The Schizophrenia Genetics Illusion—A Century of Failure and Hype

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In a 2003 edition of Science, the editors declared that the identification of genes for “mental illness” was the second most important “scientific breakthrough” of the year. “Schizophrenia, depression, and bipolar disorder often run in families,” the editors wrote, “but only recently have researchers identified particular genes that reliably increase one’s risk of disease.” The prefrontal cortex, they wrote, “is regulated in part by a gene called COMT, one of the handful associated with risk of schizophrenia.”

As it turned out, claims based on these “particular genes” didn’t hold up, including the COMT gene. When a journal as prestigious as Science says that genes for psychiatric conditions have been discovered, most people take this as fact—and remember it as fact. But in this case, it turned out not to be a fact. Despite the development of new techniques leading to current claims of gene associations based on genome-wide association (GWAS, based on common single nucleotide polymorphisms, or SNPs), polygenic risk score (PRS), and copy number variant (CNV) studies, genes shown to cause “schizophrenia”—a questionable concept in and of itself—remain undiscovered.

3D illustration of white DNA double helix against dark blue background. The center of the helix is erupting into a computer-network-like shapeThe criteria for diagnosing schizophrenia remain vague and subjective. As psychologist John Read has shown, there are 15 ways that two people can meet the DSM criteria for schizophrenia without sharing any symptoms in common. Reliability remains low, and is even decreasing. I agree with writers who reject the “schizophrenia” concept and prefer the term “psychosis.”  However, as critical psychiatrist R. D. Laing once remarked at an academic conference, “I am unhappy about using the term schizophrenia at all. But it would be somewhat whimsical to eliminate it from my vocabulary, since it is on the lips of so many.”

I became interested in the “genetics of schizophrenia” topic as a clinical psychology graduate student in the mid-1990s. The arguments fascinated me, and because I saw the genetic argument as weak, it was astonishing to hear that the debate had been largely closed in favor of genetics two decades earlier. I decided to focus my 1998 doctoral dissertation on a critical analysis of schizophrenia genetic research. I have been writing about genetic research in the social and behavioral sciences ever since, including my 2015 book The Trouble with Twin Studies.

In this article I make the case that, contrary to most of what has been written on the topic, there exists no valid evidence that genes play a role in causing schizophrenia. I make the complete case in the 2023 Routledge English-language edition of my book Schizophrenia and Genetics: The End of An Illusion (a greatly revised version of a previously self-published e-book). Here I summarize the book’s main arguments in favor of reopening the genetics of schizophrenia debate.

Family, Twin, and Adoption Studies

Science is about data, but more importantly about how scientists and others interpret data. The common claim that schizophrenia is “80% heritable,” which both justifies and guides the search for genes at the molecular genetic level, is based on a century of family, twin, and adoption research. Because similar methods are used in other areas of psychiatry and in behavioral research in general, the critique of these methods has major implications for most areas of human behavior. The production/usefulness of heritability estimates (which range from 0% to 100%) is controversial in its own right, which calls into question statements of “percentages of variance in disease liability” often used to support causal models of psychiatric conditions.

It is widely agreed upon that family studies are unable to disentangle the potential influences of genes and environment on human behavioral differences. Twin studies assume that reared-together MZ (identical) and DZ (fraternal) twin pairs grow up experiencing “equal environments,” and that the only behaviorally relevant factor distinguishing these pairs is their differing degree of genetic relationship to each other (100% versus an average 50%). Critics and even most genetic researchers, however, recognize that MZ environments are more similar than DZ environments. Although twin researchers and their supporters have developed various arguments and tests in attempts to sidestep twin studies’ glaring unequal environments problem, I show in Schizophrenia and Genetics that these arguments and tests do not hold up. Twin studies’ crucial MZ-DZ “equal environment assumption” (EEA), therefore, is false. Publications based on this obviously false assumption have produced some pretty strange “findings,” including that dog ownership, vegetarianism, and concern for nature are only somewhat less heritable than schizophrenia.

Because family studies and twin studies are unable to disentangle the potential influences of genes and environments on human behavioral differences, they supply no evidence that genes play a role in causing schizophrenia. Seventeen schizophrenia twin studies have been published since 1928. Since that time leading authorities in twin research, psychiatry, and other behavioral fields have mistakenly attributed to genetic factors the usual finding of greater MZ versus DZ behavioral resemblance (concordance).

The famous Danish-American schizophrenia adoption studies were flawed and biased to the point of constituting a not-yet-recognized scientific scandal (more below), and genetic interpretations of the few remaining adoption studies are invalid due to bias, methodological issues, and environmental confounds.

To summarize, family, twin, and adoption studies have failed to produce evidence that schizophrenia is “heritable.”

Environmental Factors

Meanwhile, studies have linked schizophrenia and psychotic conditions to childhood adversities such as having experienced bullying, emotional abuse, incest, neglect, parental loss, physical abuse, and sexual abuse, as well as the stresses of immigration, urbanicity, poverty, relative poverty, and social marginalization. Brain disease theories survive through the use of smoke and mirrors and the confusion of cause and effect. From the perspective of those who see political, economic, social, and oppressive aspects of society as causing widespread psychological harm, what psychiatry calls the “societal burden of mental disorders” is really the mental burden of societal disorders.

Molecular Genetic Research

The mistaken belief that family, twin, and adoption studies long ago established schizophrenia as a genetically based disease constitutes the fundamental error of schizophrenia gene-finding strategies. 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 called bedrock is more like quicksand.

Corporate media reporting of false-alarm “schizophrenia gene discoveries” has a long history, and continues to the present day. A widely reported yet non-replicated schizophrenia gene association was published in 1988 by the Sherrington group, who believed they had found “the first strong evidence for the involvement of a single gene in the causation of schizophrenia.” A November 10, 1988, front-page New York Times article about this study proclaimed, “Schizophrenia Study Finds Strong Signs of Hereditary Cause.” The Times also reported subsequently non-replicated schizophrenia gene discoveries in 1995, 1997, 2002, 2006, 2008, and 2013, with headlines such as “Brain-Tied Gene Defect May Explain Why Schizophrenics Hear Voices,” “Schizophrenia May Be Tied To 2 Genes, Research Finds,” “Schizophrenia as Misstep by Giant Gene,” and “Study Ties Genetic Variations to Schizophrenia.” Retractions are few and far between.

Linkage and Candidate Gene Studies. Despite much fanfare and anticipated gene-discovery “euphoria” dating back to the 1970s, the schizophrenia linkage and candidate gene eras eventually crashed and burned. In a 2002 analysis, leading schizophrenia molecular genetic researcher Lynn DeLisi and colleagues concluded, “No linkage appears to be consistently replicable across large studies.” In his 2018 book Blueprint: How DNA Makes Us Who We Are, top behavioral geneticist 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 tally, 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?” Factors such as a reliance on twin studies and heritability estimates, systematic bias, and the use of the questionable research practices I will soon discuss provide a partial explanation. Yet leading researchers (including Plomin), review writers, and the authors of influential books told the public in the 1990s and 2000s that studies had identified genes associated with schizophrenia. Similar stories of claims and hype followed by spectacular failure also played out in the areas of major depression and intelligence (IQ).

Commenting in 2008 at the height of the failed candidate-gene era, psychiatric researcher Timothy Crow wrote that although the “schizophrenia gene pond” was in fact “empty,” a “chorus of reviews…pervades the literature and will convince all but the most inquisitive that a solid foundation of evidence supports the pathophysiological relevance of these candidate genes.” When evaluating current claims of GWAS gene associations or discoveries by the world’s top researchers, we must remember that many of them were claiming gene discovery in an era they now recognize to have been a “flop.” We should keep Crow’s 2008 “chorus of reviews” comment in mind when assessing recent claims based on newer methods—same chorus, slightly modified lyrics.

A 2016 New York Times article with the title “Scientists Move Closer to Understanding Schizophrenia’s Cause” reported on a supposed discovery that variants of the C4 gene, which codes for a protein in a cascade of factors in the innate immune system and synaptic sculpting, play a role in causing schizophrenia. In 2022 this widely publicized C4-schizophrenia link was shown to be false, as another psychiatric genetic “landmark study” failed to hold up as the schizophrenia genetics story continues to unravel. (The 2022 Borbye-Lorenzen et al. study failing to find an association between C4 and schizophrenia was published as I was writing this article, too late to be included in the book.)

Enter GWAS and PRS Studies. Many current gene association claims are based on the “hypothesis-free” genome-wide association (GWAS) method, which dates back to the period 2005-2007. By definition, a scientific fishing expedition is a hypothesis-free method, where researchers base their conclusions on significant yet chance associations that in the GWAS context can pop up on a Manhattan plot. Schizophrenia GWAS publications, which can be seen as describing fishing expeditions of this type, have produced only spurious or non-causative “gene associations” (correlations). Correlation, as is well known, does not imply cause. In 2022, Thomas Insel, the biologically oriented former director of the U.S. National Institute of Mental Health, 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.”

