatric disorder of complex genetic etiology.” Many commentators have challenged these claims, and some have challenged the concept of schizophrenia itself. According to the psychologist John Read, the word “schizophrenia” is a “scientifically meaningless and socially devastating label.”2

I will begin this review by noting the continuing failure to discover “genes for schizophrenia.” Following that, I will touch on the major problem areas in schizophrenia family, twin, and adoption research, with a special emphasis on the widely cited Danish-American schizophrenia adoption studies of the 1960s-1990s. As will soon become apparent, my approach is very different from cookie-cutter academic and journalistic accounts of the “genetics of schizophrenia” topic. The authors of these works usually emphasize that genetic factors are believed to play a major role, and that environmental factors, while necessary, are not well understood.


“Scientists have not identified a single gene that would meet any reasonable standard as a ‘gene for’ schizophrenia, intelligence, depression, or extraversion.”

— Behavioral genetic researcher Eric Turkheimer, in his October, 2015 review of The Trouble with Twin Studies3

Despite Turkheimer’s accurate assessment, several research teams have claimed over the past few years to have discovered elusive susceptibility genes for schizophrenia. By 2014, leading genetic researcher Kenneth Kendler speculated that the “genetic risk for schizophrenia is widely distributed in human populations so that we all carry some degree of risk,”4 while in the same year other researchers claimed to have identified 108 regions on the genome associated with schizophrenia. And there have been other recent claims.

Subsequently unsubstantiated gene finding claims go back to at least 1973, however, when researchers claimed that their “results suggest that there may be genes linked to the Gc locus that cause psychosis in general and that there may be genes linked to the Gm and/or Rhesus systems that cause schizophrenia.”5 A widely reported yet subsequently non-replicated schizophrenia “gene discovery” was published in 1988 by the Sherrington group, who believed that they had found “the first strong evidence for the involvement of a single gene in the causation of schizophrenia.”6 A November 10th, 1988 front page New York Times article about this study proclaimed, “Schizophrenia Study Finds Strong Signs of Hereditary Cause.”

Leading psychiatric investigator C. Robert Cloninger published a 2002 article entitled “The Discovery of Susceptibility Genes for Mental Disorders” in the prestigious Proceedings of the National Academy of Sciences, where he announced that genes for schizophrenia had been “discovered” in the summer of that year by three separate research teams.7 In 2003, the editors of Science declared that the “identification” of “mental illness” genes was the second most important “scientific breakthrough” of the year.8 “Schizophrenia, depression, and bipolar disorder often run in families,” the editors of Science wrote, “but only recently have researchers identified particular genes that reliably increase one’s risk of disease.” Follow-up studies failed to confirm these “breakthroughs” and “discoveries.”

Because over four decades of (often sensationalized) gene discovery claims have not been confirmed by replication attempts, we should be extremely skeptical of recent claims. We should assume by default that current claims are false positive results as well, until proven otherwise. For more details on decades of gene discovery failures in psychiatry, readers should consult my previous postings.9

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. Due to the failure to identify genes for behavioral differences, psychiatry and other fields have developed the “missing heritability” position, which in psychiatry is an attempt to explain the failure to identify genes for psychiatric disorders by claiming that genes exist and await discovery once better methods are found, and larger samples are obtained.10

The American Psychiatric Association’s (APA) position on whether schizophrenia susceptibility genes have been discovered appeared in two versions in the spring of 2013. A May 3rd, 2013 APA press release admitted that psychiatry is “still waiting” for the identification of “genetic markers” for its disorders. In the schizophrenia section of DSM-5, on the other hand, the APA wrote that schizophrenia “liability is conferred by a spectrum of risk alleles, common and rare, with each allele contributing only a small fraction to the total population variance.”11 This was a curious claim because the DSM-5 had been conceptualized a dozen years earlier as incorporating expected “post-genomic era” psychiatric gene discoveries into its diagnostic “multiaxial system”—discoveries that never came. The main difference between the May 3rd 2013 press release and the 2013 DSM-5 is that hardly anyone knows about (or has read) the press release, whereas entire fields over a number of years will be misinformed by the DSM-5’s claim that a “spectrum” of schizophrenia “risk alleles” has been 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, especially in the era when several frequently cited genetic studies were performed.12 The criteria for diagnosing schizophrenia are so vague that, as John Read showed in Models of Madness: Psychological, Social and Biological Approaches to Psychosis, there are 15 ways that two people can meet the DSM criteria for schizophrenia without sharing any symptoms in common. And yet, establishing the reliability and validity of schizophrenia is a prerequisite for any study attempting to assess the possible role of genetic influences.13

Schizophrenia is a “highly heritable disorder” in which, as the DSM-5 reported, “most individuals who have been diagnosed with it have no family history of psychosis.”14 It is difficult to imagine schizophrenia as a “strongly genetic disorder,” when most people carrying the diagnosis have no family history of it. As schizophrenia genetic researcher David Rosenthal once wrote, “To demonstrate that genes have anything to do with schizophrenia,” the “frequency of schizophrenia must be greater in the families of schizophrenics than in the families of nonschizophrenic controls or in the population at large.”15

People diagnosed 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 Nancy Andreasen, the former Editor-in-Chief of The American Journal of Psychiatry once observed, 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.”16

Here I will briefly review the evidence that psychiatry nonetheless has put forward in support of its claim that “schizophrenia” and other psychoses are largely caused by disordered genes. The most likely reason that schizophrenia genes have not been found will become more apparent by the end of this review.


Psychiatric genetic family studies identify people diagnosed with a given condition, and then determine whether their biological relatives are diagnosed with the condition more often than are the biological relatives of a control group, or more often than the general population expectation. If a condition is found to cluster or “run” in families, the condition is familial. This is seen in schizophrenia family studies, where, in the more methodologically sound studies, the first-degree biological relatives of people diagnosed with schizophrenia are diagnosed four times more often than the 1% rate in the general population.17

The key point, however, grudgingly acknowledged by psychiatric genetics over the decades, is that “runs in the family” does not equal “genetic,” since many behavioral characteristics and medical conditions run in families for non-genetic reasons. Although the familiality of schizophrenia was once seen as conclusive proof of its genetic basis, most investigators now realize that medical conditions and behavioral characteristics can run in families for reasons such as exposure to common rearing patterns and abuse, learned behavior, diet, common exposure to environmental pathogens, and other aspects of the physical and social environment. In other words, potential genetic and environmental influences cannot be disentangled in a family study. As a leading group of psychiatric genetic researchers recognized,

“It is critical to understand…that familiality does not establish heritability. For example, religion and language are familial traits, as often all members of the same family practice the same religion and speak the same language. These facts are due not to the transmission of ‘religion genes’ or ‘language genes’ through the family, but rather to the common environment and upbringing that those family members share.”18

Genetic researchers have therefore turned to twin and adoption studies, which they argue are able to disentangle genetic and environmental factors. Many critics remain unconvinced by such claims.


Given the stunning failure to produce genes that cause schizophrenia and psychosis, psychiatry and psychiatric genetics have fallen back on emphasizing previous “classical twin method” comparisons between reared-together MZ (monozygotic, identical) and reared-together same-sex DZ (dizygotic, fraternal) twin pairs. MZ pairs are said to share 100% of their segregating genes, whereas (like ordinary siblings) same-sex DZ pairs are said to share only 50% on average.19 When both members of a twin pair are diagnosed with schizophrenia, the pair is concordant for the condition; when one twin is diagnosed but the other is not, they are discordant for schizophrenia. If a study finds that MZ pairs are significantly more concordant than DZ pairs for schizophrenia, twin researchers conclude that this points to an underlying genetic component.

Genetic interpretations of twin method results are based on twin researchers’ much-criticized MZ-DZ “equal environment assumption” (EEA). According to this assumption, MZ and DZ pairs grow up experiencing roughly equal environments, and the only factor distinguishing them is their differing degree of genetic relationship to each other (100% versus 50%). Twin researchers’ belief that the EEA is valid allows them to argue that genetic factors explain the usual finding that MZ pairs behave more similarly (or correlate higher on psychological tests) than do same-sex DZ pairs. Twin correlations or concordance rates are then factored into more complex “biometrical model fitting” procedures, which produce numerical estimates of heritability (0%-100%), and estimates of “shared” and “unshared” environmental influences.

In the 16 schizophrenia twin studies published between 1928 and 1999, the pooled MZ concordance rate was 40%, while the pooled DZ rate was 7.5%. Looking at the 10 methodologically superior studies published between 1963 and 1999, the pooled rates fall to 23% MZ versus 5% DZ, meaning that in these better-performed studies the MZ co-twin of a person diagnosed with schizophrenia is not so diagnosed about 75% of the time.20  Mainstream textbooks and academic publications often report that MZ concordance is about 50%, and that the “heritability of schizophrenia” is roughly 80%.21 This 80% heritability estimate is then widely reported in the popular press, giving the false impression that schizophrenia is largely genetically determined.

The MZ-DZ Equal Environment Assumption:
The Achilles Heel of the Twin Method

There are several important methodological problems found in schizophrenia twin research. These include:

  • The lack of an adequate and consistent definition of schizophrenia
  • The questionable reliability and validity of schizophrenia
  • The use of non-blinded diagnoses, and diagnoses that were made on the basis of inadequate information
  • The use of unreliable methods of zygosity determination (whether a pair is MZ or DZ)
  • The unnecessary, potentially biasing, use of age-correction formulas
  • The use of non-representative or small samples, or sample populations that were biased in favor of concordance (for example, psychiatric hospital populations)
  • Inadequate descriptions of the researchers’ methods
  • The use of the “probandwise” twin concordance method instead of the “pairwise” method, which leads to inflated concordance rate figures
  • The inflation of concordance rates due to questionable reanalysis practices by genetically oriented researchers not involved in the original studies, which then become the inflated concordance rates reported by the authors of textbooks and other secondary sources
  • Investigator bias in favor of genetic conclusions

Although these factors have undoubtedly inflated true concordance rates, especially in the older studies performed between 1928 and 1961, there is no doubt that the MZ concordance rate is significantly higher than the DZ rate for schizophrenia and most other psychiatric disorders and behavioral characteristics. The key question is: “Why?”

We have seen that the twin method’s critical theoretical assumption is that reared-together MZ and DZ pairs experience roughly the same childhood and adult environments. However, this “equal environment assumption” (EEA) is obviously false, since MZs clearly grow up experiencing much more similar environments than DZs.22 MZ pairs are treated much more similarly, encounter more similar environments, and experience much greater levels of “identity confusion” and attachment than DZ pairs.23 In addition, schizophrenia twin researchers have failed to assess the impact of “trait relevant” environmental factors related specifically to schizophrenia and psychosis, which are more similarly experienced by MZ as opposed to DZ twin pairs.24

Additional evidence that schizophrenia twin concordance rate differences are caused by environmental factors comes from differences between same and opposite-sex DZ pairs. Pooled schizophrenia concordance rates across all studies that compiled such figures are 11.3% for same-sex DZs, but only 4.7 % for opposite-sex DZs.25 Because both types of DZ pairs share the same genetic relationship to each other, according to genetic theory same- and opposite-sex DZ schizophrenia concordance rates should be roughly the same. But they are not.

