What Do Twin Studies Prove About Genetic Influences on Psychiatric Disorders? Absolutely Nothing


I write frequently about the fallacies of behavioral twin research, in both its “reared-together” and “reared-apart” forms. I am compelled to keep doing this because twin studies of behavior, and the claims based on them, have not gone away despite decades of critics’ airtight arguments that indicate that they should have gone away a long time ago. Assessing the validity of psychiatric twin research is very important because it relates directly to the question of whether the main causes of psychological distress and dysfunction, and socially disapproved behavior, are located inside of the human body and brain, as mainstream psychiatry claims, or outside of the body and brain, as many critics argue. Twin studies are often cited in support of psychiatry’s disputed claim that its diagnoses are valid medical/biological conditions caused by a brain malfunction or by a “chemical imbalance.”

I recently published an online in-depth critical analysis of the famous “Minnesota Study of Twins Reared Apart” (MISTRA), where I concluded that because this “reared-apart” twin study was unable to disentangle (separate) the potential influences of genes and environments on human behavior, in addition to many other reasons, the researchers’ conclusions in favor of important genetic influences on IQ, “personality,” and other behavioral characteristics must be rejected. This conclusion applies to all other published “twins reared apart” studies as well. Other than some individual cases of MZ pairs that have come to the attention of researchers since the 1920s, the only reared-apart twin study that looked into areas related to psychiatry was a 1990 MISTRA study of substance abuse/dependence and antisocial personality.

Twin studies of the major psychiatric disorders have been based on pairs who were reared together in the same family home. Since 1998 I have written about the many problems with these studies, which nevertheless form the bedrock of genetic theories and claims in psychiatry. Here I will highlight and examine the main underlying fallacy of psychiatric twin studies, and of twin studies of behavior in general. It is now widely understood that psychiatric family studies are unable to disentangle the potential influences of genes and environment, because behavior can “run in the family” due to shared environmental factors. Psychiatric adoption studies are also cited in favor of genetic influences, but critics have pointed to many major problems and biases in these studies.1

Given the spectacular half-century failure to make confirmed discoveries of genes that cause the major psychiatric conditions, the main evidence that psychiatry has marshalled in support of the genetic basis of its disorders has been the “twin method” comparison between reared-together MZ (monozygotic, identical) and reared-together same-sex DZ (dizygotic, fraternal) twin pairs. MZ pairs are said to share 100% of their segregating genes, whereas same-sex DZ pairs, like ordinary siblings, are said to share an average 50% of their segregating genes. As one group of twin researchers wrote in 2003, “For several decades, twin studies have provided a critical facet of psychiatric and behavior-genetic research.”2

When both members of a twin pair are judged to share the same psychiatric condition, the pair is concordant for the condition; when one twin is judged to have the condition but the other is not, they are discordant for the condition. Twin pair “concordance rates” are presented as a percentage ranging from 0% to 100%. A completely genetically determined condition or trait would find 100% MZ concordance, and twin researchers recognize that because MZ concordance rates for psychiatric conditions are well below 100%, environmental factors must play a role in causing them.

As a hypothetical yet representative example of a simple twin method comparison and the conclusions that researchers draw from it, after identifying 100 reared-together MZ pairs in which one twin is judged to have bipolar disorder, if in 55 of these pairs the second twin is also judged to have bipolar disorder, MZ concordance would be 55% (using the “pairwise” concordance method).3 The corresponding bipolar disorder concordance rate in a group of 100 reared-together DZ pairs in this example is 15% (15/100).4 The study found that MZ pairs were more concordant than DZ pairs for bipolar disorder at a statistically significant level (55% vs. 15%), and based on a series of assumptions (see Figure 1), twin researchers would conclude that this finding is the result of MZ pairs’ greater genetic resemblance versus DZ pairs. They would go on to calculate a heritability estimate (which ranges from 0%-100%) either by doubling the MZ-DZ concordance rate difference (80% heritability in this example), or through the use of a “model fitting” procedure. The researchers would conclude that bipolar disorder is a “highly heritable” psychiatric condition.

Social and behavioral science researchers often study people who grew up in environments that these researchers did not design, control, or observe. They must therefore make assumptions about these environments, and the conclusions they reach depend on the validity (truth) of these assumptions. An assumption is something taken for granted or accepted as true without proof. The project or investigation then treats it, and researchers arrive at conclusions, as if it were true. Whether an assumption is true or false can completely change the findings of a study.

The All-Important MZ-DZ “Equal Environment Assumption” (EEA)

As seen in Figure 1, genetic interpretations of twin method results depend on the acceptance of several key assumptions. Here I will focus on by far the most controversial of these assumptions, which has always been twin researchers’ MZ-DZ “equal environment assumption,” also known as the “EEA” (see the bolded Assumption #5 in Figure 1). According to this assumption, MZ and DZ pairs grow up experiencing roughly equal environments, and the only factor distinguishing these pairs is their differing degree of genetic relationship to each other (100% versus an average 50%). As one group of twin researchers correctly observed, the EEA “is crucial to everything that follows from twin research.”5

 twin studies

Psychiatric twin researchers’ acceptance of the five assumptions shown in Figure 1, in addition to their claim that psychiatric conditions are discrete biological entities that can be reliably identified (diagnosed), has allowed them to argue that genetic factors explain the usual finding that MZ pairs are much more concordant for psychiatric conditions than are same-sex DZ pairs, after which they engage in the above-mentioned controversial practice of estimating heritability. Psychiatric textbook writers and other authoritative authors then endorse the original twin researchers’ conclusions that most psychiatric conditions are “moderately to highly heritable,” although they usually do not closely examine or challenge the logic that the original researchers used to arrive at these conclusions. In his 2018 genetic-determinist themed book Blueprint: How DNA Makes Us Who We Are, leading behavioral geneticist Robert Plomin claimed that “genetics accounts for most of the systematic differences between us—DNA is the blueprint that makes us who we are.”6 Although this misguided claim was based substantially on twin method findings, Plomin did not mention or attempt to uphold the validity of the EEA.

