Are DSM Psychiatric Disorders “Heritable”?

Jay Joseph, Psy.D.
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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.

Criticism

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

 

Gene-Environment Interaction 

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.

Conclusion

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]

References:

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.

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39 COMMENTS

  3. Jay,
    I always enjoy reading your articles. The biggest point I took away was how faulty the assumption is that “genetic and environmental factors do not interact.” This fact dooms the heritability research. It’s further explained in Evelyn Fox Keller’s book, The Mirage of a Space Between Nature and Nurture.

    If the public clearly understood the flawed assumptions underlying heritability research, these research programs would be exposed as worthless and have to be shut down. A new paradigm of understanding the development of emotional problems based on complex dynamic interactions between environment and constitution/genes would take over.

    A while ago I daydreamed that scientists invented a new discipline called paleo-psychiatry, the study of mental illness in prehistoric creatures. In this discipline, paleo-psychiatrists would trace how disorders like borderline PD evolved from the earliest single-celled organisms, through dinosaurs and megafauna, all the way to modern man. Because if it’s heritable, there must have always been an earlier organism that had the disorder, right? 🙂 Given the current miserable state of psychiatric research, I would not be surprised if paleo-psychiatry comes into being in some form. Here below is the link to that article:
    https://bpdtransformation.wordpress.com/2015/04/05/25-who-was-the-first-borderline-from-cavemen-and-dinosaurs-to-creationism-and-the-flying-spaghetti-monster/

    • That was a good book. There is no line between nature and nurture, or mind and body. Using nineteenth century concepts and relying on fraudulent twin studies as an excuse to do yet more genetic research and to make unsubstantiated claims about heritability is a desperate attempt to prove that psychiatrists are real boys.

      Uh, scientists.

  4. Great article Jay. Very thoughtful and educational. As you bring out, the emphasis some researchers place on finding genetic influences or causes of DAM diagnoses is troublesome. The implication in the industry and certainly how it is often presented by the media is that certain people carry a “diseased gene”. Of course, this has never been found for any psychiatric diagnosis. The reality is that we all have varied traits. Different traits may lead to varying effects of certain environments. For example, a child who may have a trait of higher emotional sensitivity may react differently to an abusive home than a child who is less sensitive and more assertive. Both will be affected by abuse, but may develop different personality traits or problems later in life. Dr. Hallie Frank and myself did a study years ago on “borderline empathy”: the observation that many individuals who receive this diagnosis seem to tune in to the underlying emotions in others. Our study did find some evidence of heightened emotional perceptiveness in people diagnosed with Borderline Personality and the data seemed to indicate a constitutional variable. The important aspect in this, and in many other possible genetic correlations, is that emotional perceptiveness is not a disease, but is a potentially positive trait that under more ideal family environments is likely to lead to highly beneficial traits. Of course, this issue of emotional sensitivity brings up the whole issue of the wish of the mental health industry to numb people, rather than address societal causes that hurt our emotional development. The crucial issue, is that there are many different traits that create our amazing diversity that will lead to positive outcomes in good environment, but may shape the nature of emotional distress in poor environments. A similar argument applies to the search for a “suicide gene”. There may be traits, like for example the degree of risk aversion or pain tolerance, that may correlate with suicide. This does not mean that these are problematic genes. It will always be problematic social causes that lead to suicide. It might be helpful to know what traits may make it more likely that a person will actually commit suicide, but it will usually be more helpful to deal with the emotional and social issues involved. Genetic traits are not diseases.

      • Sir,

        Isn’t it more correct to say, that in order to analyse the causes of mental distress we must look at the brain, body AND the social and environmental factors responsible?

        I’m sure there are people who experience states of mental distress and the like with no history of trauma, but also those who exhibit those behaviours (which can be causally associated with or made worse by) environmental factors (such as abuse, trauma etc.)

        How do you explain someone, for instance, having a contamination obsession and hand cleaning compulsion (this is just an example, I don’t and have never had these particular problems) with no history of trauma, or out-of-the ordinary environmental factors?