As my colleagues and I have shown elsewhere, and as I showed in detail in Chapters 7 and 8 of The Trouble with Twin Studies: A Reassessment of Twin Research in the Social and Behavioral Sciences, the twin method’s equal environment assumption is false, regardless of how researchers have attempted to redefine and defend it.26 Schizophrenia twin studies are therefore no more able than schizophrenia family studies to disentangle the potential impact of genetic and environmental influences, meaning that all previous, current, and future genetic interpretations of these studies must be rejected outright.

Most likely, twin studies of schizophrenia and psychosis have recorded nothing more than research bias, MZ pairs’ more similar environments and treatment, MZ pairs’ higher levels of identity confusion and attachment to each other, and MZ pairs’ greater tendency to experience folie à deux (shared psychotic disorder) than DZ pairs. As Rosenthal correctly concluded in 1979,

“Many investigators have shown that the psychological aspects of being an identical [MZ] twin are quite different from those involving DZ twinship. Thus, in both family and twin studies, the possible genetic and environmental factors are confounded, and one can draw conclusions about them only at considerable risk.”27

Other Twin Studies

Two other types of schizophrenia twin studies should be mentioned. The first type studied schizophrenia rates among the biological offspring of discordant MZ pairs (one twin is diagnosed with schizophrenia, while the other is not).28 Genetic theories predict finding comparable schizophrenia rates among the offspring of these pairs, and this is what the original researchers claimed to have found. However, these studies are greatly flawed, and no valid conclusions about genetic factors can be drawn from them.29

Although no systematic schizophrenia “reared-apart” twin study has ever been published, there have been a handful of single-case reports of purportedly reared-apart MZ pairs concordant or discordant for schizophrenia. In Susan Farber’s 1981 review of these cases, she concluded that only nine MZ pairs qualified as having been truly reared-apart. However, even in these cases the twins were aware of each other’s existence, and had periodic contact. The pair that in Farber’s opinion was the “best separated set in the literature” (Craike and Slater’s 1945 “Edith & Florence”) was for her so “poorly separated” that the original authors wondered whether the twins’ knowledge of each other contributed to their “delusional systems.”30 Regardless of how many individual reared-apart MZ pairs are reported concordant for schizophrenia, they do not provide scientific evidence in favor of genetics because, among other reasons, they are anecdotal reports that were not part of a systematic study.


I have touched on the invalidating flaws and biases in twin studies of behavior only lightly, mainly because I have covered this important topic in more depth in previous postings and articles. I discuss issues in schizophrenia adoption research in more detail below. For a much more detailed analysis of the body of schizophrenia adoption research, readers should consult my previous publications.31

Because twin studies have been rightly criticized for decades as being unable to disentangle the potential influences of genes and environment, schizophrenia adoption studies were performed in an attempt to finally accomplish a clean separation between these potential influences. Adoptees inherit the genes of their biological (birth) parents, but are reared in the environment of another (adoptive) family with whom they share no genetic relationship. However, a closer look at these studies reveals many potentially invalidating problem areas.

We must always remember that the “adoptees” in these studies were children abandoned by, or taken from, their birthparent(s) for various reasons, often under difficult conditions. Many of these children experienced attachment-rupture trauma, emotional suffering, loneliness and neglect, abuse, and other types of hardships. This was especially true for the late-separated children, and for children who spent time in an orphanage. A more fitting name for this area of research would be the study of abandoned children. This term evokes a different set of emotional responses than the more positive, trauma-obscuring term “adopted children” (positive in the sense that it places emphasis on the fact that children were placed into adoptive homes, not on how they got there).32

A pair of behavioral geneticists summarized the powerful impact of the Oregon and Danish-American schizophrenia adoption studies in supporting genetic theories, writing, “When a single theory is monolithic in a field, contrary findings can break paradigms. . . . It is just this role, we believe, that the first adoption studies of schizophrenia played in the 1960s.”33 These studies also played a major role in reviving the psychiatric genetics field, with a pair of prominent supporters of that field believing that they provided “the straw that broke the environmentalist’s back.”34

The Danish-American studies by American psychiatric researchers Seymour Kety, David Rosenthal, Paul Wender, and their Danish colleagues such as Fini Schulsinger and Joseph Welner, are the most frequently cited investigations. The story that mainstream sources fail to tell, however, is that these studies’ glaring and massive flaws, biases, and arbitrary after-the-fact juggling of diagnoses helped ensure that the researchers would arrive at conclusions in favor of genetics. To find these glaring flaws and biases it is not necessary to comb the archives, or to uncover unpublished documents and smoking guns. They are found, for the most part, by reading the investigators’ publications closely, and by understanding the history and methods of psychiatric genetic research as well as the motivations and biases of the original investigators and their backers.

In the first five adoption studies of schizophrenia, the researchers compared the diagnostic rate of their schizophrenia “index” group (experimental group) adoptees or biological relatives, versus the diagnostic rate of their control group adoptees or biological relatives. Lichtenstein and colleagues did not use an adoption control group. The Kety-led and Wender-led studies began with adoptees as the first-identified relative (the psychiatric genetic term for the first-identified relative is “proband”). The Heston, Rosenthal-led, Tienari-led, and Lichtenstein-led studies began with diagnosed biological parents as the first-identified relative. These studies are as follows:

(1) Heston’s Oregon Study. In 1966, psychiatric researcher Leonard Heston assessed the rate of schizophrenia among the 47 adopted-away biological offspring of women diagnosed with schizophrenia, who were confined to Oregon state mental hospitals.35 Heston, who was not blind to the group status of the adoptees, found five schizophrenia diagnoses among his 47 experimental group adoptees, versus zero among the 50 control adoptees, a result that just reached statistical significance.36

(2) The Kety-Led Danish-American Studies. In the most-frequently cited of the three major Danish-American adoption studies, Kety, Wender, Rosenthal and their colleagues’ 1968 Danish-American “Adoptees’ Family Study” began with the records of 5,483 Danish children adopted by non-relatives in the city and county of Copenhagen between 1924 and 1947. The investigators diagnosed 33 of these adoptees with a “schizophrenia spectrum disorder.”37 These became the “index adoptees.” A matched control group was established, which consisted of 33 adoptees with no record of admission to a Danish psychiatric facility. Kety and colleagues then made blind, hospital-record based consensus diagnoses for the 306 identified biological relatives of these index and control adoptees. The same procedure was performed for the 157 index and control adoptive (rearing) relatives.

In a widely cited 1975 follow-up, the investigators reevaluated many of the 1968 Copenhagen relative diagnoses. They undertook the difficult task of tracking down and attempting to interview these index and control relatives. They believed that there were many more schizophrenia-related disorders in the population that had not come to the attention of mental health facilities or hospitals, and were therefore unrecorded. The interviews were performed by the Danish members of the research team, and were written up in English as a 35-page transcript. These transcripts were edited to remove information that could indicate the relative’s group status, and were sent to Kety, Wender, and Rosenthal, who made blind consensus psychiatric diagnoses. The code was then broken, and the relatives (and their possible diagnoses) were allocated to their respective groups. The Copenhagen biological relative group had now grown to 347 (173 index, 174 control).

After the completion of the 1968 record-based and 1975 interview-based studies based on the Copenhagen data, the investigation was extended to the remaining provinces of Denmark. The final interview-based “Provincial Sample” results were published in 1994. The Copenhagen and Provincial results were combined to produce the “Danish National Sample.”38

(3) The Rosenthal-Led Danish-American Studies. Rosenthal and colleagues’ 1971 “Adoptees Study” investigated the 76 adopted-away biological offspring of Danish parents diagnosed with schizophrenia, “schizophrenia spectrum disorders,” or manic depression.39

(4) The Wender-Led Danish-American Studies. In the least-frequently cited Danish-American study, the 1974 “Crossfostering Study” by Wender, Kety, Rosenthal and colleagues, the researchers investigated the adopted-away biological offspring of Danish parents not diagnosed with schizophrenia, but who were raised by an adoptive parent eventually diagnosed with schizophrenia.40

(5) The Tienari-Led Finnish Studies. In contrast to the earlier investigations, Pekka Tienari and colleagues’1980s-2000s “Finnish Adoptive Family Study of Schizophrenia” took the important step of looking at adoptive family environments as well as adoptees’ genetic background.41 Their index group consisted of the 190 adopted-away biological offspring of mothers diagnosed with schizophrenia and other “schizophrenia spectrum disorders.” Tienari and colleagues reported a statistically significant index versus control difference for the “schizophrenia spectrum” disorders combined. For chronic schizophrenia alone, however, there was no statistically significant difference.42 They concluded that in addition to genetic background, adoptive family environments “were a significant predictor of schizophrenia spectrum disorders in adoptees.”43

(6) The Lichtenstein-Led Swedish Study. In 2009, Paul Lichtenstein and colleagues used hospital and population records of Swedish parents and children (including some adoptees) to assess whether schizophrenia and bipolar disorder are genetically distinct disorders. Based on these records, they found an elevated schizophrenia risk among the adopted-away biological offspring of parents diagnosed with schizophrenia. They did not state how many adoptees were studied.44

Major Problem Areas of the Danish-American Adoption Studies

In all schizophrenia adoption studies, the investigators concluded that genetic factors play an important role, while Tienari added the finding that disturbed family environments also play an important role. However, these studies have been the subject of several major critical analyses. The groundbreaking Danish-American investigations headed by Kety and Rosenthal are the most frequently cited studies.45

At the close of the June/July, 1967 conference that saw the Danish-American investigators’ first public presentation of their results, Rosenthal noted that environmentally oriented researchers like to focus on people (“patients”), whereas genetically oriented researchers prefer to focus on numbers and statistics.46 The Danish-American researchers epitomized the “numbers and statistics” approach, and their publications treated schizophrenia as if it were a common medical condition. The compelling human experience of psychosis, and the relationships, environments, oppression, and other social contexts that help produce it, are largely absent from their publications. In their place are numbers, diagnoses, tables, statistical tests of significance, population and psychiatric registers, and degrees of genetic relationship—all presented in a not-so-neat package that nonetheless led to the conclusions that psychiatry and other vested interests needed.