Schizophrenia studies based on the twin method have been the model of psychiatric twin research, and most other psychiatric conditions have been studied in a similar way, with researchers arriving at similar conclusions. Schizophrenia twin studies date back to 1928, when psychiatric geneticist Hans Luxenburger published his German study. The first American study was published by Aaron Rosanoff and colleagues in 1934. In the 16 schizophrenia twin studies published between 1928 and 1999, the pooled MZ concordance rate was about 40%, while the pooled DZ rate was about 8%. These figures can be compared with the general population rate of 1% or less. Looking at the 10 methodologically superior studies published between 1963 and 1999, the pooled rates fall to 23% MZ versus 5% DZ, meaning that in these studies the MZ co-twin of a person diagnosed with schizophrenia is not so diagnosed about 75% of the time.7 Mainstream textbooks and academic publications usually report that the pooled MZ schizophrenia concordance is about 50%, with an accompanying 80% heritability estimate based largely on twin studies.

Although methodological issues and biases have undoubtedly inflated true concordance rates, especially in the older studies published between 1928 and 1962, there is no doubt that MZ pairs are more concordant for psychiatric conditions, and for behavior in general, than are DZ pairs. This proves nothing about genetics, however, as the 90-year controversy has centered on the crucial question of what causes this to occur.

We have seen that the twin method’s all-important MZ-DZ equal environment assumption (EEA) states that reared-together MZ and DZ pairs grow up experiencing similar environments. From the inception of the twin method in 1924 until the mid-1960s, the EEA was defined as the simple statement that MZ and same-sex DZ pairs grow up experiencing roughly equal environments. To cite one example of this “traditional” EEA definition, in 1967 schizophrenia twin researcher Einar Kringlen wrote:

“The basic underlying assumption for the classical twin method is, of course, that environmental conditions of monozygotic twins do not differ from those of dizygotic twins.”8

Almost everyone now agrees that this 1924-1960s traditional definition of the EEA is false, since research and common sense converge on the conclusion that MZ pairs grow up experiencing much more similar environments, and are treated much more similarly, than DZ pairs. This means that twin researchers and their critics don’t have to argue anymore about whether MZ and DZ environments are different, since almost everyone now agrees that they are different. What twin researchers and their critics currently disagree on is whether this difference matters. Twin researchers’ bottom line argument is that it doesn’t really matter; the critics emphatically argue that it matters a lot.

While conceding the point that MZs are treated more similarly and share more common experiences when growing up, psychiatric twin researchers and textbook authors much less often mention the fact that MZ pairs also experience much higher levels of identity confusion related to their twinship, attachment to each other, and emotional closeness than experienced by DZ pairs, which will (presumably) lead to greater MZ behavioral resemblance. For example, Kringlen performed a “global evaluation of twin-closeness” based on 117 Norwegian pairs, and found that 65% of the MZ pairs had an “extremely strong level of closeness,” which was true for only 17% of the same-sex DZ pairs. Fully 90% of Kringlen’s MZ pairs had experienced “identity confusion in childhood,” which was experienced by only 10% of the DZ pairs.9 These findings by Kringlen have never been cited or discussed in any psychiatric publication that I am aware of. Other researchers investigating the question of whether twins were “mixed up for each other as children,” experienced “extreme or strong closeness or interdependence in childhood,” were “hard for strangers to tell…apart,” were “never separated from [their] twin,” or were “closely attached” found that MZ twins answered yes to these questions much more often than did DZ twins.10

In light of the overwhelming evidence that MZ pairs experience much more similar environments and levels of emotional closeness and identity confusion than experienced by DZ pairs, twin researchers of the 1960s and 1970s were confronted with two main options: (1) abandon the twin method, including all previous conclusions in favor of genetics, because the EEA is false; or (2) redefine the EEA in an attempt to keep the twin method alive. Twin researchers should have chosen option #1. Instead, as evidenced by the fact that I am writing this article, they chose option #2.

The Two Main Ways That Twin Researchers Have Attempted to Validate the EEA

In redefining the EEA, twin researchers have claimed since the 1960s that the assumption is valid on the basis of one or both of the following two arguments. I have called these “Argument A” and “Argument B.”

Twin Researchers’ Argument A: The “Twins Create Their More Similar Environments” Position

Supporters of Argument A recognize that MZ pairs grow up experiencing more similar environments than experienced by DZ pairs, but they maintain that the EEA is valid because MZ pairs “create” or “elicit” more similar environments for themselves because they behave more similarly for genetic reasons, and that environmental influences on twins’ behavioral similarity should therefore be counted as genetic influences. One of many examples of Argument A is found in a 2000 article by a pair of twin researchers writing in support of the “validity of twin studies”:

“The more similar parental treatment of MZ vs. DZ twins occurs in response to the greater similarity of actions initiated by MZ pairs… It seems…likely that the increased similarity in treatment of MZ twins is a consequence of their genetic identity and the more similar responses this elicits from the environment” (italics in original).11

An early example of Argument A can be found in a 1954 article by British twin researcher James Shields, and twin researchers have been using it ever since.12