In Blueprint, Plomin described the polygenic risk score (PRS) method as a molecular genetic technique that combines statistically significant and nonsignificant individual SNP associations identified in a GWAS to produce a polygenic (composite) risk score. A 2022 study by the Schizophrenia Working Group of the Psychiatric Genomics Consortium calculated a 7% schizophrenia polygenic risk score. The study’s lengthy “Competing Interests” section showed that many of the researchers taking part in this project had financial ties to the drug companies.

In addition to the above-mentioned problems, the GWAS and PRS methods are subject to confirmation biases, environmental confounds such as population stratification (“popstrat”), financial conflicts of interest, and a reliance on questionable or false assumptions.

CNV Research. Another area focuses on potential rare risk variants, such as rare copy number variants, or “CNVs.” Many studies claiming CNV-schizophrenia associations have appeared in recent years, but they are subject to many of the problems found in the GWAS/PRS area. In 2020 Jonathan Flint and Kenneth Kendler, two of the world’s leading psychiatric genetic researchers, wrote that the “early hope that CNVs would reflect the ‘royal road’ to understanding molecular genetic effects on schizophrenia has been disappointing.”

Most likely, Robert Plomin’s final evaluation of the behavioral candidate gene era will be the future consensus evaluation of the psychiatric GWAS/PRS/CNV era as well—approaches that “failed everywhere,” and “fiascos” and “flops” that make us wonder why “so many published papers…got it so wrong.”

Misleading Information: The National Health Service Website

One of countless examples of misleading information about schizophrenia and genetics from a source most people trust is found at the U.K. National Health Service (NHS) website. I will quote from the NHS “Causes—schizophrenia” page as it appeared on 11/18/2022, accompanied by my responses.

  • Schizophrenia tends to run in families, but no single gene is thought to be responsible.”

Response: Schizophrenia running in families can be caused by nature or nurture, as most psychiatric genetic researchers readily acknowledge. And yet, as stated in the Fifth Edition of the DSM (DSM-5), “most individuals who have been diagnosed with [schizophrenia] have no family history of psychosis.” No genes shown to cause schizophrenia have been discovered.

  • It’s more likely that different combinations of genes make people more vulnerable to the condition. However, having these genes does not necessarily mean you’ll develop schizophrenia.

Response: This is speculation, not scientific fact.

  • Evidence that the disorder is partly inherited comes from studies of twins. Identical twins share the same genes.”

Response: Twin study MZ-DZ comparisons are confounded by environmental factors, and like family studies the results cannot be interpreted genetically.

  • In identical twins, if a twin develops schizophrenia, the other twin has a 1 in 2 chance of developing it, too. This is true even if they’re raised separately.”

Response: Pooled MZ twin concordance in the better-performed studies published since 1963 is less than 25%. But even if it were 50% (“1 in 2 chance”), MZ concordance alone does not establish “heritability.” MZ concordance must be compared with DZ concordance, based on the assumption that MZ and DZ environments do not differ. There are no schizophrenia studies of twins raised separately. Rather, there exist only a handful of similarity-biased anecdotal reports on individual MZ twin pairs who in most cases were only partially reared-apart.

  • In non-identical [DZ] twins, who have different genetic make-ups, when a twin develops schizophrenia, the other only has a 1 in 8 chance of developing the condition.”

Response: This result can be completely accounted for by the much less similar environments experienced by non-identical (DZ) versus identical (MZ) twin pairs.

  • While this [DZ twin rate] is higher than in the general population, where the chance is about 1 in 100, it suggests genes are not the only factor influencing the development of schizophrenia.”

Response: This result suggests nothing at all about genetic influences, since DZ twins grow up together in the same family and social environment at the same time (birth cohort), and share a twin relationship. For these non-genetic reasons, we would expect the pooled DZ concordance rate to be greater than the 1% general population rate (“about 1 in 100”). The actual pooled DZ rate in the better-performed twin studies is not 12%, as the NHS says (“1 in 8 chance”), but only around 4% (a recent 12/367 3% DZ concordance rate can be found here).

How Myths are Created and Sustained

If the mainstream genetics of schizophrenia story is wrong, the question then becomes why so many people still believe it. This story—as well as the mainstream story of the genetics of most other areas of human behavior—follows a seven-step process. Twenty-five years of research analysis has led me to conclude that this is a corrupted process, and it goes something like this: academic researchers in the fields of behavioral genetics and psychiatric genetics produce unsound research based on false assumptions and/or manipulated or genetically misinterpreted data, which is then accepted for publication in peer-reviewed academic journals → researchers producing this unsound research are often rewarded, funded, tenured, and even honored, which motivates them to produce even more unsound research, sometimes over an entire career → respected academic fields and government agencies (including health-related agencies) endorse and promote this unsound research in textbooks, websites, and other publications → the mainstream (corporate) media reports on and promotes this unsound research, often in the form of articles and news reports of new discoveries based mainly on twin research → the mainstream media regularly reports on supposedly exciting new molecular genetic behavioral gene discoveries as if decades of non-replicated false-alarm claims had never happened → books, 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 true causative gene discoveries. This leads them to accept and possibly promote various related political, social policy, scientific, and social-relations viewpoints.

Science’s “Replication Crisis”

The scientific research/publication process is in a state of crisis, which has much relevance to schizophrenia and other areas of genetic research. It is known as the replication crisis (also known as the “replicability crisis” or the “reproducibility crisis”), meaning a crisis brought about by the discovery that some key findings across various scientific fields were probably non-findings resulting from research that was poorly performed, manipulated to match researcher or funding source expectations, or even fraudulent.

Questionable Research Practices (QRPs)

Behavioral scientist Leslie John and colleagues introduced the questionable research practices (QRP) concept in 2012. “Although cases of overt scientific misconduct have received significant media attention recently,” they wrote, “questionable research practices (QRPs)…increase the likelihood of finding support for a false hypothesis.” QRPs “are often questionable as opposed to blatantly improper,” and “offer considerable latitude for rationalization and self-deception.” Not just self-deception, I would add, but deception of their colleagues and of society as a whole.

John and colleagues listed ten QRPs: (1) “Failing to report all of a study’s dependent measures,” (2) “Deciding whether to collect more data after looking to see whether the results were significant,” (3) “Failing to report all of a study’s conditions,” (4) “Stopping collecting data earlier than planned because one found the result that one had been looking for,” (5) “‘Rounding off’ a p value,” (6) “Selectively reporting studies that ‘worked,’” (7) “Deciding whether to exclude data after looking at the impact of doing so on the results,” (8) “Reporting an unexpected finding as having been predicted from the start,” (9) “Claiming that results are unaffected by demographic variables…when one is actually unsure (or knows that they [are]),” and (10) “Falsifying data.”

Where we decide to draw the line between QRPs and outright fraud is a matter of opinion. The QRP framework provides an increasingly accepted language describing how and where research goes wrong, even to the point of retraction.

The Behavioral Science Research/Publication System Remains Broken 

A long-running research/publication system that allows people—behind the scenes and prior to submitting manuscripts to journals that usually publish only statistically significant findings—to collect data, analyze results, and reach conclusions influenced by confirmation biases and possible financial conflicts of interest, is an open invitation to engage in QRPs. Plomin recognized in 2022 that the authors of “thousands of” previous behavioral candidate gene reports “commit[ted] every sin in the catalogue of questionable research practices,” an unintended yet blistering indictment of the behavioral science peer-review system that published these reports for two decades. Candidate-gene-era friendly peer reviewers, editors, and journals greenlighted these QRP-riddled studies by the thousands only a few years ago, and there is good reason to believe they continue to do so with potentially QRP-riddled GWAS, PRS, and CNV studies as well.

Among QRPs we find p-hacking, which “occurs when researchers collect or select data or statistical analyses until nonsignificant results become significant” (the conventional level of statistical significance is .05, or the GWAS level of 5 × 10−8). For example, I have shown that genetic conclusions in the famous Minnesota Study of Twins Reared Apart 1990 Science IQ study were the result of p-hacked research. In molecular genetic research, behavioral geneticist Eric Turkheimer wrote in 2016 that “genome-wide association is unapologetic, high-tech p-hacking.”

Research Preregistration. The use of QRPs and the prevalence of p-hacking in psychiatric and behavioral research (including environmental research) would be reduced by research “preregistration,” where investigators would have the option or be required to 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.

The preregistration of behavioral research would greatly reduce p-hacking and the use of other QRPs brought to light in the replication crisis. There is growing support for and use of Registered Reports, which as described at the Center for Open Science website,

“is a publishing format that emphasizes the importance of the research question and the quality of methodology by conducting peer review prior to data collection. High quality protocols are then provisionally accepted for publication if the authors follow through with the registered methodology… . It eliminates a variety of questionable research practices, including low statistical power, selective reporting of results, and publication bias, while allowing complete flexibility to report serendipitous findings.”

Behavioral research would benefit greatly by adopting Registered Reports or similar procedures, and the scientific community and the public would have much greater confidence in the results.

