In 2004 I was interviewed by Craig Newnes for The Psychologist, a journal published by the British Psychological Society. The occasion was the publication of my first book, The Gene Illusion: Genetic Research in Psychiatry and Psychology Under the Microscope. Upon publishing my fourth book, Schizophrenia and Genetics: The End of An Illusion (2023), psychologist/author Mary Boyle invited me for a new interview to discuss the book and the changes that have occurred in behavioural science genetic research since 2004. Mary’s questions, and my answers, are found below.
Mary Boyle: Jay, you were interviewed in 2004 about your book The Gene Illusion. It was a detailed critique of genetic research on “schizophrenia,” IQ and criminality and you concluded that there was little if any scientifically valid evidence in support of genetic influences on human behavioural differences. Your latest book, Schizophrenia and Genetics: The End of An Illusion has just been published. It, and your many other publications, show that a lot has happened in psychiatric and behavioural genetics research over the last 20 years. We’ll be talking about what has and hasn’t changed and whether your earlier conclusion still stands. But first, tell us how you became interested in this area and what keeps you engaged with it.
Jay Joseph: I became interested in the “genetics of schizophrenia” topic as a U.S. clinical psychology graduate student in the mid-1990s. The arguments fascinated me, and because I saw the genetic argument as weak, it was stunning to hear that the debate had been largely closed in favour of genetics by the 1980s. My desire to learn more about genetic research led me to the writings of critics of the mental health system and the medical model. I discovered several authors who had written critically about genetic research in psychiatry and psychology (including your work). Their writings inspired me to look more closely at the original studies. I’ve been publishing analyses of genetic research and theories in the social and behavioural sciences continuously since the late 1990s, including a doctoral dissertation, four books, several book chapters, peer-reviewed journal articles, and online articles.
A lot has changed since my 2004 interview for The Psychologist, but the problematic fundamentals have not. For example, the unjustified production of heritability estimates based on environmentally confounded twin studies of behaviour continues (heritability is itself a disputed concept). Behavioral gene discovery claims also continue, but as in 2004 such claims are based on gene-behavior associations (correlations) that most likely are spurious or non-causative because they are based on chance findings, false assumptions, and/or systematic error. The mainstream media usually ignores these significant problems and often reports new behavioural twin studies or gene discovery claims as “landmarks” or “breakthroughs.” The authors of these media reports believe that twin study assumptions are valid (they aren’t, as I’ll describe later), and also write as if decades of false-alarm gene discovery claims had never happened.
Mary: Psychiatric diagnostic concepts have been increasingly criticized by service users, professionals and researchers. Many psychologists – and some psychiatrists – don’t use them, including the label “schizophrenia.” Has this had any impact on genetic research?
Jay: Not much, because genetic researchers in psychiatry must continue to use these disputed labels to define the diagnoses they study. Although establishing both the reliability and validity of psychiatric conditions is a prerequisite for any attempt to search for genes or genetic influences, the literature shows both are questionable.
Nevertheless, psychiatric diagnoses are presented as illnesses or even “diseases” in mainstream textbooks, journal articles, media outlets, and at websites including those run by the UK National Health Service (NHS), mainstream psychiatry organizations, the U.S. National Institute of Mental Health (NIMH), and many other influential and respected sites. The organizations behind these and other websites assume that DSM or ICD psychiatric diagnoses are valid medical conditions and that heredity plays a key role in causing them.
Mary: There have been significant changes in research techniques and theories of genetic influence over the last twenty or thirty years. What do you see as the most important?
Jay: The main molecular genetic research methods in the 1990s and 2000s were the linkage and candidate gene association study methods. There were countless gene discovery claims based on these methods in that era (examples here and here). However, by the 2010s, the initial early-1990s excitement had given way to the crushing realization that all that researchers had found was genetic fool’s gold in psychiatry, IQ research, and other areas.