The Fallacy of Argument A. The Argument A “twins create their more similar environments” position is based on illogical circular reasoning, since the conclusion that MZ pairs behave more similarly than same-sex DZ pairs because they are more similar genetically is based on the assumption that MZ pairs behave more similarly than same-sex DZ pairs because they are more similar genetically. This assumption is based largely on genetic interpretations of the results of previous twin studies, meaning that disputed previous conclusions are used to validate disputed subsequent conclusions, and vice versa. The circular nature of Argument A is seen in Figure 2.

twin studies

Circular reasoning is the logical fallacy of assuming the very thing that one is attempting to determine, where the premise depends on or is equivalent to the conclusion. Twin researchers’ circular “X is true because Y is true; Y is true because X is true” argument seen in Figure 2 is precisely the fallacy that twin researchers using Argument A commit. (As I have shown elsewhere, the MISTRA researchers’ conclusions in favor of genetics using “reared-apart” twins were also based on a circular argument, and on the claim that environmental influences on twins’ behavioral resemblance should be counted as genetic influences.13)

Leading psychiatric twin researcher Kenneth Kendler of the Virginia Institute for Psychiatric and Behavioral Genetics has, since 1983, defended the validity of the EEA and the twin method on the basis of the Argument A position that “the behavioral similarity of monozygotic twins appears not to result from the similarity in social environment of the twins. Rather, the available evidence suggests that the similarity of the social environment of monozygotic twins is the result of the behavioral similarity of the twins.”14 Once again, supporters of Argument A attempt to save the twin method by claiming that environmental influences on twins’ behavioral resemblance should be counted as genetic influences. (Kendler has also used Argument B on numerous occasions, see below.)

In addition to illogically assuming the very thing he was attempting to prove, and counting environmental influences as genetic influences, Kendler’s argument fails because even if it were true, higher MZ versus DZ concordance for psychiatric conditions could still be completely caused by environmental factors. For the moment, let’s assume as a hypothetical example (1) that Kendler’s Argument A position is correct, (2) that experiencing severe bullying during a critical developmental period causes psychosis later in life, and (3) that a twin study finds a significantly higher psychosis concordance rate for adult MZ as opposed to DZ pairs. In this hypothetical scenario MZ pairs would be more similarly exposed to severe bullying because, due to their inherited behavioral similarity and similar physical appearance, they spend much more time together, attend school together and have common friends, elicit more similar treatment by their parents and others, and so on. However, it would be mistaken to conclude, as Kendler and other Argument A supporters likely would, that severe bullying should be counted as a genetic influence because “MZ twins create their more similar environments.” MZ twins eventually developing psychosis because they were more similarly exposed to severe bullying or other adverse psychological conditions or events—even if this more similar exposure is caused by their inherited behavioral similarity—is an environmental influence having nothing to do with any possible “genes for psychosis.” In the same way, even if “tennis playing behavior” were completely genetically determined (“100% heritable”), it would not follow that tennis elbow is a genetic disorder.

Argument A fails because it is based on illogical circular reasoning, and on the accompanying astonishing claim that environmental influences on twins’ behavioral similarities should be counted as genetic influences. Contrary to the erroneous logic of Argument A, the only relevant question is whether—not why—MZ and same-sex DZ environments are different.15

Twin Researchers’ Argument B: The “Trait-Relevant” Position

Supporters of Argument B also recognize that MZ pairs experience more similar environments than DZ pairs, but claim that the EEA remains valid until critics are able to identify “trait-relevant” aspects of the environment that MZ pairs experience to a greater degree than DZ pairs for the psychiatric condition in question. The following Argument B example/definition is found in a 1993 publication by Kendler and his colleagues:

“The traditional twin method, as well as more recent biometrical models for twin analysis, are predicated on the equal-environment assumption (EEA)—that monozygotic (MZ) and dizygotic (DZ) twins are equally correlated for their exposure to environmental influences that are of etiologic relevance to the trait under study” (italics added).16

It appears that Argument B was first put forward in 1966, without explanation or theoretical justification, by the renowned schizophrenia twin researcher Irving Gottesman (1930-2016) in a twin study of personality. This period constituted a post-World War II low point for twin research, where twin method findings were subject to increasing skepticism for several reasons.17 As one twin researcher from this era recalled in 2004, “to mainstream human genetics it seemed that twin research had been sentenced to death” by the late 1950s.18 In this context, in 1966 Gottesman redefined the traditional definition of the EEA by inserting one italicized qualifying term into it, now writing that the twin method was based on the assumption “that the average intrapair differences in trait-relevant environmental factors are substantially the same for both MZ and DZ twins” (italics in original).19 This subtle change in definition allowed twin researchers to continue their work, not because they had determined that MZ and DZ environments were similar, but because they could now bypass the obviously false equal environment assumption as it had been defined up to that point. By inserting the term “trait-relevant” into the traditional EEA definition, Gottesman overcame the sticky problem he had faced three years earlier in a different twin study of personality. In this 1963 study, Gottesman recognized that the traditional definition of the EEA, which he described as the assumption “that the within-pair environmental variance is the same for the two types of twins,” is “not necessarily true for the personality traits as measured by the tests.” He nonetheless decided to “proceed only on the assumption that such variance is not too different for the two types of twins.”20 Although Gottesman’s definition of the EEA changed between 1963 and 1966, the differing environments experienced by MZ and DZ pairs did not.