Schizophrenia Genetic Research and the Replication Crisis

A wise person once said, “Data don’t tell stories, scientists tell stories.” In the current replication crisis era, previously accepted stories researchers told about their data are receiving increasing attention and scrutiny. In the past, critics of psychiatric research didn’t have a widely agreed-upon framework and language to explain how unsound research in this field is performed, published, and validated. The QRP and p-hacking concepts now provide such a framework, enabling those of us with perspectives that differ from mainstream behavioral science positions to tell our stories in new and better ways. In Schizophrenia and Genetics, I show how schizophrenia genetic research has been characterized by the use of QRPs, by a reliance on false or highly questionable assumptions in twin research, adoption research, and other areas, and by spurious or non-causative media-hyped gene-association claims. The paradigm is poised for collapse.

The Danish-American Adoption Studies. Although still routinely cited in psychiatry textbooks and other works in support of genetics, the famous Danish-American schizophrenia adoption studies (published between 1968 and 1994) provide striking examples of massively flawed research based on several QRPs. Among many other problem areas, to arrive at desired genetic conclusions, investigators Seymour Kety, David Rosenthal, Paul Wender and colleagues (1) dismissed or minimized the impact of environmental confounds such as the selective placement of children by adoption agencies, late separation, late placement, and the non-representativeness and restricted range of adoptive family environments (John and colleagues’ QRP #9); (2) appear to have changed their planned 1968 key group comparison at the last minute because this comparison did not produce statistically significant results in the genetic direction (QRPs #6, #7, and #8); (3) for the same reason, performed a last-minute reduction of their 1994 “Provincial” study index and control adoptee (proband) groups respectively from 42 to 33, and from 42 to 24 (QRP #7); (4) broadened the definition of schizophrenia “as widely as it may have ever been reasonably conceived before” (Rosenthal), and then re-narrowed the definition when necessary, over a 26-year period (QRPs #1, #6, and #7); and (5) temporarily removed a study-defined “schizophrenia spectrum diagnosis” to achieve statistically significant results in one of their key group comparisons (QRPs #1, #6, and #7).

In the Danish-American Rosenthal-led adoption study using diagnosed parents as the first-identified relatives (probands), the researchers decided to call their 1968 results “preliminary” when they found no statistically significant genetic influences at what should have been the study’s data-collection stop-point, and then kept looking for additional diagnosed parents after 1968 in the hope of finding enough schizophrenia spectrum diagnoses among their adopted-away biological offspring to achieve statistically significant results. Rosenthal and colleagues then decided to stop counting diagnoses at the point at which the comparison dipped below the .05 level of statistical significance, and published these results in 1971. Although such maneuvering to arrive at desired conclusions may have been acceptable in 1960s-1970s psychiatry, it is now properly recognized as a classic p-hacking strategy (John and colleagues’ QRPs #2 and #4). In a different context, genetically oriented psychologist Stuart Ritchie criticized a p-hacking strategy of “not setting the sample size beforehand,” which allows “researchers to continue collecting data and testing it, collecting data and testing it, again and again in an open-ended way until they get their desired p < 0.05.” This describes to a T the p-hacking strategy Rosenthal, Kety, Wender and colleagues employed in this still-cited “landmark” schizophrenia adoption study.

Lynn DeLisi echoed mainstream psychiatric “turning point” descriptions of these adoption studies in her 2017 popular work 100 Questions & Answers About Schizophrenia: Painful Minds:

“The turning point in schizophrenia research, and probably the most important data collection and results of the 20th century in this field, came from the carefully planned and executed adoption studies of Seymour Kety and David Rosenthal….These data…turned the corner for support for ‘nurture’ to support for primarily ‘nature.’”

The reality is that the Danish-American schizophrenia adoption studies are perhaps the longest running example of p-hacked research ever seen in the behavioral sciences, and as such should not survive the replication crisis. The schizophrenia genetics story unravels even more.

Final Thoughts

Contrary to the consensus opinion in psychiatry and other behavioral sciences, there exists no scientifically acceptable evidence that schizophrenia or psychosis have an underlying genetic component, which has implications for other areas of human behavior. When it is finally acknowledged that “schizophrenia” is not “genetic” or a “disease,” society will part ways with genetic diversions and inappropriate medical approaches, and will instead focus on environmental causes, non-medical interventions, and prevention with a necessary political-change component. People might still wish to take prescribed drugs, but the process should be completely transparent, including informing people of all potential side effects and withdrawal problems. No one should be told they are being prescribed drugs to treat a genetically caused schizophrenia brain disease—not the “patient,” not the family, not anyone.

Because family, social, cultural, religious, educational, geographical, and political environments together play a powerful role in shaping human behavior, attention should be focused away from people’s brains and genes, and toward aspects of the environment that on the one hand help protect, nurture, and empower people, and on the other hand can psychologically harm people.

In his 1980 book The IQ Game, sociologist Howard Taylor described IQ-genetic researchers’ “use of assumptions that are implausible as well as arbitrary to arrive at some numerical value for the genetic heritability of human IQ scores on the grounds that no heritability calculations could be made without benefit of such assumptions.” Modifying Taylor’s description to fit schizophrenia genetic research and claims, in Schizophrenia and Genetics I describe the use of false or questionable assumptions, questionable research practices, and the promotion of spurious or non-causative gene association claims to produce schizophrenia heritability estimates and gene discovery claims, because no such estimates or claims could be made without engaging in such practices.

This is the schizophrenia game. It has been played for over a century, and it’s time to stop. A world without schizophrenia genes will do just fine.

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The author thanks Mike Jones for helpful feedback on an earlier draft of this article.

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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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110 COMMENTS

  1. Thank you, Jay, for your honest research and reporting.

    And I will say I’m quite certain that “schizophrenia” and “psychosis” should be considered iatrogenic – not “genetic” – illnesses. Given the fact that the “schizophrenia” treatments can create “psychosis,” via anticholinergic toxidrome. And the “antipsychotics” can also create the negative symptoms of “schizophrenia,” via neuroleptic induced deficit syndrome. Not to mention the antidepressants and ADHD drugs can make a person “psychotic” as well.

    But I do know from experience that those who claim to be “mental health experts” – but also claim to be ignorant of the above mentioned facts – they do have a bad habit of defaming people’s grandmothers, who they’ve never met, in an attempt to rationalize their misdiagnoses and malpractice.

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  2. Researching this subject would likely be more productive if you realized that “schizophrenia” isn’t a disease at all , but a syndrome- a collection of signs and symptoms with certain preponderences that can have any number of causes if the individual repetitive variations can’t be teased out for specific treatments.

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  3. Jay:

    I’ve got your book on order.

    I predict one day we will look back on the era of genome-wide association studies the way we now look back on Medieval scholastics debating how many angels can dance on the head of a pin.

    You look for a correlation, and if you don’t find one you just increasing the sample size until you do. Although it never seems to work the other way around. When they find a correlation, you never hear these guys say “Well maybe if you looked at another population, this correlation would disappear.”

    It’s like betting on the outcome of a coin toss, with this stipulation: heads I win, tails e keep flipping until it comes up heads.

    It’s a con game that would embarrass a used-care salesman.

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    • Truly. They find a SET of genes that has a 1.065% correlation with the “condition” in question (not even dealing with the impossibility of locating a legitimate study group with the subjective criteria used for “diagnosis”) and say, “We’ve proven that “ADHD” is genetic!!!” You look at the article and find that only 5% of the study group has this combination, while 4.7% of the control group has the exact same set of genes! How is that causation? But people lap it up. I guess if you WANT to believe something badly enough, you find a way to justify it.

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  4. It’s understandable to want to completely disregard inherited causes of psychosis when genetic research into the subject has been so corrupted.

    But family, social, cultural, religious, educational, geographical and political environments interact with inherited propensities, which should not be ignored.

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    • @Marie: Why shouldn’t we ignore them? Can you point to a single patient in a clinic anywhere in the world who has benefited from a century of psychiatric genetics research?

      You could probably find genetic variation for any trait, if you looked hard enough, and so what? When John Snow found that tainted drinking water caused cholera, the authorities didn’t commission a study on the genetics of cholera resistance. They cleaned up the water supply, and everyone benefited, whether he personally was genetically susceptible to cholera or not.

      We know what causes the complaints that fall under the diagnostic rubric of schizophrenia — child sexual abuse, physical abuse, emotional abuse, and every other category of adverse childhood experience. Unlike the human gene pool, these are factors we CAN change. Let’s work on that.

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      • I would add to that cultural dislocation and living in an urban environment.

        The example I use is that not ALL kids who get hit by cars at a crossing near a school have their legs broken. Should we do research into why certain kids have “weak bone disorder” and try and come up with some “treatment” to make their bones tougher? Or should be maybe put in a traffic light and a crosswalk?

