“Hidden Valley Road” and Schizophrenia: Do Genes Tell the Story?

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In a 2022 article I made the case that, contrary to the consensus view, there exists no valid evidence that genes play a role in causing schizophrenia (psychosis). I made the complete case in the 2023 Routledge English-language Edition of Schizophrenia and Genetics: The End of An Illusion (a greatly revised version of a previously self-published e-book). The current article is adapted from sections of Chapters 3 and 6 of Schizophrenia and Genetics, where I examined a 2020 popular work whose author promoted psychiatry’s problematic “heritability of schizophrenia” story. In this article I add expanded analyses, much new information, and updates.

The general theme of books and articles appearing since the 1980s popularizing behavioral genetic and psychiatric genetic research starts with supposedly misguided environmentalist and psychoanalytic ideas that “mental disorders” are sometimes caused by “refrigerator mothers” or “schizophrenogenic mothers.” After bashing these strawmen, the story continues that environmental theories of causation were eventually discredited by scientists performing family, twin, and adoption studies, some of whom went on to discover predisposing genetic variants (hereafter “genes”) at the molecular genetic level. That’s the story, but is it the true story?

Illustration depicting dna strands and molecule chains

The Galvin Family, Abuse, and “Schizophrenia”

Continuing these themes, in 2020 journalist Robert Kolker published Hidden Valley Road: Inside the Mind of an American Family (hereafter HVR; previously reviewed in a 2020 MIA article by Patrick Hahn). This was the tragic story of a real White middle-class family of 14. Don and Mimi Galvin had 12 children, born between 1945 and 1965. They lived at the end of an isolated unpaved road in Colorado Springs, Colorado, USA. This is how Stephen Rodrick of Rolling Stone described the Galvin family:

“On the surface, the Galvins were a postwar American dream. Don was a World War II veteran helping to jump-start the just-opened Air Force Academy in Colorado Springs alongside his witty and selfless wife. The first 10 Galvin kids, born beginning in 1945, were handsome boys who became high school football and hockey stars in their growing boomtown. Two beautiful daughters, Lindsay and Margaret, followed them. The Galvins lived on the outskirts of the city, on Hidden Valley Road, and were the envy of other families throughout Colorado Springs.”

Of the ten Galvin boys, six were eventually diagnosed with schizophrenia, including the fourth-born Brian who committed murder-suicide in 1973 at age 22. They also were diagnosed with other psychiatric conditions. Kolker recognized in an interview that “these brothers were all different and manifested their illnesses differently.” Although psychiatry lumped the brothers’ differing behavioral patterns under the “schizophrenia” umbrella, others could conclude that they experienced six different “illnesses.” In keeping with psychiatric orthodoxy, Kolker saw schizophrenia as a “complex disease” and a “brain condition.”

My specialty is analyzing genetic research in psychiatry and other behavioral science areas, and therefore the genetic research aspects of HVR are the focus of this article. The concept of “schizophrenia” is itself controversial, as are psychiatry’s criteria for determining who gets this label. The term “psychosis” to describe people’s experiences is preferable. These issues have been examined by many authors over the years.

Critics of Genetic Research Were Left Out of the Story

It is an enormously difficult task for a non-scientist journalist like Robert Kolker to jump into a field and to write a book about 100 years of research, and the at times heated controversies surrounding it. I am a clinical psychologist who has been writing on the genetics of schizophrenia topic for 25 years (including a doctoral dissertation and three books). To get the facts right (hopefully), I still need to get help from colleagues, review and edit countless drafts, reread articles and books, and stay up to date on the latest research and commentaries, which includes needing to understand molecular genetic research publications I was never trained to understand. So while I recognize and appreciate how challenging this task must have been for Kolker, I wish he had interviewed and discussed the works of genetic research critics to present all sides of the story.

Kolker did mention people who have promoted environmental theories of schizophrenia, but he did not address points raised by the critics of schizophrenia family, twin, adoption, and molecular genetic research. While I admire Kolker’s ability and willingness to jump into the contentious and complex “genetics of mental disorders” debate, I am duty bound to highlight the errors he made, and to show that the story he told about genetics is a mistaken one.

“Running in the Family” Genetic

Contrary to the commonly held view, “running in the family” does not equal “it’s genetic,” because families share a common environment as well as common genes. In the 2020 second edition of How Genes Influence Behavior, Jonathan Flint and Kenneth Kendler, two of the world’s leading psychiatric genetic researchers, recognized that a condition running in the family can be caused by the common environment families share:

“In human families, relatives can be similar because they share environments or because they share genes, or both. Relatives share all kinds of environments. They live in the same neighborhoods, often attend religious services together, eat a similar diet, are exposed to the same level of harmony or conflict in their home, and might all live close to an industrial plant that pumps out pollution into the air or water. All of these reasons and more could explain the resemblance among members of the same family.”

On this single point, that a condition running in the family cannot be interpreted genetically, psychiatric geneticists and the field’s critics are in agreement. This means that, as Flint and Kendler acknowledged, theoretically the prevalence of psychosis in the Galvin family could have been caused by environmental influences, by hereditary influences, or by a combination of both.

Kolker mentioned the “paradox” that “schizophrenia does not appear to be passed directly from parent to child.” Indeed, in a 2006 Swedish study based on a population-based cohort of over 7 million individuals, researchers found that in families where one member was diagnosed with the supposedly “highly heritable” schizophrenia condition, in more than 96% of these families there were no other similarly diagnosed members. The Galvin family psychosis cluster was an unfortunate aberration.

“Torrents” of Sexual Abuse

Kolker described how sexual abuse was rampant in the Galvin family. There was no escaping it. For the youngest child Lindsay, “it seemed as if” the second-born Galvin son Jim, who was 18 years her senior, “had taken [sexual] liberties with every young child around him.” She told her mother Mimi “that she had been sexually abused by her brother Jim countless times over several years.” Other siblings may have had similar stories.

Adding another layer of abuse and trauma, Mimi believed that a trusted Catholic priest, who was also a family confidant, had been sexually “pursuing her boys like boxes of cereal at the supermarket until he found the one he liked the best. ‘He had culled my family,’ she said. ‘He knew it was a big family of boys.’” The oldest son Donald, who had been a church altar boy and made two suicide attempts at age 12, was sexually abused by this trusted priest. His later “schizophrenia symptoms” included a preoccupation with religious matters and the reciting of prayers for days on end.

Mimi Galvin herself had been a victim of childhood sexual abuse, and was understandably overwhelmed by the task of parenting and protecting 12 children in relative isolation with a frequently absent husband.

So now we have identified sexual abuse as a major non-genetic source of psychological distress and “psychopathology” in the Galvin family. Although he acknowledged a role for environmental factors, for Kolker it’s mainly genes that tell the story of psychosis in this family, stating flatly, “Sexual abuse does not cause schizophrenia. That much is certain. Even a torrent of sexual abuse like what Mimi had envisioned still could not answer the bigger question of why there had been so much mental illness in their family.” A torrent of sexual abuse. Kolker went further and declared, “to be sure, no studies have ever suggested that abuse does cause schizophrenia.” Who was telling him such things?

