Five Decades of Gene Finding Failures in Psychiatry


Two generations of molecular genetic researchers have attempted, yet failed, to discover the genes that they believe underlie the major psychiatric disorders. The most recent failure is a molecular genetic study that was unable to find genes for symptoms of depression.1 Like most genetic researchers in psychiatry, the authors failed to consider the possibility that no such genes exist, and instead concluded that much larger samples of at least 50,000 subjects are needed to detect genes. Also like other genetic researchers in psychiatry, they based their search on the belief that previous kinship studies of families, twins, and adoptees have definitively established the genetic basis of the psychiatric disorder in question. This position is promoted by mainstream psychiatry and by supporters of psychiatric genetics, a subfield of psychiatry founded in Germany around 100 years ago and currently centered in the Unites States and Europe. The questionable validity of DSM psychiatric disorders and the “mental illness” concept are important topics, but here I will focus on genetic research using these concepts.

As far back as 1969, genetic researchers in psychiatry performed a molecular genetic study of manic-depression (bipolar disorder) and concluded that they had found proof that the condition was caused by genes: “Affective disorder in which mania occurs is probably linked on the X chromosome…  This finding clarifies some aspects of transmission. It also proves a genetic factor in manic-depressive disease.2 Like subsequent gene discovery claims in psychiatry, these results were not replicated by other research teams. As Stephen Faraone and his psychiatric genetic colleagues recognized in 2008, “It is no secret that our field has published thousands of candidate gene association studies but few replicated findings.”3 In a sense, however, these negative results are a “secret” because the media usually tells a much different story to the general public. The public has been misled by sensationalized reporting in the popular press, often in concert with leading researchers, to believe that genes for the major psychiatric disorders have been found.

Molecular genetic attempts to uncover “schizophrenia genes” go back to the beginning of the 1970s and earlier.4 In a highly publicized case a generation ago, Sherrington and colleagues believed they had identified a genetic marker for schizophrenia, but this result was not replicated.5 Despite the sequencing of the human genome and the publication of more than 1,700 schizophrenia molecular genetic studies, we have witnessed over 40 years of gene finding claims, and over 40 years of subsequently non-replicated findings. A 2012 study, co-authored by many of the world’s leading schizophrenia molecular genetic researchers, compared 732 previously identified “hypothesis-driven candidate genes” for schizophrenia with genome-wide association study (GWAS) results. The researchers found no association between these previously identified genes and schizophrenia, and concluded that their negative results “suggest, but do not prove, that many traditional ideas about the genetic basis of SCZ [schizophrenia] may be incorrect,” and that “it is possible that the next few years will lead to marked changes in major hypotheses about the genetic basis of SCZ.”6

Clearly, psychiatric molecular genetic research is massively plagued by false positive results, and systematic error appears to have been repeated year-after-year, and decade-after-decade. In this context, leading psychiatric genetic researchers have publicly asked funding sources not to “give up” on schizophrenia molecular genetic GWAS research.7 Researchers tend to downplay the implications of years of negative findings at the same time that they claim that some new technology or method will finally deliver the promised genes.

A parallel process has occurred in the behavioral genetics field,8 where many years of concerted gene finding attempts have failed to identify genes for traits such as IQ,9 personality,10 and traits studied in the social sciences.11 As critical behavioral geneticist Douglas Wahlsten wrote in a 2012 review, “In human behavior genetics…powerful new methods have failed to reveal even one bona fide, replicable gene effect pertinent to the normal range of variation in intelligence and personality.”12

Researchers in psychiatry long ago abandoned the search for a major causative single gene, and now view schizophrenia and other psychiatric conditions as “multifactorial complex disorders,” seeing them as being caused by a complex interaction of multiple genes and multiple environmental risk factors. It is important to note, however, that the failure to discover genes is currently a defining feature of “multifactorial complex disorders” in psychiatry. While continuing to search for genes, researchers frequently claim that the environmental factors contributing to the development of psychiatric disorders are unknown, or are not well understood.

In 2008, leading genetic researchers developed the “missing heritability” position to explain the fewer-than-expected gene findings for some common medical conditions, and the lack of findings for the major psychiatric disorders.13 Regarding schizophrenia, bipolar disorder, ADHD, depression, and other psychiatric conditions, proponents of this position argue that genes are “missing” because researchers must find better ways to uncover them. From the “missing heritability” standpoint, genetic variants that underlie psychiatric disorders and psychological trait variation will be found once researchers develop better methods and collect larger samples. However, psychiatric gene searches are based on the mistaken assumption that genes must exist, due to researchers’ failure to examine the numerous potentially invalidating flaws of previous psychiatric family, twin, and adoption studies. The best explanation for why psychiatry has witnessed five decades of gene finding failures, despite well-funded concerted worldwide efforts using cutting edge technology, is not that “heritability is missing,” but rather that previous and current claims that these family, twin, and adoption studies prove something about genetics are mistaken. I hope to discuss the invalidating flaws, biases, and false assumptions underlying these studies in future postings.14

Interestingly, when the environmental causes of non-psychiatric medical conditions are widely understood and recognized, in most cases society pays little attention to uncovering a possible genetic component. For example, in light of increasing head injuries and concussions, the U.S. National Football League (NFL) is currently in the process of changing professional football rules to reduce the violent head collisions that cause concussions. Although some medical researchers have looked at possible genetic factors relating to concussions, I am unaware of anyone connected with the NFL calling for twin studies of concussion, or for molecular genetic studies attempting to pinpoint concussion susceptibility genes. Few argue that we must assess NFL players for a genetic vulnerability in order to understand concussions, and no one to my knowledge is attempting to calculate concussion “heritability” estimates. The reason is clear: when the environmental causes of a condition are understood and recognized (such as blows to the head), the possibility that some people are more genetically vulnerable (predisposed) than others for developing the condition becomes largely irrelevant.

In psychiatry, despite clinical and research evidence that many people eventually diagnosed with schizophrenia and other psychotic disorders are impacted by trauma, abuse, and other adverse experiences,15 the field’s attention is largely focused on what it believes to be the genetic and biological bases of psychosis. Based on how they typically approach psychiatric disorders, if psychiatric genetic researchers were put in charge of preventing concussions in professional football, it is likely that they would (1) emphasize that concussed players have a genetically-based brain disease, (2) prioritize the use of twin studies and molecular genetic studies in an attempt to unravel the “genetic architecture” of concussions, (3) argue that the environmental causes of concussions are not well understood, (4) pay little attention to the role of head trauma, and (5) conduct genetic counseling sessions with newly drafted players. This is clearly the wrong approach, even if some players are more genetically predisposed than others to suffer concussions.

Nevertheless, politically and economically powerful groups with an interest in diverting attention away from the harmful environmental conditions they often create are very interested in supporting, financing, and promoting genetic approaches. For example, the tobacco industry has promoted the study of genetic predispositions for developing lung cancer.16 Studying possible genetic predispositions is much more than a research approach—it is one of the methods used to promote the idea that environmentally-caused medical conditions and psychiatric disorders are mainly the result of heredity.17

Although some researchers currently claim that several genes for the major psychiatric disorders have already been discovered, these claims are likely to suffer the same fate as similar non-replicated claims we have heard for decades (easily found in Google searches such as “schizophrenia gene discovery,” “ADHD gene discovery,” “bipolar gene discovery,” and in the online archives of scientific journals that have published the “thousands” of subsequently non-replicated gene finding claims). Science writer John Horgan wrote about these non-replicated claims in 2004, and the point is even more relevant today with an additional nine years of gene finding failures behind us:

“Over the past 15 years or so, researchers have announced the discovery of ‘genes for’ attention-deficit disorder, obsessive-compulsive disorder, manic depression, schizophrenia, autism, dyslexia, alcoholism, heroin addiction, high IQ, male homosexuality, sadness, extroversion, introversion, novelty seeking, impulsivity, violent aggression, anxiety, anorexia, seasonal affective disorder, and pathological gambling. So far, not one of those claims has been confirmed.”18

Statements of this type are rarely found in the popular media.