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      • @Patrick, Steve, Jay. First, I’m not advocating for genetic research. I am saying that heredity is probably a factor in mental illness, as it is in many illnesses. Maybe no one has looked into the genetic causes of cholera, but they have looked into genetic causes of numerous disorders including diabetes and breast cancer. I agree there’s no hard evidence that there is a genetic propensity for psychosis. But what hard evidence is there for other causes of psychosis? If someday we have the tools to formulate a complete description of the causes of mental illness, heredity will probably be included. Currently, such tools don’t exist.

        Also, it is very optimistic to believe that we can combat psychosis by changing cultural dislocation, urban environment, family, social, cultural, religious, educational, geographical and political factors. There’s no reason to think this will ever happen.

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      • To Jay Joseph, Marie, and others

        I think it is more correct to say that on some level, genetics is a factor in ALL aspects of human behavior. HOWEVER, it also critically important and more correct to emphasize that any kind of so-called “human predisposition” (expressed in genetic makeup) is TRIGGERED and then reinforced by the surrounding environment.

        For example, human beings are capable of behaving very violently and selfishly, especially in highly threatening and highly competitive environments where trauma is a common experience. Are there gene combinations in the human species, that allow for humans to express these behaviors as a necessity of evolutionary survival? Yes!

        At the same time, there is CLEAR evidence in the sociological history of the human species, that in some more egalitarian, less competitive (for natural resources etc.), and with less traumatic experiences, that human beings have behaved in highly cooperative and loving ways, with extremely RARE instances of violence and so-called selfish behaviors. Are there gene combinations in the human species, that ALSO allow for humans to express THESE TYPE OF BEHAVIORS (triggered by the surrounding environment) as a necessity of evolutionary survival? Yes!

        Another important example to consider: If we take two people from roughly the same environment, and subject them to extreme forms of torture – one of the those people might start to mentally breakdown (with forms of psychosis – psychologically splitting off from reality etc.) after (let’s say) 16 hours of such treatment. The OTHER person being tortured might take (let’s say) 21 hours before psychologically splitting off etc.

        Are both environmental history AND GENETICS somehow involved in the difference of the 5 hours that it took to achieve a psychological breakdown for these two individuals. Yes, I believe it correct to posit that analysis.

        HOWEVER, why!!! should our society spend one dime (instead of billions of dollars), and even one minute of time on trying to find some genetic difference between the two individuals in the above scenario???

        We SHOULD INSTEAD be spending ALL our time on finding out why we have a society with all the kind of sociological structures (in the environment) that allows for the existence of these anti-social behaviors to even exist in the first place. AND then focus ALL our attention on creating a social ENVIRONMENT that will bring forward and reinforce the very BEST qualities of the human species.

        Richard

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        • Just because certain words roll off lots of tongues, whether “schizophrenia” or “psychosis,” isn’t a reason to continue using them. Language whittles away at diverse ways of being alive. It perpetuates the most violent in cultures. If many cultures are built on the bodies-minds-hearts-spirits of others, we can choose differently. We don’t need to continue reifying a violence that begins with a presupposition that some lives matter, and others are disposable. I grieve that careers depend on explaining others’ experiences by counting, measuring, comparing variables lodged in supremacist, violent, violating foundations. Valuable human beings like Jay and Marie expend a lot of energy and consciousness, aiming not to dispose of what’s “realistic;” however, a consensus “reality” that excludes and diminishes isn’t a world or worldview that is worth parsing or maintaining. Effects are effects. Not side effects or collateral damage. Naming or fighting between two names, maintains the binary presupposition that life, being, must exist within supremacist structures. Cooperation, love, openness to questions and not-knowing offer possibilities unimaginable if we focus only on making the best of violent language, reactions, and use of power by some over, on, or for others. Searching with new eyes, hearts, consciousness will look different from the current re-search and conquer cycle that maintains the same consciousness that constructed the power-over cultures that crush living beings and the earth. Investing in mitigating “effects” only maintains and transmits corrupt, extractive, toxic systems. We have a little time left to co-create communal responses to collective problems. Co-being offers a consciousness for life, not sacrifice.

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          • Berta says:

            “Language whittles away at the diverse ways of being alive. It perpetuates the most violent in cultures…We don’t need to continue reifying a violence that begins with a presupposition that some lives matter, and others are disposable.”

            Very true. Someone should send this to the APA.

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  5. Thoughtful observers such as Marie often make the same inferential mistake. SZ is entirely an emotionally driven reaction to social life and circumstances. Any truly genetic social disadvantage (e.g., short stature, mental slowness, speech or motor impairments, unattractiveness) merely increases the probability of social defeat and regression in response to external circumstance. There are no inherited (genetic) propensities “for” schizophrenia. Put another way, all normal humans have all the genes necessary to react to social life in the schizophrenic manner. The elusive endophenotype of schizophrenia is the normal human being.

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  6. Jay Joseph quotes the editors of “Science”: “Schizophrenia, depression and bipolar disorder often run in families.”

    The editors made an amazing observation. But guess what else runs in families? Intergenerational trauma.

    Jay Joseph also says, “From the perspective of those who see political, economic, social and oppressive aspects of society as causing widespread psychological harm, what society calls the “societal burden of mental disorders”, is really the mental burden of societal disorders…”
    Absolutely.

    “Because family, social, cultural, religious, educational, geographical and political environments play a powerful role in shaping human behavior, attention should be focused away from people’s brains and genes, and toward aspects of the environment that on one hand protect, nurture, and empower people, and on the other hand can psychologically harm people.”
    This is where the focus needs to be.

    Who knew science would one day become a great tool for denying reality? It’s become its own form of psychosis.

    Define psychosis: a severe mental disorder in which thought and emotions are so impaired that contact is lost with external reality –
    This explains a lot.

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    • Also worth noting that most psychiatric genetic researchers concede the point that “running in the family” does not prove anything about genetics. For example, in the 2020 second edition of “How Genes Influence Behavior,” top genetic researchers Jonathan Flint and Kenneth Kendler recognized that a condition running in the family can be caused by the common environments families share. They wrote:

      “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 family studies cannot be interpreted genetically–psychiatric geneticists and the field’s critics are in agreement.

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  7. Jay and Steve, my husband has this question for both of you:
    “It is clear that psychosis is not 100% caused by genes because not all twins are affected. Does this mean that gene and the body do not play any role in psychosis. Could it be one influence among many?”

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    • Of course, it is possible – genes play some role in everything we do. The point is, the psychiatric profession WANTS to blame the genes and distorts the research to try and force that conclusion. And despite that, genes still fail to explain anything about any psych disorder consistently, even a small percentage.

      I look at it this way: we all have genes, they are pretty much fixed from birth. They are not something that can be changed. There are LOTS of other variables that CAN be changed, through epigenetics, through individual efforts, through improved social structures, through community supports, etc. Why focus our attention on the one thing that can’t be changed? Why not focus on the things we HAVE control over, especially as genetic research so far is a huge bust, despite billions of dollars having been invested in it?

      The other thing about genetics is often overlooked – a particular set of genes may allow vulnerability to certain conditions, but might also make other conditions possible. A hugely disproportionate number of our poets, writers, playwrights, graphic artists, etc. have had psychotic experiences. Perhaps a certain set of genes opens us to alternative experiences of life and enables artists to flourish? And snuffing out those genetic variations snuffs out a lot of creativity and motivation to change and grow in society?

      The way psychiatry approaches genetics borders on eugenics. They want to “stamp out” the “bad genes” without any real interest in understanding the purposes of those genes. Species survival depends on genetic variations. Genetic differences are not “diseases” or “disorders.” We would do best to simply understand that we have the genes we have and learn to work with them.

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      • Steve says, “The other thing about genetics that is often overlooked – a particular set of genes may allow vulnerability to certain conditions, but might also make other conditions possible. A hugely disproportionate number of our poets, writers, playwrights, graphic artists, etc. have had psychotic experiences. Perhaps a certain set of genes opens us to alternative experiences of life and enables us to flourish? And snuffing out those genetic variations snuffs out a lot of creativity and motivation to change and grow in society?”

        Yes!!! Artistic/creative people seem born with a unusual ability to see the world in unique ways. And maybe not having a chance to safely express themselves in ways that come naturally to them causes them to blow a fuse. But I think everyone is creative, so the same goes for anyone who’s need to express themselves is thwarted.

        And of course genes are the reason for it. But whatever’s involved, leave it nature alone; there’s a reason for spontaneity. It’s called evolution, which is the beauty and mystery of it all.

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      • Steve says:

        “The other thing about genetics is often overlooked – a particular set of genes may allow vulnerability to certain conditions, but might make other conditions possible. A hugely disproportionate number of our poets, writers, playwrights, graphic artists, etc., have had psychotic experiences. Perhaps a certain set of genes opens us to alternative experiences of life and enables artists to flourish? And snuffing out those genetic variations snuffs out a lot of creativity and motivation to change and grow in society?”

        YES!!! Artistic/creative/intuitive/sensitive people seem born with an ability to experience the world uniquely. And maybe not having a chance to safely express this in ways that come naturally to them causes them to blow a fuse. But I think everyone is creative, so the same goes for anyone whose need to express themselves is thwarted.