The major problem areas in the Danish-American adoption studies are discussed below, although by no means are they the only problem areas. The following points have been made by the critics over the years, and I have added a few new ones for good measure.

• The Danish-American investigators decided to expand the definition of schizophrenia to include what they called schizophrenia spectrum disorders, and they would not have found statistically significant results without such an expansion. Danish-American schizophrenia spectrum disorders (also referred to here as “spectrum” disorders), as described in the 1968 Kety-led study, included “chronic schizophrenia,” “acute schizophrenia,” “borderline schizophrenia” (also called “latent schizophrenia”), “uncertain chronic schizophrenia,” “uncertain acute schizophrenia,” “uncertain borderline schizophrenia,” and “inadequate personality.” The researchers decided to count all these, including the “inadequate personality” and “uncertain” cases, as schizophrenia.

The 1968 Kety-led study found zero cases of chronic schizophrenia among the 65 identified first-degree biological relatives of the index adoptees, and the 1971 Rosenthal-led study found that only 1 of the 76 adopted-away biological offspring of a parent diagnosed with a schizophrenia spectrum disorder had received a hospital diagnosis of chronic schizophrenia. Had the researchers decided to count only these chronic cases—as schizophrenia was defined in Denmark—they would have had found no evidence that schizophrenia has a genetic component.47 As Rosenthal subsequently admitted, “If we had relied only on hard-core, process [chronic schizophrenia] cases, we would have found no significant difference between our index and control subjects.”48

• Although the investigators cited other reasons in their most important publications, the main reason that they decided to widen the definition of schizophrenia to include “schizophrenia spectrum disorders” was to have enough cases to be able to conduct their study. In a little-known 1971 article, Rosenthal basically admitted as much.49 Rosenthal also acknowledged elsewhere, “It seems somewhat ironic that…Paul Wender and I…in concert with Seymour Kety [were] in effect broadening the concept of schizophrenic disorder as widely as it may have ever been reasonably conceived before.” The researchers, according to Rosenthal’s account, “strained to encompass all disorders that shared salient clinical and behavioral manifestations with process [chronic] schizophrenia and to group these as a spectrum of schizophrenic disorder.”50

Although the researchers described the spectrum in their original 1968 publication, there is no evidence that they created this expanded definition of schizophrenia before they searched the Danish adoptee and relative records, and arrived at their initial diagnoses. The necessity of creating a spectrum was due to the investigators finding only 16 cases of chronic schizophrenia among the 5,483 identified adoptees, when 38-40 cases would have been expected on the basis of population statistics.51 This sample of 16 chronic schizophrenia adoptees was, as Rosenthal acknowledged, a “lower than expected yield,”52 which was “too small to make any of these studies meaningful.”53

• “Uncertain” diagnoses should not have been counted as “schizophrenia” in these studies, and certainly not the doubly vague “uncertain borderline schizophrenia” diagnosis. According to Kety, “in the case of the relatives, questionable or uncertain schizophrenia had to be added if relatives with less certain diagnoses were not to be lost.”54 Perhaps so, but Kety could have prevented these relatives from becoming “lost” without counting them as schizophrenia in his study’s statistical calculations.

In the 1975 Kety-led study, “uncertain” diagnoses represented 35% (13/37) of all index biological relative spectrum diagnoses, and another 13 were diagnosed with “schizoid or inadequate personality” (which the researchers called “Category C”). Together, these “uncertain” and “inadequate personality” diagnoses accounted for over 70% (26/37) of all index biological relative diagnoses.55

• Schizophrenia and the spectrum disorders were poorly defined by the investigators, with Kety admitting, amazingly, that their diagnostic descriptions were “necessarily vague,”56 with a “lack of sharp boundaries.”57 Kety and colleagues frequently claimed that they based their diagnoses on Eugen Bleuler’s original 1911 descriptions of schizophrenia and “latent schizophrenia,” and they used the terms “borderline schizophrenia” and “latent schizophrenia” interchangeably in the Copenhagen study. Bleuler, however, believed that “only a few isolated psychotic symptoms can be utilized in recognizing” schizophrenia, and therefore demanded a “very high diagnostic threshold value” for identifying it. Bleuler believed that mild or “simple” schizophrenia could only be diagnosed retrospectively, after a person had manifested much more serious symptoms.58 Kety and colleagues, on the other hand, explained that they diagnosed people with latent schizophrenia in the “absence of frank delusions or other psychotic symptoms.”59

• The investigators claimed that the Kety-led 1968 and 1975 results showed that “borderline schizophrenia” was genetically related to chronic schizophrenia, because it was significantly concentrated in the index biological relative group compared with the control group. They made a similar claim about the 1994 Kety-led Provincial Sample study.60 However, they used improper methods of counting and combining diagnoses to arrive at this conclusion. An examination of their results, based on proper methods of counting, leads to the opposite conclusion.61

• The 1975 Kety-led study found an 11% schizophrenia spectrum disorder rate (19/174) among all control biological relatives. Based on the prevailing Danish chronic schizophrenia population expectation of about 0.7%, we would expect one or two of these 174 biological relatives of non-diagnosed control adoptees to have been diagnosed with chronic schizophrenia by chance.62 This indicates that the researchers expanded the definition of schizophrenia so widely, that it produced roughly a ten-fold increase of “schizophrenia” in Denmark.

• Although the purpose of the Kety-led studies was to determine whether genetic factors play role in causing schizophrenia, the spectrum concept itself implicitly assumed that chronic schizophrenia is genetically based. The researchers then attempted to determine whether the various spectrum disorders were “genetically related” to an already assumed-to-be-genetic “chronic schizophrenia.”

• The purpose of the Rosenthal-led studies was to test the components of the “assumed diathesis” (genetic predisposition) of schizophrenia, and one of the study’s four assumptions was that “heredity was an important contributor to schizophrenia.”63 However, in their 1971 report the investigators concluded that “the evidence supports the theory that heredity plays a significant role in the etiology of schizophrenia spectrum disorders.”64 This conclusion is not valid, as a goal of the study was to investigate the components of an already assumed genetic basis of schizophrenia. The study therefore revolved around the investigators’ circular argument which saw them assume and conclude the very same thing.

• The investigators engaged in the unsound research practice of “data dredging” (also known as a “data fishing”), which involves searching through the data in an attempt to find statistically significant trends or differences, without testing a prior hypothesis. They assessed their data through the after-the-fact selection and creation of diagnoses and comparisons that allowed them to conclude in favor of genetics.

In 1976, after the publication of the Kety-led 1968 and 1975 studies, the researchers wrote, “The schizophrenia spectrum was and still is a hypothesis or group of hypotheses on which we hoped our continuing studies might cast some light.”65 Data dredging occurs when researchers commit the error of testing a hypothesis and reaching a conclusion based on that hypothesis, in the same study. Identifying correlations and potential factors can be useful to help arrive at a hypothesis, but the hypothesis must then be tested on a new set of data. As the authors of a medical textbook put it, in their discussion of data dredging:

“The scientific process requires that hypothesis development and hypothesis testing be based on different data sets. One data set is used to develop the hypothesis or model, which is used to make predictions, which are then tested on a new data set” (emphasis in original).66

Yet Kety, Rosenthal, Wender, and their Danish colleagues’ method was to develop and test their hypotheses at the same time, in the same study. It has been said that this method is similar to drawing a bullseye (the hypothesis) around a shot arrow (the data), and then claiming that the bullseye was hit, as opposed to shooting an arrow towards the bullseye in an attempt to hit it.

 In the Kety-led studies, the researchers counted spectrum diagnoses among first-degree biological relatives (e.g., siblings, 50% genetic resemblance) and second-degree biological relatives (e.g., half-siblings, 25% genetic resemblance) with equal weighting. Contrary to genetic predictions, there were more spectrum diagnoses among the half-siblings. Amazingly, 25% of the index half-sibs received a spectrum diagnosis in the 1975 study.67 In the mid-1970s, some leading schizophrenia researchers pointed to this excess of half-sibling spectrum diagnoses, with one noting that “genetic theory predicts a much higher risk for full siblings.”68 Another critic wrote, “This finding is peculiar and contradictory. It shows, in effect, that the less consanguinity, the greater the ‘genetic’ effect.”69 As Rosenthal once wrote, in order to “demonstrate that genes have anything to do with schizophrenia,” an investigator must show that “the frequency of schizophrenia in relatives of schizophrenics [is] positively correlated with the degree of blood relationship to the schizophrenic index cases.”70 The Kety-led studies failed this test.

 The Kety-led 1975 study found a significant concentration of spectrum disorders among their index versus control biological relatives. The researchers viewed this result as “compatible with a genetic transmission for schizophrenia, but it is not entirely conclusive.”71 Because of possible factors such as prenatal or perinatal trauma, and early mothering experiences, in the 1975 study they wrote, “One cannot, therefore, conclude that the high prevalence of schizophrenia illness found in these biological relatives of schizophrenics is genetic in origin” (emphasis added).72 This statement, unfortunately, did not prevent numerous commentators and textbook authors from concluding that this “high prevalence” did indeed show that schizophrenia is “genetic in origin.”

Kety and colleagues then made their case for the discovery of “compelling evidence” in support of the “significant operation” of genetic factors, on the basis of a comparison between the biological paternal half-siblings of their index and control adoptees:

“The largest group of relatives which we have is, understandably, the group of biological paternal half-siblings. Now, a biological paternal half-sibling of an index case has some interesting characteristics. He did not share the same uterus or the neonatal mothering experience, or an increased risk in birth trauma with the index case. The only thing they share is the same father and a certain amount of genetic overlap. Therefore, the distribution of schizophrenic illness in the biological paternal half-siblings is of great interest.”73

The researchers counted 16 spectrum diagnoses among these paternal half-siblings, but found a “highly unbalanced” diagnostic distribution (14/63 index, versus 2/64 control). They concluded, “We regard this as compelling evidence that genetic factors operate significantly in the transmission of schizophrenia.”74 However, Kety and colleagues would have found no statistically significant difference if they had included all schizophrenia spectrum diagnoses in this comparison. In the 1968 and 1975 Kety-led studies, and in the Rosenthal-led studies, the investigators still counted “schizoid or inadequate personality” (Category C) as a schizophrenia spectrum disorder.75 However, they removed Category C diagnoses from their “compelling” 1975 paternal half-sibling comparison. As seen on page 418 of a 1976 Danish-American publication, the index versus control spectrum diagnosis difference is not statistically significant when spectrum Category C is included (18/63 index, versus 11/64 control; probability = .094).76 In order to obtain the desired results, in their 1975 publication Kety and colleagues excluded Category C from their paternal half-sibling comparison, but not from the (constantly changing) spectrum itself.