Some of us argued back in 2004-2005 that claims then being made about discoveries of “genes for behavior” and “genes for psychiatric disorders” were based on a genetic mirage. For example, in a 2005 exchange with leading psychiatric genetic researcher Kenneth Kendler in the American Journal of Psychiatry, I wrote that we should consider “the possibility that genes for the major psychiatric disorders do not exist.” Kendler pointed to several “positive” psychiatric linkage and candidate gene results in response. It subsequently developed that the critics had been right all along about the genetic mirage. As Jonathan Flint, Kendler, and a colleague wrote in the 2020 (2nd) edition of How Genes Influence Behavior, “Literally thousands of papers reporting the results of physiological candidate gene association tests. … are now considered to be false positives.” This discovery led them to conclude that “it’s not too harsh to say simply that these studies have taught us nothing useful about the genetic basis of psychiatric disease.” In his 2018 book Blueprint: How DNA Makes Us Who We Are, top behavioural geneticist Robert Plomin called behavioural candidate gene research a “flop,” a “fiasco,” and an “approach [that] failed everywhere.”
Another research area focuses on rare genetic variants, such as copy number variants or “CNVs,” accompanied by many claims of gene association. However, as Flint and colleagues wrote in How Genes Influence Behavior, “the early hope that CNVs would reflect the ‘royal road’ to understanding molecular genetic effects on schizophrenia has been disappointing.”
Currently, genome-wide association studies (GWAS) and calculations of polygenic risk scores (PRS) derived from GWAS results are a major focus of attention. These methods involve the idea that many genetic variants each make a small contribution to a characteristic or “disorder.” The GWAS era began in 2005-2007.
A GWAS, CNV, or PRS study might find an association (correlation) between genetic variants and a given diagnosis or behavioural characteristic (IQ, for example). But these methods don’t provide evidence that genes play a role in causing the diagnosis or characteristic. Correlations and PRS “predictions” are not causes and may be spurious and/or the result of systematic error, as earlier behavioural linkage and candidate gene researchers learned the hard way. In 2022, Thomas Insel, the biologically oriented former director of the NIMH, recognized that “in contrast to the mutations discovered for cancer or rare diseases, none of the genetic variants associated with mental illness can be considered causal.”
Other GWAS/PRS major problem areas include the questionable validity of psychiatric diagnoses and behavioural characteristics such as IQ and personality, population stratification confounds, a lack of individual predictive value, the practice of increasing sample size to find statistically significant gene associations, the frequent inability to replicate gene associations in independent samples, low PRS generalizability across global populations, that “variation explained by” does not mean “caused by,” and the potential “fishing expedition” aspect of “hypothesis-free” studies in which researchers base their conclusions on statistically significant yet chance associations.
GWAS publications have reported all kinds of improbable gene associations (“hits”) in the past few years, including characteristics such as getting concussions, self-reported childhood maltreatment, crying habits, ice cream flavour preferences, loneliness, musical beat synchronization, regular attendance at a sports club, pub, or religious group, and white wine liking. I see these “discoveries” as giant GWAS red-flag warnings of systematically biased research, and they bear an uncanny resemblance to earlier candidate gene association study red flags.
For the past 15 years, genetic researchers have been struggling with what they call a “missing heritability” problem, that is, the gap between (misleading) heritability estimates from twin studies (see below) and the disappointing results of molecular genetic research. The most likely explanation for the missing heritability problem in psychiatric genetic research is that causative genes are “missing” because they do not exist. I said as much in my 2004 interview, in my 2006 book The Missing Gene: Psychiatry, Heredity, and the Fruitless Search for Genes, and in a 2012 article. I continue to hold this view in 2023.
Mary: How have researchers responded to what seem like unpromising outcomes?