        And of course genes are the reason. But whatever’s involved, leave it alone; there’s a reason for spontaneity, it’s called evolution, which is the beauty and mystery of it all.

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    • Hello. The pooled identical (MZ) concordance rate for schizophrenia is less than 25% in the better-performed studies, which can be explained by non-genetic influences. In the most recent study the MZ rate was 14.8%. There is no scientifically valid evidence that genes have anything to do with schizophrenia/psychosis. That doesn’t prove that genes play no role, but only that currently there is no evidence that they do play a role.

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  8. Good points Steve but (as you said in an earlier post in reply to Marie, I think) we don’t have “to simply understand that we have the genes and learn to work with them” because the “genes” are nonexistent. Not a single angel dances on the head of this pin. Genes (or large mutigenic structural variants, such as CNVs) that confer competitive disadvantages and social vulnerabilities may predispose to extreme social defeat in children and adolescents but they do not cause schizophrenia. Social defeat does (including fear, inferiority, abuse, abandonment, forced immigration, discrimination and so forth, in combinations that are always individually unique). As Lidz presciently said in 1958, at a time when “biological” psychiatry was just starting its rise, “schizophrenic outcome is a possibility inherent in the developmental process which must be anticipated, rather than a condition to be regarded as incomprehensible or as the manifestation of a disordered cerebral apparatus.” He also said, “I wish to remark somewhat parenthetically, in response to a question raised repeatedly, that the problem of why one child among several in a family becomes schizophrenic does not appear to be insurmountable when one grasps the dynamics of role relationships within the family, the vicissitudes of the family, and the different stresses linked to being a member of one sex or the other in the given family.” Over 95% of all cases of SZ ascertained by national registries and hospital records do not have a 1st, 2nd or even 3rd degree relative with SZ. By the way, MZTs reared together are only concordant ~13%, barely above the fraternal sibling recurrence risk (SRR, usually given as ~8%). (Furthermore, even the SRR is inflated d/t the family size effect and ascertainment biases, and of course the gratuitous definitional creep of schizophrenia that Joseph exposes in his books and papers). That small percentage (~13%) is shockingly low for a presumed genetically-based condition that encompasses every domain of personality. In contrast, in the infamous separated twin studies, Bouchard reported “separated” MZTs who were highly concordant for such trivial and arbitrary things as pet names and hair styles. This disparity is the greatest of all embarrassments to MISTRA. How is it possible that genes can control individual hair styles of “separated” twins over space and time, yet fail so miserably to produce concordance for schizophrenia in MZTs who are reared together? As so poignantly detailed in Jay Neugeboren’s autobiographical essay “Imagining Robert”, his schizophrenic twin brother was repeatedly sexually abused by someone the family trusted, a fact that didn’t come out for years after his brother’s diagnosis. And by the way, if you are an investor, the big money in GWAS/PGS phenotypic prediction is in selling test kits full of caveats and other fine print indemnifying the vendors.

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    • I pretty much agree with all you said, except that I don’t think “social defeat” is caused by the genetic phenotype, it’s caused by the society’s unwillingness/inability to be flexible enough to deal with the wide range of “phenotypes” that are around. “ADHD” is the best example. It is caused almost entirely by inflexible social expectations in schools. Kids who go to school a year later have a 30% lower chance of being “diagnosed.” Kids with an “ADHD” diagnosis in open classrooms are virtually indistinguishable from their “normal” peers. A great study showed that groups of 3 with an “ADHD” kid in the group did FAR better solving problems than groups of 3 “normal” kids. If we didn’t expect young people to sit still for extended periods of time “studying” subjects they have no interest in or have already mastered, “ADHD” would mostly disappear, regardless of the fact that some kids will always be ‘more active’ than others in any group.

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  9. @Marie:

    “But what hard evidence is there for other causes of psychosis?”

    I am glad you asked. There is OVERWHELMING evidence that the complaints that fall under the diagnostic rubric of schizophrenia are caused — not triggered, caused — by child sexual abuse, physical abuse, emotional abuse, and every other category of adverse childhood experience. The correlation is robust, reliable, and dose-dependent. It cuts across income brackets, ethnic identiies, and national boundaries. There are so many studies we now have systematic reviews of the systematic reviews.

    As if all this were not enough, the connection between trauma and psychosis has been confirmed in a macabre way. In the 1990’s, there was a huge excess of Holocaust survivors in mental hospitals in Israel.

    What common sense tells us is true: bad things happen, and they can drive you crazy.

    “Also, it is very optimistic to believe that we can combat psychosis by changing cultural dislocation, urban environment, family, social, cultural, religious, educational, geographical and political factors. There’s no reason to think this will ever happen.”

    That sounds incredibly pessimistic.

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    • Actually there is no OVERWHELMING evidence that childhood abuse causes schizophrenia. Certainly, some studies show an association, but most research is flawed and it’s obvious that there are other causes for schizophrenia than childhood abuse, which seems to put too much of the blame for the illness on parents.

      Bad things indeed do happen, and can drive certain people crazy. I knew a man who had a psychotic breakdown because he feared his wife was having an affair and he’d lose his family. But most people facing divorce don’t react that way.

      I also think there’s a huge difference between being pessimistic and realistic.

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      • Certainly, the correlations between childhood abuse and “schizophrenia” labels being assigned is orders of magnitude higher than the most optimistic estimate of “genetic contribution.” We’re talking over 80% vs. at best single digits, and that’s not even allowing for the biased research and reporting you properly identify. Plus, childhood abuse is something we CAN do something about!!!!

        Someone simply doesn’t want that information to be discussed! I wonder who?

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  10. Thanks Steve for pointing that out. I didn’t mean it that way. “Social defeat” is not caused by genetic phenotype any more than it is caused by genes. It is caused by social interaction and that is that. Children with certain neurodevelopmental CNVs – which are well characterized and highly syndromic – have exceptionally high rates of SZ, as well as social anxiety and depression. They also have exceptionally – actually phenomenally – high exposure to bullying, sexual abuse, family separation, and ridicule.

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      • @GPM & Steve:

        “Genes (or large mutigenic structural variants, such as CNVs) that confer competitive disadvantages and social vulnerabilities may predispose to extreme social defeat in children and adolescents but they do not cause schizophrenia.”

        Agreed. CNV number variants are a known risk factor for low IQ, which in turn may be a risk factor for bullying, social isolation, etc. So if anything, they’ve discovered a risk factor for these pernicious social factors, which in turn are risk factors for the complaints we group under the diagnostic label “social anxiety,” “ADHD,” “schizophrenia,” etc.

        I’m also reminded of the 22q deletion, which is a known risk factors for a diagnosis of schizophrenia, with a ten-so-thirty-fold increase in absolute risk of a diagnosis. This falls short of Kenneth Kendler’s criterion of a 100-fold odds ratio needed to call something “a gene for,” and the great majority of people born with this deletion are never diagnosed with schizophrenia, but this still is a phenomenon that demands explanation.

        We know the 22q deletion causes a whole host of physical deformities, which in turn may be risk factors for the pernicious social influences mentioned above. It is not “a gene for schizophrenia,” by any means.

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  11. This whole nature nurture ‘genetics or environment’ debate is such a crock of shit. There is no such thing as an infant with schizophrenia, so obviously it’s developmental. Maybe there are infant tempermants that are more predisposed to psychosis developing down the line idk, but temperament is not ‘genetic’ in the reductive sense either: maternal levels of cortisol influence temperament; the womb is an ENVIRONMENT.

    Development, which is what is proper to us humans, is nature via nurture all the way down, which means there is no possibility of the environment not being involved. The other day I told a friend of mine I had sleep apnea and she said ‘oh is that environmental or genetic?’ I had to roll my eyes. The airway is developed THRU the attachment dynamic, I.e. breastfeeding. behaviors that the infant engages in with the caregivers are the catalysts for genes to become active in the development of the airway.

    There is not a single gene that spontaneously manifests without an environmental stimulus and context, and so you simply cannot say that anything at all is purely genetic. Epigenetics should put the nature nurture debate to bed as an oversimplified, overly reduced way of thinking about an organism. But then again psychiatry loves nothing more than to be overly simplified, reduced, and rigidly mechanistic with no concept of organic development.

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    • Rasx says:

      “Development, which is what is proper to us humans, is nature via nurture all the way down, which means there is no possibility of the environment not being involved…”

      “There is not a single gene that spontaneously manifests without an environmental stimulus and context….”

      “Epigenetics should put the nature nurture debate to bed as an oversimplified, overly reduced way of thinking…”

      “But psychiatry loves nothing better than to be overly simplified, reduced, and rigidly mechanistic with no concept of organic development.”

      Psychiatry isn’t a medical association; it’s a medical dissociation.