Environmental Factors

As reviewed by psychologist John Read in several chapters in the 2013 second edition of Models of Madness and in a later publication, since the turn of the 21st century studies have linked schizophrenia and other psychotic conditions to childhood adversities such as having experienced bullying, emotional abuse, incest, neglect, parental loss, physical abuse, and sexual abuse—adversities and trauma that clinicians who work with people diagnosed with psychotic disorders are well aware of. Since then, other studies have supported a link between schizophrenia/psychosis and childhood adversity and trauma.

The Galvin sons also were abused by the psychiatric establishment. At one point Peter Galvin was taking six different prescribed neuroleptic (“anti-psychotic”) drugs at the same time: Geodon, Risperdal, Risperdal Consta (a long-acting injectable form of Risperdal), Zyprexa, Prolixin (another long-acting injectable), and Thorazine. Jim and Joe Galvin both died at the age of 53 from a condition known as “neuroleptic malignant syndrome,” which refers to poisoning caused by years of taking prescribed neuroleptic drugs. According to Kolker, Mimi “had no compunction about saying that Jim and Joe both died of the medicine that was supposed to help them.”

Enter Robert Freedman and Lynn DeLisi

Having knocked down the beleaguered “schizophrenogenic mother” strawman yet again, and after eliminating trauma and even “torrents” of sexual abuse as possible causes of schizophrenia and psychosis, Kolker promoted gene-centered explanations while largely overlooking the fact that reared-together siblings influence each other’s behavior and are not diagnosed with schizophrenia independently of each other. He believed that diagnosing schizophrenia is “more of an art than a science.” Because there are no biological tests for schizophrenia, one aspect of this “art” has always been that doctors’ and psychiatrists’ diagnoses are influenced by the idea that “if your siblings (or your identical co-twin) have schizophrenia, the behavior that brought you to my office makes me think you probably have it too.”

Kolker featured the work of two psychiatric researchers who, with the help of Galvin family blood samples, supposedly had helped uncover schizophrenia’s biological/genetic roots. The two were Robert Freedman of the University of Colorado Medical Center in Denver, who pinned hopes on the CHRNA7 gene, and Harvard professor of psychiatry Lynn DeLisi, who focused on the SHANK2 gene in collaboration with neurobiologist Stefan McDonough and others. Freedman “was on the hunt for a physiological understanding of” schizophrenia, whereas DeLisi, “wanted to track down the genetic components of schizophrenia.” What DeLisi and Freedman would learn from the Galvin family, wrote Kolker, “helped unlock our understanding of the disease.” (Kolker also mentioned another group’s 2016 finding of a supposedly landmark association between the C4 gene and schizophrenia. A 2022 study, however, found no evidence for a C4-schizophrenia link.)

Kolker didn’t say it’s a proven fact that SHANK2 and CHRNA7 play a role in causing schizophrenia, but for him the likelihood that they do was strong enough to portray Freedman and DeLisi as gene discoverers (he referred to their work as gene “discoveries” on pages 246, 247, and 272). Undoubtedly, Freedman and DeLisi were motivated by a desire to prevent and better treat human suffering and dysfunction, but the winners of the “genes for schizophrenia” hunt also stand to receive prizes and professional honors, and possibly to reap financial rewards.

In theory, scientific research is the unbiased process of identifying the underlying causes of observed phenomena in nature. In the world we currently live in, this process is often distorted and even corrupted by the needs of corporations and governments to increase profits and to justify maintaining the social and political status quo, which includes financially rewarding people and institutions that help them achieve these goals. There’s a gold rush aspect of psychiatric molecular genetic research.

While recognizing that environmental factors or triggers are necessary to produce schizophrenia, Kolker portrayed Freedman and DeLisi as having helped seal the case against the misguided supporters of purely environmental (non-genetic) theories. He emphasized that Hidden Valley Road “is a work of non-fiction,” but as I will show, there are fictional aspects to the story he told about CHRNA7 and SHANK2.

The Historic Candidate Gene Era “Flop”

Both Freedman and DeLisi studied the Galvins and other families in search of “candidate genes” that play a role in causing schizophrenia. A psychiatric candidate gene association study attempts to identify genetic influences on a condition by generating hypotheses about it, and then identifying genes that might play a role in causing it. Genes become schizophrenia “candidates” based on their role in influencing brain functions believed to be related to the condition. A candidate gene has been defined as “a gene believed a priori to be involved in the pathophysiology of the disorder.”

What Kolker didn’t tell us, presumably because he didn’t know, is that the psychiatric candidate gene effort that began in the early 1990s ended as an expensive bust. The major depression candidate gene literature, for example, turned out to be, as psychiatric drug researcher Derek Lowe wrote in a 2019 Science article, “all noise, all false positives, all junk.” In his 2018 book Blueprint: How DNA Makes Us Who We Are (which I reviewed in the Winter, 2022 edition of the American Journal of Psychology), one of the world’s leading behavioral geneticists, Robert Plomin, described over two decades of behavioral candidate gene research as an “approach [that] failed everywhere,” a “fiasco,” and a “flop.” By Plomin’s 2018 count, for schizophrenia alone “over 1,000 papers reported candidate gene results for more than 700 genes.” Plomin then asked, “how can so many published papers have got it so wrong?”

In the 2020 edition of How Genes Influence Behavior, Flint and Kendler (and Ralph Greenspan) conceded that in the end, “literally thousands” of physiological candidate gene papers “have taught us nothing useful about the genetic basis of psychiatric disease.” As psychologist Stuart Ritchie commented in 2020, “reading through the candidate gene literature is, in hindsight, a surreal experience: they were building a massive edifice of detailed studies on foundations that we now know to be completely false.”

Patrick Sullivan co-founded the Psychiatric Genomics Consortium (PGC) in 2007, and is one of the world’s leading psychiatric genetic researchers. In a 2017 article, he described psychiatric candidate gene studies, which cost hundreds of millions of dollars, as being based on “guesswork,” and that his “field was pretty bad at guessing.” Sullivan concluded that “historical candidate gene studies didn’t work, and can’t work,” and “I strongly suggest that we abandon candidate gene guesswork (as historically applied) as they have only provided false directions and wasted effort.”

The initial excitement and numerous subsequent discovery claims accompanying psychiatry’s candidate gene goldrush eventually gave way to the crushing realization that all that had been found was genetic fool’s gold, and that the method should be “ditched.”

The CHRNA7 Gene

Linkage study failure. Kolker wrote in HVR that a 1997 Freedman et al. molecular genetic linkage study “identified CHRNA7 as the first gene ever to be definitively associated with schizophrenia. He and his colleagues had made history.” However, schizophrenia linkage research (described here), which began with high hopes in the 1980s, also turned out to be a flop. In a 2000 article, Lynn DeLisi concluded that “on close inspection,” Freedman’s 1997 study found no linkage to the schizophrenia “illness,” based on “8 families afflicted with schizophrenia.” And in a subsequent analysis by DeLisi and colleagues, appearing five years after Freedman’s supposedly “historic” schizophrenia linkage discovery, the authors concluded, “No linkage appears to be consistently replicable across large studies. Thus, it has to be questioned whether the genetic contribution to this disorder is detectable by these strategies…”

Kolker’s source for his claim that “Freedman discovered the first gene ever to be definitively associated with schizophrenia” was Denver Post staff writer Carol Kreck, the author of a 1999 article for the newspaper. It is unclear whether Kreck came up with this “first discovery” claim on her own, or whether someone fed it to her.