The Fallacy of Argument B Supporters of Argument B attempt to reverse the burden of proof onto critics for showing that MZ and same-sex DZ pairs differ in terms of their exposure to “trait-relevant” environmental factors. According to Kendler, Ming Tsuang, and their psychiatric genetic colleagues, “It would seem that the burden of proof rests with critics of the twin method to demonstrate that ‘trait-relevant’ environmental factors are more similar for identical than same-sex fraternal twins.”21

However, a basic principle of science is that the burden of proof falls squarely on the people making a claim, not on their critics. For example, if astronomers announce that they discovered a new planet in our solar system, they bear the burden of proof for demonstrating that this new planet exists; their skeptical colleagues and others are not required to prove that the planet does not exist. In a similar way, psychiatric twin researchers using Argument B bear the burden of proof for identifying the specific and exclusive trait-relevant environmental factors involved in the psychiatric condition in question, and then they must show (1) that twins did not experience such factors, or (2) that MZ and DZ pairs experienced such factors to roughly the same degree. Although we have seen that most twin researchers now recognize that MZ and DZ environments are different, they have been unable to identify specific and exclusive trait relevant environmental factors that play a role in causing the major psychiatric disorders, and then determine whether MZ and DZ pairs were similarly exposed (or not exposed) to these factors. Argument B fails in part because, as any psychotherapist will tell you, sexual, physical, or emotional abuse, racism, trauma, bullying, living in poverty, and countless other potential adverse environmental factors are “of etiologic relevance to” various psychiatric conditions. At the same time, twin researchers have failed to assess the impact of several identified “trait-relevant” environmental factors related specifically to schizophrenia and psychosis, which neuroscientist Roar Fosse and colleagues showed are more similarly experienced by MZ as opposed to DZ twin pairs.22

* * *

Interestingly, the circular Argument A position that twins create more similar environments because they are more similar genetically potentially supersedes Argument B. This is because, even if critics show that MZ pairs experience more similar trait-relevant environments than experienced by DZ pairs, twin researchers could still argue (and have argued) that MZ pairs “created” or “elicited” these more similar trait-relevant environments. The validity of the EEA and the twin method, therefore, rests mainly on the acceptance or rejection of Argument A.

The “EEA-Test” Studies

In a series of “EEA-test” studies spanning several decades, which were designed to test the validity of the equal environment assumption, twin researchers measured aspects of twins’ environmental similarity, such as whether they shared the same bedroom growing up, had common friends, were dressed alike, attended school together, and so forth. Kendler has written that these studies tested the EEA in several different ways, and he concluded in a 1993 edition of a leading American psychiatry journal, “With some uniformity, the available empirical evidence suggests that the EEA is probably at least approximately correct for the normative traits and psychiatric disorders studied.”23 This single sentence by the world’s leading theoretical defender of psychiatric twin studies and the EEA contains hedged terms such as “some uniformity,” “available empirical evidence,” “suggests,” “probably,” “at least,” and “approximately.” It is hardly a ringing endorsement of the EEA, which is understandable because, as I have attempted to show here, the EEA is indefensible.

Paradoxically, the starting point of most “EEA-test” publications is the recognition that MZ and same-sex DZ childhood environments are indeed unequal. After analyzing twin data, the authors of these publications usually argue that the greater environmental similarity and treatment of MZ twins does not contribute to their greater behavioral similarity, or that environmental factors have only a minimal impact on concordance rate differences, or that environmental influences on twins’ behavior should be counted as genetic influences. EEA-test researchers typically conclude in favor of the EEA and the twin method on the basis of Argument AArgument B, or both.

To better understand what “EEA-test” studies are about, imagine that several teams of researchers decide to conduct studies to test the hypothesis that the sun never shines on New York City. Let us also imagine that their closely held beliefs, academic careers, research funding, personal and professional relationships, and affiliations depended on confirming this hypothesis. The researchers decide to perform their studies only between the hours of 11:00 pm and 3:00 am, and they unanimously conclude that “the available evidence supports the hypothesis that the sun never shines on New York City.” EEA-test studies are performed in a similar way, because researchers focus narrowly on evidence that they claim supports the EEA, while completely overlooking the massive body of evidence, and countless real-world examples, that contradict this claim.

The results of “twins reared apart” studies such as the MISTRA are sometimes put forward in support of the twin method and the EEA, since the twins in these studies supposedly were reared apart from each other (most pairs were in fact only partially reared apart from each other), and therefore avoided the twin method’s EEA problem. As I and other critics have shown, however, and as I mentioned at the beginning of this article, reared-apart twin studies are based on several questionable or false assumptions, and contain numerous invalidating methodological flaws and biases. The studies published to date, therefore, cannot be used to validate the EEA.

Conclusion: Genetic Interpretations of Psychiatric Twin Studies Must Be Rejected

Since the 1920s, the twin method has been based on the assumption that reared-together MZ and DZ twin pairs grow up experiencing similar environments, even though most people—including most leading twin researchers—now understand that MZ and DZ environments are different. This has compelled these researchers to concoct illogical arguments to allow them to continue their work, and authoritative psychiatric texts and popular media outlets continue to endorse the original twin researchers’ mistaken interpretations of their results in favor of genetics. Psychiatric studies based on the twin method should have disappeared by the early 1960s, following the publication of psychiatrist Don Jackson’s classic 1960 debunking of schizophrenia twin research.24 But as we know, that didn’t happen.

Critics of psychiatric twin studies have correctly argued that, because MZ pairs experience much more similar environments than experienced by same-sex DZ pairs, these studies are no more able than psychiatric family studies to disentangle (separate) the potential impact of genetic and environmental influences. That is, in both family studies and twin studies, genetic interpretations of the results are confounded by environmental factors. It goes way beyond psychiatric twin researchers merely “overestimating the heritability” of various diagnoses. Because the EEA is false, we cannot reject the “null hypothesis” position that psychiatric twin studies have recorded nothing more than MZ pairs’ much more similar environments and treatment, MZ pairs’ much higher levels of identity confusion and attachment to each other, research bias, and in the case of psychosis, MZ pairs’ greater tendency to experience folie à deux (shared psychotic disorder).