This means that the comparison identified by Kety and colleagues as providing “compelling evidence” in support of genetics was not statistically significant according to their own 1975 definition of the schizophrenia spectrum—a fact that no mainstream psychiatry or psychology textbook that I am aware of has ever mentioned.

The 1975 paternal half-sibling comparison is an obvious example of data dredging. The investigators searched through their results until they found a comparison that they believed supported the genetic transmission of schizophrenia, and then concluded that this comparison provided compelling evidence in favor of such transmission. The proper method would have been to refrain from reaching this conclusion, but instead to note that the comparison generated an interesting hypothesis that could be tested in a future study. In the subsequent Provincial Sample attempt to “replicate” the Copenhagen results, there were 40 identified biological paternal half-siblings of the 29 chronic schizophrenia index adoptees. Not one of these paternal half-siblings was diagnosed with chronic schizophrenia.77

• In the Kety-led 1968 study, the researchers appear to have changed the study’s design after the initial relative group comparisons failed to obtain statistically significant results in the genetic direction.78

• For Rosenthal, it was enough for a person to be “cold, distant and inadequate, or odd and eccentric” to qualify as having a “schizophrenic-like type of disorder.”79 Being judged as a “pervert” also qualified.80 The researchers referred to same-sex attraction as a symptom of schizophrenia in all but one of their original 1968 spectrum diagnoses.81  Although they based these diagnoses on DSM-II descriptions, sexual orientation (or “homosexuality”) was not mentioned in any of the DSM-II descriptions of schizophrenia.82

• In the Rosenthal-led studies, the researchers counted “manic-depression” as a “schizophrenia spectrum disorder”83 despite their insistence elsewhere that schizophrenia and manic-depression are “genetically distinct and different disorders.”84 Without these manic-depressive cases, Rosenthal and colleagues would not have been able to claim statistically significant results in the genetic direction in their 1971 publication.85 In a 1978 publication that saw the first-ever reporting of the researchers’ final Adoptees Study consensus diagnoses, there was no statistically significant difference (33% versus 25%) between the index and control adoptees on the basis of an investigator-defined schizophrenia spectrum consisting of chronic schizophrenia, borderline schizophrenia, and “schizophrenic personality.”86

• In the Kety-led studies, there were inconsistencies in the way that the researchers decided to count and diagnose dead or unavailable relatives.

• The researchers failed to provide case history information for adoptees or relatives, and failed to study important environmental variables.

• In the Kety-led studies, a critic noted in 1976 that the “procedure of counting up all the possible relatives of each index case and pooling them as if they were independent samples . . . would allow some families to disproportionately affect the results.”87 Although Kety and colleagues did address this issue, their decision to emphasize the diagnostic rate among individual relatives, as opposed to individual families, violated the assumption of independent observations underlying the statistical methods they used. Because family environments may play a role in causing schizophrenia and psychosis, genetic study diagnoses given to people raised in the same family environment are not independent observations, because they shared this environmental factor in common.

• The researchers decided to include many late-separated and late-placed adoptees (abandoned children) in their samples. Therefore, during sensitive developmental periods, these adoptees (1) were reared for a certain period of time by their biological parent(s), (2) suffered a disruption of attachment bonds with their biological parent(s), and/or (3) were placed in unstable environments between separation and adoption.

• Substandard interviews were used to make diagnoses. In the Kety-led studies many of these “interviews” never took place, but instead were fabricated by the investigators on the basis of hospital records.88 In the raw data Kety called them “pseudointerviews,” but no mention of their existence appeared in any Danish-American publication. Of the interviews that were conducted, the researchers believed that they could make a psychiatric evaluation of a reluctant interviewee on the basis of a five-minute doorstep conversation.89

• Problem areas in the Kety-led 1994 “Provincial Sample” attempt to “replicate” the earlier Copenhagen results in the rest of Denmark include the following points: (1) The study was subject to most of the problems and biases found in the 1968 and 1975 studies, and there was selective placement bias in the sample (see below). (2) Without adequate justification, the investigators decided to reduce the size of their control group from 42 to 24, seventeen years after beginning the study.90 (3) The two diagnoses used in the study were “latent schizophrenia” (similar to the Copenhagen “borderline” diagnosis) and “chronic schizophrenia,” and there was no statistically significant first-degree biological relative index group elevation of the former when compared with controls.91 (4) The symptoms of “latent schizophrenia” were vague, and were often indistinguishable from non-spectrum psychiatric diagnoses. (5) The researchers counted a total of 3 diagnoses of “chronic schizophrenia” among the 24 first-degree biological full-siblings of the 29 index adoptees with the same diagnosis. However, all three were members of the same family, suggesting that family environment, rather than genetic background, best explains this clustering of chronic schizophrenia among three siblings reared in the same family.92

• Problem areas in the Wender-led 1974 “Crossfostering Study” include: (1) The use of global mental health ratings in place of diagnosing schizophrenia. (2) The use of post data-collection comparisons to support the genetic position. (3) The failure to find statistically significant differences between important comparison groups. (4) The investigators’ failure to consider non-genetic explanations of their results. (5) The average age of the crossfostered adoptees at the time of their parent’s diagnosis was 12 years old.

• Subsequent “independent” reanalyses of the Danish-American data by other groups, based on “operationalized diagnostic criteria,” contained numerous flaws and biases, and did little to “confirm” the original researchers’ (incorrect) conclusions in favor of genetics.93

* * *

The basic story of the Danish-American schizophrenia adoption studies is that, after several years of painstaking research in Denmark in the early-to-mid 1960s, the investigators found no evidence that chronic schizophrenia was caused by hereditary factors. Instead of acknowledging this, and publishing these negative results with little fanfare or recognition of scientific discovery, Kety, Rosenthal, Wender and their Danish colleagues decided to risk opening up a “Pandora’s box” by greatly expanding the definition of schizophrenia94 — Rosenthal admitted that they “strained” to do so—in an attempt to find results that confirmed their pre-existing belief that genetic factors underlie schizophrenia.

As seen clearly in their published works, the investigators used admittedly “vague” diagnostic criteria while expanding the definition of schizophrenia “as widely as it may have ever been reasonably conceived before,” arbitrarily and fallaciously included and rejected various spectrum diagnoses, changed definitions and comparison groups after obtaining and reviewing the data, removed spectrum diagnoses from “compelling” index-control comparisons to achieve significant results, counted “uncertain borderline schizophrenia” and “inadequate personality” diagnoses as “schizophrenia,” counted “manic-depression” as a schizophrenia spectrum disorder, included being gay (“homosexuality”) as a diagnostic indicator of schizophrenia, misinterpreted E. Bleuler’s original diagnostic descriptions, assumed the genetic basis of schizophrenia in the processes of testing for it, violated statistical assumptions, failed to provide adoptees’ life history information, and used differing and inconsistent methods of counting diagnoses and relatives.

This illustrates how conclusions drawn from ostensible scientific experiments are transformed into a statement of the investigators’ beliefs. Genetic research has a long history of these types of conclusions, going all the way back to Galton. The “results” of these massively flawed studies are then rubber stamped by psychiatry textbooks and review articles, and by similar publications in the related fields, and generations of students, clinicians, “patients,” researchers, and others are greatly misled about the true causes of schizophrenia and psychosis.

Selective Placement:
The Achilles’ Heel of Schizophrenia Adoption Research

A critical aspect of psychiatric adoption research is the often unstated “no selective placement assumption.” This requires investigators to assume that factors relating to the adoption process (including the policies of adoption agencies) did not lead certain groups of adoptees to be placed into environments contributing to a higher rate of the condition in question. The investigators must assume that children were not systematically placed into adoptive homes correlated with the socioeconomic status—or presumed genetic status—of their biological families. In many psychiatric adoption studies, however, the evidence suggests that experimental (index) group adoptees did experience more psychologically harmful rearing environments than those experienced by the control adoptees. Children with a biological family history of mental disorders were seen as inferior potential adoptees, and therefore were placed into more chaotic and psychologically harmful (and potentially “schizophrenogenic”) adoptive families.

Most adoptees (abandoned children) were placed in the early-to-middle part of the 20th  century in Denmark, the United States (Oregon), and Finland. The Swedish study index relatives were born between 1932 and 2002. Although rarely mentioned by the original authors or by the authors of secondary sources, all four regions had laws permitting the compulsory eugenic sterilization of people labeled “schizophrenic,” “insane,” “feeble-minded” and so on. Society and scientists alike viewed as axiomatic that the offspring of “insane” people were the undesirable and dangerous carriers of “hereditary taint,” worthy of sterilization and other eugenic measures. Mid-20th century schizophrenia researcher Manfred Bleuler (the son of Eugen Bleuler) described the “sinister shadow” of “familial tainting” during this era, which obviously played a major role in the adoption process:

“If one knows schizophrenics and their families well, it is sometimes a matter for despair to see how much they suffer under the terrible concept of ‘familial tainting.’ Like a sinister shadow it darkens the lives of many people and of entire families. The stifling, uncertain fear of coming from an ‘inferior breed,’ of carrying within one’s self the seeds of something pathological, morbid, and evil (I am speaking in the jargon the afflicted apply to themselves), like a curse that you must pass on to someone else, causes oppressive feeling of inferiority.”95

Denmark. In 1929 Denmark became the first European nation to pass a eugenics-inspired sterilization law.96 This law (a stronger law passed in 1935) was in force until well after the last studied Danish adoptees were placed (placements were made between 1924 and 1947). The forced sterilization of the “insane” and others in Denmark continued well into the 1960s.

The Danish adoption agencies checked a potential adoptee’s perceived genetic family background to determine his or her suitability (or desirability) for adoption. When an agency suspected a family history of mental disorders, it consulted the Danish Institute of Human Genetics, which was the keeper of the Danish National Psychiatric Register.97 The Register was established in 1937, and included the names of people diagnosed with mental disorders, and people who had been psychiatrically hospitalized.98 It was established at a time when eugenic ideas were at their high point in Denmark (and in the world as a whole), and was used to aid eugenic selection programs. It is therefore ironic that the Psychiatric Register, which enabled the Danish-American adoption studies to be performed, was established in order to aid eugenic programs and eugenics-influenced adoption placement decisions.

According to one account, “Every weekend (at least in the 1930s), Danish people who wished to adopt would visit the orphanages and pick children. . . . Children whose selection by an adoptive parent is delayed may be less attractive physically and behaviorally.”99 Many children were also perceived as being less attractive genetically. Clearly, the most loving and stable potential adoptive parents, who were usually informed of “deviance” in the adoptee’s family background, would not have picked children “tainted” by a family history of mental disorders.