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  12. The “environment” also includes the other genes in the environment of a gene, the milieu of transcription factors etc, and above all the overall metabolic/physiologic state of the cell which calls upon genes as resources; in turn the totality of the cell is hopelessly coupled to its cellular environment, etc etc. This “cytological” or “cytosocial” environment is only partially Markovian (independent of previous state): it has a memory; previous environments affect future environments. It is also unfathomably sensitive to the sequence of environments as well their frequency, duration and magnitude. That complexity is what makes it impossible to assign a simple value to any trauma or other experience; it is historical and context dependent. It is this overwhelming complexity and sensitivity to initial and unfolding conditions, particularly in early social development, that results in the butterfly effect of stochastic experiences on personality. DNA cannot possibly contain enough information to determine this process ab initio. The DNA polymer functions as a factory organelle just like any other evolved accouterment that the earliest forms of life started tacking on. Life – that is, the living state, or “life itself” – invented DNA. The activity of genes, just like the activity of proteins and every other countless inanimate molecule in the living thing, is “controlled” by the living state, not the other way around. Life preceded DNA by millions of years. The idea that DNA is the blueprint of life is absurd. We should be worshiping (reverently pursuing the knowledge of) the living state, not a polymer. This absurdity is the twin of another absurdity, the EEA. Together, they form the porous foundation of the most colossal scientific folly in history.

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  13. @Marie:

    “Actually there is no OVERWHELMING evidence that childhood abuse causes schizophrenia.”

    Where is the evidence for a genetic cause of the complaints that fall under the diagnostic label of “schizophrenia?” They’ve spent billions of dollars looking and the evidence isn’t there.

    Where is the evidence for a common neural substrate underlying the complaints that fall under the diagnostic label of “schizophrenia?” They’ve spent billions of dollars looking and the evidence isn’t there.

    Where is the evidence for the role of child sexual abuse and other adverse childhood experiences in causing these complaints? EVERYWHERE you look. Can you show me one study that has looked for a correlation and not found one?

    “it’s obvious that there are other causes for schizophrenia than childhood abuse, which seems to put too much of the blame for the illness on parents.”

    Agreed. I already mentioned the huge excess of schizophrenia cases among Holocaust survivors.

    BTW, one major risk factor for a diagnosis of schizophrenia is losing a parent at an early age. In plain English, if the parent cannot be there for the child because the parent is DEAD, that is a major risk factor for a diagnosis of schizophrenia. Is that “blaming the parents?”

    “Bad things indeed do happen, and can drive certain people crazy. I knew a man who had a psychotic breakdown because he feared his wife was having an affair and he’d lose his family. But most people facing divorce don’t react that way.”

    Can’t argue with that. I’d like to know what else happened to this fellow that made it so easy for him to go over the edge.

    “I also think there’s a huge difference between being pessimistic and realistic.”

    If I understand you correctly, you are saying we cannot do anything about child sexual abuse and other adverse childhood experiences. Can we do something about the human gene pool? What did you have in mind?

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    • Yeah, I’m just going to come out and say I’m very sick of this societal knee-jerk aversion to ‘parent blaming.’ Something like 95% of people in inpatient psychiatric wards have disorganized attachment, which is entirely due to misattuned, neglectful, overwhelming or abusive behavior towards infants by primary caregivers. The early studies on complex trauma revealed that of the countless people who came together to report they’d been abused by a few notorious pedophiles in the catholic priesthood, only a fraction developed the symptoms we call ‘cptsd’ now, and all of them had disorganized attachment. Secure attachment is probably THE number one protective feature against everything we label ‘mental illness,’ and developmental psychopathology as a field uses the paradigm of insecure attachment as the bedrock for explaining later pathology. So if you have a psychiatric presentation, it’s EXTREMELY likely that your parents fucked your up, that they did so young, and that they did so repeatedly. ‘Blame’ is a moral term and we shrink away from ‘parent blaming’ because it puts a bad taste in our mouth, but that’s because of a moral and cultural prejudice and nothing more, and it’s a prejudice that prevents most victims of familial abuse — and we are many — from ever coming forward. The data from the ‘hard’ sciences like neuroscience to the ‘soft’ sciences like psychology overwhelmingly supports that we SHOULD ‘blame’ the parents in many if not most cases; that is, their behavior almost invariably factors into the etiology of the ‘mental illness.’ Almost ALL of the ACES relate to the parent child dynamic. But this doesn’t have to mean that parents are evil or bad: trauma is inter-generational; disorganized attachment is transferred behaviorally from parent to child and so on because of unprocessed trauma that the parent suffered at the hands of THEIR parents, until someone breaks the cycle. So hurt parents hurt kids unless they heal themselves. A moral prejudice against ‘blame’ for parents changes nothing about these facts, no matter how people may want to thrash about and think moral admonitions against ‘parent blaming’ somehow serve as a compelling argument against a massive body of evidence from attachment science and beyond. Parents factor prominently into their children distress and that is that.

      Honestly, I think we have to start asking ourselves, who is it we’re trying to help here? Because the medical model that de-contextualizes kids from their families and adults from their childhoods serves very nicely as a way to avoid ‘parent blaming.’ In fact, I know of many parents — mine included— that were DESPERATELY searching for a diagnosis for the express purpose of putting to rest their own feelings of failure and the pressures from the outside to change their behavior and the family environment. I get it, I do, no parent wants to feel like they failed their kids. But I will tell you that when I put together that I was an abused kid and that my distress was coherent with my current context IN THE CONTEXT of my overall development, that was the catalyst for my own healing and liberation, and other people who I began to tell that I had been abused and traumatized by my family began to express respectful compassion instead of fear and confusion around my previous ‘broken brain’ explanations. But my parents HATED this paradigm shift. And if you look at the evidence, self-stigma and stigma from the outside decreases proportionately with how much of the narrative around the ‘pathology’ is psychosocial and developmental. So, will we protect parents to the death with a biomedical paradigm that gets everyone off the hook, EXCEPT the patient, in denial and defiance of the evidence, and to the detriment of the patient themselves? Will we keep telling them they’re incoherent and broken to protect anyone and everyone from ‘blame?’ Or will we change and look at people as coherent responses to their context and development including their usually disfunctional families, who they had no control over as infants and young children? But I will tell you for sure parents of ‘patients’ will continue to fight against this paradigm shift no matter HOW helpful it would ultimately be to the people we are supposed to be trying to help.

      So if our goal as a society is to keep parents free from feelings of guilt, shame and the responsibility to change, then yeah let’s go for biopsychiatry and genetic reductionism. But let’s not pretend that this is a move meant to ‘help’ the patient or tell the truth about the evidence.

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          • Rasx

            You have a powerful story and very well told. You also present many insights into how psychiatry and the medical model divert people’s attention from the very direct experiences of abuse and trauma within family life that is at the heart of why people present with so much psychological distress that gets labeled as “mental illness.”

            However, I think it is essential for all of us to move this particular narrative to another level of analysis.

            Most of these dysfunctional and abusive parents and their entire backward family cultural did not develop out of nowhere, and is not, somehow, the product of “bad genetics.”

            Most abusive parents, themselves, were also the victims of traumatic and abusive histories. This does NOT excuse their behaviors, but should make us DEEPLY analyze all the inherent forms of inequality, prejudice, misogyny, patriarchy, daily trauma, and mind crippling forms of poverty in a class based and profit based economic and political system.

            At the highest level of assessment of all that is wrong with psychiatry and the medical model, is how it DOES EVERY THING POSSIBLE to divert our attention and finger pointing away from examining all the many oppressive institutions that prop up this system.

            For in the final analysis, if we really want to end the medical model (and all its forms of oppression) we will need to make major systemic changes throughout the entire society.

            Richard

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      • Adding to this to make the ‘in the context of one’s life’ point more evident, the original ACES study was begun because of a doctor working at an obesity clinic looking to find why so many of his clients who lost weight ended up dropping out and gaining it back. He began to find to his overwhelming surprise that many of them had been sexually abused, usually BY a family member, usually BY a parent. They would encounter a man or woman who looked like their abuser and made an advance, and would plunge back into binge eating and leave the program. Why? Because ‘overweight is invisible,’ as the first woman the doctor interviewed famously said. So you could look at that and say ‘oh most people don’t respond to sexual advances that way, therefore there’s something inherently wrong with people that do.’ And you would be totally wrong in saying that, because the REASON they responded that way is because they were traumatized IN THE PAST. The history of relational trauma makes the present ‘disfunction’ into a coherent response at the developmental level: this was the premise that inspired the ACES study and the results speak for themselves: 1,222% more likely to commit suicide if you have 4 or more severe adverse experiences before 18.

        I think Freud maybe serves as the best example of where denying the effect of developmental and relational trauma
        In the family gets us: this moral and cultural outrage against ‘parent blaming.’ Freud found that the majority of his hysteria patients reported childhood sexual abuse when they opened up to him. His original theories had to do with dissociating from these painful experiences as a source of pathology. But he suffered so much backlash because people didn’t want to believe so many women were being sexually abused by their parents. So he completely changed his theory, now operating on the premise that they had made up the abuse as an infantile fantasy! Gaslight the patient to save the parent. Now so many years later with attachment science, trauma science and the massive literature on ACES were finding that his original theories were more accurate.