Candidate gene study failure. Returning to candidate gene research, Kolker apparently was unaware of the 2015 schizophrenia candidate gene analysis published by M. S. Farrell and leading researchers who concluded, specifically in relation to CHRNA7 and other schizophrenia candidate genes, “We can state with high confidence that the large common variant genetic effects originally reported in many initial candidate gene studies are highly unlikely to be true.” In a 2017 assessment of CHRNA7 and 24 other widely studied schizophrenia candidate genes, Emma Johnson and colleagues found that “variants in the most-studied candidate genes were no more associated with schizophrenia than were variants in control sets of noncandidate genes.” Final nails in the CHRNA7 coffin, it would seem.

Although schizophrenia candidate gene research had already achieved “flop” status by the time Kolker was researching and writing his book, he described how one of the Galvin daughters “remembered champagne being popped as she walked into Freedman’s lab,” where the supposed “CHRNA7 discovery” was being celebrated as she sought advice on whether she and her husband should have children.

Presumably no champagne flowed in the aftermath of a 2008 candidate gene study Freedman himself co-authored, with the title “No Significant Association of 14 Candidate Genes With Schizophrenia in a Large European Ancestry Sample: Implications for Psychiatric Genetics.” This study found no significant association between CHRNA7 and schizophrenia. The results, according to Freedman’s own study, “were consistent with chance expectation.” This 2008 study was not mentioned or referenced in HVR. Similarly, Freedman failed to mention or reference it in his 2010 book The Madness Within Us: Schizophrenia as a Neuronal Process, where he called CHRNA7 a “gene associated with schizophrenia.” In a 2006 chapter Freedman co-wrote with Patrick Sullivan and others in The American Psychiatric Publishing Textbook of Schizophrenia, CHRNA7 was not listed among the nine “best current candidate genes for schizophrenia.”

Patenting CHRNA7. Freedman told Kolker he was an “unpaid advisor” to the drug companies. However, although unmentioned in HVR, Freedman and a colleague applied for a CHRNA7 patent in 2003 (backed by a 104-page application-support document), and they were granted this patent in 2009. A disclosure statement published that year in the American Journal of Psychiatry, which Freedman edited at the time, stated, “Dr. Freedman holds a patent through the VA [U.S. Department of Veterans Affairs] for discovery of a genetic variant in schizophrenia.” A 2015 Freedman publication stated that this patent was for CHRNA7: “Dr. Freedman has a patent on the genomic structure of CHRNA7 and SNPs in the promoter through the Department of Veterans Affairs. He derives no income from this patent.” The statement did not say whether he stood to earn future income from the patent, but it is likely that the VA and others would profit from the production of future drugs and tests based on CHRNA7, were it shown to be a true biological marker for schizophrenia. It seems that Freedman patented the gene in part to profit in the future from tests in the same way as Myriad Genetics had patented the BRCA1 and BRCA2 breast cancer genes for that purpose in the 1990s. What Freedman told Kolker about CHRNA7 in their “extensive interviews” may have been influenced by the former’s financial and professional stake in the gene.

The ability to patent genes is controversial (the U.S. Supreme Court ruled against some aspects of gene patenting in 2013), and the ethics of researchers and institutions patenting existing parts of the human body, and potentially harming patients and discouraging future research by doing so, is questionable (see this video). The website disclosing information about Freedman’s CHRNA7 patent called it a “method of identifying individuals predisposed [to] schizophrenia.” The website shows that the patent expired in September, 2017 due to a “failure to pay maintenance fees,” but was renewed at a later date and is currently paid through February, 2024.

The previously mentioned articles and analyses by leading psychiatric genetic researchers and others documenting the failure of CHRNA7 and the entire behavioral candidate gene era were available as Kolker was researching and writing his book. Had he been aware of these publications and understood their implications, he might have described the Freedman laboratory’s champagne party as one of countless examples of “surreal” celebrations of failed psychiatric candidate gene “guesswork.”

The SHANK2 Gene

Turning to DeLisi’s SHANK2 gene, schizophrenia genetic review articles rarely mention it. In a biologically oriented 2022 review article on schizophrenia appearing in The Lancet, for example, there was no mention of SHANK2 (or CHRNA7). A January, 2023 PubMed.gov search for the combined terms “SHANK2” and “schizophrenia” returned only 21 articles since the publication of a 2016 article DeLisi co-authored on the topic, where she and her colleagues wrote that SHANK2 “represents a compelling candidate for a high penetrance variant.” Four years later, in the wake of the candidate gene collapse, DeLisi received the International Society of Psychiatric Genetics “Ming Tsuang Lifetime Achievement Award,” in addition to a similar award in 2022 from the Schizophrenia International Research Society. In the statements describing her achievements, there is no mention of SHANK2.

In the 2017 (most recent) edition of DeLisi’s popular book 100 Questions & Answers About Schizophrenia: Painful Minds, despite devoting many pages to genetics, the terms “SHANK” or “SHANK2” do not appear even once. Scientists usually mention their discoveries in the books they write.

DeLisi published an academic journal article on schizophrenia genetics in 2022, where she wrote of gene discovery in multiplex families like the Galvins as a goal for future research, but not as a something that had been achieved. (In “multiplex” families, multiple individuals are affected by a specific disease or condition.) Towards the end of her long career in psychiatric genetic research, DeLisi could not claim any gene discoveries in multiplex families:

“Unfortunately, so many gaps exist in our understanding of normal brain development and variation, that it is difficult to put together this puzzle in its complete form so far by finding unique mutations in multiplex families.”

DeLisi mentioned Kolker and Hidden Valley Road in this 2022 article, writing that Kolker “suggests with some ‘literary license’ that science has made lots of progress.” DeLisi said that Kolker “describes how several years of persistent research on this family paid off with the finding that a mutation in the SHANK-2 gene appeared to be present in all the affected individuals,” but she distanced herself from Kolker’s description. SHANK2 also was found in the “unaffected mother” (Mimi Galvin), wrote DeLisi, and later was “found to be present in one of the unaffected female siblings and her female offspring…All three of the females had a previous lifetime history of major depression, but none had a psychosis.” The source DeLisi gave for these findings was “DeLisi, unpublished data,” and the question then becomes why these findings were not published.

The SHANK2 candidate gene theory that DeLisi at best saw as inconclusive, and which was not mentioned in her book on schizophrenia or in lifetime achievement award statements, was presented to the world by Kolker as the likely gene “mutation responsible for the [Galvin] family illness,” and as a major component of “the genetic flaw that caused schizophrenia in the Galvin boys.”