Kety believed that his “Adoptees’ Family” design was less vulnerable to selective placement factors because it began with diagnosed adoptees, in contrast to studies that began with diagnosed parents.100 However, although he and his colleagues did not mention this, in 8 of the 33 Copenhagen index adoptive (rearing) families, but in none of the 34 Copenhagen control adoptive families, a parent had been admitted to a mental hospital at some point.101 This suggests that Kety’s index adoptees were placed into more psychologically unstable adoptive homes than were the control adoptees.

Oregon. Similar conditions existed in Oregon, where adoptees were placed between 1915 and 1945. Although Heston failed to mention it, Oregon passed a law in 1917 creating a “State Board of Eugenics,” whose duty was to authorize the compulsory sterilization of “all feeble-minded, insane, epileptic, habitual criminals, moral degenerates and sexual perverts,” because they might produce “inferior” offspring.102 An additional Oregon law passed in 1919 stipulated that, if a person had been admitted to a mental hospital, this constituted “prima facie evidence that procreation by any such person would produce children with an inherited tendency to feeble-mindedness, insanity, epilepsy, criminality or degeneracy.”103 The author of a 1925 article wrote approvingly that while sterilization laws in many U.S. states were limited to “inmates of institutions,” in Oregon “there is a Eugenics Commissioner, who has authority to comb the state for degenerates and enforce sterilization.”104 Because Heston’s index adoptees were born to women hospitalized with schizophrenia, it is very unlikely that the “tainted” children they gave birth to were placed into the same types of adoptive homes as were the “non-tainted” control children.

A 1929 article by eugenicist Paul Popenoe captured the thinking of the times. He believed, in general, that American adoptees’ “ancestry” was not “up to par,” although “the best are sorted out early by the child-placing agencies. The remainder, collected in orphanages, represent predominantly the inferior levels and usually show up badly in tests.” Indeed, 25 of the 47 Heston index adoptees had spent months or years “collected in an orphanage.”105 Popenoe advised potential adoptive parents to “pick out a child with as good ancestry as possible,” which in “the mother is always known.”106 Clearly, the “inferior” biological offspring of “insane” mothers were not seen as desirable potential adoptees.

Finland and Sweden. In 1935 the Finnish Parliament passed the Sterilization Act, which allowed the compulsory eugenic sterilization and castration of “idiots,” “imbeciles,” and the “insane,” which included people diagnosed with schizophrenia and manic-depression.107 In 1950, Finland passed the Castration Act, which permitted the compulsory castration of criminals, the mentally retarded, and the “permanently mentally ill.” Compulsory eugenic sterilization was not legally abolished in Finland until 1970. Significantly, up to one-third of Tienari’s index adoptees were placed after their mother was diagnosed as psychotic.108 Sweden also had a long history of eugenics and compulsory eugenic sterilization.109


It appears that selective placement factors introduced a major environmental confound  into all schizophrenia adoption studies, suggesting that like family and twin studies, the results can be explained by non-genetic factors. Adding this factor to these studies’ other massive methodological problems and biases, they clearly provide no scientifically acceptable evidence that disordered genes play a role in causing schizophrenia and psychosis.


The “established fact” in psychiatry that schizophrenia is caused in large part by disordered genes speaks volumes about the discipline’s failure to critically analyze the methods and assumptions of its own research, a practice that occurs in other behavioral fields as well. In countless textbooks in psychiatry, psychology, and the related fields, we find the same uncritical acceptance of the conclusions of twin and adoption researchers. Too often, these textbooks provide an inaccurate presentation of the evidence supporting the genetic position, and only a handful attempt some kind of critical analysis. It follows that few psychiatrists or behavioral scientists question the twin method’s equal environment assumption, or read through the often tedious original schizophrenia adoption study publications.

Psychiatry’s largely uncritical acceptance of the conclusions of schizophrenia twin and adoption researchers is an appalling development in the history of scientific research, and can be understood in part by its interest in maintaining itself as a viable and legitimate branch of medicine. Genetic theories also aid the interests of the social and political elites, and the interests of the psychopharmaceutical industry, to locate the causes of psychological dysfunction and psychosis within people’s bodies and brains, as opposed to the real causes, which are psychologically unhealthy aspects of their familial, social, and political environments.110 It is not surprising, therefore, that despite psychiatry’s failure to identify biological or genetic markers for its disorders, these groups continue to channel research funding in the genetic and biological direction.

As superbly reviewed by John Read, since the turn of the 21st 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, sexual abuse —findings that are well known to clinicians who work with people diagnosed with psychotic disorders.111 Read reviewed the evidence linking schizophrenia and other psychotic disorders to social environments 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.”112 Psychological processes through which childhood adversities may lead to symptoms of psychosis later in life include attachment, dissociation, dysfunctional cognitive processes, psychodynamic defenses, problematic coping responses, impaired access to social support, behavioral sensitization and revictimization.113

The ongoing failure to make confirmed discoveries of schizophrenia susceptibility genes is the result not of a “missing heritability” problem, but of psychiatry’s “missing critical analysis of schizophrenia family, twin, and adoption research” problem. Once this is understood, science and society will at last be able to focus on the real causes of schizophrenia and psychosis.

The time has come to call a halt to the massive failure that has characterized schizophrenia molecular genetic research, and to undertake a thorough reassessment of the original family, twin, and adoption studies, which inspired the fruitless search for genes in the first place. As the mainstream authors of an article on the “facts” of schizophrenia concluded, “A reconsideration of our basic strategies and fundamental assumptions may be in order.”114 Indeed, this is long overdue, and the environmental causes of “schizophrenia” and psychosis must become the main focus of both research and societal attention.115

* * * * *


1. Bailey, J. M., & Pillard, R. C., (1993), Reply to Lidz’s “Reply to ‘A Genetic Study of Male Sexual Orientation’” [Letter to the Editor], Archives of General Psychiatry, 50, 240-241, p. 241.

2. Read, J., (2013d), “The Invention of Schizophrenia,” in J. Read & J. Dillon (Eds.), Models of Madness: Psychological, Social and Biological Approaches to Psychosis (2nd  ed.; pp. 20-33), London: Routledge, p. 32.

3. Turkheimer, E., (2015), Arsonists at the Cathedral, PsycCRITIQUES, 60 (40), 1-4. DOI: a0039763. For a response to Turkheimer, see my November, 2, 2015 MIA blog posting.

4. Kendler, K. S., (2014), A Joint History of the Nature of Genetic Variation and the Nature of Schizophrenia, Molecular Psychiatry, 20, 77-83, p. 77.

5. Elston et al., (1973), Possible Linkage Relationships between Certain Blood Groups and Schizophrenia or Other Psychoses, Behavior Genetics, 3, 101-106, p. 105.

6. Sherrington et al., (1988), Localization of a Susceptibility Locus for Schizophrenia on Chromosome 5, Nature, 336, 164-167, p. 164.

7. Cloninger, C. R., (2002), The Discovery of Susceptibility Genes for Mental Disorders, Proceedings of the National Academy of Sciences, 99, 13365-13367.

8. Anonymous, (2003), Scientific Breakthrough of the Year: The Runners-Up, Science, 302, 2039-2045, p. 2039.

9. Previous postings/articles on the fruitless search for genes in psychiatry include:
Five Decades of Gene Finding Failures in Psychiatry, The Latest Gene Finding Claim in PsychiatryTwin Studies and the “Nonreplication Curse” in Psychiatric Molecular Genetic Research, and Quotations From the Genetics “Graveyard”: Nearly Half a Century of False Positive Gene Discovery Claims in Psychiatry.

10. Joseph, J., (2012), The “Missing Heritability” of Psychiatric Disorders: Elusive Genes or Non-Existent Genes?, Applied Developmental Science, 16, 65-83. See also Chaufan, C., & Joseph, J., (2013), The Heritability of Common Disorders is “Missing”: Should Health Researchers Care?, International Journal of Health Services, 43, 281-303.

11. American Psychiatric Association, (2013), Diagnostic and Statistical Manual of Mental Disorders (5th ed. [DSM-5]), Arlington, VA: Author, p.103.

12. Kirk et al., (2013), Mad Science: Psychiatric Coercion, Diagnosis, and Drugs, New Brunswick, NJ: Transaction.

13. Read, J., (2013b), “Does ‘Schizophrenia’ Exist?,” in J. Read & J. Dillon (Eds.), Models of Madness: Psychological, Social and Biological Approaches to Psychosis (2nd ed.; pp. 47-61), London: Routledge.

14. American Psychiatric Association, 2013, p. 103.

15. Rosenthal, D., (1974b), “The Genetics of Schizophrenia,” in S. Arieti & E. Brody (Eds.), American Handbook of Psychiatry (2nd ed., pp. 588-600), New York: Basic Books, p. 589.

16. Andreasen, N. C., (2000), Schizophrenia: The Fundamental Questions, Brain Research Reviews, 31, 106-112, p. 109.

17. Some schizophrenia family studies found no significant elevation among first-degree biological relatives; see Joseph, J., (2006), The Missing Gene: Psychiatry, Heredity, and the Fruitless Search for Genes, New York: Algora, Chapter 6.

18. Glatt et al., (2008), “Psychiatric Genetics: A Primer,” in J. Smoller et al., (Eds.), Psychiatric Genetics: Applications in Clinical Practice (pp. 3-26), Washington, DC: American Psychiatric Publishing, pp. 6-7.

19. Research performed in the 21st century has called into question the basic twin study assumption that both members of an MZ pair are genetically identical throughout their lives; see Charney, E., (2012), Behavior Genetics and Postgenomics, Behavioral and Brain Sciences, 35, 331-358.

20. Joseph, J., (2013), “‘Schizophrenia’ and Heredity: Why the Emperor (Still) Has No Genes,” in J. Read & J. Dillon (Eds.), Models of Madness: Psychological, Social and Biological Approaches to Psychosis (2nd ed.; pp. 72-89), London: Routledge, p. 74.

21. Sullivan et al., (2003), Schizophrenia as a Complex Trait: Evidence from a Meta-Analysis of Twin Studies, Archives of General Psychiatry, 60, 1187-1192.

22. See also Fosse, R., Joseph, J., & Jones, M., (2015), Schizophrenia: A Critical View on Genetic Effects, Psychosis (published online September 14th). DOI: 10.1080/17522439.2015.1081269

23. Joseph, J., (2015), The Trouble with Twin Studies: A Reassessment of Twin Research in the Social and Behavioral Sciences, New York: Routledge. See also Jackson, D. D., (1960), “A Critique of the Literature on the Genetics of Schizophrenia,” in D. Jackson (Ed.), The Etiology of Schizophrenia (pp. 37-87), New York: Basic Books.