Jay: They often respond by implying that GWAS-identified associations constitute gene discoveries, and that better methods and larger samples will produce more discoveries and increased “GWAS heritability” in the future. Although researchers and the media announce new behavioural gene “discoveries” almost daily, the failed behavioural candidate gene era provides a telling example of how a widely promoted scientific structure can produce thousands of gene-discovery claims over two-plus decades, and then come crashing down upon the discovery that the structure produced only false-positive non-findings.
The best example is the frequently cited claim that people experiencing “stressful life events” are more likely to be diagnosed with depression if they carried a 5-HTTLPR gene variant. Despite the publication of at least 450 research papers about this variant, by 2018 or so it became clear that the 15-year-old 5-HTTLPR depression story did not hold up: “There Is No ‘Depression Gene,’” read the title of a 2019 article published in Science. (My review of the “genetics of major depression” literature here.)
In his 2014 book Misbehaving Science: Controversy and the Development of Behavior Genetics, sociologist Aaron Panofsky described behavioural geneticists’ “coping strategy” of “technological optimism” in the face of gene discovery failures. By this, he meant the “optimism that the next level of technology will overcome past disappointments.” Disappointing results from PRS studies, including a study of “educational attainment” based on three million individuals, suggest that currently employed “next level” methods such as GWAS and PRS will suffer a fate similar to the earlier failed linkage and candidate gene methods in psychology, psychiatry, and related fields. Psychiatric Genomics Consortium co-founder Patrick Sullivan concluded in 2017 that the “historical candidate gene studies” he and many others had previously promoted “didn’t work, and can’t work,” and he “strongly suggest[ed] that we abandon candidate gene guesswork…as they have only provided false directions and wasted effort.” It is likely that the authors of future publications will arrive at similar evaluations of psychiatric genetic CNV, GWAS, and PRS research.
Mary: You mentioned twin studies earlier. These and adoption studies have been especially influential in research on areas such as “schizophrenia,” IQ, “personality,” “bipolar disorder” and criminal behaviour. Yet you and other critics have forensically shown that they don’t support genetic explanations. You devote several chapters of your new book to them as well as your 2015 book The Trouble with Twin Studies: A Reassessment of Twin Research in the Social and Behavioral Sciences. Why do you think it’s so important to keep these studies – some of which are now 90 and more years old – in the limelight?
Jay: It is important to keep twin studies in the limelight because they (and, to a lesser extent, adoption studies) continue to supply the evidence most often cited in support of substantial genetic influences on a wide range of behavioural characteristics, and because twin study heritability estimates guide molecular genetic research. Support for twin studies is seen in journal articles, textbooks, websites, and across social and traditional media. Yet twin studies are based on accepting a key assumption that is clearly wrong, and adoption studies have their own set of problem areas. Neuroscientist/geneticist Kevin Mitchell wrote in 2009, “Familiality and twin concordance data are the bedrock on which all psychiatric genetics, including GWAS, is based and justified.” What Mitchell saw as bedrock is more like quicksand.
Most twin studies find that reared-together MZ (monozygotic, identical) twin pairs behave more similarly than do reared-together same-sex DZ (dizygotic, fraternal) twin pairs. These findings are rarely disputed. What is disputed is what these findings mean. Twin researchers interpret their findings genetically by assuming that MZ and DZ environments are similar, and that the only behaviorally relevant factor distinguishing these pairs is their differing degrees of genetic relationship to each other (100% vs. an average 50%).
Critics, on the other hand, have argued since the 1930s that the MZ-DZ “equal environment assumption” (EEA) as it relates to behavioural twin studies is false because, when compared with same-sex DZ pairs, MZ pairs grow up experiencing (1) more similar treatment by parents and others; (2) more similar physical and social environments; (3) more similar treatment by society due to their sharing a very similar physical appearance; (4) a much greater tendency to spend time together, to have common friends and peer influences, and to model their behaviour on each other; and (5) identity confusion and a much stronger level of emotional attachment to each other.
