A key psychiatric genetic concept is heritability. The concept was originally developed as a tool to help predict the results of selective breeding programs of farm animals,1 but has been extended in the past few decades as an indicator of the strength or magnitude of genetic influences on various psychiatric disorders and behavioral characteristics. Numerical heritability estimates have been a mainstay of the field of behavioral genetics, but here I would like to focus on problems with the heritability concept in psychiatry, while keeping in mind that most of the points made here and by previous critics apply to the use of heritability estimates in all areas of human behavior, including other controversial areas such as IQ and personality. In this brief discussion I will try to explain the main issues surrounding heritability as clearly as possible, while recognizing that for many people this “extraordinarily misunderstood” concept is difficult to comprehend and to articulate.2
Kenneth Kendler, a leading psychiatric genetic researcher, defined heritability as “the proportion of variation due to genetic factors.”3 The key word here is “variation,” which in this context refers to how psychiatric disorders and characteristics are distributed in the population. In human genetic research, heritability is said to measure the extent to which variation among people is explained (accounted for) by genetic influences. A group of leading behavioral geneticists argued that assessing the causes of variation allows researchers to estimate “how much genetics contributes to a trait,” and allows them to quantify the “relative importance” of genetic and environmental influences.4 According to Michael Rutter, a prominent genetically oriented researcher and author, within certain “constraints,” it “is possible, and meaningful, to quantify the strength of genetic influences on individual differences with respect to psychological characteristics or mental disorder as they occur in the populations studied.”5
Heritability estimates are derived from correlations among relatives, which include twins, adoptees, siblings, and other types of family relationships. Although heritability assesses the causes of variation in a population, it does not address developmental processes that cause individuals to develop various characteristics and abilities.6
Other leading psychiatric geneticists have written that heritability estimates measure “the degree to which the vulnerability to develop a disorder is influenced by genes.”7 Psychiatric genetic researchers usually present heritability estimates to other researchers and to the general public as a percentage figure between 0% and 100% (or as a number between 0.0 and 1.0). They believe that 0% heritability indicates that the vulnerability to develop a psychiatric disorder is “due entirely to environmental influences,” whereas 100% heritability “indicates that the liability can be explained entirely by genes.”8 Estimates usually fall between these two extremes, and researchers argue that as heritability rises, so does the strength of the genetic influence. Psychiatric disorders in the 20-40% range are seen as having “moderate heritability,” in the 40-60% range as having “moderately high heritability,” in the 60-80% range as having “high heritability,” and in the 90-100% range as having “very high heritability.”9
Heritability estimates are often calculated from twin data by doubling the reared-together MZ (monozygotic, identical) versus DZ (dizygotic, fraternal) correlation or concordance rate10 difference, or by claiming that the reared-apart MZ twin pair correlation “directly estimates” heritability (reared-apart twin studies are not performed in psychiatry). Using basic twin method reared-together twin data, if a sample of MZ pairs shows 50% concordance for schizophrenia, and the DZ sample shows 10% concordance, psychiatric geneticists double the difference and estimate the “heritability of schizophrenia” in the sample as 80%.
Researchers frequently use “model fitting” statistical analyses (structural equation modeling) to calculate heritability, which attempt to test the “fit” between a model of genetic and environmental relatedness against the observed data. All heritability estimates based on twin method MZ-DZ comparisons depend on the validity of the method’s “equal environment assumption,” which critics have convincingly argued is not supported by the evidence.11 And as I showed in my recent book on twin research, model fitting analyses are based on an additional set of very questionable assumptions about people, society, and genetics.
The authors of mainstream psychiatric and psychiatric genetic publications believe that the major psychiatric disorders are “moderately to highly heritable.” Examples of pooled heritability estimates for various disorders include schizophrenia 84%, bipolar disorder 84%, ADHD 75%, borderline personality disorder 69%, panic disorder 43%, PTSD 38%, major depression 37%, and social phobia 25%.12 The remaining portion (100% minus heritability) is attributed mainly to environmental influences, usually separated into “shared” and “non-shared” components.