24. Fosse R., Joseph J., & Richardson, K, (2015), A Critical Assessment of the Equal Environment Assumption of the Twin Method for Schizophrenia, Frontiers in Psychiatry, 6:62, DOI: 10.3389/fpsyt.2015.00062

25. See Joseph, 2006, p. 129. The pooled DZ schizophrenia concordance rates are same-sex 59/523 (11.3%), and opposite-sex 20/422 (4.7%). An additional 2007 study of 29,602 Swedish twin pairs, which recorded hospitalization rates for psychosis and other psychiatric disorders, revealed that same-sex DZ psychosis correlations again were 2-3 times higher than the opposite-sex DZ correlations. See Prescott et al., (2007), Twin Pair Resemblance for Psychiatric Hospitalization in the Swedish Twin Registry: A 32-Year Follow-Up Study of 29,602 Twin Pairs, Behavior Genetics, 37, 547-558, p. 553.

26. Joseph, J., Chaufan, C., Richardson, K., Shultziner, D., Fosse, R., James, O., Latham, J., & Read, J., (2015), The Twin Research Debate in American Criminology, Logos, 14 (Nos. 2-3), published online 8/9/2015.

27. Rosenthal, D., (1979), “Genetic Factors in Behavioural Disorders,” in M. Roth & V. Cowie (Eds.), Psychiatry, Genetics and Pathography: A Tribute to Eliot Slater (pp. 22-33), London: Oxford University Press, p. 25.

28. Fischer, M., (1971), Psychoses in the Offspring of Schizophrenic Monozygotic Twins and their Normal Co-Twins, British Journal of Psychiatry, 118, 43-51; Gottesman, I. I., & Bertelsen, A., (1989), Confirming Unexpressed Genotypes for Schizophrenia, Archives of General Psychiatry, 46, 867-872.

29. For a critical analysis of research on the offspring of discordant MZ pairs, see Joseph, J., (2004), The Gene Illusion: Genetic Research in Psychiatry and Psychology under the Microscope, New York: Algora, pp. 187-193; Torrey, E. F., (1990), Offspring of Twins with Schizophrenia [Letter to the Editor], Archives of General Psychiatry, 47, 976-977. Briefly, the design itself appears unable to adequately separate potential genetic and environmental influences, and small samples make it unlikely that statistically significant differences will be found between these offspring groups. In addition, the discordant co-twins grew up in the same family, and likely experienced similar environments and treatments. Most of the environmental factors that could have contributed to a schizophrenia diagnoses in one of the twins were probably also experienced by their “well” co-twin, who could have manifested deviant rearing patterns toward his or her offspring. There are also doubts about the accuracy of the diagnoses, especially since most of the offspring were not personally examined by the researchers. Torrey considered the case material handed down by Fischer to be “markedly unsatisfactory,” and found that none of the MZ pairs “met the basic criteria for twins with clearly diagnosed schizophrenia in the index twin and verifiable (i.e., based on interview) normality in the co-twin.”

30. Farber, S. L., (1981), Identical Twins Reared Apart: A Reanalysis, New York: Basic Books, p. 156. For more on this pair, see Joseph, 2004, pp. 185-186.

31. For my previous analyses of schizophrenia adoption research, see Joseph, 2004, Chapter 7; Joseph 2006, Chapters 3, 5, and 6.

32. Cassou et al., (1980), Génétique et Schizophrénie: Réévaluation d’un Consensus [Genetics and Schizophrenia: Reevaluation of a Consensus], Psychiatrie de l’Enfant, 23, 87-201.

33. Rowe, D. C., & Jacobson, K. C., (1999), “In the Mainstream,” in R. Carson & M. Rothstein (Eds.), Behavioral Genetics: The Clash of Culture and Biology (pp. 12-34), Baltimore: Johns Hopkins University Press, pp. 14-15.

34. Gottesman, I. I., & Shields, J., (1976), A Critical Review of Recent Adoption, Twin, and Family Studies of Schizophrenia: Behavioral Genetics Perspectives, Schizophrenia Bulletin, 2, 360-401, p. 364.

35. Heston, L. L., (1966), Psychiatric Disorders in Foster Home Reared Children of Schizophrenic Mothers, British Journal of Psychiatry, 112, 819-825.

36. For a critical analysis of Heston’s study, see Joseph, 2004, pp. 204-212.

37. There were actually 34 index adoptees. One consisted of the members of an MZ twin pair with the same relatives, who were counted as one adoptee.

38. Kety et al., (1968), “The Types and Prevalence of Mental Illness in the Biological and Adoptive Families of Adopted Schizophrenics,” in D. Rosenthal & S. Kety (Eds.), The Transmission of Schizophrenia (pp. 345-362), New York: Pergamon Press; Kety et al., (1975), “Mental Illness in the Biological and Adoptive Families of Adopted Individuals who Have Become Schizophrenic: A Preliminary Report Based on Psychiatric Interviews,” in R. Fieve et al., (Eds.), Genetic Research in Psychiatry (pp. 147-165), Baltimore: The Johns Hopkins Press; Kety et al., (1994), Mental Illness in the Biological and Adoptive Relatives of Schizophrenic Adoptees: Replication of the Copenhagen Study to the Rest of Denmark, Archives of General Psychiatry, 51, 442-455.

39. Rosenthal et al., (1971), The Adopted-Away Offspring of Schizophrenics, American Journal of Psychiatry, 128, 307-311.

40. Wender et al., (1974), Crossfostering: A Research Strategy for Clarifying the Role of Genetic and Experiential Factors in the Etiology of Schizophrenia, Archives of General Psychiatry, 30, 121-128.

41. Tienari, Sorri, et al., (1987), Genetic and Psychosocial Factors in Schizophrenia: The Finnish Adoptive Family Study, Schizophrenia Bulletin, 13, 477-484; Tienari et al., (2003), Genetic Boundaries of the Schizophrenia Spectrum: Evidence from the Finnish Adoptive Family Study, American Journal of Psychiatry, 160, 1587-1594.

42. Based on figures from Tienari at al., 2003. For a critical analysis of Tienari’s study, see Jackson, G. E., (2003), Rethinking the Finnish Adoption Studies of Schizophrenia: A Challenge to Genetic Determinism, Journal of Critical Psychology, Counselling and Psychotherapy, 3, 129-138; Joseph, 2004, Chapter 7, pp. 261-271. In their 2003 publication (p. 1590), Tienari and colleagues diagnosed DSM-III-R schizophrenia in 7 out of 137 index adoptees whose biological mothers were also diagnosed with DSM-III-R schizophrenia (5.1%). DSM-III-R schizophrenia was diagnosed in 3 of the 192 control adoptees (1.6%). Using Fisher’s Exact Test, one-tailed, the probability value for this difference = .065, which is not statistically significant at the conventional .05 level of significance.

43. Tienari et al., (2004), Genotype-Environment Interaction in Schizophrenia-Spectrum Disorders, British Journal of Psychiatry, 184, 216-222, p. 216.

44. Lichtenstein et al., (2009), Common Genetic Determinants of Schizophrenia and Bipolar Disorder in Swedish Families: A Population-Based Study, Lancet, 373, 234–239.

45. Critical analyses of the Danish-American schizophrenia adoption studies include: Benjamin, L. S., (1976), A Reconsideration of the Kety and Associates Study of Genetic Factors in the Transmission of Schizophrenia, American Journal of Psychiatry, 133, 1129-1133; Boyle, M., (2002), Schizophrenia: A Scientific Delusion? (2nd ed.), Hove, UK: Routledge; Cassou et al., 1980; Joseph, 2004, 2006, 2013; Lewontin et al., (1984), Not in Our Genes, New York: Pantheon; Lidz, T., (1976), Commentary on a Critical Review of Recent Adoption, Twin, and Family Studies of Schizophrenia: Behavioral Genetics Perspectives, Schizophrenia Bulletin, 2, 402-412; Lidz, T., & Blatt, S., (1983), Critique of the Danish-American Studies of the Biological and Adoptive Relatives of Adoptees who Became Schizophrenic, American Journal of Psychiatry, 140, 426-435; Lidz et al., (1981), Critique of the Danish-American Studies of the Adopted-Away Offspring of Schizophrenic Parents, American Journal of Psychiatry, 138, 1063-1068; Pam, A., (1995), “Biological Psychiatry: Science or Pseudoscience?,” in C. Ross & A. Pam (Eds.), Pseudoscience in Biological Psychiatry: Blaming the Body (pp. 7-84), New York: John Wiley & Sons.

46. Rosenthal, D., (1968), “The Heredity-Environment Issue in Schizophrenia: Summary of the Conference and Present Status of our Knowledge,” in D. Rosenthal & S. Kety (Eds.), The Transmission of Schizophrenia (pp. 413-427), New York: Pergamon Press.

47. For example, Kety, Rosenthal, and Wender wrote that chronic schizophrenia “is the only syndrome which merits the designation of schizophrenia in Denmark.” Kety et al., (1978), “Genetic Relationships within the Schizophrenia Spectrum: Evidence from Adoption Studies,” in R. Spitzer & D. Klein (Eds.), Critical Issues in Psychiatric Diagnosis  (pp. 213-223), New York: Raven Press, p. 214.

48. Rosenthal, D., (1972), Three Adoption Studies of Heredity in the Schizophrenic Disorders, International Journal of Mental Health, 1, 63-75, pp. 73-74.

49 Rosenthal, D., (1971b), A Program of Research on Heredity in Schizophrenia, Behavioral Science, 16, 191-201, p. 194.

50. Rosenthal, D., (1975b), “The Spectrum Concept in Schizophrenic and Manic-Depressive Disorders,” in D. Freedman (Ed.), Biology of the Major Psychoses (pp. 19-25), New York: Raven Press, p. 19.

51. For more details, see Joseph, 2006, Chapter 3.

52. Rosenthal, 1972, p. 65.

53. Rosenthal, 1971b, p. 194.

54. Kety, S. S., (1987), The Significance of Genetic Factors in the Etiology of Schizophrenia: Results from the National Study of Adoptees in Denmark, Journal of Psychiatric Research, 21, 423-429, p. 424.

55. Kety et al., 1975, p. 154.

56. Kety, S. S., (1983b), Mental Illness in the Biological and Adoptive Relatives of Schizophrenia Adoptees: Findings Relevant to Genetic and Environmental Factors in Etiology, American Journal of Psychiatry, 140, 720-727, p. 724.

57. Kety, S. S., (1983a), Dr. Kety Responds [Letter to the Editor], American Journal of Psychiatry, 140, 964.

58. Bleuler, E., (1950), Dementia Praecox or the Group of Schizophrenias, New York: International Universities Press (Originally published in 1911), pp. 238-239, 294. For a discussion of E. Bleuler’s views on schizophrenia and latent schizophrenia, versus the Danish-American researchers’ accounts of his views, see Joseph, 2006, Chapter 3, pp. 74-77.