The time has come to suspend psychiatric molecular genetic research and to undertake a thorough public reassessment of the original family, twin, and adoption studies that inspired the fruitless search for genes in the first place. At the same time, the familial, social, and political causes of psychiatric conditions must become the focus of attention.19

In a mocking jab at critics such as R. D. Laing and Thomas Szasz, psychiatric investigator Seymour Kety, the lead researcher of the influential yet severely flawed Danish schizophrenia adoption studies, famously wrote in 1974: “If schizophrenia is a myth, it is a myth with a strong genetic component!”20 Schizophrenia molecular genetic research was relatively new in those days, but now the results of decades of molecular genetic research are in: There appear to be no genes for schizophrenia. We could therefore revise Kety’s position to bring it in line with current scientific results: “If schizophrenia is a genetic disorder, it is a genetic disorder without any genes.”

Further Reading

Boyle, M. (2002). It’s All Done with Smoke and Mirrors. Or, How to Create the Illusion of a Schizophrenic Brain Disease. Clinical Psychology, 12, 9-16.

Joseph, J. (2011). The Crumbling Pillars of Behavioral Genetics. GeneWatch, 24 (6), 4-7.

Joseph, J. (2012). The “Missing Heritability” of Psychiatric Disorders: Elusive Genes or Non-Existent Genes? Applied Developmental Science, 16, 65-83.

Krimsky, S. & Gruber, J. (Eds.). (2013). Genetic Explanations: Sense and Nonsense. Cambridge, MA: Harvard University Press.

Latham, J., & Wilson, A. (2010). The Great DNA Data Deficit: Are Genes for Disease a Mirage? The Bioscience Research Project.

Lewontin, R. C. (2009, May). Where are the Genes? Genewatch.


1 Hek et al. (2013). A Genome-Wide Association Study of Depressive Symptoms. Biological Psychiatry. Advance online publication. DOI: 10.1016/j.biopsych.2012.09.033; see also “Depression Gene Search Disappoints”

2 Reich et al. (1969). Family History Studies: V. The Genetics of Mania. American Journal of Psychiatry, 125, 1358-1369.

3 Faraone et al. (2008). The New Neuropsychiatric Genetics. American Journal of Medical Genetics Part B (Neuropsychiatric Genetics) 147B, 1–2

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

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

6 Collins et al. (2012). Hypothesis-Driven Candidate Genes for Schizophrenia Compared to Genome-Wide Association Results. Psychological Medicine, 42, 607-616.  For an opposing viewpoint within psychiatric genetics, in 2012 Michael Owen claimed that “possibly thousands” of schizophrenia genes have been discovered: “We now have molecular genetic evidence that a very large number of genes, possibly thousands, contain risk alleles for schizophrenia in the population.” See Owen, M. J. (2012). Implications of Genetic Findings for Understanding Schizophrenia. Schizophrenia Bulletin, 38, 904-907.

7 Sullivan et al. (2012). Don’t Give Up On GWAS. Molecular Psychiatry, 17, 2-3

8 Joseph, J. (2011). The Crumbling Pillars of Behavioral Genetics. GeneWatch, 24 (6), 4-7.

9 Chabris et al. (2012). Most Reported Genetic Associations with General Intelligence are Probably False Positives. Psychological Science, 23, 1314-1323.

10 Plomin, R. (2013). Child Development and Molecular Genetics: 14 Years Later. Child Development, 84, 104-120; Wahlsten, D. (2012). The Hunt for Gene Effects Pertinent to Behavioral Traits and Psychiatric Disorders: From Mouse to Human. Developmental Psychobiology, 54, 475-492.

11 Benjamin et al. (2012). The Genetic Architecture of Economic and Political Preferences. PNAS, 109, 8026-8031; Charney, E., & English, W. (2012). Candidate Genes and Political Behavior. American Political Science Review, 106, 1-34.

12 Wahlsten, 2012.

13 Maher, B. (2008). The Case of the Missing Heritability. Nature, 456, 18-21; Manolio et al. (2009). Finding the Missing Heritability of Complex Diseases. Nature, 461, 747-753.

14 For problems with family, twin, and adoption studies, see Joseph, J. (2004). The Gene Illusion: Genetic Research in Psychiatry and Psychology Under the Microscope. New York: Algora. (2003 United Kingdom Edition by PCCS Books); Joseph, J. (2006). The Missing Gene: Psychiatry, Heredity, and the Fruitless Search for Genes. New York: Algora; Joseph, J. (2010). Genetic Research in Psychiatry and Psychology: A Critical Overview. In K. Hood, C. Tucker Halpern, G. Greenberg, & R. Lerner (Eds.), Handbook of Developmental Science, Behavior, and Genetics (pp. 557-625). Malden, MA: Wiley-Blackwell.

15 Kessler et al. (2010). Childhood Adversities and Adult Psychopathology in the WHO World Mental Health Surveys. British Journal of Psychiatry, 197, 378-385; Read, J. (forthcoming). Childhood Adversity and Psychosis: From Heresy to Certainty. In J. Read & J. Dillon (eds.). Models of Madness (2nd ed.). London: Routledge; Read et al. (2009). Time to Abandon the Bio–Bio–Bio Model of Psychosis: Exploring the Epigenetic and Psychological Mechanisms by Which Adverse Life Events Lead to Psychotic Symptoms. Epidemiologia e Psichiatria Sociale, 18, 299–310.

16 Proctor, R. N. (1995). Cancer Wars: How Politics Shapes what we Know and Don’t Know About Cancer. New York: Basic Books; Wallace, H. (2009). Big Tobacco and the Human Genome: Driving the Scientific Bandwagon? Genomics, Society and Policy, 5, 1-54.

17 See Chaufan, C. (2007). How Much Can a Large Population Study on Genes, Environments, Their Interactions and Common Diseases Contribute to the Health of the American People? Social Science and Medicine, 65, 1730–1741.

18 Horgan, J. (2004, November 6th). Do Our Genes Influence Behavior? Chronicle of Higher Education.

19 Belle, D., & Bullock, H. (2013). Poverty, Unemployment, Economic Inequality, and Mental Health. In M. Shally-Jensen (ed.), Mental Health Care Issues in America: An Encyclopedia (Vol. 2; pp. 541-546). Santa Barbara, CA: ABC-CLIO.