Although heritability estimates are widely used in psychiatric genetics and mainstream psychiatry as an indicator of the strength of genetic influences on a given disorder, their usefulness and validity has, in the words of developmental psychologist David Moore, “been the subject of unrelenting criticism from philosophers, biologists, and psychologists for nearly four decades.”13 The writings of these critics include (but are not limited to) the following points:
- Heritability estimates do not measure the strength of genetic influences on psychiatric disorders and behavioral characteristics, nor do they assess the relative importance of genetic and environmental influences, and are misleading and potentially harmful when they are presented this way.
- Although heritability estimates are based on the assumption that genetic and environmental factors are separate (additive) and do not interact, they clearly do interact.
- Even when heritability is high, or even when it is 100%, a simple environmental change or intervention can have an important preventative or curative impact. In most cases, therefore, heritability estimates tell us nothing about the potential effectiveness or non-effectiveness of an environmental intervention, or to what extent a psychological characteristic is or is not changeable.
- Heritability is the property of a population, not of the characteristic or disorder itself.
- Because it is a population statistic, heritability does not describe the importance of genetic factors as they relate to an individual.14
- Heritability estimates apply only to a specific population, at a specific time, and in a specific environment. Estimates can change substantially under different environmental conditions.
- Heritability estimates are based on research methods that (to varying degrees) are unable to disentangle the potential influences of genes and environment on behavior, such as family, twin, and adoption studies.
- A finding of high heritability within different populations does not mean that genetic differences exist between different populations (such as different ethnic groups).
- Recent findings that gene expression switches on and off “epigenetically” in response to environmental events and challenges provide additional important evidence that genetic and environmental influences are not additive, but are interactive.15
- The continuing decades-old failure to discover genes at the molecular genetic level for psychiatric disorders, and for behavioral differences in general, provides additional evidence against the “heritability” of these disorders and behaviors.16
A leading group of psychiatric genetic investigators wrote that heritability estimates “measure the degree to which genetic factors influence variability in the manifestation of the phenotype [disorder],” and that a disorder’s variability “is presumed to arise from two independent factors: genetic variability…and environmental variability.”17 According to behavioral genetic twin researcher Nancy Segal, model fitting analyses that produce heritability estimates assume that “genetic and environmental effects are independent from each other, and [that] genetic and environmental effects combine additively.”18
Many critics, however, have argued that genetic and environmental factors are not independent, and that gene–environment interaction reduces or even invalidates heritability estimates.19 As the population geneticist Richard Lewontin wrote, “If these causes ‘interact’ in any generally accepted meaning of the word, it becomes conceptually impossible to assign quantitative values to the causes of that individual event. Only if the causes are utterly independent could we do so.”20 According to developmental researcher Michael Meany, “research in biology reveals that the genome cannot possibly operate independent of its environmental context.”21 Simple examples of potential gene–environment interactions include physically attractive people who experience much different responses from their social environments than do physically unattractive people, and children with great musical talent who are sent to an expensive music academy to maximize their talent.
Flamingos provide an example from nature of the fallacy of partitioning genetic and environmental factors into separate additive influences. Flamingos become pink by ingesting a diet of shrimp and other foods rich in alpha and beta carotenoid pigments. Those whose diet does not include carotenoid pigments do not become pink. Flamingos are therefore born with a genetic potential to have pink feathers, but require environmental influences to achieve this potential.
Rutter cited flamingos as an example of gene-environment interaction.22 He noted that both genes and environment play a crucial role in the ability of flamingos to turn pink, and that “you could feed seagulls for ever on the same diet and they would never turn pink.” He concluded that “it would make no sense to say that flamingos’ color was 50 percent due to genes and 50 percent due to diet. It is 100 percent due to genes (which have to be present) and 100 percent due to the environmental diet (which has to be present).”
Even if, for the sake of argument only, we allow that DSM psychiatric categories are valid discrete disorders with a genetic component, like flamingo color it “makes no sense” to say, for example, that schizophrenia is 84% genetic and 16% environmental, that panic disorder is 43% genetic and 57% environmental, or that major depression is 37% genetic and 63% environmental. In such cases both genetic and environmental factors are essential interacting influences whose contributions jointly, as opposed to additively, combine to produce the observed characteristic (phenotype).