59. Kety et al., 1994, p. 445.

60. According to Kendler and Diehl, who inspected the Kety-led Provincial Sample data while in preparation, “Latent and uncertain schizophrenia was not found to be significantly more common in the biologic relatives of the schizophrenia adoptees than in those of the control adoptees (6.5% vs. 5.5%, respectively).” See Kendler, K. S., & Diehl, S. R., (1993), The Genetics of Schizophrenia: A Current, Genetic-Epidemiologic Perspective, Schizophrenia Bulletin, 19, 261-285, p. 265.

61. For a detailed explanation of how the researchers incorrectly counted “borderline schizophrenia” and other spectrum diagnoses, see Joseph, 2006, Chapter 3. See also Joseph, 2004, Chapter 7. Most individual spectrum disorders retained by the Danish-American researchers did not, as they often put it, “discriminate between genetic relatives of schizophrenic adoptees and controls.” In the 1975 Kety-led study, there was no statistically significant “borderline schizophrenia” elevation in the index versus control biological relative groups (see Joseph, 2006, p. 67). Kety and colleagues found statistically significant results only by combining this diagnosis with chronic schizophrenia and “uncertain” spectrum diagnoses, and then concluding that all were genetically related to chronic schizophrenia. In doing so, they skipped a crucial step in determining the relationship between chronic and borderline schizophrenia. That is, they decided that individual diagnoses, standing alone, did not have to cluster significantly among their index versus control biological relatives.

62. The mid-20th century chronic schizophrenia rate in the Danish population has been given as 0.69%. See Slater, E., & Cowie, V., (1971), The Genetics of Mental Disorders, London: Oxford University Press, p. 13.

63. Rosenthal et al., (1968), “Schizophrenics’ Offspring Reared in Adoptive Homes,” in D. Rosenthal & S. Kety (Eds.), The Transmission of Schizophrenia (pp. 377-391), New York: Pergamon Press, p. 380.

64. Rosenthal et al., 1971, p. 310.

65. Kety et al., (1976), Studies Based on a Total Sample of Adopted Individuals and their Relatives: Why They Were Necessary, What They Demonstrated and Failed to Demonstrate, Schizophrenia Bulletin, 2, 413-427, p. 417.

66. Jekel et al., (2007), Epidemiology, Biostatistics, and Preventive Medicine (3rd ed.), Philadelphia: Saunders-Elsevier, p. 206.

67. Kety et al., 1976, p. 418, Table 2a.

68. Gottesman & Shields, 1976, p. 370.

69. Benjamin, 1976, p. 1131, emphasis in original.

70. Rosenthal, 1974b, p. 589.

71. Kety et al., 1975, p. 156.

72. Kety et al., 1975, p. 156.

73. Kety et al., 1975, p. 156.

74. Kety et al., 1975, p. 156.

75. Joseph, 2004; Lidz & Blatt, 1983. Kety and colleagues continued to count Category C “schizoid or inadequate personality” as a schizophrenia spectrum disorder in the 1975 Kety-led study. It was listed and counted as a spectrum disorder in Table 3 of this 1975 publication, and on page 155 they wrote, “We are not prepared to dismiss the possibility that there is a schizoid or inadequate personality which is genetically related to schizophrenia.” In a different 1975 publication (found in the same edited book), Rosenthal defended the retention of Category C in the spectrum. See Rosenthal, D., (1975a), “Discussion: The Concept of Schizophrenic Disorders,” in R. Fieve et al., (Eds.), Genetic Research in Psychiatry (pp. 199-208), Baltimore: The Johns Hopkins Press.

76. Kety et al., 1976, p. 418, Table 2a, probability = .094, by Kety and colleagues’ own calculation. This comparison is not statistically significant at the conventional .05 level of statistical probability.

77. Kety et al., 1994, p. 448, Figure 1.

78. The evidence suggests that the researchers’ original plan had been to compare diagnostic rates between their index biological versus index adoptive families, and to then do the same for the control adoptees. See Rosenthal, D., (1967), “An Historical and Methodological Review of Genetic Studies of Schizophrenia,” in J. Romano (Ed.), The Origins of Schizophrenia: Proceedings of the First Rochester International Conference on Schizophrenia, March 29-31, 1967 (pp. 15-26), New York: Excerpta Medica Foundation, p. 25; Kety, S. S., (1959), Biochemical Theories of Schizophrenia, Part II, Science, 129, 1590-1596, p. 1594. On page 25 of the 1967 Rosenthal publication, which was a paper he presented at a March, 1967 conference, Rosenthal wrote,

“In Denmark, with the collaboration of Dr. Fini Schulsinger and others, we began with adoptees who are now schizophrenic. We compare the incidence of schizophrenic disorders in their biological and adoptive families. The same procedure is carried out for a matched group of normal adoptees, who serve as controls.”

For more details, see Joseph, 2004, pp. 220-222.

79. Rosenthal, 1979, p. 23.

80. Rosenthal et al., (1968), p. 380. This index adoptee’s complete “schizophrenia spectrum diagnosis” was listed as “border-line schizophrenia or pervert.”

81. Kety et al., 1968, p. 252, Table 3.

82. American Psychiatric Association, (1968), Diagnostic and Statistical Manual of Mental Disorders (2nd ed. [DSM-II]), Washington, DC: Author, pp. 33-35.

83. See Rosenthal et al., 1971, p. 309.

84. Rosenthal, D., (1971a), Genetics of Psychopathology, New York: McGraw-Hill, p. 124.

85. Rosenthal et al., 1971. For more on this point, see Joseph 2004; Lidz et al., 1981.

86. Haier, R. J., Rosenthal, D., & Wender, P. H., (1978), MMPI Assessment of Psychopathology in the Adopted-Away Offspring of Schizophrenics, Archives of General Psychiatry, 35, 171-175, p. 174, Table 3.

87. Benjamin 1976, p. 1130.

88. Kendler, K. S., & Gruenberg, A. M., (1984), An Independent Analysis of the Danish Adoption Study of Schizophrenia, Archives of General Psychiatry, 41, 555-564, p. 556; Lewontin et al., 1984, p. 224.

89. Paikin et al., (1974), “Characteristics of People Who Refused to Participate in a Social and Psychopathological Study,” in S. Mednick et al., (Eds.), Genetics, Environment and Psychopathology (pp. 293-322), New York: American Elsevier, pp. 308-310.

90. For more on the reduction of the Provincial Sample control group, see Joseph, 2004, pp. 243-245.

91. Joseph, 2004; Kendler & Diehl, 1993.

92. Kety et al., 1994, p. 448, Figure 1.

93. For more on the independent reanalyses of the Danish-American adoption study data, see Boyle, 2002, Chapter 6; Joseph, 2004, Chapter 7; Joseph, 2006, Chapters 3, 5, and 6.

94. Rosenthal, D., (1974a), “The Concept of Subschizophrenic Disorders,” in S. Mednick, et al., (Eds.), Genetics, Environment, & Psychopathology (pp. 167-176), New York: American Elsevier, p. 167. Rosenthal’s use of the term “Pandora’s box” in reference to creating the schizophrenia spectrum is taken directly from this publication.

95. Bleuler, M, (1978), The Schizophrenic Disorders: Long-Term Patient and Family Disorders, New Haven, CT: Yale University Press, p. 473.

96. Hansen, B. S., (1996), “Something Rotten in the State of Denmark: Eugenics and the Ascent of the Welfare State,” in G. Broberg & N. Roll-Hansen (Eds.), Eugenics and the Welfare State: Sterilization Policy in Denmark, Sweden, Norway, and Finland (pp. 9-76), East Lansing, MI: Michigan State University Press; Kemp, T., (1957), Genetic-Hygienic Experiences in Denmark in Recent Years, Eugenics Review, 49, 11-18.

97. Mednick, S. A., & Hutchings, B., (1977), “Some Considerations in the Interpretation of the Danish Adoption Studies in Relation to Asocial Behavior,” in S. Mednick & K. Christiansen (Eds.), Biosocial Bases of Criminal Behavior (pp. 159-164). New York: Gardner Press.

98. Häfner, H., & der Heiden, W., (1986), The Contribution of European Case Registers to Research on Schizophrenia, Schizophrenia Bulletin, 12, 26-51.

99. Mednick, S. A., (1996), “General Discussion III,” in G. Bock & J. Goode (Eds.), Genetics of Criminal and Antisocial Behavior (pp. 129-137), New York: John Wiley and Sons, p. 134.

100. Kety et al., 1994.

101. Lewontin et al., 1984, p. 223. Kety and colleagues reported that there were 33 control families in the 1968 study, and 34 control families in the 1975 study. It is not clear why the number increased from 33 to 34.

102. Olson, C. P., (Ed.), (1920), Oregon Laws: Showing all the Laws of a General Nature in Force in the State of Oregon (Vol. 2), San Francisco: The Bancroft-Whitney Company. See also Joseph, 2004, pp. 204-212.

103. Olson, 1920, p. 3176.

104. Anonymous, (1925), Galton Society, Eugenical News, 10, 69-71, p. 71.

105. Heston, L. L., & Denny, D. D., (1968), “Interactions between Early Life Experience and Biological Factors in Schizophrenia,” in D. Rosenthal & S. Kety (Eds.), The Transmission of Schizophrenia (pp. 363-376). New York: Pergamon Press, p. 365.

106. Popenoe, P., (1929, September), The Foster Child, Scientific Monthly, 29, 243-248.

107. Hemminki et al., (1997), Sterilization in Finland: From Eugenics to Contraception, Social Science and Medicine, 45,1875-1884; Hietala, M., (1996), “From Race Hygiene to Sterilization: The Eugenics Movement in Finland,” in G. Broberg & N. Roll-Hansen (Eds.), Eugenics and the Welfare State (pp. 195-258), East Lansing, MI: Michigan State University Press.

108. Tienari, Lahti, et al., (1987), “The Finnish Adoptive Family Study of Schizophrenia: Possible Joint Effects of Genetic Vulnerability and Family Interaction,” in K. Halweg & M. Goldstein (Eds.), Understanding Major Mental Disorder: The Contribution of Family Interaction Research (pp. 33-54), New York: Family Process Press, pp. 44-45.

109. Broberg, G., & Tydén, M., (1996), “Eugenics in Sweden: Efficient Care,” in G. Broberg & N. Roll-Hansen (Eds.), Eugenics and the Welfare State (pp. 77-149), East Lansing, MI: Michigan State University Press.

110. Read J., & Dillon, J., (Eds.), (2013), Models of Madness (2nd ed.), London: Routledge. See also Hill, D., (1983), The Politics of Schizophrenia: Psychiatric Oppression in the United States, Lanham, MD: University Press of America.