20 Kety, S. S. (1974). From Rationalization to Reason. American Journal of Psychiatry, 131, 957-963.


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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  1. While you make a compelling case for abandoning gene research for psychiatric disorders, and I agree, don’t go overboard on this one by asserting the primacy of familial, social and political contributors in creating these conditions. There is still lots of room for scientific research that doesn’t involve gene research. A case in point: The new bestseller, Brain on Fire, describes the author’s descent into what had all the hallmarks of madness, but what turns out to be a rare autoimmune disease. Or is it so rare? She was the beneficiary of the latest scientific research that happened to fit her particular case (viral encephalitis). Why must we favor psycho/social factors over possible medical causes? Recovery for every person is unique to who they are. It would be a shame to convince people that their problems are societal when in fact, they may be the beneficiaries of research into previously ignored medical areas. But, I get it. Geneticists have had their chance, and now it’s time to move on.

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    • You are so right! Why not look at medical causes? Auto-immunity is just beginning to be understood. If it can be implicated in MS and so many other diseases why could it not affect the brain in various ways? They need to continue research on medical causes.

      Nobody who as ever lived with a psychotic person would ever say that “familial, social and political” factors cause psychosis.

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      • I have lived with someone who was “psychotic” (multiple diagnosis including schizophrenia) and I believe, as does he, that familial and sociological factors caused his madness. He is doing fairly well now, largely becuae of the social support he got including talking about and putting into context the family truamas that freaked him right out of his head.
        Richard Bentall is a UK psychologist who has done extensive research on this, while I havn’t read his work I have seen him talk at a conference and asked him a question about the link between homophobia and psychosis as I thought I had detected this – he said twice the rate of psychosis amongst the LGBT community. So there is a social factor for you. Others are surviving childhood sexual assault, family violence, bullying at school and racism.

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      • Madincanada, “Nobody who as ever lived with a psychotic person would ever say that “familial, social and political” factors cause psychosis,” are you serious?

        You are quite in the dark.

        There are many professionals besides Richard Bentall, as John Hoggett mentioned, who are more than ready to explain the familial, social, and political factors that can lead to such conditions as “schizophrenia,” etc. Bert Karon, Ty Colbert, the International Society for Psychological and Social Approaches to Psychosis, for starters.

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        • There are MANY people who HAVE lived with “schizophrenics” who do see it as something different than “biological,” and who have true stories of healing, recovery and faith in the human condition. Schizophrenics who have completely recovered, are understood, have stories to tell.

          Whether it’s “familial, social and political” factors or spiritual, or conceptual, or artistic or many others: there are MANY people who have amazing stories; and yet profession this is almost completely overlooked by the “medical” profession. As are many biology based theories about what might contribute to “schizophrenia” involving nutrition, vitamins and intestinal health.

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          • I wonder about the issue contained in your last sentence, knowing that stress contributes to (causes?) many intestinal conditions, I tend to wonder about which comes first… is the “sz” in these cases caused by the intestinal problem or is stress causing both of them….

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      • “Nobody who as ever lived with a psychotic person would ever say that “familial, social and political” factors cause psychosis.”

        That’s completely a fallacy, in fact the people who have decided to look at familial, social and political factors regarding psychosis are EXACTLY the ones that have promoted healing, and whose methods consistently and statistically correspond the MOST with healing!

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    • My mild criticism of Jay’s post came about because of the football concussion analogy. It is not that “obvious” to me that familial trauma or sociopolitical events can be broadly interpreted to apply to everybody with a mental health label. Everybody with an MI label has some obvious or not so trauma in their past, but this doesn’t necessarily translate as being the cause of their condition. Many people believe trauma to be at the root of their condition, and claim successful recovery when they directed their attention to clearing the trauma. So, they are right within their own experience. There has been too much focus on finding a gene, that is absolutely true, but to me, the gene obsession has prevented meaningful research into other possible biological causes. There are many trauma related therapies (my son has done several) but where do you turn if you think you still have an underlying biological problem? There is really nothing out there. I’ve subscribed to the trauma theory for quite a while because I figured it should never be overlooked, and I’ve seen a lot of progress not only with my son but with healing the family dynamics. Speaking only for me, I’m thinking there may be more to the picture than just trauma.

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    • Dear Rossa,

      Almost by definition, psychiatric disorders are not medical conditions. If they are shown to have a biological basis, they cease being psychiatric disorders and are transferred to other areas of medicine, such as neurology. Thomas Szasz made this point repeatedly. Thus far, there is no evidence that DSM “mental disorders” are true medical conditions, but if such evidence comes in, they will be treated as medical conditions and not psychiatric disorders.

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      • Jay,
        You say that almost by definition, psychiatric disorders are not medical conditions, because, if they are, the patient gets transferred to some other branch of medicine (yes, that’s indeed what happens), but aren’t you also asserting, that the “disorder” that produces the behavior is always familial/psycho/social? I know there are lots of people, many MIA readers, in fact, who also believe that it all comes down to trauma. You are a psychologist, so it’s understandable that you are championing this approach because this is how you make your living. In a practical sense, for the individuals who want to improve their mental health, isn’t a disservice being done by therapists proclaiming the superiority of the trauma model, when the person may discover years later that his/her particular problems could have been addressed by being more open-minded to other healing modalities? The opposite also applies, of course. The majority of people for the past several decades have been told that their problems are not trauma-related, instead opting to believe the disease or the unproven genetic model, and they may have cheated themselves out of a fuller or better recovery. It is very possible that the psychiatrist of the future will take a more holistic approach to treating the individual patient, not just focusing on assuming that it’s all trauma or it’s all biology. Right now, most of us are like the blind man describing the entire elephant by touching only one part of it. It is well known that “schizophrenia” is a collection of symptoms and no two people have the same symptoms. The problem with scientific research to date, is that all the research money goes into one or two areas
        (genes and dopamine)leaving everything else, an orphan. And, of course, there’s no big money in psychotherapy, so it has been sidelined, too. I don’t expect a big change in the future because soon the immune system or something else will become the flavor du jour, and research will continue on in its tunnel visioned way. The only thing that might change is where psychiatry decides to place its bets.
        Thanks for stimulating a good discussion.

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        • This is quite misleading, to put it “mildly.”

          When what’s called a disease is seen as being caused by the familial/psycho/social environment in a modality that actually corresponds with healing and this evidence is SUPPRESSED by the medical profession; this is NO WAY suddenly makes people pointing this out to be suppressing other modalities, when they point out: “heh, there’s this method that DOES heal.”

          There are also many factors that alternative methods have brought out which ARE perhaps related to biology such as nutrition and rest. And there’s more. A reduction of stress would also be beneficial. Not expecting a person to have to deal with the amount of false logic, false advertising, peer pressure, social pressure and intimidation, taking away of personal freedoms and other mechanizations of the proponents of the false biological method that ABOUNDS would also CLEARLY reduce stress. As would not having to deal with “oh excuse me, there’s also this way that hasn’t been proven to work, takes up most of the money, everyone is supposed to follow, is forced on people, has no real scientific basis; but when you point out methods that do work, you are discriminating against it because somewhere in the future it might be proven to work.”

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        • Dear Rossa,

          Thanks for your thoughtful post. Traumatic events are only one aspect, since there are many other environmental conditions that cause psychological harm to people. Living in poverty or being the victim of oppression are two examples. The problem with giving weight to biological causes is that, claims by the psychiatric establishment notwithstanding, there is no evidence that they cause mental disorders, and this emphasis serves mainly to distract from focusing on environmental causes. As I mentioned, if biological causes are found one day, the condition will cease to be a mental disorder and will be transformed into a medical condition.