Even though the evidence overwhelmingly shows that MZ environments are much more similar than DZ environments, psychology, psychiatry, and other behavioural science areas continue to endorse genetic interpretations of twin study results. Nevertheless, twin study MZ-DZ comparisons cannot be interpreted genetically because such comparisons are unable to disentangle the potential influences of genes and environments. Behavioural twin researchers, it seems, have been engaged in a century-long scientific folly of epic proportions.
Turning to so-called “twins reared apart” studies—a method still recovering from the Cyril Burt scandal of the 1970s—I showed in a 2022 analysis that the actual result of the famous 1990 “Minnesota Study of Twins Reared Apart” (MISTRA) article published in Science was a failure to find genetic influences on IQ (0% heritability). The researchers arrived at their conclusion in favour of 70% IQ heritability by using methods that included (1) suppressing their DZ-apart full-sample control group IQ correlations (which have never been published), (2) counting environmental influences as genetic influences, (3) failing to acknowledge that most twin pairs they studied were only partially reared apart, (4) keeping their raw data off-limits to independent reviewers, and (5) mistakenly assuming the non-existence of behaviour-shaping cohort influences experienced by two people of the same sex who are born and grow up at the same time in the same historical era. Twin study results never speak for themselves; interpretation is everything.
Mary: In your new book, you situate psychiatric genetics research within the context of the replication crisis and questionable research practices in the behavioural sciences. What do you think this adds to our understanding of what’s going on in this area?
Jay: There is a growing realization that the scientific research/publication process is in crisis. It is known as the replication crisis, meaning a crisis brought about by later independent analysts’ discovery that they could not replicate some key scientific research findings. The original findings were probably non-findings resulting from poorly performed research or from data and conclusions manipulated by researchers to match their own or their funding sources’ expectations.
A wise person once said, “Data don’t tell stories; scientists tell stories.” Previously accepted stories researchers told us about their data are receiving increasing attention and scrutiny, and we can now evaluate behavioural and psychiatric genetic research using replication crisis concepts and terms, such as the questionable research practices (QRPs) described by behavioural scientist Leslie John and colleagues in 2012. These researchers found that the use of QRPs as reported anonymously by academic psychologists was “surprisingly high.”
An aspect of the QRP concept is p-hacking, which describes the practice of researchers consciously or unconsciously manipulating definitions and data, either openly or behind the scenes, to transform non-findings into publishable career-enhancing “findings” that reach the conventional .05 level of statistical significance. P-hacking is a significant problem in behavioural research (the MISTRA, for example) and extends into the molecular genetic realm. In 2016, behavioural geneticist Eric Turkheimer wrote that “genome-wide association [research] is unapologetic, high-tech p-hacking,” where if “no significant results are discovered the first time around, the process is repeated with even larger samples, continuing until something significant finally emerges.”
As I described in detail in Schizophrenia and Genetics, the famous schizophrenia adoption studies performed in Denmark between 1968 and 1994 by American researchers Seymour Kety, David Rosenthal, Paul Wender and their Danish colleagues provide a disturbing example of how psychiatry, psychology, and other behavioural science fields continue to pass off massively flawed studies as “landmark” research. To match their genetic confirmation biases and to achieve statistically significant results in the genetic direction, the Danish-American adoption investigators (1) dismissed or minimized the impact of environmental confounds such as selective placement, late separation, and late placement; (2) openly manipulated data and temporarily removed diagnostic categories from key comparisons; (3) called one of their studies “preliminary” and decided to collect data past the study’s data collection stop-point; (4) changed key group comparisons; and (5) broadened the definition of schizophrenia “as widely as it may have ever been reasonably conceived before” (Rosenthal), and then re-narrowed the definition, over 26 years.
For Kety, Rosenthal, Wender et al., concluding that heredity did not contribute to schizophrenia was unacceptable. Far from objectively evaluating their results, they reasoned that if their data showed no evidence of assumed genetic causes—as it did at several key points—there must be something wrong with the data, or with the study design, that they needed to fix. That’s not how science is supposed to work.