        • Hello. Psychiatric researchers have been looking for faulty brains and faulty genes for decades, and have found none, as the APA officially admitted in 2013 (see below). They have found nothing, yet they continue searching while largely ignoring environmental causes because they mistakenly see psychiatric disorders as “highly heritable brain diseases.”

          There are many environmental causes of dysfunction and distress other than “trauma.” The hand cleaning compulsion you mention is caused by people believing that they will contract a dangerous disease if they don’t wash their hands repeatedly. So it is necessary to help them question this belief, and to understand this belief in the context of their history and the social environment they grew up in and continue to experience. As Szasz pointed out many times, if a brain disease is discovered, the condition ceases to be a psychiatric disorder, and becomes a neurological disorder.

          For the APA admission that they have found no genes or biomarkers, see http://www.psychiatry.org/advocacy–newsroom/newsroom/statement-from-dsm-chair-david-kupfer-md

          • “The hand cleaning compulsion you mention is caused by people believing that they will contract a dangerous disease if they don’t wash their hands repeatedly”

            This is true. And challenging this belief is what psychiatrists/psychologists do in clinical settings (in addition to prescribing drugs if needed). However, why is it that most people do not have this belief while some develop them and have a hard time with getting rid of them even if given the same not-out-of-the-ordinary environmental factors?

            There have been (to my knowledge) no specific genes found for intelligence or personality either. But that they have no influence on those traits is absurd.

            “So it is necessary to help them question this belief, and to understand this belief in the context of their history and the social environment they grew up in and continue to experience”

            Again, this is true. I’ve seen this being done in clinical settings. But I don’t live in the US, so I don’t know how it works there.

            Ignoring environmental and social causes is a bad thing.

            I agree that psychiatric labels (though helpful for categorisation and research purposes, just like labels in gastroenterology such as irritable bowel syndrome, which is a symptom based descriptive label) can hide the very real problems in living people face.

            But if you’re claiming that there are no genetic influences, as opposed to environmental and social causes not being given enough consideration, then you’re wrong, aren’t you?

            The generally accepted notion of causation is interacting biological, psychological and social factors.

    • That is a very thoughtful comment, especially “Genetic traits are not diseases.”.

      As for why psychiatry is forever looking for THE GENE is very simple and you sort of spelled it out: “It will always be problematic social causes”. Psychiatry cannot deal with that because it is not in the business of changing society but in the business of keeping the status quo. They’re looking for a fault in an individual and so any mention of the environment has to be dismissed as unimportant since that’s something they don’t want to touch or even think about.

      I’d add – it’s not only in psychiatry. We are now looking for medical ways to address obesity epidemics while it is clear that the place to look is in our collective lifestyle and not biochemistry.

  5. I must confess, I am amazed at how much genetics is seemingly involved in familial traits, after raising my two children, and seemingly seeing it first hand. However, I raised my children, as a stay at home mom, with love and tried to help them in every way and instill self confidence, as my mother did, which would be a ‘nurture’ distortion in today’s society. A girlfriend of mine, who was also an active volunteer and stay at home mom, and I used to joke that “We’re raising our fathers,” despite us both trying to instill something other than the antiquated paternalistic values our ethical banker fathers had been raised with. Maybe it worked, despite it not seeming to, when our children were little? Our children are now big into accepting others as equals, and down on our current society’s divide and conquer tactics. Although, I must confess, today’s unethical bankers who are buying into the old, evil European Federal Reserve banker’s strategies, do seem to be wreaking havoc within our society now.

    I’m grateful for your insight into the differences between “heritability” and “inherited,” since I was unaware of this distinction. And I was terrified, after having been defamed with “depression caused by self,” “paranoid schizophrenia,” and “bipolar,” all within three weeks by three different doctors. There is no validity, nor reliability, to the DSM disorders. I was misdiagnosed, according to the DSM-IV-TR, due to antidepressant discontinuation syndrome (antidepressant fraudulently given under the guise of a “safe smoking cessation med”), NSAI known to cause “confusion,” and an opioid drug, given under a different name, adverse drug effects. Since I knew ‘bipolar,’ and especially ‘schizophrenia,’ were claimed to be “genetic” illnesses. And I did not want my children to ever be defamed with these supposedly “genetic” illnesses, due to my doctors’ misdiagnoses. I had to find the medical explanation for my supposed “life long incurable, genetic, mental illness” that only lasted as long as I was miss-medicated. Thankfully, I did.