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      • Dear Jay,

        I would argue the exact opposite. Psychiatry is a branch of medicine. Therefore, almost by definition psychiatric disorders are medical conditions. Perhaps there are disorders (personality disorders, relationship dysfunction, etc) which might be more effectively labeled psychological disorders. Biology being the substrate of all thought and behavior, they are still all biological in the strictest sense of the word.

        I also reject the idea that once a ‘biological basis’ has been identified for a disorder it becomes the domain of neurology. As an example, think of someone who is psychotic due to amphetamine exposure or depressed due to a thyroid problem – those are cared for by psychiatrists and I think they would meet your criteria for having a biological basis. They are also in the DSM.

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    • The only reason the person with a rare Auti-immune disease wouldn’t be seen as having something biological going on is because of the erroneous biological base for mental illness, that is WHY people stop looking and believe they know the answer, BECAUSE they believe it’s biological NOT because there hasn’t been enough research into whether it is or not, when in regards mental illness (NOT regards Auti-immune disease) there’s NEVER been any proof.

      If you want to find the cause for biological disease, you don’t support research in areas where it’s NEVER been found; where the cure is found outside of the biological model, and yet the cure is suppressed and there’s another new and improved story about what’s biological that goes nowhere, and have for the greater part of a century.

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    • doth the lady protest too much? Please, we are having a hard enough time already getting people to pay attention to & understand the trauma angle. I don’t think anyone’s arguing that real biological medical conditions can’t cause these problems, or that they should be ignored, but the trauma angle is already known (by many) to be a huge player yet is routinely neglected in our society. People, doctors, scientists, are only too ready to look for & accept medical conditions as causers of this distress, but trauma, abuse, neglect, social problems etc. are much more likely to be ignored/avoided/discounted, especially because they implicate other people who DON’T WANT TO BE IMPLICATED. That’s why we have to make such a case for them. Medical conditions are generally blame-free thus much more palatable to our society.

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  2. Rossa, I think the point here is that hundreds of millions of tax-payer dollars have been wasted in recent decades looking for genes that don’t exist in support of an obviously unsupportable theory. There ARE clearly familial, social and political antecendents to extreme mental and amotional states, many of them associated with trauma, and why shouldn’t those be looked at? At the same time, there are, as you point out, many actual physical diseases that have symptoms that look like so-called mental illness, and any doctor worth his/her salt should rule those out before deciding the problem is mental/emotional. But I didn’t see that the writer was suggesting that we ignore these.

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  3. Thanks for writing here. I have been very impressed by the clarity and soundness of previous articles I have read from you, and next on my list is reading your “The missing gene” book.

    You say: “researchers frequently claim that the environmental factors contributing to the development of psychiatric disorders are unknown, or are not well understood.”. If you mostly disagree with that claim, and had to name one book (for a general audience) that is a good reference for valuable knowledge about environmental factors in psychiatric disorders, which one would that be?


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  4. I don’t know why anyone capable of the slightest degree of intellectual vigor would assume a genetic cause for a “disease” that is “diagnosed” by a behavioral checklist. Normally, one finds the gene and then defines the disease based on the cause. Anyone with half a brain would realize that just because two people are depressed doesn’t mean they’re suffering for the same reason. Real science would start to break down these situations and look for possible root causes of the “syndrome”, and only when the causes are found would the “diseases” be established.

    It’s like calling a rash a disease. A rash could be caused by poison ivy, measles, or syphillus. The treatments and possible outcomes would be radically different. Yet each condition causes a rash. The rash is not the disease – the thing that causes the rash is what needs to be treated. That’s just elementary scientific logic, of which the psychiatric profession is apparently incapable.

    The psychiatric establishment is remarkably deluded. Thanks for giving us this kind of hard data to help spread the new concept that DSM diagnoses are not disease states. 40 years of trying to prove something and failing at every attempt is pretty darned good proof that your original hypothesis is false.

    — Steve

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    • Brilliantly said, common sense says what you have just summed up. One could not pass a high school science subject doing the research they do, but they claim it as some sort of miracle and lifesaving research!!??

      How they ever made it through medical school is beyond me. How they even managed to get the marks to enter medical school is beyond me, given the research they now produce.

      Two plus two equals four is clearly something they just have not mastered yet!!

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  5. This is very good and clear summary of the position in genetics in psychiatry, but I wonder if you comment on the DISC1 (disoreded in schizophrenia!) gene, which a colleague of mine is always going on about. I think he’s talking crap, but he has lots of ‘science’ to back up his arguments, and I only have conjecture.

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    • DISC1 is one of the many genes claimed to underlie schizophrenia, but none have been substantiated. There are continuing claims like this for most psychiatric disorders. It should also be noted that even if a gene is associated with a disorder, it doesn’t necessarily mean that it causes the disorder. Correlation does not equal cause, but in psychiatry they don’t even have consistently replicated correlations.

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      • Even if some gene (or combination thereof) is found to be strongly correlated with schizophrenia, AND even if a genetic variation is found to be a necessary condition for schizophrenia, it is still not necessarily a DEFECTIVE gene. It can simply be connected with a trait that is not well received in the social environment. “Sensitive” children can grow into strong, caring adults if they are not treated as though the only acceptable thing to be is a middle linebacker (to stick with Jay’s football analogies – go Ravens, by the way) as opposed to a hair stylist.

        “Strengths” can be made into weaknesses, and vice verse, depending on how they are nurtured or squashed. Changing analogies now – if you hitch a quarter horse to a plow, you get a lame horse. Run a Clydesdale in the Kentucky Derby and you get a lame horse. Neither is a case of defective genes. It is up to adults to recognize who children are and nurture them accordingly.

        There is a lot of evidence that experience (“trauma” is just the most obvious) strongly influences all kinds of mental problems; as Jay has shown, there’s little honest, credible evidence to support genetic flaws as culprits. But of course nobody knows the whole story. The problem lies in emphasis: evidence of environmental influence is all over the place and nobody in power cares, while any unverified scrap of genetic (or other medical) evidence is greeted like the holy grail. If psychiatry and PhARMA weren’t so desperate to sell the medical model, there wouldn’t be so much harm in people poking around genes. The trouble comes when unverified genetic “discoveries” are used as reasons to sell drugs that “correct” chemical imbalances that don’t exist.

        In any case, the biggest question is not how schizophrenia starts, but how people recover from it. Evidence is accumulating that psychosocial approaches are more effective than what psychiatry offers now, after spending hundreds of billions.on real or phony research. Read the book and articles on Open Dialogue’s work with first episode psychosis – the results have been remarkable for over twenty years; they even indicate that good psychosocial intervention may actually prevent the development of psychosis and schizophrenia. The psychosocial approach could have been recognized and improved on long ago, but the mental health industry turned its back on the results of Soteria House and Burt Karon’s work for decades.

        Psychosis and schizophrenia can be terrifying and confusing, and seem utterly intractable. That by itself doesn’t necessarily make it the product of physics defects or medical illnesses. Open Dialogue has demonstrated people really can recover, with little or no psychiatric drugs.

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        • “how people recover from it”

          Actually, I need to correct myself. It’s misleading to even accept psychiatry’s definition of “schizophrenia,” as Mary Boyle and others have shown so well. And I don’t know if “recover” is the best word either – “respond to” or “process the experience of” or “work their way through” the experience of what is labelled “schizophrenia.” We really don’t know that much about it, and a number of people with “lived experience” have different perspectives on what works and doesn’t work for them, and what they view as satisfying, meaningful lives. They need to be listened to very carefully.