There seems to be no end to far-fetched and even comical “findings” and heritability estimates produced by twin method MZ-DZ comparisons, which use methods similar to those used in psychiatric twin research. Among these we find a twin study whose authors concluded in favor of a genetic basis for being a “born again Christian,” a twin study that found important genetic influences on tea and coffee drinking preferences, a twin study that “found relatively high heritabilities for entrepreneurship,” a twin study that found that “drunk-driving is under significant genetic influence,” a twin study that found genetic influences on “differences in humor styles,” a twin study that found genetic influences on loneliness in adults” and another than found that “subjective well-being” (happiness) is moderately heritable, a twin study that found genetic influences on “problematic masturbatory behavior,” twin studies that found that the “belief in God” is substantially heritable, a twin study that found a substantial genetic component in British election voting choices, and a twin study of the “frequency of female orgasm.” These publications seem more appropriate for the Science and Technology section of the satirical news source The Onion than they do for publication in scholarly academic journals.

MZ pairs behave much more similarly than DZ pairs behave for just about everything—we get it. It’s just that there is no reason to believe that this has anything to do with the direct influence of genetics in general, or with genes that psychiatry believes cause behavioral differences or psychiatric disorders in particular. As the political scientist Evan Charney concluded in 2013, “That twin studies generate results that even partisans of the methodology acknowledge as absurd is further evidence that they are to many what they have always seemed to be: an obviously confounded, unreliable methodology.”25

Not surprisingly, then, the search for genes in psychiatry, which dates back to the 1960s, has been a colossal failure. A major planned feature of the 2013 DSM-5, as its creators had conceptualized it almost a dozen years earlier in 2002, would have been the incorporation of “post-genomic era” psychiatric gene discoveries into a revision of the DSM’s “multiaxial diagnostic system”—gene discoveries that psychiatry had anticipated on the basis of previous twin (and adoption) studies, but which never came.26 This led to the APA’s decision to abandon the multiaxial system altogether in DSM-5, but did not lead to the creation of an APA “task force” charged with taking a much closer objective look at twin studies and the EEA.

Given the decades of sensationalized yet non-replicated claims of gene discoveries for psychiatric disorders, the media and the public response to claims based on genome-wide association studies, or to claims based on more recent studies using the “polygenic risk score” (PRS) method, should be extreme skepticism and caution. In Plomin’s 2018 book Blueprint, he referred to the recently developed PRS method as a “new fortune telling device” for predicting behavior and psychiatric disorders.27 Plomin did not mention his previous 40-year track record of making claims of behavioral gene discoveries that could not be replicated.28 The first such claim appeared in 1978, when the Bee Gees ruled the pop music charts and the price of gasoline in the United States was 65 cents per gallon.

It is crystal clear that the twin method is unable to separate the potential influences of genes and environments on psychiatric conditions and on behavior in general, leading to the conclusion that genetic interpretations of all past, present, and future MZ-DZ twin method comparisons in psychiatry must be rejected outright. The time has come to part ways with diversionary genetic and medical approaches to psychological distress and dysfunction—and twin studies have played a major role in supporting and maintaining such diversionary approaches—so that society and science can instead focus on environmental causes and prevention, social interventions and political change, and non-medical treatment approaches.