The language developed since the early 2010s to describe unsound research practices has enabled those of us with perspectives that differ from mainstream behavioural science positions to tell our stories in new and better ways. The Danish-American schizophrenia adoption studies are perhaps the longest-running example of openly p-hacked research ever seen in the behavioural sciences and constitute a half-century-long scientific deception in psychiatry that should not survive the replication crisis.
The current behavioural science research/publication system provides an open invitation for researchers to engage in QRPs and p-hacking. In his 2020 book Science Fictions: How Fraud, Bias, Negligence and Hype Undermine the Search for Truth, psychologist Stuart Ritchie acknowledged that “the system of peer review and journal publication” is “badly broken.” The system is broken in part because it allows researchers—behind the scenes and before submitting their manuscripts to academic journals—to collect data, analyze results, and reach conclusions consistent with their confirmation biases.
The replication crisis has led to increasing calls to require research preregistration in behavioural research, where investigators would submit their research rationale, hypotheses, design and analytic strategy, and planned data collection stop-point to a journal for peer review before collecting and analyzing data. Preregistration methods in the form of register reports have been adopted by hundreds of scientific journals in the past decade. Research preregistration alone cannot fix a broken system, but it’s a good place to start.
Mary: Also in Schizophrenia and Genetics, you discuss two well-known family studies, the “Genain Quadruplets,” all of whom were diagnosed as “schizophrenic” and the Galvin family (discussed in the book Hidden Valley Road), where six boys were given that diagnosis. You show how researchers and commentators have downplayed or even ignored the horrific abuse and trauma these children suffered in favour of a genetic explanation. These are extreme examples but are there other ways researchers keep genetics in the foreground in the face of a weak evidence base?
Jay: Yes. For example, Robert Plomin argued in Blueprint that most environmental influences on behaviour are actually genetic influences, and that the remaining true environmental influences are “mostly random—unsystematic and unstable—which means that we cannot do much about them.” By this logic, because society “cannot do much about” the environment and cannot do much about heredity either, there is no need to spend millions of dollars on behavioural genetic research.
Plomin justified counting most environmental influences as genetic influences by arguing that “we select, modify and even create our experiences in part on the basis of our genetic propensities,” meaning that “children make their own environments, regardless of their parents.” Similar faulty arguments have been put forward by others about childhood maltreatment, implying that children partly “create” family environments containing physical, sexual, and emotional abuse. Do people who suffer from racism and other oppressive aspects of society create their suffering? Are some people genetically less bothered by these adversities? In any case, environmental influences are environmental influences, not genetic influences. (My review of Blueprint was published in 2022.)
Despite poor returns, molecular genetic researchers in psychiatry and psychology also help keep genetics in the foreground by using language that is often optimistic, including phrases such as “spectacular advances,” “momentum of genomic science,” “revolutionary genetic research,” “golden post-genomic era,” and “the future looks bright.” As seen in Blueprint, public statements of excitement, optimism, and discovery by leading researchers are at times accompanied by private feelings of disappointment and failure.
Mary: There’s a lot of talk now about conflicts of interest in medical and psychiatric research, and especially about the role of pharmaceutical companies. There’s not yet much public discussion about vested interests and conflicts of interest in genetic research. How much of an issue is this and should we be worried about it?
Jay: Conflicts of interest are a major issue we should be concerned about since there is a symbiotic relationship between psychiatry, psychiatric genetics, supporters of neoliberal political policies, and drug companies. All have a vital and mutual interest in convincing the public that “mental disorders” are individual-based largely genetic brain diseases in need of medication “like other diseases.” However, the evidence for neurotransmitter or genetic causes, even for diagnoses like schizophrenia and major depression, is weak. A leading group of neuroscientists concluded in 2022, “Despite three decades of intense neuroimaging research, we still lack a neurobiological account for any psychiatric condition.”