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          • I think that’s an extremely important point you make, Peter, and entirely correct. As behavioral geneticists become more desperate they seem to be retreating into this idea of a ‘genetic predisposition’ which is then ‘triggered’ by environmental factors; some sort of hereditary weakness which, needless to say, needs to be medicated (ideally, I presume, before symptoms start and it is “too late”). But nothing seems to point to that kind of hereditary weakness and I think that model makes very little sense from an evolutionary point of view.

            To use yet another analogy after football and horses: if an individual has some genes that make his gut better at absorbing nutrients that is not in any way a genetic weakness – in normal circumstances it should in fact be beneficial and positively selected. But if that individual is exposed to contaminated food, his greater ability to absorb nutrients might in fact work against him, and make him ill while individuals without this gene which eat the same food remain healthy, or at least asymptomatic. Clearly the genes coding for better absorption are not the cause of the disease, the contaminated food is. Efforts should be directed at identifying the contaminated food as well as ways to remove the toxins from the already affected individual – and, if permanent damage has occurred, then to devising coping strategies to help the individual live with the damage. But the one thing you don’t need to do is ‘treat’ the gene, or even find out which gene it is because there is absolutely nothing wrong with it (although I suppose that identifying the gene might help identify the toxin – but that’s a long roundabout way of going about it).

            Having said all that (and it went on for a bit longer that I intended, sorry) I personally don’t think there is any strong association between any of the symptoms of ‘mental illnesses’ and any genes or even any epigenetic processes.

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  6. Great article, many thanks indeed.

    I can’t help feeling however that there’s a large elephant in this room, the most resounding failure of behavioral genetics yet, although I realize it’s a very touchy subject: sexual orientation.
    The parallels with schizoprenia research in particular are impossible to ignore (flawed twin studies followed by hundreds of genetic studies, etc.)

    See this for a taste and tell me if it doesn’t sound awfully familiar:

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  7. I stand corrected then, it is obviously not a touchy subject.

    I just can’t help wondering how can the very same people who are so consistently wrong about every single other mental illness be so consistently right about sexual orientation? It must be the exception that proves the rule. Or a miracle.

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    • Are you suggesting heterosxuality is a mental illness? Surely no more so than bisxuality or homosexuality?

      You write about every other mental illness and then sexual orientation in the same sentence in a way that implies that you do.

      Only asking – but it sounds a bit wierd to me if you do.

      I don’t know much about behavioural genetics but the mental health research has spent lots of money and found just about nothing. Maybe the stuff on left/right handedness or some other interestig human behaviour like sexual preference or taste in home furnishings is partly genetic but I’m not sure if either handedness, a liking for bright colors or sexuality is an illness. Homosexuality certainly hasn’t been listed in the DSM as such for quite a while. Mind you, the fact that it once was rather proves that DSM and similar classifications are all a bit of nonsense anyway if you ask me.

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      • And not only a nonsense but partly, if not largely, a political document that backs up whatever predjudices are current in society. This maybe slightly off topic but mental illnesses are partly down to fashion, both in what is defined as an illness and also in how people choose to display their distress (we don’t here much of conversion hysteria these days but it once very popular, anorexia did not exist in Japan until the newspapers wrote of it). So the idea of studying genetic causes of perticular mental illnessses when what is defined as an illness varies from year to year and when how people express distress varies from culture to culture and from decade to decade seems in many cases quite questionalbe to me.

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  8. John, I’m sorry, I should have written mental illness in quotation marks: “mental illness”.

    In my first comment I was just trying to draw attention to the fact that the exact same bad science that supports the current consensus on schizophrenia (or bipolar disorder, or ADHD, etc.) as a genetic “chemical imbalance of the brain” also supports the consensus that sexual orientation is an unchangeable inborn trait. But it is not easy to discuss this fact – and it is a fact – when it is instantly countered with accusations of homophobia (incidentally, some people within the APA have for a while now been trying to include homophobia as a mental disorder; no doubt that if they succeed they’ll quickly find out it responds very well to psychoactive drugs.)

    Anyway, I’m sorry if I don’t explain myself very well; I’m sure Jay Joseph, who clearly has a good understanding of the science on this issue could explain it much better than me.

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    • I’m not bothered whether sexuality is inherited or not or whether sexuality is a partly inherited characteristics. I am bothered by any statements which decry homosexulity. And while you’re post may not have been intentionally homophobic by associating homosexuality and mental illness you are making an association which worries me. People do not report genetic studies on sexuality in a morally neutral way. Studies are not reported as looking into the genetic basis of heterosexuality, yet both heterosexualit and homosexuality are valid expressions of human (and animal) sexuality.

      A quick google search on the genetic of sexuality shows conflicting ideas. It reminds me of everything I used to hear about the genetic of schizophrenia – I used to hear that it turned out that schizophrenia is 50% genetic and usually said with great certainty. Yet it turned out to be rubbish.

      The fact that the APA has tried to include homophobia as a mental illness just adds to my point that DSM and similar diagnostic systmes are political documents. At one time slaves who ran away were supposed to have a mental illness now they would be seen as people fleeing for their freedom. At one time drug companies were looking into drugs to “treat” violence in men. This would have helped many people, many woman and children. Now I think trying to stop men being violent using drugs is appaling but the drug companies stopped this research mainly becuase they thought that there was no market. What is described as a mental illness is so often a political decision.

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  9. I enjoyed reading the article.I will leave any discussion of sexuality and all its issues to those in the LBGT and queer community who are the experts in my eyes.
    I would like to refer again to the April 2012 TED talk by Juan Erniquez. I think it’s really important to this and many discussions.So many, many questions. And so few professionals who are able to say I don’t know. Maybe that’s a beginning of a true dialogue.

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  10. One more thing for this thread. National Geographic 125th Anniversary has an article on this genetic theoretical quagmire entitled “Restless Genes”. Part of the discussion centers on the interaction of genetics with environment. Something to think on.

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  11. This is a great treatment of a fascinating and significant topic. The Plomin (2013) article cited in the references had some subtle but potentially huge arguments that I think are worth highlighting as a complement to the main post:

    “If a disorder is influenced by many genes—and this is the conclusion that emerges from GWA research—its genetic liability is likely to be normally distributed. Thus, in terms of genetic liability, common disorders are quantitative traits (Plomin, Haworth, & Davis, 2009). In other words, genes that are found to be associated with disorders in case-control studies are predicted to be correlated with the entire range of variation throughout the normal distribution. Stated more provocatively, this means that from a genetic perspective there are no common
    disorders, just the extremes of quantitative traits….

    Three important implications follow from this conclusion that common disorders are quantitative traits. First, at all levels of analysis from biology to brain to behavior, it should stimulate research on quantitative dimensions rather than qualitative disorders. Although the extremes of these quantitative dimensions are important medically and socially, there seems to be no scientic advantage in reifying diagnostic constructs that have evolved historically on the basis of symptoms rather than etiology. Focusing on quantitative dimensions could lead to a new
    approach to psychopathology based on etiology rather than symptoms (Plomin et al., 2009). Second, research on quantitative dimensions leads away from the notion of curing diagnosed ‘‘cases’’ toward a public health model that focuses on preventing problems and promoting health rather than curing illness once it occurs (Brownson, Fielding, & Maylahn, 2009)”

    The implications of Plomin’s arguments to me are that genetic researchers need to move to a model of using genetic variations as clues to unravel the biological mechanisms involved in the spectrum of behavioral traits without the misleading and reductionist assumption that an independently existing (reified) disease process or genetic mistake is occuring that clearly differentiates normal from pathological (or even extremely resilient) traits.