Show 28 footnotes

  1. For much more on the problems found in psychiatric adoption studies, see Joseph, J., (2006), The Missing Gene: Psychiatry, Heredity, and the Fruitless Search for Genes, New York: Algora.
  2. Eaves, L., Foley, D., & Silberg, J., (2003), Has the “Equal Environments” Assumption Been Tested in Twin Studies? Twin Research, 6, 486-489, p. 486.
  3. A published twin study of bipolar disorder (manic-depression) finding results similar to this example is Bertelsen et al., (1977), A Danish Twin Study of Manic-Depressive Disorders, British Journal of Psychiatry, 130, 330-351.
  4. Using the “pairwise method,” twin concordance is equal to the percentage of twin pairs concordant for the psychiatric disorder in question. For example, if both twins are judged to have the condition in 30 out of 100 pairs, pairwise concordance would be 30/100 = 30%. Since the 1960s, the “proband method” has gained wider acceptance. (In the psychiatric genetics literature, a person through which other relatives are identified is often referred to as a “proband.”) Using this method, which yields a “probandwise” concordance rate, concordant twin pairs are double-counted if each twin was found independently from his or her co-twin, and the number of concordant pairs is added to the total number of pairs. Based on the above example, but now using the proband concordance method, if both twins are judged to have the same psychiatric condition in 30 out of 100 pairs, probandwise concordance would be 60/130 = 46%. Because the number of concordant pairs is doubled, the proband method always produces higher concordance rates, especially in the lower concordance rate range.
  5. Alford et al., 2005, Are Political Orientations Genetically Transmitted?, American Political Science Review, 99, 153-167, p. 155.
  6. Plomin, R., (2018), Blueprint: How DNA Makes Us Who We Are, Cambridge, MA: MIT Press, p. 186.
  7. Joseph, J., (2013), “‘Schizophrenia’ and Heredity: Why the Emperor (Still) Has No Genes,” in J. Read & J. Dillon (Eds.), Models of Madness: Psychological, Social and Biological Approaches to Psychosis (2nd ed.; pp. 72-89), London: Routledge, p. 74. A list of schizophrenia twin studies published up to 2013, and accompanying concordance rates, can be found in this publication.
  8. Kringlen, E., (1967), Heredity and Environment in the Functional Psychoses: An Epidemiological-Clinical Study, Oslo: Universitetsforlaget, p. 20.
  9. Kringlen, 1967, p. 115.
  10. Joseph, J., (2015), The Trouble with Twin Studies: A Reassessment of Twin Research in the Social and Behavioral Sciences, New York: Routledge, Table 7.1.
  11. Evans, D. M., & Martin, N. G., (2000), The Validity of Twin Research, GeneScreen, 1, 77-79, p. 78.
  12. Shields, J., (1954), Personality Differences and Neurotic Traits in Normal Twin Schoolchildren, Eugenics Review, 45, 213-246, p. 240. For a list of quotations by researchers using the “twin create their more similar environments” Argument A over a 60-year span, see Joseph, 2015, Appendix C.
  13. Joseph, J., (2018), Twenty-Two Invalidating Aspects of the Minnesota Study of Twins Reared Apart (MISTRA) (Full Version), published online November 6th, 2018, URL: https://www.madinamerica.com/wp-content/uploads/2018/11/Twenty-Two-Invalidating-Aspects-of-the-MISTRA-by-Jay-Joseph-Full-Version.pdf
  14. Kendler, K. S., (1983), Overview: A Current Perspective on Twin Studies of Schizophrenia, American Journal of Psychiatry, 140, 1413-1425, p. 1416.
  15. Argument A also portrays twins (and children in general) as behaving according to an inherited behavioral blueprint, but implies that parents (and other adults) are easily able to change their behavior and treatment in response to the twins’ behavior—in effect being flexible enough to let twins “create their own environments.” However, parents are people too, and the “twins create their more similar environments” scenario ignores the fact that, according to this scenario, adults’ “parenting response” behavior must be far more unchangeable than the twins’ supposed “parent response eliciting” behavior. This is because, in addition to the parents’ presumed strong genetic predispositions, they have experienced decades of peer, family, religious, cohort, and other behavior-molding influences.
  16. Kendler et al., (1993), A Test of the Equal-Environment Assumption in Twin Studies of Psychiatric Illness, Behavior Genetics, 23, 21-27, p. 21.
  17. For more on the history of twin research, see Chapter 2 of Joseph, J., (2004), The Gene Illusion: Genetic Research in Psychiatry and Psychology Under the Microscope, New York: Algora.
  18. Parisi, P., (2004), Twin Research, and Its Multiple Births and Expressions: A Short, Personal Voyage through Its Scope, History, and Organization, Twin Research and Human Genetics, 7, 309-317, p. 310.
  19. Gottesman, I. I., (1966), Genetic Variance in Adaptive Personality Traits, Journal of Child Psychology and Psychiatry, 7, 199-208, p. 200.
  20. Gottesman, I. I., (1963), Heritability of Personality: A Demonstration, Psychological Monographs, 77, (9, whole volume 572), 1-21, p 8.
  21. Lyons, M. J., Kendler, K. S., Provet, A. G., & Tsuang, M. T., (1991), “The Genetics of Schizophrenia,” in Tsuang et al., (Eds.), Genetic Issues in Psychosocial Epidemiology (pp. 119-152), New Brunswick, NJ: Rutgers University Press, p. 126.
  22. See also Fosse, R., Joseph, J., & Jones, M., (2015), Schizophrenia: A Critical View on Genetic EffectsPsychosis (published online September 14th, 2015, DOI: 10.1080/17522439.2015.1081269), URL: https://www.tandfonline.com/doi/full/10.1080/17522439.2015.1081269
  23. Kendler, K. S., (1993), Twin Studies of Psychiatric Illness: Current Status and Future Directions, Archives of General Psychiatry, 50, 905-915, p. 907.
  24. Jackson, D. D., (1960), “A Critique of the Literature on the Genetics of Schizophrenia,” in D. Jackson (Ed.), The Etiology of Schizophrenia (pp. 37-87), New York: Basic Books.
  25. Charney, E., (2013), Nature and Nurture, [Review of the Book Man Is by Nature Political Animal, by P. Hatemi & Rose McDermott (Eds.), Perspectives on Politics, 11, 558-561, p. 560.
  26. See D. Charney et al., (2002), “Neuroscience Research Agenda to Guide Development of a Pathophysiologically Based Classification System,” in Kupfer et al. (Eds.), A Research Agenda for DSM-V (pp. 31-83), Washington, DC: American Psychiatric Association.
  27. Plomin, 2018, p. vii.
  28. For more on Robert Plomin’s long history of making behavioral gene discovery claims that turned out to be false positive results, see Joseph, 2015, Chapter 10.


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  1. Jay you started to lose me with the title and then with all the different stats. I appreciate your efforts.
    When I was an inpatient psych unit social worker and having been involved in a new sexual abuse team service – I started asking the folks if they had abuse and or trauma in their histories almost to a one they had experience or experiences. This reflects what Dr Bessel van dear Klerk did on his own as well.
    So if research is using DSM dx and the diagnostic process is becoming more and more fraudulent then why put all the work and time and effort in rebuttal instead of just saying / especially with twins- we need the real experts- twins, their parents, their siblings, their teachers, their friends to explain why this and not that.
    Margret Mead had the bright idea of field studies and if you really want to know about twins a nice longitudal study might work.
    I would ask why?
    There are so so so many issues that needfurther exploration and research this seems like a scientific red herring.
    The two issues that do come to mind our twin loss and disability issues in sets of twins.
    Other than that – please look into trauma, sexual abuse, power and control in the mental health systems.
    Thanks for the work. I hope it helps out somehow.