Genetic Insider Accounts and Genome-wide Association Studies (GWAS)

Although a major theme of Hidden Valley Road was that CHRNA7 and SHANK2 were real or probable schizophrenia gene discoveries—even as the evidence suggested they were in fact non-discoveries—Kolker did provide some interesting insights into how schizophrenia molecular genetic researchers privately viewed their results, based on the many conversations and interviews he had with them. DeLisi favored the approach of looking for schizophrenia genes in multiplex families like the Galvins, whereas the GWAS (“genome-wide association study”) approach beginning in the period 2005-2007 compares genes among large groups of diagnosed and non-diagnosed people. A GWAS might indicate an association (correlation) between genetic variants and a given condition, but it does not provide evidence that genes play a role in causing the condition. Correlations are not causes, and may in fact be spurious correlations and/or the result of systematic error, as schizophrenia linkage and candidate gene researchers learned the hard way (see this excellent analysis by Evan Charney).

DeLisi shared her thoughts about schizophrenia GWAS research with Kolker. “I don’t believe that these hundred genes or markers are going to lead to anything,” she told him (in reference to a 2014 GWAS). Indeed, “hypothesis-free” GWAS publications have reported all kinds of improbable “findings” in the past few years, including the discovery of statistically significant gene associations (“hits”) for characteristics such as getting concussions, self-reported childhood maltreatment,  crying habits, female sexual dysfunction, food liking, household income, ice cream flavor preferences, leadership traits, loneliness, being a morning person, musical beat synchronization, risk taking behavior, regular attendance at a sports club, pub, or religious group, sexual behavior, and white wine liking. These supposed findings are enormous red flags for potentially spurious results in schizophrenia GWAS investigations, just as similar candidate gene “findings” were enormous red flags during the candidate-gene era. The behavioral GWAS era will likely experience the same fate as the failed linkage and candidate gene eras.

Kolker described earlier GWAS investigations as a “blistering disappointment,” which led researchers to “double down” and resolve “to build a bigger and better GWAS.” The disconnect between researchers’ private “blistering disappointment” and public discovery claims and dauntless optimism is stunning, as the issue now seems more related to institutions maintaining government and corporate grants, individual researchers protecting salaries and corporate “consultation fees,” the possibility of striking it rich with drug patents and direct-to-consumer and other types of tests, reputations, and being published in prestigious journals.

Speaking about the candidate gene era, Plomin hinted in Blueprint at corrupted aspects of the behavioral science research publication process when he attributed failure in part to “chased” probability values and “cheating,” practices otherwise known in the current scientific replication crisis as “p-hacking.” P-hacking describes the practice of researchers consciously or unconsciously manipulating definitions and data, behind the scenes, to transform non-findings into publishable career-enhancing “findings” that fall below the conventional .05 level of statistical significance.

DeLisi, Freedman, and Kolker on the Danish-American Schizophrenia Adoption Studies

Psychiatry justifies molecular genetic research by the belief that previous family, twin, and adoption studies established schizophrenia as a genetically based disease, beyond any doubt. As I argued in Schizophrenia and Genetics, this belief constitutes the fundamental error of schizophrenia gene-finding strategies. DeLisi, Freedman, and Kolker all saw Seymour Kety, David Rosenthal and colleagues’ 1968 Danish-American adoption studies, which used three main research designs, as signaling a historic turning point in support of psychiatric genetic theories of schizophrenia, yet none appeared to understand the basic design of these studies.

DeLisi

In the 2017 edition of 100 Questions & Answers, DeLisi wrote that in the Kety-led 1968 study, the “investigators showed that an excess of schizophrenia was present in the biological relatives of individuals with schizophrenia, but not the adoptive relatives.” In fact, Kety and colleagues did not make that comparison, and Kety himself called such a comparison “fallacious” and “improper.”

DeLisi, Freedman, and Kolker said that the Danish-American researchers counted diagnoses of “schizophrenia,” when in fact they counted what Kety and Rosenthal called “schizophrenia spectrum disorders” ranging all the way down to “uncertain borderline schizophrenia,” “uncertain acute schizophrenia,” “inadequate personality,” “vague schizoid tendencies,” and “perversion.” Anyone who reads the original research publications will see that Kety, Rosenthal et al. counted these vaguely defined mostly non-psychotic conditions/judgements as “schizophrenia.” In the previously mentioned DeLisi 2022 publication, she continued to misrepresent and misunderstand how the Danish-American studies were performed.

As Rosenthal once admitted, he and his colleagues “broadened the definition of schizophrenia as widely as it may have ever been reasonably conceived before.” Even this was an understatement, in part because Rosenthal counted “manic-depressive psychosis” as a schizophrenia spectrum disorder at the same time as he viewed schizophrenia and manic-depression as “genetically distinct and different disorders.”

The molecular genetic studies that DeLisi, Freedman and many others performed were based on schizophrenia diagnostic criteria found in the 1994 fourth edition of American psychiatry’s Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), meaning that they defined schizophrenia very differently from the way the adoption researchers who inspired their work defined it. Schizophrenia molecular genetic researchers continue to study a very different “disorder” from the one Kety and Rosenthal studied.

Freedman

In The Madness Within Us, Freedman wrote, in reference to earlier twin studies, that the “environmental factors” experienced by MZ (identical) and DZ (fraternal) twin pairs “should about equalize in the two different types of twins.” Whether or not these environments should equalize, they don’t by a longshot, as almost everyone else in the world—including most twin researchers—understands.

Freedman believed that the Danish-American adoption studies provided the “most dramatic proof that schizophrenia is a heritable illness.” As he wrote in The Madness Within Us:

“The demonstration that the risk for schizophrenia in children of mothers who have schizophrenia remains, even if the child is adopted by another mother close to the time of birth, was historically the most dramatic proof that schizophrenia is a heritable illness and hence a biologically based outcome, rather than a psychologically based outcome.”

This is a rough description of the design used in the Rosenthal-led “Adoptees” study, which started with schizophrenia spectrum disorder biological parents as the first-identified relatives or “probands.” However, Freedman cited a Kety et al. 1971 article that described the Kety-led “Adoptees’ Family” study, where the design used adoptees, not parents, as the probands.

Kolker

A major reason why Kolker believed that the case for genetic explanations was airtight, and that family dynamics explanations were weak or discredited, was that the Danish-American adoption studies had confirmed the earlier alleged “gold standard” findings from twin research. Kolker said that the famed psychiatrist Emil Kraepelin published the first schizophrenia twin study in 1918. In fact, Kraepelin never performed or published such a study. In Schizophrenia and Genetics, I explained in two chapters why twin studies fail to provide any evidence in favor of genetic influences.

Kolker believed that the Danish-American adoption studies showed that family environments play little if any role in causing schizophrenia or psychosis. In Chapter 14 of HVR, he briefly described these studies as they were first presented at a famous 1967 conference on schizophrenia research, held at Dorado Beach, Puerto Rico and published in book form the following year. His descriptions were at times inaccurate, and he did not seem to have a firm grasp on how these studies were performed. For example, Kolker said that the Kety-led study’s control group consisted of “schizophrenia patients who grew up in their own families,” which is not true. The actual control group consisted of the first- and second-degree biological relatives of adoptee probands not diagnosed with a schizophrenia spectrum disorder.