    And it likely relates to both the supposedly highly “heritable” / genetic DSM disorders, “bipolar” and “schizophrenia.” Both “bipolar” and “schizophrenia” patients are regularly given the “gold standard treatment” for “schizophrenia,” the neuroleptic drugs. And I’ve found that the neuroleptic drugs do, in fact, cause both the positive and negative symptoms of “schizophrenia.” Via, at least, the central symptoms of neuroleptic induced anticholinergic intoxication syndrome and neuroleptic induced deficit syndrome. See evidence below:

    “neuroleptics … may result in … the anticholinergic intoxication syndrome … Central symptoms may include memory loss, disorientation, incoherence, hallucinations, psychosis, delirium, hyperactivity, twitching or jerking movements, stereotypy, and seizures.” These are an almost exact description of the positive symptoms of ‘schizophrenia,’ but of course, today’s psychiatrists never confess their “gold standard treatment” can cause the positive symptoms of their most serious “mental illness.”

    “Neuroleptic induced deficit syndrome is principally characterized by the same symptoms that constitute the negative symptoms of schizophrenia—emotional blunting, apathy, hypobulia, difficulty in thinking, difficulty or total inability in concentrating, attention deficits, and desocialization. This can easily lead to misdiagnosis and mistreatment. Instead of decreasing the antipsychotic, the doctor may increase their dose to try to ‘improve’ what he perceives to be negative symptoms of schizophrenia, rather than antipsychotic side effects.”

    I completely agree, “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.” I hope and pray this happens, especially since the psychiatric industry is in denial their “gold standard treatment” for bipolar / schizophrenia is an environmental factor that does, indeed, cause both the positive and negative symptoms of bipolar / schizophrenia.

  6. It helps get an easy answer yeah ? Grease the skids.

    This one can be diabolical because not only did someone in the family’s past potentially get screwed over but it can be used as an excuse to screw over someone from the next generation.

    • It is diabolical, you’re right. As my moronic psychiatrist was creating the symptoms of “bipolar” / schizophrenia via the central symptoms of anticholinergic intoxication syndrome, he was also claiming “there must be someone else in family” and defaming my sweet, non-psychotic grandmother, as psychotic. One would think doctors would be intelligent enough to know that defaming someone’s deceased grandmother was inappropriate behavior, unfortunately at least some psychiatrists are not intelligent enough to comprehend this. I have since gotten a scrip from my grandmother’s former doctor confessing to the reality that my grandmother was never psychotic.

      My grandmother was psychic, however, she knew when people were going to die. Which is not a pleasant foreknowledge to have. And it has been my experience that the psychiatric industry does not understand the difference between the words psychic and psychotic either. My grandmother’s psychic abilities did land her a brief prescription for Stelazine, one of the old neuroleptics, but she was quickly taken off of it because she suffered a severe allergic reaction to it. She was never labeled or ever put on any other psychiatric drugs, doctors of old were intelligent enough to comprehend some people are allergic to the neuroleptic drugs.

      I, too, suffered a severe allergic reaction to the first antipsychotic I was put on, resulting in a medically confessed “Foul up.” But, obviously, today’s psychiatrists cover up severe allergic reactions to today’s antipsychotics, with massive tranquilizations, rather than just taking a person with no family history of “mental illness,” except an allergic reaction to an old neuroleptic, off the neuroleptic that resulted in the medically confessed “Foul up.”

      And this type of psychiatric cover up of a 2001 “Foul up” with Risperdal in a grown adult did allow the psycho / pharmacutical industries to later get Risperdal approved by the FDA for use in childhood bipolar, schizophrenia, and autism.