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        • Dear Rasx,

          Thank you for your outstanding comments on this subject. Copies should be sent to university psychology departments worldwide, especially the one on 12/18/22 at 12:06 am; it says everything that needs to be said from every point of view.

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        • What Freud did to protect himself caused decades of damage to many, many people, most of whom were women.

          And a tragic example is that of author Virginia Wolf. She was sexually abused by family members and then told by psychiatrists that her memories were delusional.

          So, yeah, Freud was one helluva guy!

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        • Rasx says, “….because the REASON they responded that way was because they were traumatized IN THE PAST.”
          Very true.

          And these traumas aren’t forgotten; they’re stored in the unconscious BECAUSE they’re overwhelming, which the reason for an unconscious.

          And memories, both good and bad, are triggered in unexpected ways. And there’s nothing “inherently wrong” with THAT —

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      • Rasx says, “…95% of people in inpatient psychiatric wards have disorganized attachment…”

        Tell that to the psychiatrists.

        “Secure attachment is probably THE number one protective feature against everything we label ‘mental illness’; and developmental psychopathology as a field uses the paradigm of insecure attachment as the bedrock for explaining later pathology.”

        Tell that to the psychiatrists.

        “Almost ALL of the ACES relate to the parent child
        dynamic.”

        Tell that to the psychiatrists.

        “So if our goal as a society is to keep parents free from feelings of guilt, shame and the responsibility to change, then yeah let’s go for biopsychiatry and genetic reductionism. But let’s not pretend that this is a move meant to ‘help’ the patient or tell the truth about the evidence.”

        On second thought, don’t bother telling the psychiatric industry – – too many of them have got “MMD”: Myopic Mind Disorder

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  14. These things are hard to grasp as long as we cling to the notion that SZ is a “disease”. Rather, SZ is one of many possible responses, perhaps the most extreme short of physical suicide, to the terrors and heartbreaks that life offers to the young and vulnerable. SZ, as a form of psychosocial suicide, is as “human” as becoming Bernard Madoff or Mother Teresa, war, grief, joy, love, xenophobia, murdering cuckolders and kissing babies. Patrick Hahn asks, correctly, what other experiences might have predisposed the divorced man to “react that way”. Think of allergies, like bee stings, which cause anaphylactic shock in a minority of people, but only mild and brief irritation in most others. As in bee stings, when and why a person becomes psychotic in apparent reaction to a proximal (recent, direct) social stimulus (the affair in this case) is not merely conditioned by the apparent severity of the stressor, but also the entire life history of exposure to other stressors or trauma in the domain of social relationships. It can also be conditioned on the lack of exposure to such stressors (one of the main causes of asthma is spending infancy and childhood in an allergen-free “protected” environment). That’s why an apparently trivial stimulus can seem to precipitate a severe psychotic episode in some people. Or why a “happy” stimulus results in something very unhappy: Why one woman is overjoyed by childbirth and another plummets into a psychotic postpartum depression. The response to these transitions is conditioned on the person’s life history, which in turn is heavily conditioned by the multigenerational transmission of emotional “information”. It also helps to understand why the first major psychotic “schizophrenic” episode in a young adult is often precipitated by some upheaval in the social network and roles, such as death in the family, marriage of a sibling, leaving home, living independently, establishing separate quarters, getting married (or divorced), joining the military or having a baby. The decisive events predicating the response are buried in the past, in prior attachments and other socioenvironmental factors. Divorce can induce profound infantile rage, desperate attempts to prevent or punish abandonment, panic attacks, somatic symptoms, major depression and hysterical conversion behavior in mature adults. Or indifference, or even joy less commonly. The matter is complicated by the anecdotal nature of the case; did this man in question have a bona fide psychosis? I don’t know. Even so, I would probably trust Marie’s anecdote more than the “imaginary interviews” that the Danish adoption study fraudsters conducted. Most clinicians have seen countless cases of psychological regression and collapse associated with divorce – in the divorcing couple, and often, perhaps more commonly, in the children of the couple. Also, consider how such a profound emotional reaction could actually be adaptive, or at least preferable to some alternatives. It could have prevented a double homicide, which is far more socially destructive than privately retreating into psychosis for a while. OJ Simpson could have saved society and his children a lot of anguish and expense and prevented a few calamitous riots if he’d become psychotically incapable of the complex goal directed behavior of confrontation and decapitation. Or was it a Colombian gene cartel, as the gene hunters believe?

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  15. Hi Jay,
    I always appreciate your articles which explain the science in an understandable way for a layperson. I especially appreciate your expertise addressing the twins studies which seemed irrefutable until I read a previous article of yours here on MiA. But I’ll be honest, I haven’t worked my way thru this article completely because I got derailed on your statement in the beginning that your prefer ‘psychosis’ to ‘schizophrenia’.

    I have walked with my wife thru her DID, outside the system and without psych drugs for the last 15 years. In the DID world I have read that if the voices a person hears seem ‘outside’ the person, then they “have” schizophrenia, but if they seem ‘internal’ then they “have” DID (don’t know if that is accurate…just saying). So, even though I have zero experience with someone who has ‘schizophrenia’, I’ve always kind of viewed it as the mirror image of what I’ve walked thru with my wife.

    Now until I started frequenting MiA, I didn’t even know what ‘psychosis’ was, but it seemed like such a big deal once I got here. Now I’ve never seen my wife as ‘psychotic’ and there are two reasons I still don’t view her that way even after I tried to become more educated about what ‘psychosis’ is. 1) I don’t think ‘psychosis’, accurately describes what is occurring in the person: at least not my wife. I think all her ‘psychosis-like’ symptoms are better understood as natural consequences of extreme dissociation caused by the trauma she suffered as a 2-year old…and once I adjusted my perspective to align with what was happening internally with her, then most of that stuff she experienced made sense to me. And thus, 2) I think using that term makes those of us on the outside lazy because rather than putting the effort into understanding what is really happening internally, we just say ‘she’s psychotic’ and so what would be the point of trying to understand something that’s just ‘crazy’, right?

    I also saw another comment mention attachment issues, and yes, that’s what we’ve used, with me as her primary attachment figure, to help her heal and tear down the dissociation which has slowly resolved the ‘psychosis-like’ symptoms. One by one her dissociated ‘parts’ have securely attached to me and then (it seems) that attachment helped each connect to the rest of her greater personality.

    There’s so much more I could say, but I won’t bore you unless you have interest.
    Sincerely,
    Sam

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  16. Sam’s unease about the term “schizophrenia” (SZ) is well placed. SZ is just the most recent inadequate placeholder to describe a process, or socioemotional/sociocognitive/sociobehavioral syndrome, that baffles the “normals” who call themselves psychiatrists and neurologists. The previous term, dementia praecox, was even worse. At least “SZ” implies some sort of dignifying and humanizing internal psychological conflict or distress actively generating the symptoms in response to social stimuli, whereas DP describes a passive, progressive and irreversible neurodegenerative condition like Alzheimer’s. In a move that Western psychiatry has mostly ignored, 20 years ago the Japanese addressed this (from Wiki):

    The old term for schizophrenia, “Seishin-Bunretsu-Byo” (Mind-Split Disease), has been replaced by “Togo-Shitcho-Sho” (Integration Disorder) in Japan.

    The Japanese apparently have more genes for psychological insight than we do. This is a step forward, but a long way to go. The term SZ should be abolished in the West and replaced by understanding. This is all part of the complete overhaul of psychiatric nosology that is desperately needed. A new edition of the DSM will not do it. The DSM needs to be trashed too. The completely failed “operationalization” or “biologization” or “geneticization” of the diagnostic criteria pushed by Insel and others is itself a type of cognitive pathology that ought to be the only entry in DSM6. The idea that suffering, worried, scared, conflicted, traumatized people have genetic brain diseases is barbaric and Medieval and even nutty. For instance, take a look at this paper, published yesterday online:

    https://doi.org/10.1038/s41380-022-01776-4

    “The genome-wide neurodevelopmental CNV burden identified explains 0.034% of the variation in PTSD symptoms.”, it says. That’s a whopping 17/50,000th of the variation “explained”. It explains nothing, but is barely non-zero, which is the threshold that apparently justifies further funding. These people are looking for a very monetizable prize: a screening test that police, military and others can use to identify those whose genes are too weak for the kind of violent work that strong-gened people can do while whistling. Such a discovery would rake in millions (or save millions from the VA budget), and that’s why funders, who are often as fooled by this grift as the general public, pony up the money. No other reason. The last thing they care about is human well being. After all, perpetual war and crime and sexual abuse are inevitable and unpreventable. Genetic intervention (genetic counseling, matchmaking, gene editing, selective abortion, career guidance, etc) is all that can be done, so press the donate button.

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    • GPM says, “The DSM needs to be trashed too. The completely failed “operationalization” or biologization” or “geneticization” of a diagnostic criteria pushed by Insel and others is itself a kind of cognitive pathology that ought to be the only entry in the DSM.”