Kolker is far from being the only writer to get the Kety-led study’s control group wrong. In Schizophrenia and Genetics and earlier publications I showed that the authors of textbooks and important works, including leading psychiatric and psychiatric genetic researchers, routinely misrepresent adoption studies’ methods and results.

Kolker wrote that at Dorado Beach, Rosenthal “discredited the idea that bad parenting created the [schizophrenia] disease.” I am not aware of Rosenthal making such a statement, and in his Dorado Beach conference summary chapter, Rosenthal concluded only that “intrafamilial” and other environmental factors had not been “proved.” He didn’t say these factors were discredited.

Rosenthal’s own study found no evidence in support of genetics. It is fascinating to note that the famous and widely cited Adoptees study Rosenthal and colleagues presented at Dorado Beach, and published in 1968, produced no statistically significant results in the genetic direction, and Rosenthal did not claim to have obtained such results. Based even on Rosenthal’s 1968 extraordinarily broad definition of what counted as a schizophrenia spectrum disorder, the results were Index group adoptees 13/39 (33%) versus Control group adoptees 7/47 (15%). The one-tailed probability value for this Index-Control group comparison is .07, not statistically significant at the .05 level used in the Danish-American studies and most areas of science. The actual result of Rosenthal’s 1968 study, therefore, was a failure to discover genetic influences on schizophrenia (a result confirmed ten years later in this Rosenthal publication).

Kolker said that at Dorado Beach, Rosenthal “declared that biology…appeared to explain nearly every single documented instance of the illness,” and that it “seemed to” Rosenthal that his findings provided “proof that nature, not nurture, won the argument.” Whatever Rosenthal may have declared or allegedly proved about schizophrenia, the negative results of his own 1968 Adoptees study led to the opposite conclusion.

In contrast to Rosenthal’s 1968 Adoptees study, Kety’s 1968 Adoptees’ Family study did report statistically significant results. However, Kety and colleagues achieved these results only by engaging in “questionable research practices” such as greatly expanding the definition of schizophrenia after unexpectedly failing to find enough traditionally defined cases to perform the study, by dismissing or downplaying the impact of potential environmental confounds (such as the selective placement of adoptees), by including “homosexuality” as a schizophrenia diagnostic indicator, and by changing group comparisons at the last minute to avoid statistically non-significant results (see Chapter 6 of Schizophrenia and Genetics).

Instead of endorsing psychiatry’s and other behavioral science fields’ ongoing support of the massively flawed and openly p-hacked Danish-American adoption studies, and twin studies based on obviously false assumptions, had Kolker approached his project with a more critical eye he might have concluded that Rosenthal’s 1968 negative-result (failure to reject the null hypothesis) study discredited the idea that genetics “created the disease.”

Conclusion

The “schizophrenia as a strongly heritable disease” story doesn’t become true because it is repeated ad nauseum in online postings and articles, in the social media, in textbooks, in popular books, in scholarly review articles, in the opening paragraphs of most molecular genetic research publications, and in books by famous scientist authors. Instead, it is necessary to closely examine the original studies and their assumptions to determine whether they support this story. The biopsychiatrists Kolker relied on say they do. The critically minded authors Kolker mostly ignored say they don’t. Replication crisis scrutiny certainly extends to the review of books such as HVR that help popularize scientific research, where unsupported gene discovery claims reach and influence a general audience, and are endorsed by famous celebrities and even former U.S. Presidents.

In Blueprint, Plomin recalled that “hundreds of candidate gene stories…that…were not true…led to hundreds of media reports about ‘genes for intelligence’ or ‘the gene for schizophrenia.’” Apparently, Kolker didn’t “get the memo” about the historic schizophrenia candidate gene collapse. Because he (albeit mistakenly) believed that CHRNA7 and SHANK2 were real or probable causative gene discoveries, his account of the genetic aspects of the Galvin family’s story produced a Hollywood-like hopeful and triumphant message in the face of otherwise tragic events—a Lorenzo’s Oil-type discovery theme, only this time based on non-discoveries. Kolker would have done better to have arrived at a more realistic conclusion, similar to the one arrived at by Sam Dolnick, the New York Times reviewer of his book:

“If there were justice in the world, the Galvins’ genes would have provided the key to understanding and preventing schizophrenia, perhaps redeeming some measure of their pain. Unfortunately, science doesn’t indulge in narrative satisfaction….The Galvins’ genes seem to hold no silver bullet, no Rosetta Stone.”

Overall, despite some glimpses into the tragic world of a family riddled with abuse and dysfunction, in addition to glimpses into the behind-the-scenes world of molecular genetics insiders, Hidden Valley Road reproduced psychiatry’s long-running yet unsupported “genetics of schizophrenia” narrative. The author presented a story of persevering medical scientists using the genes of multiplex families to make historic discoveries. Others might see the “genes for schizophrenia” story as a half-century-long train wreck.

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The author thanks Mike Jones for helpful feedback on an earlier draft of this article. All opinions expressed in this article are the author’s own.

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Mad in America hosts blogs by a diverse group of writers. These posts are designed to serve as a public forum for a discussion—broadly speaking—of psychiatry and its treatments. The opinions expressed are the writers’ own.

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27 COMMENTS

  1. Jay, thank you so much for such a thorough, engaging and comprehensible piece (and for the provided links/ references). It really is heartening to know that there are people like you in this field i.e. unafraid to tell the truth. I look forward to reading your books.

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  2. “Sexual abuse does not cause schizophrenia.” No it doesn’t, but the “mental health” industries’ inability to bill to help child abuse survivors – and their faustian “partnership” with some of the mainstream religions, to function as their child abuse cover uppers – does result in a lot of misdiagnosis of innocent child abuse survivors, and/or their legitimately concerns mothers, with the scientifically “invalid” DSM disorders.

    “if your siblings (or your identical co-twin) have schizophrenia, the behavior that brought you to my office makes me think you probably have it too.”

    Yes, such genetic assumptions are a big problem within the “mental health” industries. To the point that when one’s mother tells a psychologist that one’s grandmother was made ungodly ill on an old antipsychotic, and quickly taken off of it. That psychologist will turn this into a lie to her client’s psychiatrist, that “her grandmother” – who none of my “mental health” workers ever met – “was psychotic.” And even my grandmother’s former doctor wrote me a note pointing out that my grandmother was “never psychotic.”

    Not to mention, I’ve even been defamed as having a family history of “mental illness,” by researchers, who I’ve volunteered to be interviewed by. The ass-U-Me-ing about genetic causes of “mental health” etiologies, by the “mental health professionals,” is out of control.

    “he described psychiatric candidate gene studies, which cost hundreds of millions of dollars, as being based on ‘guesswork,’ and that his ‘field was pretty bad at guessing.'”