  7. How troubling that in this entire article that comes across as terribly scientific and technical, the author reifies “psychiatric disorders.” Indeed, referring to them as though they are real, reliable, and valid entities — in the context of the citation of theory and statistics about heritability — is stunningly misleading. Why worry so much about alleged heritability of entities that have been used to cause so much harm, including to so many of the people who read MadinAmerica?

    • Paula,

      It doesn’t appear that you read the entire article. Towards the end, I wrote:

      “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. 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.”

      In any case, the article was about the claims of people who do see these categories and valid, reliable, and “heritable.” This was not the place to go into an elaborate debunking of the of psychiatric disorder (“mental illness”) concept, which many other MIA authors have done very well, and for the most part I agree with them on this point and have said so in previous books and articles.

      • I’m so glad I stumbled into this discussion! First, sorry I haven’t replied yet to you, Paula, regarding “Johnny&Jane Marching Home…” You’re still in my active “IN” box!
        And Jay, I’m in the middle of reviewing your comments, and work here at MIA. I’m a “late arrival” here at MIA, but I read Breggins’ classic “Toxic Psychiatry” in the early 1990’s, so that should give you an idea where I’m coming from, and how long I’ve been coming from there! Back to you, Paula: “How troubling”? Relax, Paula, you’re correct up to a point in your (mis)perception, but I think Jay is coming from a much more clinical perspective. You and I, Paula, are more “in the trenches”, and out “on the streets”, where real people live, work, and play. So, yes, I think you’re BOTH correct! Now, that makes at least *3* of us! Do we have a quorum? >*grin*< Thank-you both. Now, back to WORK…..
        The APA's ("psychiatric") admission of NO BIOMARKERS EXISTing was sadly suppressed in both popular and common media.~B.

    • I don’t think it does this site favour in general either to take maybe too extreme positions.

      “Indeed, referring to them as though they are real, reliable, and valid entities — in the context of the citation of theory and statistics about heritability — is stunningly misleading. ”

      I don’t think it’s “stunningly misleading”. Currently Jay’s articles are some of the few ones published on this site I actually consider reading and thinking more thoroughly. Maybe it’s because I feel I don’t understand genetics and the related studies done it well enough.

  8. Another great article Jay; I appreciate scientific criticism of the pseudoscience of psychology and psychiatry.

    It is hard for me to consider behavioral genetics past is foundation on the “equal environment assumption” of twin studies. Identical twins and fraternal twins obviously create different environments for themselves. Your work debunking this pseudoscience is classic.

    Best wishes, Steve

  9. Much time and energy could be saved and more productive and precise dismantling of psychiatry could more possibly happen and strategies become clearer if people simply read Edwin Black’s book “War Against The Weak”. One of the cheapest places I’ve found to buy books new or used is http://www.abebooks.com Black’s books, a source book of documented facts like no other and of course a must read as long as truth is important .It is a day by day document by document hidden history of eugenics and its origins in America how after World War ll it was decided that the word eugenics could not now be used openly by its elite advocates and how it continues under different descriptive labels and how and who the “elite” financiers of eugenics have been and still are . It exposes eugenic’s main players and how they have operated and now adapted to the present and more . It reveal a lot of inconvenient truths .

    • Dear Fred,

      Thanks. Black’s book is excellent. I would also highly recommend Allan Chase’s classic 1977 book on eugenics, “The Legacy of Malthus.” Simply a must read.

      The word “eugenics” stopped being used openly in the 1960s and early 1970s. It was still used frequently in a positive sense until then, when journals such as “Eugenics Quarterly” became “Social Biology” only in 1968. Between 1944 and 1965, the American Journal of Psychiatry had an annual “Review of Psychiatric Progress,” with a “Heredity and Eugenics” section authored by Franz J. Kallmann.

      • Jay, thanks for the tips to what to read about this subject. I’ve been interested in this topic at least since I read a related book by Chorover. I live in Finland and I know there was plenty of eugenics movement here. Finland was even allied with Germany in much of the early parts of 20th century. I have some articles on my to-read list concerning this particular point in history.