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    • I am puzzled by the statement:“Normally, one finds the gene and then defines the disease based on the cause.” Having been involved in the identification of the gene that causes spinocerebellar atrophy it was, like Huntington, known to be an identifiable, autosomal dominant disease long before the gene was discovered.
      All medical science depends on statistical probability. No-one is perfect in diagnosis or treatment but increased effort can lead to increased accuracy . Psychiatry seems to have forgotten the principle of differential diagnosis. It has been established several times that most of diagnosis depends on what the patient tells you that should lead to appropriate questioning and dialogue. What ever happened to the fifty-minute hour that at least allowed for the possibility of such interaction? Professor Robert Kendell was one of my instructors at the University of Edinburgh and was horrified by his own research into the time psychiatrists took to reach a diagnosis – less than ten minutes.
      To continue with causes let’s consider “Forty years on from Robins and Guze, what empirical evidence is there that disordered brain function is causally related a psychiatric diagnosis like ‘schizophrenia’?” One has to ask, what empirical evidence is there that the cause is not disordered brain function? As one of the thirty percent who hallucinate on Demerol I can assure you that I know what an hallucination is and I know the cause.
      It is repeatedly written that antipsychotics such as olanzapine increase weight. Yes, they do. But by what means? They increase appetite, that’s how. I have watched patients on olanzapine eat meals that would be too much for a lumberjack. We do know what substances control appetite, among them dopamine. We also know that most psychotropic drugs are lipophilic, heading straight for body fat where they hang around for a long time making withdrawal syndrome longer and more difficult. It is discouraging for those of us trying to improve the whole disaster of failed psychiatry and drug-soaked treatment to find an almost universal reluctance to open the mind and reject what has become a received wisdom that there is no such thing as mental illness. This dogma, just as the previous one, is going to help no-one.

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      • Ah, but it is not necessary scientifically to prove that the cause is not disordered brain function. Otherwise, we can put out any hypothesis and say, “You haven’t proven this is wrong yet, so it is true.”

        It is the responsibility of the person postulating the theory to provide the proof. If there is no proof that brain function is disordered in a psychotic person, then from a scientific perspective, we have to assume that disordered brain function is not a cause. Even if there are brain differences in a psychotic person, those putting forth the chemical imbalance theory would have to prove that these differences are the pre-existing cause of the hallucinations, rather than the result of them or something that just happens at the same time as them.

        For instance, let’s assume that depression is associated with a certain chemical condition in the brain (which has not been proven, not even close). It is possible that a person’s thoughts lead to feelings of depression which are accompanied by certain changes in brain chemistry. The thought could cause the change, but the change and the depressed feelings occur together. The chemistry difference doesn’t cause the depression, they just happen to be associated.

        As an example, there was a PET-scan study done where people thought of depressing things while hooked up to the device, and their brains changed to a pattern that was associated with depression. When they thought of happy things, their brains changed back to a different state. The person apparently controlled his/her brain utilization patterns based on what s/he thought.

        I don’t think that anyone here would suggest that there is no such thing as mental/emotional/spiritual distress. And it’s feasible that some part of that may be the result of inherent biological characteristics, but that proposition has not been proven, despite a hell of a lot of research trying to prove it is true.

        I think the objection here is to taking a set of behaviors that have been arbitrarily determined to be a “problem” based on cultural and social norms, and decide that the person with this “problem” has a medical disease. If there is an underlying pathology of some kind that made EVERYONE depressed, and we could identify that and reliably alter it in a safe fashion, then depression as an illness makes sense. But it should be clear that there are many, many reasons why a person is depressed, and many, many approaches they can take to move forward and heal or recover or whatever word we want to use, most of which have no relationship to the field of medicine.

        It’s not that there is no such thing as the distressing states described in the DSM as “mental illness” – it’s that calling it “mental illness” makes one think that it’s a “disease like diabetes” that can be “treated” with “medicine.” There is at this point little to no evidence that this last statement is remotely true, and as I stated above, in the realm of science, a hypothesis is properly considered false until proven otherwise, and is then true only as long as further evidence continues to support it. “Mental illness” as a physiological disease just doesn’t meet the scientific criteria for truth.

        —- Steve

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      • Irene, when you say that you knew spinocerebellar atrophy was an autosomal disease, I imagine this was so because you had strong evidence from family studies. Now, where does the evidence that schizophrenia has a genetic aetiology come from? Also from family studies, mainly adopted twin studies. I’d suggest you look at those studies and honestly ask yourself whether they are in any way convincing and whether they aren’t riddled with methodological flaws (most notably not assessing whether some form of abuse or trauma had taken place in the adoptive families). You might find this of interest:

        You ask “what empirical evidence is there that the cause [of schizophrenia] is not disordered brain function?”, but I’m afraid that is the wrong question. I’m certain that schizophrenia -or rather the symptoms gathered under that name- are cause by ‘disordered’ brain function (which is not the same as a brain disorder). The question however is not that, the question is what is the aetiology of that disordered brain function.

        In the first reply to your comment Steve raises something that I think is crucial here: “It is possible that a person’s thoughts lead to feelings of depression which are accompanied by certain changes in brain chemistry. The thought could cause the change, but the change and the depressed feelings occur together. The chemistry difference doesn’t cause the depression, they just happen to be associated. ” I don’t agree that they just happen to be associated, but where I think Steve is correct is in suggesting that direction of causality is not only brain>thoughts, but also thoughts>brain. In fact, although I know many will find this controversial, I would suggest that the relationship between thoughts (mind) and brain is not one of causality at all, but one of identity – this is however too complex a subject to discuss here.

        I think it is clear from your comment that you subscribe to a epiphenomenalistic view of the relationship brain-mind and I think it is something you should question. Coincidentally Philip Thomas has just published a very interesting article here in MIA touching on this: “Pinball Wizards and the Doomed Project of Psychiatric Diagnosis” which you might find interesting.

        I know absence of evidence is not evidence of absence, but I think there is by now plenty of evidence to suggest that schizophrenia (to say nothing of depression or bipolar disorder) is not a genetic disorder – and this is not just because the genes have not been identified, but there are also serious questions from an evolutionary perspective.
        So if it is not genetic, what then? Because it certainly is something. How about a pathogen? How about a pathogen called “abuse”, or “trauma”? Does this seem far-fetched? I confess I’m always surprised when I hear psychiatrists talk about conditions with a physiological cause vs conditions with a psychological cause. What exactly is a psychological cause? In what sense is psychology not physical?

        Take this example: a child is continuously subjected to verbal abuse and develops low self-esteem. The abuse is never ‘physical’ in a conventional sense, but it is of course a physical process in the sense that the abusive words are soundwaves that reach the child’s ear, stimulate nerves, produce biochemical reactions in the brain, and cause a ‘disordered brain function’: low self-esteem. Similarly, if the child is then consistently praised this might ‘re-order’ brain functioning – or not, if the abuse was too prolonged, or at a crucial stage of brain development, etc. Call it psychological if you will but you are referring to a process which is as physical as a virus infection. The identity between psychology and physiology (the identity mind-brain) raises of course important questions and many people immediately jump to the erroneous conclusion that it precludes free-will or genuine decision-making. This is not so but as I said before the issue is too complex and this comment is already far too long!