Some contemporary behavioral genetic researchers, while continuing to support twin research and other basic positions of their field, now recognize that heritability estimates have little meaning. According to Eric Turkheimer, “the relative magnitudes of the various components were supposed to tell us something about the importance of genetic and environmental causes underlying a trait, but they do not.”23 He continued, “In the real world of humans…the magnitudes of the proportions are variable from situation to situation, and have nothing whatsoever to do with the causal properties of genes and environment for the trait in question.”24 Elsewhere, Turkheimer wrote that “heritability is a distraction.”25
Behavioral genetic twin researchers Wendy Johnson, Turkheimer, Thomas Bouchard, and Irving Gottesman wrote in 2009 that “little can be gleaned from any particular heritability estimate and there is little need for further twin studies investigating the presence and magnitude of genetic influences on behavior.”26 In their view, once the role of genetic influences is accepted, “it becomes clear that specific estimates of heritability are not very important.”
The obvious conclusion is that the use of heritability estimates as a measure of the relative importance of genes and environment on psychiatric disorders and other behavioral characteristics should be abandoned.
Heritability ≠ Inherited
Some writers have noted the common confusion between two different uses of the word “heritability.” The technical meaning of heritability refers to the proportion of individual differences in a population that can be attributed to genetic factors. In contrast, people commonly yet mistakenly use the word “heritable” to mean “inherited,” or “hereditary.” According to the late critical behavioral genetic researcher Jerry Hirsch, “heritability” and “heredity” are “two entirely different concepts that have been hopelessly conflated.” Because they sound alike, he wrote, “when we hear one of the two words, automatically we think the other.”28 As Hirsch repeatedly pointed out, a heritability estimate is not a “nature-nurture ratio” of the relative contributions of genes and environment. The author of The Mirage of a Space between Nature and Nurture, Evelyn Fox Keller, found it unfortunate that “authors and readers alike routinely slide from one meaning [of heritability] to the other, wreaking havoc on the ways in which legitimate scientific measurements are interpreted.”29 Behavioral geneticist Douglas Wahlsten, a critic of heritability estimates, argued that “the only practical application of a heritability coefficient” is its original purpose of “predict[ing] the results of a program of selective breeding.”30
Variation ≠ Cause
Lewontin showed long ago that a “trait can have a heritability of 1.0 [100%] in a population at some time, yet could be completely altered in the future by a simple environmental change.”31 An example is phenylketonuria (PKU), a genetic disorder of metabolism that causes intellectual disability. Although PKU is a “highly heritable” single gene disorder, the administration of a low phenylalanine diet to the at-risk infant during a critical developmental period prevents PKU from causing intellectual disability.
As an example of how heritability estimates do not measure the “strength” or “magnitude” of genetic influences, imagine “Country A,” where all citizens (100%) carry the gene predisposing them to favism (glucose-6-phosphate dehydrogenase deficiency), a disease marked by the development of hemolytic anemia. Favism is caused by an inherited deficiency of glucose-6-phosphate located on the X chromosome, combined with the consumption of fava (broad) beans or the inhalation of fava bean pollen. In other words, both “beans and genes” are necessary for favism to appear. Let us then imagine that 3% of the citizens of Country A, all of whom are of course genetically predisposed to develop favism, consume fava beans and are subsequently diagnosed with favism. In this case, because all citizens carried the gene but only some ate fava beans, all favism variation in Country A would be caused by environmental factors (fava bean exposure), and the heritability of favism therefore would be 0%. At the same time, it obviously would be mistaken to conclude that genes play no role in developing the disease in Country A, or that the genetic influence is weak or irrelevant. A genetic predisposition is, in fact, a prerequisite for developing favism.32
On the other extreme, in “Country B,” 100% of the citizens eat a diet that includes fava beans, but only some citizens carry the favism gene. All favism variation in Country B therefore would be caused by genetic factors (carrying or not carrying the gene), and the heritability of favism in Country B would be 100%. As we see, heritability estimates assess variation as opposed to cause, and do not at all indicate the strength or weakness of the genetic influence—or by implication the strength or weakness of the environmental influence.