        • Dear Hermes,

          Eugenic ideas and practices were widespread in Finland and other Scandinavian countries for much of the 20th century. A well researched academic book on the topic of Scandinavian eugenics is:

          Broberg, G., & Roll-Hansen, N. (Eds.). (1996). Eugenics and the Welfare State: Sterilization policy in Denmark, Sweden, Norway, and Finland. East Lansing, MI: Michigan State University Press.

          • Thanks, Jay. I actually have also that book on my to-read list. I found the reference to it in one pro-graduation study I stumbled on, concerning eugenics in Finland.

  10. So, when certain individuals with no previous “mental health history” become acutely suicidal or psychotic or “depressed” after taking Chantix or Accutane or Risperdal when others do not, is this a “genetic predisposition”? This mental disturbance is not related to trauma or social problems. Is the drug an “environmental”
    factor? Do these physiological responses to toxic drugs qualify as “brain diseases” or neurological disturbances?

    • One of the things in pharmacology is that different people have different responses to the same drug. So for example, if you have back pain, you may be prescribed tylenol+codeine. For a subset of people who have a certain variant of the CYP2D6 gene (which is involved in metabolising codeine), the body does not turn codeine into its biologically active form as desired. So this prescription does not have much of an effect on them. People who have yet another variant of the same gene get severely affected by the same prescription because more of it is converted into its biologically active form than in the average person. Things like this form the basis for the emerging field of pharmacogenomics.

      However, if a doctor who is prescribing drugs does not warn you about the dangers of the drug, or doesn’t recognise adverse drug reactions (like antidepressant induced mania/psychosis), or covers it up dishonestly, then it is really a cause for concern. The fact that you respond in one manner to a drug and others in another manner, is no excuse for the doctor’s lack of judgement or honesty or the fact that he/she has withheld information, and you should be able to sue him.

  12. Another great read. I feel like I can tell someone what heritability versus heredity is, but then when I try to explain it beyond that, I have to shrug my shoulders.

    Have there been MZTRA studies done that show how different identical twins can be too? The Minnesota study is slow to mention those. Of course those would never be publicized, since they don’t have the same shock and awe factor. That really is the only compelling thing for me are the anecdotal stories of identical twins, both raised together and apart, that are so alike in every little mundane way (even past where I would think genetics could even touch)

    I have recently been really struggling with the fact that personality is being boiled down to a mix of genetics and womb environment. And the idea of shared environment counting as almost nothing vs. non-shared environment (Judith Harris’ work) really gets my goat, since it seems so contrary to what I see and changes people make. As parents, we can take the innate tendencies and then help guide kids to healthy lifestyle choices that can make them realize their full potential. Maybe this is the Christian part of me speaking, but I believe many non-Christians would agree, and many phsychologists see it every day in their work. They see kids have disorders from parents/environments that get mended, they see disorders that may be genetic get mended, etc. They see how environment can drastically affect a person’s well being by either being positive or negative towards their tendencies. I always have personally believed (off mere observation, no formal education in genetics or psychology or the like) that personality is made up of a mix of both that definitely interact, but if you had to find a percentage, maybe 20% genes, the rest all types of environment. Completley arbitrary, I know, and based on nothing scientific. 🙂

    Anyway, thanks for being a differing voice. Why are there not more of you?

    • Hello. I have a MIA posting on reared-apart twin studies entitled “Studies of Reared-Apart (Separated) Twins: Facts and Fallacies.” Many of the main points are covered there, and my recent book “The Trouble with Twin Studies” covers these studies in depth.

      For a number of reasons, individual stories of the supposed similarities of reunited reared-apart MZ pairs prove nothing about genetics. Dissimilar pairs, of which there are many, are not interesting news stories and do not support the typically pro-genetic orientation of twin researchers who conduct reared-apart twin studies.