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        • Great post! I agree very much with your line of thinking, that the origins of these mind states are very complex and attempts to reduce them to simple genetic or biological causes is very unlikely to be the case. And the twin studies aren’t even convincing without the methodological flaws – supposing even 50% of identical twins with “schizophrenia” (and also ignoring the impossibility of 100% accurate “diagnosis” of this rather vaguely defined malady), what happened to the other 50%? If it’s genetic, and identical twins have the same genetic material, shouldn’t we see more like 98% concordance? Clearly, genetics can’t provide the entire answer of causality, even in the most optimistic interpretation of the known data.

          I’d disagree on one point, though – I don’t think there is evidence that brain and thought are an identity. It appears to me more that emotion and brain activity track together, i.e. a state of anxiety is experienced and expressed physiologically in response to a thought. For instance, a person who believes they are in danger will generally experience heightened cortisol, which is associated with anxiety and fear. But this fear may be based on a real danger (a charging bear) or a belief (my mom is probably going to yell at me) or a fantasy (the CIA is trying to track me down.)

          What actually generates a thought, as well as where a thought resides and what impact it has on the body/brain, remains a very large mystery scientifically. I think we move into the area of philosophy when we start talking about thought, and as you say, it’s way too big a topic for this forum. But so much of psychiatry’s false underpinning is bad philosophy (unstated assumptions taken as proof) that I think it’s important for us to draw the line pretty firmly between what we know and what we believe or assume to be true.

          Nice post!

          — Steve

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          • Thanks Steve. I agree with you on the basics and disagree on the details – but we have indeed strayed onto philosophy and it is too big a topic!

            Still, anyone interested on epiphenomenalism please follow this link to what I think is a good, concise introduction (maybe I should be posting this on “Pinball Wizards”):


            Just one last thing: just as I think the division between psychology and physiology is spurious, I also think the division between morphology and physiology is to a large extent spurious, particularly when it comes to the brain. The division morphology/physiology comes from mechanistic analogies that do not hold true for biological systems and do not take into account basic things like ‘self-repair’: the fact that in any biological system a fundamental aspect of its physiology is to repair its own morphology. Again, the causation is not just morphology>physiology but also physiology>morphology. There’s constant ‘feedback’ in the system.

            I think this is important because neurologists in particular (sorry, Irene) tend to make a sharp distinction between the two when it comes to ‘mental illness’. They tend to see normal functioning as physiology and consider atypical morphology as evidence of a disorder, whereas in fact atypical morphology can also be explained as the result of atypical experiences. The brain is an organ whose physiology is precisely to continuously alter its own morphology in response to stimuli from the ‘environment’ (the environment being any information which reaches the brain either from the body or from the ‘outside world’ through the senses). This idea is, if you like, the translation into scientific terms of the philosophical question of epiphenomenalism.

            By the way, this just reminded me of something I read some time ago: neuroscientists had studied people who had practised martial arts for a long time and found differences in the morphology of their brain areas controlling motor skills, compared to a control group. So… maybe people born with brains that give them superior motor skills naturally gravitate towards martial arts? But then the differences only showed on those who had been practising for a long time (the ‘black belts’)…

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  12. Great post and very interesting and “emotive” comments on the Family and its generational embodiment of emotive styles of coping, which can and do result in the major and historically known emotional disorders of schizophrenia and manic-depression. After decades of manic-depressive experience, only re-learning a sense-of-self which was dysregulated by circumstances early in my life, has set me free from a “missed” developmental need.

    Here on MIA just as throughout wider society we speak with a assumption of perception which is self-decieving, because the core of the human-self is discovered in “implicit” not “explicit” experience. Only through becoming aware, through a “felt-sense” process of self-exploration was I able to sense my missing developmental needs, of which my very first experience of “mania” was a subconscious attempt to achieve.

    A subconscious motivation completely misread by fearful others and this self-deceiving, predominately left-brained sense of a human self, which falsely assumes that “education” has given it a fully conscious sense of itself and others. Please consider the writing of Allan N Schore, one the few who consistently seeks to understand the “bigger picture,” rather than simply satisfying his own self-preservation needs;

    “Offering data at the neuropsychological, cultural, and historical levels, McGilchrist (2009) echoes this principle: “If what one means by consciousness is the part of the mind that brings the world into focus, makes it explicit, allows it to be formulated in language, and is aware of its own awareness, it is reasonable to link the conscious mind to activity almost all of which lies ultimately in the left hemisphere” (p. 188). He adds, however, “The world of the left hemisphere, dependent on denotative language and abstraction, yields clarity and power to manipulate things that are known, fixed, static, isolated, decontextualized, explicit, disembodied, general in nature, but ultimately lifeless” (p. 174).

    In contrast, “the right hemisphere … yields a world of individual, changing, evolving, interconnected, implicit, incarnate, living beings within the context of the lived world, but in the nature of things never fully graspable, always imperfectly known— and to this world it exists in a relationship of care” (p. 174). Indeed, the “emotional” right hemisphere “has the most sophisticated and extensive, and quite possibly most lately evolved, representation in the prefrontal cortex, the most highly evolved part of the brain” (p. 437). An essential tenet of McGilchrist’s volume (2009) is expressed in its title:

    the right hemisphere is the master, and the left the emissary, which is willful, believes itself superior, and sometimes betrays the master, bringing harm to them both. Offering interdisciplinary evidence that spans the sciences and the arts, he convincingly argues that the left hemisphere is increasingly taking precedence in the modern world, with potentially disastrous consequences.

    I agree that especially western cultures, even more so than in the past, are currently overemphasizing left brain functions. Our cultural conceptions of both mental and physical health, as well as the aims of all levels of education, continue to narrowly overstress rational, logical, analytic thinking over holistic, bodily based, relational right brain functions that are essential to homeostasis and survival. It is ironic that at a time when clinicians and researchers are making significant breakthroughs not only in right brain social-emotional models of optimal development but also in right brain models of the etiologies and treatment of a wide range of psychopathologies, strong economic and cultural inhibitory restraints and cutbacks are being felt by practitioners. How can we understand this? We are constantly told that the reason for this lies in objective economic factors. But the paradigm shift in psychology and neuroscience suggests subjective unconscious forces are at play here. Listen to McGilchrist’s (2009) description of what the world would look like if the left hemisphere were to become so far dominant that, at the phenomenological level, it managed more or less to suppress the right hemisphere’s world altogether. He imagines that this left-brained world would lead to an increasing specialization and technicalizing of knowledge, as well as the following: increased bureaucratization, inability to see the big picture, focus on quantity and efficiency at the expense of quality, valuing technology over human interaction, lack of respect for judgment and skill acquired through experience, and devaluing of the unique, the personal, and the individual. Even more specifically; 

    Knowledge that came through experience, and the practical acquisition of embodied skill, would become suspect, appearing either a threat or simply incomprehensible.… The concepts of skill and judgment, once considered the summit of human experience, but which come only slowly and silently with the business of living, would be discarded in favor of quantifiable and repeatable processes.… Skills themselves would be reduced to algorithmic procedures which could be drawn up, and even if necessary regulated, by administrators, since without that the mistrustful tendencies of the left hemisphere could not be certain that these nebulous “skills” were being evenly and “correctly” applied.… [F] ewer people would find themselves doing work involving contact with anything in the real, “lived” world, rather than with plans, strategies, paperwork, management and bureaucratic procedures.… Technology would flourish, as an expression of the left hemisphere’s desire to manipulate and control the world for its own pleasure, but it would be accompanied by a vast expansion of bureaucracy, systems of abstraction and control. (McGilchrist, 2009, p. 429)  

    Sound familiar? I suggest that this “imagined” left brain worldview now dominates not only our culture but also the current mental health field in the following forms: an overemphasis on psychopharmacology over psychotherapy, an undue influence of the insurance industry on defining “normative” and “acceptable” forms of treatment, an overidealization of “evidence-based practice,” an underappreciation of the large body of studies on the effectiveness of the therapeutic alliance, a trend toward “manualization” of therapy, a training model that focuses on the learning of techniques rather than expanding relational skills, and a shift of psychotherapy from a profession to a business.”