In the above example, the heritability of favism is 0% in Country A, and 100% in Country B, even though the causes of favism are the same in both countries. As Moore concluded, “Because heritability statistics are about accounting for variation and not about causation, they do not actually reflect the strength of influence of genes on the development of a trait, even if it seems like they do.”33
Heritability and Psychiatric Disorders
The irrelevance and misleading nature of heritability estimates in psychiatry is seen in the example of autism. For many years, based mainly on the results of three or four small twin studies, leading researchers variously described autism as showing “strong genetic determination,”34 and as being “under a high degree of genetic control.” Although the evidence in favor of genetics is surprisingly weak36 reviewers commonly estimate autism heritability at roughly 90% (0.9), based on Anthony Bailey and colleagues’ 1995 twin study and review.37 At the same time, leading autism researchers such as Michael Rutter recognize the role of environmental risk factors, “and the evidence suggests that they are likely to involve physical causes during the prenatal or early postnatal periods.”38
Suppose a team of researchers conclusively proves that all children who eventually develop autism had eaten “Baby Delight Apricot Baby Food” between the ages of four and six months, and that further investigation had shown that the ingestion of a rare chemical found only in this brand of apricot baby food by genetically predisposed children, during this sensitive developmental period, caused autism. The government immediately removes Baby Delight Apricot Baby Food from the market, confiscates existing inventories of the product, and issues warnings to parents. What would happen to the rate of new autism diagnoses a few years later? The answer is that it would be reduced to virtually zero. Like PKU, presumed genetic factors appear to be “under a high degree of genetic control” (and difficult to change) only in the absence of (or denial of) identified environmental causes and triggers.
An example in the twin research literature illustrating this important point is found in Segal’s description of a British reared-apart MZ pair who suffered from headaches and irritability, due to their shared allergy to foods containing gluten. Although medical researchers believe that gluten sensitivity is “strongly heritable,”39 and that “genetic predisposition plays a key role,”40 according to Segal one twin’s “health and spirit improved dramatically” upon “eliminating wheat from his diet,” and his twin brother “agreed to make the same dietary changes when he returned home.”41 As this example shows, an environmental intervention cured a “strongly heritable” condition in the same way as it would have cured a “weakly heritable” condition. This pair’s story again shows that a heritability estimate does not indicate the strength or “relative importance” of the presumed genetic component, or the potential effectiveness or ineffectiveness of an environmental intervention.
Philosophy professor Neven Sesardic published Making Sense of Heritability in 2005, a book devoted to defending what he viewed as the importance of heritability estimates in the behavioral sciences. Sesardic believed, contrary to the views of the critics but consistent with the way heritability estimates are usually presented in psychiatry, that “the more heritable a variation, the less environmentally modifiable it is….Heritability does place a constraint on malleability.”42 However, the above examples and countless other real and potential examples show that there is little support for this position.
Establishing the reliability and validity of a psychiatric disorder is a prerequisite for any study attempting to estimate heritability. Reliability in psychiatry refers to the ability of psychiatrists to consistently agree on a diagnosis. A disorder must be valid in addition to being reliable. Validity refers to whether the concept actually exists as a true disorder. Many critics of psychiatry have argued that psychiatric disorders are not reliable or valid discrete illnesses, but rather describe people’s varying psychological responses to having experienced adverse events and environments, or are socially disapproved behaviors that psychiatry labels as mental disorders.
In their 2013 work Mad Science: Psychiatric Coercion, Diagnosis, and Drugs, Stuart Kirk, Tomy Gomory, and David Cohen showed that there are serious reliability and validity problems in psychiatry, suggesting that research is impaired when it relies on the DSM to diagnose people with similar problems.43 A lack of reliability and validity has important implications for psychiatric genetic family, twin, and adoption studies—and accompanying heritability estimates—because many people diagnosed in these studies may not actually “have” the condition at all.44
It is not the task of critics to establish the “true heritability” of schizophrenia, depression, and other psychiatric conditions, or to demonstrate that it is zero, but rather to show that, on many levels, the “heritability of psychiatric disorders” does not qualify as a valid concept.