    I do agree, there’s way too much “guessing” and assuming going on within the psych fields. But I’ve got an idea, since our country’s broke, maybe our government should stop spending “hundreds of millions of dollars” on researching into this “bullish-t”?

    “The disconnect between researchers’ private ‘blistering disappointment’ and public discovery claims and dauntless optimism is stunning, as the issue now seems more related to institutions maintaining government and corporate grants, individual researchers protecting salaries and corporate ‘consultation fees,’ the possibility of striking it rich with drug patents and direct-to-consumer and other types of tests, reputations, and being published in prestigious journals.”

    Yes, I agree, that’s pretty much where we are. It’s all about the money. And as we all know, “It Is Difficult to Get a Man to Understand Something When His Salary Depends Upon His Not Understanding It.”

    “Rosenthal’s 1968 negative-result (failure to reject the null hypothesis) study discredited the idea that genetics ‘created the disease.'”

    Yes, and as to the real etiology of “schizophrenia” … since the “schizophrenia treatments,” the “antipsychotics”/neuroleptics, can create both the positive and negative symptoms of “schizophrenia,” via anticholinergic toxidrome and neuroleptic induced deficit syndrome. I’d say the primary etiology of “schizophrenia” is most likely iatrogenic, not genetic.

    “Others might see the ‘genes for schizophrenia’ story as a half-century-long train wreck.” My anticholinergic toxidrome poisoning story began with me, “on a run away train, never coming back.” And now it does seem it is time for the incorrectly assuming “mental health” industries to be “on a run away train, never coming back.”

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  3. This is quite something. I had never heard of this book, which was a NEW YORK TIMES NUMBER ONE best seller!?

    It just goes to show what an issue, what goes into something being “compelling.”

    I had mentioned this before, wasn’t going to go back to it, but with THIS turning up!

    How people can be so compelled to find out what’s going on with “schizophrenia” that they look towards anything THIS misleading.

    TWO big time Hollywood actors: Brad Pitt and Johnny Depp both have made a movie about “mental illness.” Johnny Depp also starred as a homosexual, and Brad Pitt wanted to, as a part in a movie.

    I didn’t know these people, but then I had for a couple of years had past lifetime feelings that I had been Vaslav Nijinsky. This got around, because I talked about it, and BOTH of those actors could frequent my city (I live in Grand Rapids, Michigan) where there never are, that I EVER have seen paparazzi.

    And they BOTH without EVER having talked to me about it, started referring to me by that name. Clearly only from gossip or small talk.

    Brad Pitt was hanging out at a coffee house I frequented, like multiple times a week. He was taking a math course at a local college, because of his interest in Architecture, and others from his class were there as well. It was kind of funny, because he can’t sit still, and he would often get something wrong in calculations, ask another to look at his work, and you’d see something akin to someone looking at what he did as if they are changing someone’s diapers, or this concerned look as when you’re trying to calm someone down. This millionaire that can hire tutors. Bouncing around making an object of himself getting college students who could afford none of that to help him.

    I was intrigued by him, and he clearly started having feelings for me, and I could feel it. I also was having such. And I was so out of it and insecure at that time. Then I got into one of these periods where you’re more not there, and would more just be taking in what’s going on than even thinking about it. Comes from trauma, the mental health system, not being given a voice, not knowing who you are. He had this group of people that I later referred to as his Humpty Dumpy Band, and one of them walked into the coffee house, and they gave each other high fives (which had become customary). Mr. Pitt was sitting behind me, one chair over, and the other came and sat on the other side of that table, while I was on a higher chair, the height of a bar stool. I was looking at a Schumann score, which I remember because I later asked to used his pen, or pencil to write Hemiola where this is a Hemiola in the music. I didn’t want to scrounge around in my backpack looking for a writing utensil. They had gone through their high fives. Mr. Pitt being such a store, the other started going on about wanting a bigger apartment with an extra room, but Pitt was trying to discourage him. He then, it seems for all I know, thought he was cute referring to his CD player as being and E drive, since you only have those on computers. (the D drive is usually the CD-drive but the E drive something else, back then) Maybe I got that wrong (was he referring to the grade he would get?), but he seemed to be entertaining acting like a “schizophrenia,” because I was there behind him. CDs aren’t E drives, that’s on computers, but to confuse them is cute “schizo” stuff, and I a real one was right there behind him!? I don’t know, it was pretentious to me. I really made me laugh, if that’s what he was trying to portray, which I don’ really know. Maybe I got that wrong. At one point the other said: “Are you accusing me of dating too many bar maids?” Which might have had something to do with the extra room. THEN, there was a moment of silence, and then we got to hear: “She’s STILL mad at me…..” Another pause. and we hear THAT again: “She’s STILL mad at me,” as who she was was elevated to that we all are supposed to know who he’s getting together with, because it’s all in the stuff you have to pass by at the store to actually pay the cashier. The tabloids. No mention of who she was, so I have to mention that at that time it was reported that he was dating Jennifer Aniston. This was just when or before Fight Club came out. Not that I’ve seen it. He doesn’t mention HER name, but then says: “Maybe, she’s mad at me because she KNOWS I want to have sex with Vaslav Nijinsky.”

    WOW! Let’s get Vaslav Nijinsky, whose life was torn apart by sexual exploitation involved with THIS! By an actor. No, I didn’t get involved with him. I WAS thinking about it. When I came out of such a vulnerable state, where I couldn’t respond to what was going on, I got pretty angry. I could just SEE myself having to deal with all of that. Namely given the media and how they tear anyone apart in such a “venue” as his environment. THAT MUCH I knew, that I was vulnerable. THAT made me quite angry afterwards, such insensitivity. Beyond what the media might do would they get their hands on such, he’s supposed to be an actor, and have insight into what’s going on with others, after having portrayed a “mentally ill” person in the movie 12 monkeys.

    AFTER he did 12 monkeys.