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  2. the title of this blog seems to imply that genes
    having absolutely nothing to do with mental
    illness….I don’t believe that genes have
    nothing to do with it knowing the family that
    I came from…and I use mental illness without
    quotes because I have a mental illness…you all
    may not have it but I do…

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    • Hello. The title does not say or imply that genes have “nothing to do with mental illness.” What it does say/imply is that twin studies fail to provide scientifically acceptable evidence that genes play a role. Psychiatric conditions and behavior in general can “run in families” due to the shared environments experienced by family members. Most genetic researchers now recognize this.

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        • Very, very little. The most optimistic estimate I’ve read is that 15% of the variation in behavior/mood related to “mental disorders” is correlated to a set of over 100 genetic markers. And these markers didn’t correlate with a specific “disorder,” but with people who were diagnosed with “ADHD,” “Bipolar,” “Schizophrenia” and/or “Major depressive disorder,” I believe. So these genes, considered as a WHOLE, might represent something like sensitivity to others’ emotions, or a tendency toward getting angry more easily than the average, or a tendency to worry, or something completely unrelated.

          As a contrast, any “mental illness” you consider has high correlations with abuse, neglect, and stress. 80% or more for “schizophrenia,” for instance, and the more trauma experienced (especially sexual abuse), the higher the rates of “psychotic” symptoms.

          So the correlation with environmental factors is MUCH higher than even the most optimistic estimates of genetic “vulnerability.” Yet psychiatry as a profession insists on spending all its time and money on drugs and physiology and genetic research and brain scans. That’s where the disconnect is. There may be genetic contributions to mental/emotional distress, but whatever they are, they pale in comparison to the known contribution of environmental factors, and yet psychiatry pretends it’s the other way around.

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          • As far as mental states go, we do not stay in one mental state all the time. Our thoughts change as we age and we can alter them with enough effort.

            Our brains are living organs continually being reconfigured through our thoughts. Not blocks of rock shrinks can chisel into whatever hideous forms THEY think best.

            (Many of them seem to have minds of concrete. All mixed up and permanently set. Heh heh.)

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    • “I don’t believe that genes have nothing to do with it” is a double negative statement .

      Alcoholics like to say alcoholism is a disease , so that they do not feel guilt, so they do not feel the responsibility for their bad choices. This belief in disease is good for the feeling of guilt a person can have can make people go back to drinking in order to try to feel better.

      In the religion of Christianity, Jesus died on the cross to provide the way for people to receive forgiveness from their sins.

      In the religion of psychiatry. people like to blame DNA and unbalanced brain chemicals for their sins, to remove feelings of guilt and responsibility for bad behaviour, and it works! How do you find forgiveness? You find a scapegoat. Those bad molecules and genes are responsible, not me/not my loving father/not my loving mother!
      I find it far more easy to forgive someone if I think they are mentally ill. I am no longer angry at their bad choices and bad behavior because they are not responsible, they did not do it on purpose. Finding forgiveness….

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      • “I don’t believe genes have nothing to do with it,” is a double negative. But, given the context, it’s correctly used.

        Littleturtle believes genes have something–if only a little–to do with “mental illness.” I don’t believe in it myself since the very term “mental illness” means existing in one’s mind rather than the physical world. Brain problems can cause weird thoughts and feelings. But those are physical illnesses since the brain is a physical organ. TBI, epilepsy, brain cancer, Parkinsons, and Lou Gehrigs are brain diseases as opposed to “bipolar” and “schizophrenia” which are “mental illnesses.”

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      • Forgiveness is impossible if a person is not responsible for bad behaviors. This helps explain the conflicted views of “mentally ill” people our society holds.

        They’re not to blame for horrible behaviors and crimes because their existence itself is viewed as a crime. Hence the stigma since they can never be anything but deviant/criminal/insane.

        In a survey people said they’d rather have a convicted felon as a neighbor than a “severely mentally ill” person. Why? The answer was “Felons can change.” If wickedness is hard wired into your brain and DNA you will always be a menace and a nuisance.

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      • Brw, Mark, Jesus referred to Himself as the Great Physician to heal us from our sins. I never left the church but often puzzled over what behaviors were sins (willful) versus symptoms. Now I believe they were all willful but many were harmless eccentricities that annoyed people–neither illegal nor immoral. A lot of sinful behaviors are considered respectable and therefore “mentally healthy.” Remember the people Jesus really got mad at?

        A lot of church goers should puzzle over why after 2000 years a bunch of people need drugs for salvation. (My dad has.) Only nobody thinks about deep issues now. Churches I go to are filled with super loud shallow, meaningless songs and the messages are often shallow too. I heard one preacher say people were complaining over a book’s doctrine. But he read it and found it sound…because it made him FEEL GOOD. That explains why church goers fall for anything advertised by pastel cartoon commercials of dancing pills, smiling picnickers and lemonade. No discernment or depth of thought anywhere.

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  3. Thank you for your work Jay Joseph.

    T. Szasz wrote psychiatry is the medicalization of morals. Where “bad” behaviours were previously called “sins”, behaviours made by choice , made by freewill , are now considered a disease.

    Most obvious is the childhood disease of short attention span/playing games renamed “ADHD”, where in the past, fear of corporal punishment kept most in line, but today, corporal punishment no longer socially acceptable, authority switched to using drugs , drugging children obedient.

    The child now believes they are a disease( for not being a orderly robot), have disease inside them because authority tells them so. This is far worse than a physical punishment( like from a spanking), as they feel/think their diseased soul needs medication. Authority is lying to them and they have no other option but to believe the lie, from the evidence of their own hands/minds playing when they are not supposed to.