    Excerpts from: “The Science of the Art of Psychotherapy,” by Schore, Allan N. N.

    And from my own attempts to decipher the Familial role in the generational nature of emotional regulation;

    The Familial Face of Affect-Regulation?
    The reality of “affect” is seen most clearly on the human face where its “involuntary” nature cannot tell a lie. The brain-nervous systems “pattern-match” all current experience with past experience, aiding our survival with previously “safe” reactions. This “involuntary” nature of affect-regulation lies at the heart of our human “attachment” needs. Real attachment need is an overwhelmingly subconscious phenomena, constantly monitored at a subconscious level of nervous-system reactivity. Our early life experience of the Familial face of affect, becomes our familiar expectation of the subconscious world of affective self-regulation and getting our vital attachment needs well met.

    61 years later, my birth and developmental experience is written on my face. Its the “intensity” in my eyes & hard set jaw-line, of residual trauma affect.

    Its the human face that “attunes” communication between people, long before we utter a single word to each other. In the subconscious world of affect-regulation and securing attachment needs, communication occurs at the millisecond speeds of the nervous systems and for those of us suffering from the residual effects of traumatic experience, we normally operate on a level of tense “neuroception,” constantly scanning for safety concerns, rather than with the relaxed easy flowing spontaneity, which reflects an inner security of well met attachment needs. Wanphen and I share a similar life history of insecure attachment as reflected in our faces.

    The eyes are well known windows to the soul through their direct affect on the nervous regulation of the heart. Like a kind of neural wifi, the eyes transmit subconscious information directly between two nervous systems when we share a mutual gaze, and no other gesture communicates to others as fast as a sudden shift in eye movement during our face to face interactions, in which the eyes convey real intent, regardless of our spoken words. Please consider a neuroscience understanding of the importance of the human face and our eyes, during early life development.

    “Mirroring Gaze Transactions and the Dyadic Amplification of Positive Affect:
    Dyadic mirroring gaze transactions thus induce a symbiotic, physiobiologically attuned affect amplifying merger state, in which a match occurs between the expression of rewarding arousal. This process of interpersonal fusion generates dynamic ‘vitality affects.’ Sustained facial gazing mediates the most intense form of interpersonal communication. Eye to eye contact gives non-verbal advanced notice of the other. The temporal structure of gaze, the most immediate and purest form of inter-relation, provides clues to the readiness or capacity to receive and transmit social affect. Facial actions in emotional expression, regulates blood supply to the brain for oxidative metabolism.

    The development of internal representations of external objects – such as faces – that consistently provide stimulating responses to the infant. The elements which mediate this function are found in a “neural network or connection matrix,” and the creation of the architecture of this network depends on pulses of electro-chemical energy through the infants brain “at critical developmental junctures” As these pulses flow through the brain, synaptic connections are established and strengthened and the firing rates of groups of neurons are set. The result is that certain kinetic pathways are established, making it more likely that these patterns will guide future energy flows” Excerpts from “Affect Regulation & The Origins of the Self” by Allan N Schore.

    Best wishes to all,

    David Bates.

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  13. Jay Joseph, how would you interpret this latest study

    Primary source: Lancet
    Source reference:
    Smoller JW, et al “Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis” Lancet 2013; DOI: 10.1016/S0140-6736(12)62129-1.

    Additional source: Lancet
    Source reference:
    Alessandro Serretti, Chiara Fabbri “Shared genetics among major psychiatric disorders” Lancet 2013; DOI: 10.1016/S0140-6736(13)60223-8.

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    • Love to hear from Jay on this.

      My take: first off, they found correlations, which are large-scale statistical probability findings. This is very far from saying that every case of these 5 “disorders” involves this gene alteration, and it’s even further from saying that this genetic pattern plays a causal role.

      Second, they have lumped together 5 different “disorders” to get these results! This would suggest that either the “disorder” definitions are close to meaningless (which, of course, is absolutely true), or that they had to pool all this data from different disorders to get a statistically significant result (which could certainly be true), or it simply means that this genetic array is associated more commonly with certain personality types who are somehow more vulnerable to the stresses of our current, insane social system. There could be other explanations. It certainly doesn’t convince me of anything. It seems like almost meaningless research to me.

      Others take on this?

      — Steve

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    • Dr. Joseph,

      I, too, would greatly appreciate it if you would interpret the study cited by Altostrata.

      I am very, very grateful for all of your fine work debunking the self serving eugenics genes claims about bogus DSM stigmas past and present.

      I was very, very discouraged to see this article and psychiatry in bed with BIG PHARMA and our increasingly fascist government making the neverending latest fraud claims of great genetic breakthroughs in finding the genes for their VOTED IN unproven “disorders” based more on BIG PHARMA revelation than any science whatever per Dr. Marcia Angell.

      It boggles my mind that they can claim they studied a huge number of people with and without these bogus disorders for which they have no proof, reliability or validity or any tests to prove anyone has them while ignoring all severe social stressors as you and Dr. Boyle so brilliantly point out to come up with this latest great breakthrough in psychiatry!!

      The following is the most depressing news I read this morning:

      Do you agree that coming up with supposed genes for voted in bogus stigmas that are so loosely applied to just about everyone to push the same lethal drugs for the most part is rather absurd or am I missing something? I suppose it is good enough to keep hoodwinking a brainwashed public. Yet, I continue to contemplate why nobody remembers the enlightening tale of the boy who cried wolf too many times and his fate. But, I suppose he wasn’t backed by BIG PHARMA and government billions to continue his spin.

      Would it be possible for you to debunk this article with your usual brilliant research and publish it so the public might be better informed?

      Thank you again for all you have done and continue to do by providing the necessary research and science we need to validate our reality rather than the constant invalidation of biological psychiatry. I highly recommend the book, PSEUDOSCIENCE IN BIOLOGICAL PSYCHIATRY too.

      Again, thank you for your great work that continues to give me hope that some day maybe things might change if it isn’t too late already.

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  14. The solution is quite simple really. The fundamental basics of psychiatry are inherently flawed causing a wide array of false positives in all categories making finding a true common genetic component impossible.

    It’s like finding proof the earth is flat.

    Practically all disorders stem from an original observational root, refined over time. Since an observation is as good as the one who observes it, scientifically it has no real value.

    Trying to prove scientifically (genetics) disorders which are anything but is a Sisyphus task.

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