The heritability statistic was developed as a means of predicting the results of selective breeding programs in agriculture. It is not an indicator of the degree of genetic influence on psychiatric disorders, and has no valid meaning as it relates to them other than to predict the results of a program attempting to breed psychiatric disorders out of the human population. Although contemporary psychiatric genetic researchers do not advocate such programs,45 the implementation of eugenic and “racial hygienic” policies was a major goal and activity of the field of psychiatric genetics in the first half of the 20th century in Germany and elsewhere.46
Biologist Steven Rose correctly concluded that the “heritability measure…except in the very specific context for which it was originally devised (agricultural breeding experiments) [is] rarely applicable, widely misunderstood and in most cases meaningless.”47
The words “heritability” and “inherited” have different meanings, and heritability estimates do not indicate the relative magnitude of environmental and presumed genetic influences on psychiatric disorders. Although researchers will continue to use family, twin, and adoption studies to claim that various behavioral characteristics are influenced by genetic factors, assigning a numerical heritability estimate to such claims is meaningless and misleading. Therefore, its use in psychiatry and other behavioral fields should be discontinued.
* * * * *
Portions of this article were adapted from The Trouble with Twin Studies: A Reassessment of Twin Research in the Social and Behavioral Sciences, 2015, New York: Routledge. [Chapter Summaries]
1. Bouchard, T. J., Jr., (2009), Genetic Influence on Human Intelligence (Spearman’s g): How Much?, Annals of Human Biology, 36, 527-544, p. 527; Lush, J. L., (1949), Heritability of Quantitative Characteristics in Farm Animals, Hereditas (Suppl.), G. Bonnier & R. Larsson (Eds.), 356-375.
2. Moore, D. S., (2008), Espousing Interactions and Fielding Reactions: Addressing Laypeople’s Beliefs about Genetic Determinism, Philosophical Psychology, 21, 331-348, p. 338.
3. Kendler, K. S., & Prescott, C. A., (2006), Genes, Environment, and Psychopathology: Understanding the Causes of Psychiatric and Substance Abuse Disorders, New York: Guilford, p. 41.
4. Plomin et al., (2013), Behavioral Genetics (6th ed.), New York: Worth Publishers, pp. 86-87.
5. Rutter, M., (2006), Genes and Behavior: Nature-Nurture Interplay Explained, Malden, MA: Blackwell, p. 179.
6. For more on this point, see Gottlieb, G., (2003), On Making Behavioral Genetics Truly Developmental, Human Development, 46, 337-355; Tabery, J., & Griffiths, P. E., (2010), “Historical and Philosophical Perspectives on Behavioral Genetics and Developmental Science,” in K. Hood et al., (Eds.), Handbook of Developmental Science, Behavior, and Genetics (pp. 41-60), Malden, MA: Wiley-Blackwell.
7. Faraone, S. V., Tsuang, M. T., & Tsuang, D. W., (1999), Genetics of Mental Disorders, New York: Guilford, p. 32.
8. Faraone et al., 1999, p. 32.
9. Kendler & Prescott, 2006, pp. 44-45.
10. Twin pairs are concordant for a disorder when both members of the pair are diagnosed with the same disorder. Twin pairs are discordant when one member is diagnosed with the disorder, while the other is not.
11. Joseph, J., (2004), The Gene Illusion: Genetic Research in Psychiatry and Psychology under the Microscope, New York: Algora; Joseph, J., (2015), The Trouble with Twin Studies: A Reassessment of Twin Research in the Social and Behavioral Sciences, New York: Routledge.
12. Glatt, S. J., Faraone, S. V., & Tsuang, M. T., (2008), “Psychiatric Genetics: A Primer,” in J. Smoller, B. Sheidley, & M. Tsuang (Eds.), Psychiatric Genetics: Applications in Clinical Practice (pp. 3-26), Washington, DC: American Psychiatric Publishing.