There’s a gold rush aspect of psychiatric molecular genetic research. Drug companies still believe they can design and patent drugs targeted at a person’s genotype and stand to profit even more in the future. Other ways genes can be monetized include the development of patented diagnostic tests, direct-to-consumer (DTC) genetic tests such as 23andMe, and products aimed at marital partners and post-conception embryo selection. There are frequent declared and non-declared conflicts of interest in psychiatric molecular genetic research. It’s difficult for researchers, institutions, and academic journals to remain objective when salaries, “consulting fees,” grants, endowments, profits, royalties, advertising revenues, potential patent fortunes, and scientific recognition are at stake.
As in 2004-2005, psychiatric genetic researchers continue to discover only “gene association” fool’s gold, most likely because that’s all there is to discover. But as long as the system keeps going and staves off a candidate-gene-style GWAS/PRS/CNV collapse, the insiders will continue to profit. More and more, the entire enterprise resembles a smaller scientific version of the U.S. “military-industrial complex.”
Mary: What you’re saying suggests that genetic research in the behavioural sciences, and the ways it’s communicated, is something we should be concerned about not just as researchers, service-users or professionals, but as citizens….
Jay: We should be very concerned because we are being fed a false and harmful narrative. The mainstream story about the genetics of most areas of human behaviour follows a seven-step corrupted process, which goes something like this:
Academic researchers in the fields of behavioral genetics and psychiatric genetics produce unsound research (accompanied by misleading heritability estimates) based on false assumptions and/or genetically misinterpreted data, which is then accepted for publication by peer-reviewed scientific journals → researchers producing unsound research are often rewarded and even honored, which motivates them to produce even more unsound research → respected academic fields and government agencies (including health-related agencies such as the NHS and the NIMH) endorse and promote this unsound research in textbooks, websites, and other publications → the mainstream media reports on and promotes unsound research, often in the form of articles and news reports of supposed new discoveries based mainly on twin studies, including selectively reported stories about individual pairs of reunited “separated twins” supposedly displaying “spooky” behavioral similarities (for example, the “Jim Twins”) → the mainstream media regularly reports on supposedly exciting new molecular genetic behavioral gene discoveries as if five decades of false-alarm claims had never happened → books (e.g., Hidden Valley Road and The Gene: An Intimate History), videos, online articles, and social media posts by journalists and some highly respected researchers and authors promote and celebrate unsound research, while the works of critics are usually ignored, distorted, or dismissed → students and teachers in the academic world, political policy makers, and the general public are convinced by the above process that what are in fact unsound studies and false-alarm or non-causative behavioral gene association claims are actually sound studies and causative gene discoveries.
The above process describes how corporations, the mainstream media, and the politically powerful attempt to “manufacture consent” in the area of human behavioural differences, just as they manufacture consent for their domestic and especially foreign policy positions and actions. The process encourages people to accept and possibly promote various related political, social policy, scientific, and social-relations viewpoints. It also supports practices such as psychiatric genetic counselling programs, selective adoption placements, producing genetic risk profiles, prioritizing funding of genetic over environmental research, and even the promotion of eugenic interventions that involve selecting for “desirable traits.” People diagnosed with “schizophrenia” or another “mental disorder” may worry that they are carrying faulty genes they might pass on to their children. Others may fear that they harbour predisposing genes if other family members are diagnosed. These are important ethical issues that don’t get nearly enough attention.
Mary: How do you see psychologists’ and others’ responsibilities and influence in this area?
Jay: Psychologists and other behavioural scientists should ensure that the research they cite and endorse is methodologically sound and is based on well-founded assumptions. Unfortunately, the replication crisis has demonstrated that we cannot rely on the peer-review process to prevent the publication of methodologically unsound research based on false assumptions and QRPs (e.g., candidate gene association studies and twin research). Psychologists and psychiatrists should be willing to challenge psychiatric and behavioural genetic claims that their fields have integrated into their consensus positions. We all understand that a field’s consensus views are not always correct, especially in the politically charged social and behavioural “soft sciences.” By necessity, critical analysis of behavioural and psychiatric genetic research includes consulting the works of critics of these fields and giving their arguments due consideration, and exploring alternatives to diagnosis and medicalization. We are responsible for ensuring that teaching curricula include critical analyses of genetic research (which may be omitted from standard textbooks) and that this informs our discussions with clients, colleagues, teachers, students, and the media.