    Vice and Virtue
    1 Lust Chastity
    2 Gluttony Temperance
    3 Greed Charity
    4 Sloth Diligence
    5 Wrath Patience
    6 Envy Kindness
    7 Pride Humility
    “In our fervor to medicalize morals, we have transformed every sin but one into sickness.
    Anger(5), gluttony(2), lust(1), pride(7), sloth(4) are all the symptoms of mental diseases.
    Only lacking compassion (kindness) is still a sin.”

    All humans might choose to sin, or be forced to, so all must have the same “defective” DNA.

    Who/what would humans be without our “defective” DNA? We would be robots.

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  4. Given the reality that the ADHD drugs and antidepressants can create the “bipolar” symptoms, as shown in Whitaker’s research. And given the reality that the antipsychotics/neuroleptics can create both the negative and positive symptoms of “schizophrenia,” via neuroleptic induced deficit syndrome and antipsychotic and/or antidepressant induced anticholinergic toxidrome.


    And, of course, there are zero medical tests which can be used to make sure people are initially properly diagnosed with either of these “serious mental illnesses.” Since the psychiatric drugs can create the symptoms of both “bipolar” and “schizophrenia,” it is highly likely that the primary actual etiology of both these “serious mental illnesses” is iatrogenic, not genetic.

    I agree, “Assessing the validity of psychiatric twin research is very important because it relates directly to the question of whether the main causes of psychological distress and dysfunction, and socially disapproved behavior, are located inside of the human body and brain, as mainstream psychiatry claims, or outside of the body and brain, as many critics argue.”

    Given the reality that the vast majority of those labeled as “borderline” or with the “psychotic and affective disorders” (“depression,” “anxiety,” “bipolar,” or “schizophrenia”) are actually misdiagnosed child abuse survivors. And child abuse is a crime that occurs outside of an individual’s brain.


    All this misdiagnosis of child abuse survivors is due to the fact that helping child abuse survivors is NOT an insurance billable DSM disorder for any “mental health professional” today.


    This is evidence that the primary actual function of our “mental health” industry today is silencing and turning child abuse survivors into the “mentally ill” with the psychiatric drugs. And covering up rape was historically the primary function of the psychological industry as well.


    Since profiteering off of silencing and covering up rape and other child abuse is the number one actual function of both extremes of our “mental health system.” And since this is actually illegal behavior, perhaps it’s time to get rid of our scientifically “invalid,” criminal “mental health” industries?

    Especially since covering up child abuse, on the massive scale at which our “mental health professionals” are collectively doing such, either wittingly or unwittingly, does also function to aid, abet, and empower the child abusers and human traffickers. And living in a society controlled by “satanic pedophiles” and “human traffickers,” as our world leaders are describing Western civilization today, is not actually in the best interest of the majority within humanity.


    The “dirty little secret of the two original educated professions,” that the number one function of our “mental health professionals” is rape profiteering and covering up, does die hard though. How sick that America has a multibillion dollar, primarily child rape covering up, group of “mental health” industries.

    This should end, and America should start arresting the child molesters and traffickers instead. But, of course, pointing these disgusting societal problems out is “socially disapproved behavior.”

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  5. steve says [very very little]
    are you teasing me….
    how can you say this steve…
    we know some about genes…
    not much…but MOST we don’t know..
    and don’t genes determine brain..
    and doesn’t brain determine mind…
    and doesn’t brain determine emotions…
    and doesn’t brain drive survival and reproduction…
    true biology will not go away…

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    • Do genes determine brain? To an extent, yes – they appear to determine development potential. But the Decade of the Brain research and more recent research into “epigenetics” has proven unequivocally that large structural and functional changes in the brain occur as a direct result of personal experience. So the idea that genes determine brain is not entirely true – genes PLUS experience determine brain.

      Does brain determine mind? This is a question that transcends the realm of science. No one really knows that the “mind” is, and the assumption that the mind is a direct result of the brain is based on the philosophical school called “materialism,” that assumes there can be nothing that is not observable and measurable in the physical world. Of course, quantum physicists have already shown that this school of thinking doesn’t explain everything, including such fascinating phenomena as a particle being able to move from one place to another without occupying the space in between, or the fact that you can’t measure anything to 100% accuracy, so in fact, all scientific measurements are approximations, which is not a big deal with big objects, but gets very significant when looking at tiny things like electrons. So the idea that “Brain determines mind” is not established scientifically, but is a conclusion drawn from a particular philosophical school. There are many schools of philosophy that draw different conclusions on that question.

      “Brain determines emotions” – True in a very physiological sense, though apparently gut and other organs can also influence emotions dramatically. But without knowing what MIND is, to say that “brain determines emotions” cuts out the possibility that mind affects brain which then determines emotions as a result. That’s the reality I observe.

      Brain drives survival and reproduction – for sure this is true, but again, without the question of what MIND is being answered, we can’t really say that all is driven only by the brain.

      I suppose I’d ask you the question: do you believe humans can exercise free will?

      Depending on your answer, I might present some other questions or arguments that have a bearing on this. Suffice it to say, it is not such a simple question as you seem to want it to be, in my view. The interaction between brain and mind is the biggest mystery of human beings, and anyone who tells you this mystery has been solved scientifically is blowing smoke. The main reason that decades of genetic research has turned up close to nothing regarding genetic underpinnings of mental/emotional/behavioral phenomena is that, in most cases, such underpinnings either don’t exist or are so incredibly complex and subtle that they provide no explanation whatsoever as to why a person is acting the way they are.

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