13. Moore, D. S., (2013b), “Current Thinking about Nature and Nurture,” in K. Kampourakis (Ed.), The Philosophy of Biology: A Companion for Educators (pp. 629-652), Dordrecht: Springer, p. 636.
14. Chaufan, C., (2008), Unpacking the Heritability of Diabetes: The Problem of Attempting to Quantify the Relative Contributions of Nature and Nurture, DataCrítica: International Journal of Critical Statistics, 2, 23-38.
15. Charney, E., (2012), Behavior Genetics and Postgenomics, Behavioral and Brain Sciences, 35, 331-358; Moore, D. S., (2013a), “Behavioral Genetics, Genetics, and Epigenetics,” in P. D. Zelazo (Ed.), Oxford Handbook of Developmental Psychology (pp. 91 – 128), New York: Oxford University Press; Meaney, M. J., (2010), Epigenetics and the Biological Definition of Gene x Environment Interactions, Child Development, 81, 41-79, p. 42.
16. See Joseph, 2015, Chapters 9 and 10.
17. Glatt et al., 2008, p. 9.
18. Segal, N. L., (2012), Born Together—Reared Apart: The Landmark Minnesota Twin Study, Cambridge, MA: Harvard University Press, p. 63.
19. For example, see Chaufan, 2008; Goldberger, A. S., (1979), Heritability, Economica, 46, 327-347; Layzer, D., (1974), Heritability Analysis of IQ scores: Science or numerology?, Science, 183, 1259-1266; Lewontin, R. C., (1974), The Analysis of Variance and the Analysis of Causes, American Journal of Human Genetics, 26, 400–411; McGuire, T. R., & Hirsch, J., (1977), “General Intelligence (g) and Heritability (H2, h2),” in I. Uzgiris & F. Weitzmann (Eds.), The Structuring of Experience (pp. 25-72), New York: Plenum Press; Taylor, H. F., (1980), The IQ Game: A Methodological Inquiry into the Heredity-Environment Controversy, New Brunswick, NJ: Rutgers University Press; Wahlsten, D., (1990), Insensitivity of the Analysis of Variance to Heredity-Environment Interaction, Behavioral and Brain Sciences, 13, 109-120; Zuk et al., (2012), The Mystery of Missing Heritability: Genetic Interactions Create Phantom Heritability, PNAS, 109, 1193-1198.
20. Lewontin, 1974, p. 402.
21. Meaney, 2010, p. 42.
22. Rutter, 2006, p. 24.
23. Turkheimer, E., (2011a), Commentary: Variation and Causation in the Environment and Genome, International Journal of Epidemiology, 40, 598-601, p. 598.
24. Turkheimer, 2011a, p. 598.
25. Turkheimer, E., (2011b), Still Missing, Research in Human Development, 8, 227-241, p. 239.
26. Johnson et al., (2009), Beyond Heritability: Twin Studies in Behavioral Research, Current Directions in Psychological Science, 18, 217-220, p. 218.
27. Hirsch, J., (1997), Some History of Heredity-vs-Environment, Genetic Inferiority at Harvard (?), and The (Incredible) Bell Curve, Genetica, 99, 207-224; Stoltenberg, S. F., (1997), Coming to Terms with Heritability, Genetica, 99, 89-96.
28. Hirsch, 1997, p. 220.
29. Keller, E. F., (2010), The Mirage of a Space Between Nature and Nurture, Durham, NC: Duke University Press, p. 59.
30. Wahlsten, 1990, p. 119.
31. Lewontin, 1974, p. 400.
32. Paradoxically, if fewer Country A citizens were genetically predisposed (say 60%), some favism variation in the population would be attributable to genetics, and heritability would be well above zero.