Mary: Some, maybe many readers may be saying at this point, “But surely our genetic endowment must have some impact on our mental life and behavior and we need to research this.” What would you say to them?
Jay: I would say to them that although genes are of course involved in most aspects of human functioning, focusing on genetics to understand who we are psychologically and how humans differ behaviorally is a mistaken approach lacking scientific support.
Psychiatric and behavioural geneticists argue that heredity plays an important role in producing “individual differences in behavior.” To understand how these differences arise, they say we should focus on reared-together twins, reared-apart twins, adoptees, brains, genes, IQ scores, biological-relative IQ correlations, “personality,” a range of statistical modelling techniques, “mental disorders,” crime statistics, GWAS hits, polygenic risk scores, and heritability estimates. Supporters of this approach sometimes depict those who focus on environmental causes of behavioural differences as suggesting that people are born as psychological “blank slates.” Steven Pinker attributed this view to environmentalists in his 2002 book The Blank Slate: The Modern Denial of Human Nature, and it has continued since then.
However, so-called “blank slatism” is a straw man because few who focus on environments hold such views as they relate to cognitive and other abilities and temperament. They usually argue that while there may well be inborn differences among people in these areas, it is perinatal, family, social, cultural, religious, educational, geographical, and political environments (including oppression) that together play a decisive role in shaping human behaviour and abilities and that focusing on “individual differences” and problematic heritability estimates implies limited changeability and distracts our attention from the need to improve or radically change these environments.
Instead, those of us who focus on environments point to the many characteristics, potentials, needs, desires, biological similarities, and abilities we all share, and prioritize progressive policies and programs related to healthcare, education, jobs, housing, nutrition, disease prevention, maternity/paternity leave, anti-discrimination, poverty alleviation, wealth redistribution, war prevention, and so on.
Regarding DSM and ICD “mental disorders,” although many people see it as axiomatic that disordered genes are an important underlying cause of major psychiatric diagnoses such as schizophrenia, bipolar disorder, ADHD, and depression, there is no scientifically valid evidence supporting the direct role of genes, even if genes play some role in differences in abilities and temperament.
After decades of research, the psychiatric and behavioural genetics fields have produced no findings beneficial to the human condition as they relate to the major psychiatric diagnoses and psychological characteristics such as IQ and personality. In various ways, though, they have produced harm. The psychiatric genetics field has harmed people not only because of its eugenic (“racial hygiene”) history and origins but because it diverts our attention from evidence-backed causes of human suffering and dysfunction. The behavioural genetics field’s misplaced emphasis on genes and supposedly high within-group “IQ heritability” is sometimes cited by “race scientists” to claim that “races” and classes differ genetically in “measured intelligence,” and is also cited in support of regressive political policies. Supporters of psychiatric and behavioural genetic research need to explain how these fields are contributing valid information that benefits society. If a better world finds no one funding or engaging in “genes for behavior” research, I doubt any of us would suffer from it.
Boyle, M., & Johnstone, L. (2020). A Straight Talking Introduction to the Power Threat Meaning Framework: An Alternative to Psychiatric Diagnosis. PCCS Books.
Kirk, S. A., Gomory, T., & Cohen, D. (2013). Mad Science: Psychiatric Coercion, Diagnosis, and Drugs. Routledge.
Panofsky, A. (2014). Misbehaving Science: Controversy and the Development of Behavior Genetics. University of Chicago Press.
Richardson, K. (2022). Understanding Intelligence. Cambridge University Press.