    It doesn’t end there. He got married to Aniston. And it STILL bothered me such uncouth behavior. Also because he feels free to say such remarks, it NEVER has been something he’s talked about in interviews, to make himself that vulnerable that he has such homosexual feelings. Instead he has, and had such an image that’s marketable because he WASN’T open, and so far HASN’T been. That he would SIMPLY with SUCH BILLING state that he HIMSELF has homosexual feelings, he’s wanted to make love to a guy, or simply mention love itself, rather than sex. Would he state that he has sexual feelings for other guys, HIMSELF. I can’t see but that quite a NUMBER of guys who don’t know what to think about themselves would possibly be prevented from committing suicide. SIMPLY because someone with such billing dared to make themselves vulnerable.
    That REALLY bothered me. Still was bothering me years later. I did a search online for Brad Pitt is gay, and the ONLY place that turned up regarding such was in gaypornblog. I actually posted about his behavior, and then: 1) I got TWO nasty phone call messages. Someone that sounded like Jennifer Aniston left a message: “hello..HELLO……(all in this rather out their tone, and not negative in projection, but then we get) YOU PRICK!” I can’t say that was her, but I wouldn’t know who else would call me like that, haven’t had any calls like that since at all, from anyone. Rather peculiar timing if it wasn’t. And there was another message with profanity in it, which I thought was just some repressed person, but after hearing what he hauled out with his family, on a flight when he was drunk, and how he couldn’t go a day without alcohol or marijuana, or something else (even when married), with such a result. Stuff we only know because his NEXT x-wife wanted to anonymously see the police report after the incident regarding a divorce, and it got out when she didn’t want it to, which then is blamed on her. I can’t say that wasn’t him, nor that it was. Couldn’t think it was, till after this report that wasn’t supposed to get out. And then that blog lost ALL of their posts, suddenly. Given the caliber of that blog that could have easily been a payoff rather than some computer glitz. Again, I can’t say I know one way or the other. If it’s non related and chance, it fits quite well that one would think it’s something else. We do all know that Brad Pitt and George Clooney found it funny to hire gay escorts from a site, and send them to each other’s shoots on set. That was all over the news some years ago, and then that site got closed down. What else could people have found out regarding who was hiring such, beyond this “fun” of those two!? Brad Pitt also thought it was worth telling people that George had put, which I now read were TWO stickers on his car. Although I remember Mr. Pitt as saying it was one: I’m gay and I vote,” and “Small Penis on board.” Everyone is honking at him, and he thinks it’s funny says Matt Damon thinking it’s because he’s Brad Pitt (Matt Damon ALSO has done a gay role, but as far as we know isn’t, and I remember some remark stereotyping a character he did i don’t even remember in which movie and stating THAT character was narcissistic)….

    And Johnny Depp who portrayed someone on this whole fantasy, who “magically” comes to when taking a neuroleptic. Quite non reality based, as those drugs go. I think Don Juan de Marcos would first have to as addicted to whatever Johnny has been on on both sides of the counter and beyond to be “stabilized” which would be because of withdrawal symptoms. And this whole affair with HIS x-wife, as if with everything he was on, he could remember what he’d done. You would need Hollywood and the media to back that vacancy up. Johnny Depp also referred to me as “Nijinsky,” without ever even starting a conversation asking me about it, himself. Numerous time, in different places. When he was not together with the mother of his children anymore, and before his relationship with his not yet x- wife was in the media, I was waiting at a bus stop. And he came along, stumbling like a drunk, and I thought: “oh, here it comes…..” I DID NOT want to have to deal with a drunk person, and their idea of social interaction. I had ENOUGH going on at that time, and told him to drop dead several times. he THEN actually grabbed my arm, as if he was doing something gentlemanly, and said in a tone I can only describe as childish, although I wouldn’t want to insult a child about it: “No, I want to torment you.” I was supposed to think this was cute, part of his image, his food for the multitudes. Fortunately, after I spouted some more at him, he left. STILL stumbling from intoxication, or rather wobbling along. I wonder whether he even could remember what he’d done. I so had enough of it, told him he’d grabbed my arm, and that I’d call the police. That anyone, going through what I already had, and then this “Nijinsky” connection, would have to deal with him thinking I’m some playground for this game of him thinking something he calls “tormenting” is cute. And the whole what I might call “Peter Pan” image media game, although I wouldn’t want to insult J M Barrie using his character for such reference. I have to add that I had read somewhere that he would wear even a band-aide his daughter had given him, and would describe her behavior as loving to “torment” daddy. Before that, before he had children, I saw him in a bar so loaded that he was all over the place, jumping at impulses while he wouldn’t remember any of it. And I’m sorry, but I don’t think Amber Heard has lied at all. She was holding back from any of what has come out to be in the media, she thought he would come around. And she held back from even naming him, only in an op-ed stating how she had become an object as a woman who spoke out about domestic violence. Because she was harassed, after divorcing him. Got death threats, had to get a new phone every week or something, was black-listed. That’s how women are treated in Hollywood. When Lynn Collins was in X-men and the movie didn’t do well, as the female lead, she was ditched by Hollywood, although the male lead did fine. And recently Tar with this Femme Fatal character again, while there are NUMEROUS male conductors who have on record done exactly what no female conductor even could do, since none of them have held such a position. And it really has nothing to do with classical music the weird banter supposedly involving it, the end is quite anti-asian. It’s just convenient to use a woman as such a character, because of what sells, and then Cate Blanchet jumps for it. What I think is that Amber Heard had to deal with a guy so full of controlled substances on both sides of the counter, that when reality kicked in regarding what he actually would do when his short term memory was turned off by the controlled substances, and he wouldn’t nor couldn’t remember behavior that otherwise might have been nothing but a dream while asleep in his bed, a dream that would just be a dream, not behavior aggressively grating against his image, and provoking such guilt he wouldn’t be able to deal with remembering it. Feelings he doesn’t know how to deal with, that Hollywood isn’t helping with, that the media isn’t helping with, that his psychiatrist and the drugging doesn’t help with, that the mafia he gets his drugs from doesn’t help with, that the alcohol and cigarettes don’t help with, nor the other legal substances. That’s what I think. And what’s sad is that if he really wanted to offer food for the multitudes, would he actually realize what the substance abuse lead to, and the psychiatric drugs, and the image games and addictions, and saw what the result was, and acknowledged it, then he’d truly be making change. That’s what I think, would I have an opinion of what really happened. Same as Brad Pitt would he actually state openly about his homosexual feelings, despite image marketing….

    As commodities go, and then we have the mental health system.

    I’ve posted about this stuff, but then asked Steve to remove the posts. But then reading about this book, a best seller that Oprah and Obama found one of their best reads, that supposedly is an amazing scientific piece of detective work. And what I’ve been through regarding, I thought OK. I’m not going to hold this back anymore.

    YES it’s a very compelling issue. So compelling and people want such an answer, want to know what’s going on, and want so much to be heroes that it doesn’t matter to what extent they get it quite wrong, and end up being EXTREMELY insensitive without knowing it…..

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    • By the way, regarding this “aside:” “(Matt Damon ALSO has done a gay role, but as far as we know isn’t, and I remember some remark stereotyping a character he did i don’t even remember in which movie and stating THAT character was narcissistic)” I don’t even know whether it was a role Mr. Damon played, or another character, but in one interview, regarding someone that’s “mentally” ill he actually went on a whole “delineation” regarding how such people display narcissism. This is a HOLLYWOOD actor maintaining an image talking about…..

      And he was actually serious about this. I could go on about this. And it isn’t that I haven’t encountered him and a few others showing the same……..

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  4. Thanks for your interesting comments. Just for the record, I didn’t directly say that “Rosenthal’s 1968 negative-result (failure to reject the null hypothesis) study discredited the idea that genetics ‘created the disease.’” One study cannot do that. I was saying that the author of Hidden Valley Road could have reached that conclusion if he had read the study carefully, and if he had read what critics had to say about the study. He did neither of those, and he reached the opposite conclusion–that Rosenthal’s research showed that nature won the schizophrenia/psychosis nature-nurture argument.

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  5. Jay:

    I enjoyed reading this. I also enjoyed our recent little dust-up on Twitter with Kolker.

    “to be sure, no studies have ever suggested that abuse does cause schizophrenia.”