33. Moore, 2013b, p. 636. As another example, imagine a society where everyone (like MZ twin pairs) is genetically identical. Because genes do not vary from person to person in this society, all variation in psychiatric disorders and behavior would be caused by environmental factors, meaning that the heritability of all behavioral characteristics, psychiatric disorders, medical conditions—basically everything—would be zero. Once again, population variation and cause are different concepts
34. Folstein, S., & Rutter, M., (1977), Genetic Influences on Infantile Autism, Nature, 265, 726-728, p. 728.
35. Bailey et al., (1995), Autism as a Strongly Genetic Disorder: Evidence from a British Twin Study, Psychological Medicine, 25, 63-77, p. 63.
36. For a critical review of autism genetic research, see Joseph, J., (2006), The Missing Gene: Psychiatry, Heredity, and the Fruitless Search for Genes, New York: Algora, Chapter 7.
37. Bailey et al., 1995.
38. Rutter, M., (2013), Changing Concepts and Findings on Autism, Journal of Autism and Developmental Disorders, 43, 1749-1757.
39. Hadjivassiliou et al., (2010), Gluten Sensitivity: From Gut to Brain, Lancet Neurology, 9, 318-330, p. 320.
40. Sapone et al., (2012), Spectrum of Gluten-Related Disorders: Consensus on New Nomenclature and Classification, BMC Medicine, 10, (1), 13, p. 4, doi:10.1186/1741-7015-10-13.
41. Segal, 2012, p. 227.
42. Sesardic, N., (2005), Making Sense of Heritability, Cambridge: Cambridge University Press, p. 163.
43. Kirk, S. A., Gomory, T., & Cohen, D., (2013), Mad Science: Psychiatric Coercion, Diagnosis, and Drugs, New Brunswick, NJ: Transaction.
44. I placed the word “have” in quotation marks because, lacking a proven biological basis, someone cannot “have” a psychiatric disorder in the same way as someone can have a real biologically based medical condition.
45. According to heritability critic Douglas Wahlsten, “If one intends to use heritability to anticipate the results of breeding for higher values of a phenotype, it makes a major difference whether heritability is judged to be 30, 40, 50 or 60%. On the other hand, the value of so-called heritability in this broad range of possibilities has no valid implications for the educational or health policy of a nation.” See Wahlsten, D., (2003), Airbrushing Heritability, Genes, Brain and Behavior, 2, 327-329, p. 327.
46. For discussions of the eugenic and racial hygiene origins of psychiatric genetics, see Baron, M., (1998), Psychiatric Genetics and Prejudice: Can the Science be Separated from the Scientist?, Molecular Psychiatry, 3, 96-100; Joseph, 2004, 2006; Joseph, J., & Wetzel, N., (2013), Ernst Rüdin: Hitler’s Racial Hygiene Mastermind, Journal of the History of Biology, 46, 1-30; Müller-Hill, B., (1998), Murderous Science, Plainview, NY: Cold Spring Harbor Laboratory Press (original English version published in 1988); Roelcke, V., (2006), “Funding the Scientific Foundations of Race Policies: Ernst Rüdin and the Impact of Career Resources on Psychiatric Genetics, ca 1910-1945,” in W. Eckart (Ed.), Man, Medicine, and the State: The Human Body as an Object of Government Sponsored Medical Research in the 20th Century (pp. 73-87), Stuttgart: Steiner; Roelcke, V., (2010), “Medicine During the Nazi Period: Historical Facts and Some Implications for Teaching Medical Ethics and Professionalism,” in S. Rubenfeld (Ed.), Medicine after the Holocaust: From the Master Race to the Human Genome and Beyond (pp. 18-27), New York: Palgrave Macmillan; Roelcke, V., (2012), Ernst Rüdin – Renommierter Wissenschaftler, Radikaler Rassenhygieniker [Ernst Rüdin – Distinguished Scientist, Radical Racial Hygienist], Der Nervenarzt, 83, 303-310; Weber, M. M., (1996), Ernst Rüdin, 1874-1952, American Journal of Medical Genetics (Neuropsychiatric Genetics), 67, 323-331; Weiss, S. F., (2010), The Nazi Symbiosis: Human Genetics and Politics in the Third Reich, Chicago: University of Chicago Press.
47. Rose, S., (1997), Lifelines: Life beyond the Genes, New York: Oxford University Press, p. 293.