      Yes. People who believe in the DSM are the ones with a problem.

      “The idea that suffering, worried, scared, conflicted and traumatized people have a genetic brain disease is barbaric and Medieval and even nutty.”

      Yes. It’s barbaric and nutty.

      I took a look at the paper, and was not surprised. My gut has always told me that stuff like this, i.e. foolish scientific extravaganzas, i.e. “molecular psychiatry” are products of a particular type of dissociated mind, its key feature being the uncontrollable urge to concoct excruciatingly complicated scientific explanations for easily explained phenomena. These types of seemingly rational activities are actually a function of the unconscious mind’s efforts to shield the conscious mind from painful emotional realities. It’s a classic form of dissociative distraction, with no connection to the real world. Simply put, it’s scientific escapism.

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  17. @Steve & @Birdsong:

    When I was writing my first book, I was uncertain about whether or not to include the information about the trauma Joanne Greenberg (author of I Never Promised You a Rose Garden) experienced as a child. It sounded bad, but not horrible. I finally decided to include that information and let the reader make up his mind about its significance.

    I am sure there are people who have experienced worse trauma but who never were diagnosed with schizophrenia. On the other hand, after three years at Chestnut Lodge, Greenberg went on to become a professor and a famous author.

    It could be that creative, sensitive people are more likely than others to be diagnosed with schizophrenia — after all, if your life is unbearable, and there is no realistic prospect of that changing, it’s actually a pretty neat trick to be able to escape into a world of one’s own making. And I cannot rule out the possibility that the ability to do this may be in part genetically-based. But to whatever extent that is the case, instead of regarding these genes as disease genes, we ought to regard them as gifts that require proper stewardship by the individual and society at large.

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    • I think being sensitive is both a gift and a curse. But strong feelings can be too intense for the conscious mind to process, especially when something traumatic is involved. Minds break from reality for a reason, and psychosis protects the conscious mind, and art is an expression of the mind’s unconscious.

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    • People have been known to “go insane” i e. “psychotic” when placed in intolerable circumstances, for instance, POW’s subjected to torture. But just too much stress in good situations can cause temporary breaks with reality. And too much stress makes it harder for the conscious mind to suppress painful (but unprocessed) thoughts, feelings, experiences, in other words, “trauma”.

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    • Life can be harder for sensitive people, especially for those who don’t fit in. And people get ostracized/labeled for not fitting in.

      I use to wonder what happened to the kids who labeled/teased/bullied others. I think a lot grew up to be psychologists or psychiatrists, because I knew some who did!

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      • I read an article on here once about how narcissistic folks and bullies in indigenous societies would’ve been the ones pathologized for not gearing into society in a compassionate way, whereas in our society it is their victims who bear this burden. The narcissists and bullies are more likely to be elected president.

        Reminds me of the shot down suggestion that men who beat their significant others should be given a diagnostic criteria in the DSM instead of the women who stick up for them, which is what our culture encourages. Really goes to show how socially constructed these things are. All you have to do is put some words together to construct a diagnostic criterion for something you observe, put it in print and all of a sudden it is reified, causa sui, incoherent and bad. The best example of this I think is drapetomania. The slave owners are normal; the slaves who seek freedom are diseased. And then maybe if we find some physiological element common to freedom-seeking slaves, then the conclusion is freedom-seeking is a contextually incoherent disease! Would the same logic hold for the slave owners I wonder? As a person who ‘got out’ of a disfunctional family system and a psychiatrized life I sometimes I think drapetomania is my true diagnosis. Probably a lot of us on these forums are the same.

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        • Rasx,
          I agree completely. There’s nothing more sensitive to the environment than an infant, both in the womb and after.

          I agree with Jerome Kagan in concluding that “different temperaments will express their attachment styles differently”, and with your statement that “high reactivity or sensitivity is a complex developmental outcome”, and that “attachment style is nonetheless determined by parental behavior”. And I also agree that sensitivity isn’t a risk factor for ‘mental illness’ later in life.

          But I still think people are born with their own unique personality, and also with their own abilities: artistic, athletic, intellectual etc. But ultimately, all this come down to, as you say, nature via nurture.

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        • And the DSM is, as you say, socially constructed:

          “All you have is do is put some words together to construct your diagnostic criterion for something you observe, put in in print and all of a sudden it is reified…”

          Which means the DSM a totally subjective piece of socially biased junk. And your example of drapetomania shows exactly how, which means anyone tagged with a psychiatric diagnosis is suffering from “drapetomania”, to one extent or another.

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      • Not entirely inherited. For instance as I mentioned above in the prenatal period maternal levels of cortisol affect what we eventually call infant temperament. And attachment trauma can lead to what you might call ‘sensitivity,’ for instance sensory integration issues are a common outcome of attachment trauma and lead to infants who are much more sensitive to environmental input. Insecure attachment also leads to relational hypervigilance which is a kind of emotional sensitivity. Jerome Kagan is the ‘temperament guy’ and he warned against reducing temperament to genetics due to its inherent complexity. Jerome Kagan also tried to reduce attachment to temperament and couldn’t, ultimately concluding that different temperaments will express their attachment styles differently but attachment style is nonetheless entirely determined by parental behavior. Furthermore as my trauma therapist told me it’s ludicrous to think that there would be such a thing as a ‘low reactive newborn.’ A newborn can’t regulate itself and is entirely dependent on the parent to do so. ‘High reactivity’ would therefore be a complex developmental outcome. Finally, ‘high reactivity’ or sensitivity isn’t a risk factor for ‘mental illness’ later in life in isolation. What does constitute a risk factor is high reactivity AND a misattuned caregiver that cannot provide regulation for a sensitive child. It’s the same with temperaments: what some people might call a ‘difficult temperament’ turns out only to be predisposing to a ‘mentally ill’ presentation in the presence of a specific suite of parental responses to such a temperament. That is why early interventions that focus on improving parental attunement and responsiveness (it wouldn’t really make sense for an early intervention to be different from this, as infants inherently can’t regulate their own systems and so expecting them to change on their own is absurd — though I really feel this way about childhood interventions in general), if the parent is willing to engage, are successful in ameliorating the child’s difficulties.

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        • Rasx,
          the problem is…in our dysfunctional culture where independence and individualism are overprized, no one wants to be told that another’s mental health or mental health healing (as in my wife’s case) is almost 100% on the primary attachment figure…or me (or her parents originally)…but that is the gist of how I read attachment theory even though it is anathema to nearly everyone…even the book I was asked to write…one of the reasons it got canceled was because someone read between the lines and realized that I understood the amount of sacrifice it required of me to help my wife heal 40 years after her parents had abdicated their roles as primary attachment figures….how sad that even the survivors have accepted the tenets of our dysfunctionally, hyper-independent culture.
          Sam

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    • I don’t think losing touch with your surroundings means anything other than losing touch with your surroundings. But I do think artistic or creative people are more sensitive to their surroundings, which doesn’t mean anything other than artistic and creative people are more sensitive to their surroundings. And I don’t mean to imply that artistic, creative, or sensitive people are more likely to experience “mental illness” later in life.

      Labeling people with psychiatric disorders mostly helps the people doing the labeling, which means some people are hung up on controlling the people in their surroundings.

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  18. I looked up the difference between personality and temperament. According to my resources, people are born with certain temperaments, whereas personality is influenced by experience. It’s all very confusing to me.

    But the overriding factor is definitely the type (or lack thereof) of emotional bond/attachment between a baby and its parents/caregivers.

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    • ‘Born with’ doesn’t mean unaffected by experience. The baby in the womb has an experience of their environment, insofar as they interact with and are changed by their interaction with their environment. And their primary environment IS their caregiver, literally. The varying states of the caregiver’s body — and by extension the nature of the caregiver’s own environment — throughout pregnancy will therefore have an influence on the temperament of the baby after the umbilical cord is cut.

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    • Don’t mean to be arguing with you, Birdsong. I’m not an expert on temperament either. Also thanks for all the positive feedback earlier I really appreciate it. Always enjoy your posts.

      In other news I will probably be signing off of here for a while, MIA has been a great, validating hopeful resource for me for awhile now and I’ve enjoyed reading all your comments for some time even though I only started participating recently. On the other hand I’ve gotten a little compulsive with reading up on these things to combat my conditioning — the self doubt from years of gaslighting is massive for me: as Sam says I am one of those brainwashed survivors trying to make my way out the other side. But I don’t think just encountering the information is enough for me to do so, to believe myself down to the cellular level.

      Sam also have really enjoyed your posts and your website: it’s a damn shame your book didn’t get published and I felt a lot of sadness that I didn’t have someone like you in my life when I was younger while reading through your stuff. Thankfully now I have a great attachment based therapist.

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  19. @Birdsong @Rasx:

    I use a timekeeping metaphor. You can kick a sundial around the yard and it still will do what a sundial is designed to do. You can’t do that with a fine watch. But, properly handled, a fine watch can do so much more than a sundial.

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