111. Read, J., (2013a), “Childhood Adversity and Psychosis,” in J. Read & J. Dillon (Eds.), Models of Madness (2nd ed.; pp. 249-275), London: Routledge; Read, J., (2013c), “Psychosis, Poverty, and Ethnicity,” in J. Read & J. Dillon (Eds.), Models of Madness (2nd  ed.; pp. 191-209), London: Routledge.

112. Read, 2013c, p. 205.

113. Read et al., (2014), The Traumagenic Neurodevelopmental Model of Psychosis Revisited, Neuropsychiatry, 4, 65-79.

114. Tandon et al., (2008), Schizophrenia “Just the Facts”: What we Know in 2008. 2. Epidemiology and Etiology, Schizophrenia Research, 102, 1–18, p. 12.

115. I thank M.C. Jones and Ken Richardson for providing helpful feedback on an earlier draft of this article.


  1. Jay,

    Wow! This is a seminal article. I have been a fan of your work ever since I first read The Gene Illusion some years ago. I hope you will spread this article far and wide.

    This review makes clear what I’ve believed for a long time: there is no major proven genetic contribution to so-called schizophrenia, nor is there even such a demarcable, separable condition as “schizophrenia.”

    In my opinion, in your earlier work you pandered to the psychiatrist writers by indulging their belief in the existence of schizophrenia (as opposed to the existence of severe psychotic symptoms along a continuum). I suppose in a way you had to do this to refute their false assertions on their level. But in reality, as you probably know more than you let on in your writing, schizophrenia is a totally invalid, useless, unscientific concept. It supposes that one can neatly and reliably cut off severe human suffering point at some borderline and say, “This is schizophrenia, and that isn’t”. And that’s bullshit. It is amusing to read these studies by supposedly serious psychiatric researchers when you realize the studies are all based on a fake diagnosis.

    I have one quibble with something you said, Jay. You said it is established that “schizophrenics” (a word it would be better we do not use) do not often have children. However, this is not universally true. In poor countries such as India and Columbia where drugs are rarely used and people are not discouraged from returning to a life of work and social involvement, people once-labeled as schizophrenic frequently return to a normal live and have children at a high rate approaching the normal population. This fact was detailed in companion papers to the original World Health Organization studies by Hopper and Wanderling. Furthermore, many young people given intensive psychotherapy of various kinds, such as those in Open Dialogue or by ISPS therapists, have improved to the point where they return to work, have relationships and families.

    Yet these people are not included in the sources you cite, because those sources including as “schizophrenics” only the most unfortunate 1% of the population who get no significant psychotherapy, are loaded up on brain-damaging drugs for years, given horrible disease messages, and not encouraged to return to work and normal social interaction. So the message, Jay, should be that a full return to work and social involvement is much more possible for people labeled schizophrenic than has previously been thought in these studies that suffer from that most insidious of biases: Courtenay Harding’s “clinician’s illusion.”

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    • Thanks for your reply. Since the topic was an examination of the alleged evidence that schizophrenia is caused by disordered genes, I mentioned the issues relating to birthrates, and the validity of the “schizophrenia” concept, only in passing. But of course, they are important issues in their own right, and have been covered very well by others. To clarify, I did not use the term “schizophrenic” or “schizophrenics” in the article. When these terms do appear, they are always found in quotations taken from other writers.

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  2. This is an excellent example of the kind of results you’re going to get when you use behavioral diagnoses to study biophysical ailments. Just like depression, schizophrenia is a syndrome- a collection of symptoms and signs of a certain nature that can have differing causes. No surprise you won’t get constant results from groups of guys lumped together in the back wards of some institution. And you can’t treat them as well as the better institutions of the 19th century, which had 50% recovery rates without the amenities (or the meds)of today’s institutions.

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  3. I absolutely appreciate the work put into this article. But for me this is what it all boils down to:

    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…And yet, establishing the reliability and validity of schizophrenia is a prerequisite for any study attempting to assess the possible role of genetic influences.

    As in, let’s find an actual unicorn before engaging in scientific arguments about its lifestyle?

    Substitute “witchcraft” for “schizophrenia” in any of these studies and decide for yourself whether it makes any less sense.

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  4. This article follows the old saying, ‘When you’re going to lie, and you want people to believe you, make the lie a great big lie”. The author has done a great job of that.

    I don’t even have the endurance to catalogue all the lies in this article. But lie #1 is that there has never been a valid twin study done(or one that shows schizophrenia isn’t genetic). It’s a bold lie, but it’s still a lie.

    Sad, very sad that people still believe such tripe as well as still swallowing the ‘kitchen sink’ causal theory of schizophrenia. That same lie exists in autism crowds, but it does just as much damage there. Authors of this tripe don’t care who they hurt. It’s all about money, and getting ‘disciples’.

    But it confirms another old saying, “If you repeat something often enough, people will eventually believe you”.
    Forget proof. If you just say it over and over, you’ll eventually develop an army of blind disciples. Who cares about the people with schizophrenia and their families, who are harmed by it? Other people clean up that mess, and they are invisible, voiceless.

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    • Where is any proof to back up any of your claims. This is your typical way of dealing with anything that you don’t like here on MIA, you state that it’s all lies and so on but you never, ever come up with anything to verify anything of what you state. The twins studies have been debunked numerous times but you seem to have some secret study or studies that you can point to that prove that schizophrenia is caused by genetics. Okay, show us your study or studies.

      I jus don’t even have the endurance to continue with all of this. I think I’m wasting my time since everyone else seems to be ignoring you. I admit it, I was the only one to bite and take the bait and respond to you.

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    • Tusu,

      If you can’t take the heat, get out of the kitchen. And if you don’t have the endurance to make real arguments, why bother? Making a non-argument like you did just makes you look weaker.

      Come back when you’re ready to have a real debate about any of the points in the article.

      As for it being about money, Jay Joseph isn’t profiting from these articles or books; he probably barely makes enough money to cover the research and publication costs. On the other hand, the lies that drugs help people labeled “schizophrenic” have better outcomes in the long-term, as well as the lie that schizophrenia is a biological disease, are very profitable indeed. They give great benefit to psychiatrists and drug companies, while causing great harm to suffering people and their families, who you seem to care so much about.

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    • ” It’s all about money, and getting ‘disciples’.”

      What are you talking about, tusu? We aren’t getting paid to point out the harms of psychiatry, we’re here trying to learn and share our research with others, to help protect others.

      Where’s your research disproving Jay’s findings? Attacking the messenger is inappropriate, and unconvincing.

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    • I do not know you but I know science and Jay is advocating real science in contrast to the pseudoscience pushed by careers and an unbelievably strong confirmation bias. A confirmation bias is a powerful force in support of our social construction of “mental disorders;” only an intense confirmation bias allows twin studies to pass for real science.

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    • there has never been a valid twin study done(or one that shows schizophrenia isn’t genetic

      How’s that for backwards? Assuming (incorrectly) that such a disease exists, the scientific procedure would be to see if one can directly show that it is genetic, not rely on the alleged absence of disproof.

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      • But what’s great for the psychiatric industry is there is medical proof that the “schizophrenia,” “cure,” the neuroleptics, can in fact, create both the positive and negative symptoms of “schizophrenia,” all by themselves.

        And the psychiatrist can NOT distinguish between the symptoms of the “disease,” and the adverse drug reactions.

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        • Someone Else

          As regards the drugs creating the illness you are completely right!
          This is even (now) medically acknowledged.

          I think that when a person arrives at a ‘clinic’ the doctors look at the statistics and figure out if they can create another “schizophrenic”. If not then the person is put on standby with an intermediary diagnosis, for the time being.

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  5. Trivial, but something similar occurred in the early moral treatment institutions in this country in the early 19th century. They were able to recover about 50% of their patients while not having access to antipsychotic drugs.
    Another trivial interesting item: India has had antipsychotic medicine for centuries- reserpine, the alleged active chemical found in snakeroot, which was used in infusions from its herbal source.

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  6. Wow, that’s a LOT of extremely unscientifically done research, the psychiatric industry really should be ashamed. Thank you for pointing it all out.

    I was so glad you concluded with Read’s research. Because my research has led me to the disheartening theory that it is likely, that the most common actual etiology of “schizophrenia” today, is psychiatrists misdiagnosing child abuse or ACEs issues, as “psychosis.”

    And, realistically, when you give a child abuse victim (a rightfully distressed, but non-psychotic / non-“brain diseased” person) a neuroleptic to “cure” the pains and injustice of rape or other abuse. The neuroleptics can cause the negative symptoms of “schizophrenia,” via neuroleptic induced deficit syndrome, which is almost always misdiagnosed as “schizophrenia.” And further mistreated by increasing, rather than decreasing, the dose of the neuroleptic.

    And too much of a neuroleptic (which can be even a small dose, for a person who is not actually initially “psychotic”) can cause one to suffer from neuroleptic induced anticholinergic intoxication syndrome, aka anticholinergic toxidrome, as well. The central symptoms of which are indistinguishable from the positive symptoms of “schizophrenia” to the medical community:

    “Central symptoms may include memory loss, disorientation, incoherence, hallucinations, psychosis, delirium, hyperactivity, twitching or jerking movements, stereotypy, and seizures.”

    Thus get misdiagnosed as “the classic symptoms of schizophrenia,” at least they were in my medical records.

    And, given the reality the “cure,” can mimic the symptoms of the “disease.” It strikes me this makes any certainty that “schizophrenia” ever could be, or today even still can be, reliably diagnosed, next to nil. Especially given the psychiatric industry’s denial (at least in the DSM) of these neuroleptic induced potential causes of the symptoms of “schizophrenia.” (And any DSM disorder treated with the neuroleptics.)

    I do think it is likely that 2/3’s of “schizophrenics” today, are child abuse or ACE’s victims who may very likely have been turned into “schizophrenics” with the neuroleptics, themselves. And I really hope the psychiatric industry will stop profiteering off of covering up child abuse. Because such is wrong, and harmful to all of society, in the long run.

    Thanks for your tireless efforts, Jay.

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  7. I was diagnosed schizoaffective and I’ll read this article and try to understand it but I looked at the intro and conclusion and barely know anything about behavioral genetics but I’ll try to contribute. I believe schizophrenia is a result of neural pathways being wired during development such that behaviors which are normal according to our genes become expressed at extreme levels through learning in an abnormal external environment. The genes themselves cannot regulate environment nor pick an ideal state to develop to where brain activity is perfectly attuned to function perceptively and logically. They compose the cellular structure and the necessary actions of neurons, but after these are formed enough to serve as a working mind, genes are irrelevant because the organ is only doing what it has learned over time.

    Walking, for example, is coded into our genes for movement. But the genes don’t decide when to walk, our brain does. The same brain decides what it will see and hear, how to speak and socialize, etc.

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