    In fact, there are so many studies showing this we now have systematic reviews of the systematic reviews.

    Kolker’s mendacity knows no bounds. But what from someone who dismisses the plight of individuals who were raped, sodomized, and had God knows what else done to them when they were small and defenseless with sneering remarks about “blaming Mommy and Daddy?”

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    • It is so obvious how biased they are toward the evidence by how they talk about it. For abuse to have CAUSED “schizophrenia,” apparently we need proof beyond a reasonable doubt that EVERY case of “schizophrenia” is caused by abuse, despite there being no reason to assume all cases of “schizophrenia” are caused by any one thing, it being a behavioral syndrome that could have many causes. But for biological causation, a tiny correlation of hundreds of genes associated with less than a tenth of cases is evidence that “schizophrenia has a biological cause,” even though correlations with childhood abuse are ten or a hundred times stronger. How is it that the world of science and medicine is still willing to entertain and publish such obviously biased nonsense?

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      • Alinsky tactics. Hold your enemy to standards which you aren’t held to yourself. The burden for causation by abuse…… beyond a reasonable doubt. The burden for causation by genes….. “edit” the documents, and ‘verbal’ the results.

        Truth does not mind being questioned…. a Lie does not like being challenged. (author unknown)

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        • Oh, and if your ever in doubt about abuse causing ‘schizophrenia’, take a look at the deterioration of inmates in Abu Ghraib or Guantanamo Bay as a result of their ‘treatment’.

          I was also wondering about a ‘chemical waterboard’ after hearing recently from a brother (Maajid Nazem) about the use of a medazolam and morphine cocktail being used on people after issuing blanket Do Not Resusitate orders.

          One Dr Stuart Wilkie describing the process as a feeling that your drowning….. though unlike waterboarding, the ‘patient’ doesn’t actually survive. The possibility of resuscitation with flumazenil always an option if the intention is to torment (or what’s the term? “enhanced coercive techniques”?), and obtain the answers the State wants. And at present, they want the gene thing to be true, so I’d be careful questioning their delusional reality.

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  6. “In the 2020 edition of How Genes Influence Behavior, Flint and Kendler (and Ralph Greenspan) conceded that in the end, “literally thousands” of physiological candidate gene papers “have taught us nothing useful about the genetic basis of psychiatric disease.” As psychologist Stuart Ritchie commented in 2020, “reading through the candidate gene literature is, in hindsight, a surreal experience: they were building a massive edifice of detailed studies on foundations that we now know to be completely false.””

    It seems to me that starting with a false premise of “psychiatric disease” would guarantee that the entire edifice would crumble. If we were talking about any other species than Homo sapiens, we would be discussing “behavioral syndromes”, not diseases. Psychiatry creates “diseases” to justify its existence as a field of human medicine, but true animal behaviorists would balk at claims that behavioral syndromes are diseases.

    Psychiatry would benefit from a deep dive into true animal behavior research. Then again, there is a tremendous amount of money tied up in the whole psychiatric disease scam, so I won’t hold my breath hoping that psychiatry might find some humility.

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    • Some colleagues and I are carrying out a study of NIMH grant proposals. It has been an eye-opening experience.

      Lots of these researchers propose to systematically torment mice or rats or monkeys and then use all sorts of gee-whiz technologies to study the effects on their brains, or on gene expression.

      It seems to me they’ve just said it. In order to put these animals into a state they say is comparable to “mental illness” in humans, they had to systematically torment them. These mice or rats or monkeys were fine before the researchers got hold of them.

      Here’s my modest proposal: instead of pouring more billions into brain-based or gene-based research of “mental illness,” why don’t we just assume that being systematically tormented is a bad thing, and if mice or rats or monkeys are being tormented put a stop to it?

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      • Touche! It is fascinating that the psychiatric mainstream claims that these “mental illnesses” are all or mostly genetic, yet they have to use torture of animals to create similar circumstances. Wasn’t the “wire monkey” set of experiments sufficient to establish that early childhood mistreatment/neglect leads to a host of “mental illnesses” for adults? How many times do we have to do the same experiments and still fail to see the real results?

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      • As someone who worked for a time as a Laboratory Animal Veterinarian at a large research university, I can say pretty clearly that, at least in the 1990s and before, animals used in many kinds of experiments, especially behavioral, endured treatments sufficiently stressful to negate many of the findings of those research studies. i terminated an especially egregious experiment and then had to deal with the political backlash from the main investigator. Universities stand to lose millions of dollars in research funding when this kind of information comes to light. This is a problem that is polluting the results of many studies.

        Chronic stress alters many physiological parameters. We know the pathways. Physiology is closely linked to behavior. Epigenetics is the study of the effect of the environment on gene expression. Psychiatry, to the extent it claims to have an interest in the genetics of behavior, should be studying the epigenetic effects of chronic stress leading to behavioral changes, rather than trying to make associations between certain gene alleles with what they claim are “mental illnesses”. This would have much more relevance for human emotional suffering.

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      • I have several times signed petitions about this. They do the most….. you know when someone is on ritalin, and start doing repeated things, and are put on anti-depressants because that’s seen as a sign of depression, then are seen as bipolar because of that….

        https://investigations.peta.org/nih-monkey-torture/

        “repeated obsessive behavior”

        But torture monkeys for how long and get no results, and also promote a logic that’s…..

        I’m at a loss for words….

        Giving people chemical imbalances to say you’re treating it, and try to make out that what turns out to be one (an imbalance) comes from the treatment, till that has to be straightened out (shrinking of the frontal cortex, the brains stem swelling, dopamine deficiency because the brain stops making as much when their dopamine antagonism)….

        And this is genetic? How?

        Dehumanize people and animals as an excuse to say you’re trying to reinstate their humanity looking for something that doesn’t turn up time and time again!?

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  7. Jay, great article: let’s prove you right! A (scientific) Study of Identical Twins Separated at Birth and Reunited in Adulthood (AFTER the study) will prove Jay correct; this has proven impossible with human subjects (as Jay has clearly explained previously and herein) but can be done easily with primates. With support from the community, scientists at primate research centers can easily disprove Behavioral Genetics and promote a breakthrough in “mental health” care.

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  8. You’d think at least one critic would have asked the million dollar question about that quack “research”: What if it had never been done? What if the Galvin “sick boys” had all just abandoned their “family” and psychiatry forever?

    Real science wouldn’t make everyone petrified to ask what might happen if its subjects chose to live beyond it.

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  9. Or how about this thought experiment I decided to leave out of the article: What if all ten Galvin boys had been adopted away at birth and placed immediately with ten different randomly selected adoptive families. How many of them would have developed psychosis? My guess is zero.

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  10. Dr Lewis A Opler, a distinguished psychiatrist at ColumbiaUniversity, toldme that the causes of schizophrenia are “heterogenous.” I believe he is right. It’s a combination of genes and environment. I am reading Hidden Valley Road. It is valuable to me to learn about another family’s experiences with schizophrenia: the theories, treatments, attitudes, drugs, etc. Our family went through it also. This book really helped me.

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