      • Thanks! Makes sense to me! Thoughts about my other question below? Do you think somatic mutations within an MZ pair could account for some of the differences, or do you see them as negligible? I’m not informed enough to know if 300 copy errors could cause a big enough difference to affect personality traits or larger mental illnesses like Schizophrenia

      • I think the question is not if the “predispositions” can be heritable – they clearly are as we see personality traits passed down the generations. But these are quite different from being “mental illnesses”. The fact that one person has more “predisposition” to become obese eating too many burgers does not mean obesity is a genetic disease, nor does it mean that feeding anyone such a diet is a good idea. It boils down to pathologizing normal human traits while what really is pathological is the environment.

  13. Another question–do you think somatic mutations between identical twins could account for displayed differences within a pair, whether mental illness, personality? Researchers have found on average, one MZ twin may have just over 300 variations in their genome from somatic mutation early on. In my understanding, a majority of these mutations will never have any affect, but when they do, it can lead to differences like schizophrenia and other disorders. Therefore providing a genetic link. What I can find in somatic mutation is that it does not always do anything, but when it does, it’s usually a negative affect. Just a question on how you take this into account. I

    • Thanks Jay! So, to clarify, any somatic mutations would most likely not affect personality either (slight differences that fall within the “normal” range)

      I agree about mental disorders. So much of what I see in my family and in others has pretty strong correlations to major environmental factors.

      I look forward to future posts, and thank you for putting up with my questions. 🙂

  15. I don’t think we should be throwing out genetics. For instance, as a few of you might know, my main complaint was an eating disorder. In fact, until psych got its hands on me, it was my only complaint. (I sure wish MIA would pay more attention to ED since it is a serious problem that more people die of than schiz or bipolar or depression, but that’s another story. More die of psychiatry!) Anyway, if a person’s “mental illness” (depression, bipolar, ADHD, or whatever) came from, say, increased need for one of the B Vitamins, or perhaps hypoglycemia, both of which can run in families, then family history, or what can be gleaned from memory, is vital. My mother’s anorexia, I believe, originated from hypoglycemia. From what I can gather, she had it between 1940 and 1942 and cured it on her own with the loving support of her two sisters. I truly believe I inherited the precise same eating disorder, never mind I looked exactly the same as my mother! Trust me, this embarrassed me all my life! The worst was when I had my Bat Mitzvah and all the aunts pinched my cheeks and reminded me of it. When she became elderly, my brother received frantic calls from her neighbors, telling him that they’d seen her wandering around, seeming confused, disoriented, and dizzy. That’s when I remembered. After a few horrendous Yom Kippur holiday bouts of illness, her doctor had given her very strict orders: Don’t fast again, and never skip a meal. That’s the moment I figured it out. I believe that low blood sugar and forgetting to eat contributed to her early dementia.

  16. Personality traits are inheritable; yet they are not. Since “mental Illness” is a way to pathologize “the human condition” for monetary gain and Orwellian control; it is totally not possible. I would say illogical; but logic is not one of my strengths. However, I will say many times I have heard my mother or my father say to both my sister and me as to a behavior, talent, skill, ability, or personality trait; “Where did you get that from? It didn’t come from me or my parents!” I had heard that traits are heritable for five generations; but, now through genetic ancestral testing; they can determine your “racial” hereditary for up to about 1,000 years (I think.) You see, we really know very little about where we got came from. Although, interesting and at times beneficial to undertake either a personal or wider range study of this; it might be more beneficial to us if we concentrate on what make us unique and what good we can contribute to an ailing society. I have found Gardner’s Multiple Intelligences, the Learning Styles of Visual, Kinesthetic, and Auditory, Right Brain/Left Brain Thinking, Myers-Briggs, Temperament Theory, and even style and color theory to be liberating and hopeful. All of these appreciate what is good about me; and not what is sick, disordered, diseased, or defective. Lets not worry about what we inherit. Let’s celebrate who we are; our special uniqueness that only God could give us and be more concerned about leaving the world a better place than when we found it no matter our religious or philosophical beliefs. One of the problems with this society is that we seek to have each person conform to a false image in all areas of life. This is not the will of God. This is not in the best interest of humanity and of the glorious creation of God. Thank you.