Notes

[←1]

Chambers, C., (2017), The Seven Deadly Sins of Psychology: A Manifesto for Reforming the Culture of Scientific Practice, Princeton, NJ: Princeton University Press, p. 175.

[←2]

Bailey, J. M., & Pillard, R. C., (1993), Reply to Lidz’s “Reply to ‘A Genetic Study of Male Sexual Orientation’” [Letter to the Editor], Archives of General Psychiatry, 50, 240-241, p. 241.

[←3]

Goldman, D., (2011), Molecular Etiologies of Schizophrenia: Are We Almost There Yet?, American Journal of Psychiatry, 168, 879-881, p. 880.

[←4]

Leo, J., (2016), The Search for Schizophrenia Genes, Issues in Science and Technology, 32 (2), 68-71.

[←5]

Arieti, S., (1974), Interpretation of Schizophrenia (2nd ed.), New York: Basic Books.

[←6]

Bleuler, E., (1950), Dementia Praecox or the Group of Schizophrenias, New York: International Universities Press (Originally published in 1911).

[←7]

Szasz, T. S., (1976), Schizophrenia: The Sacred Symbol of Psychiatry, New York: Basic Books, p. 12.

[←8]

Szasz, T. S., (1997), Insanity: The Idea and its Consequences, Syracuse, NY: Syracuse University Press (originally published in 1987).

[←9]

Szasz, T. S., (2004), “Reply to Bentall,” in J. Schaler (Ed.), Szasz under Fire: The Psychiatric Abolitionist Faces His Critics (pp. 321-353), Chicago: Open Court, p. 322.

[←10]

Eugenics is a doctrine which holds that humans can be “improved” by selective breeding to eradicate “undesirable” hereditary traits in society. Eugenicists argue that many social problems and psychiatric disorders are caused by inherited genetic traits in people, which can be bred out of the population for the benefit of future generations. Many German eugenicists of the first half of the 20th century preferred the term racial hygiene to eugenics.

[←11]

Chase, A., (1980), The Legacy of Malthus: The Social Costs of the New Scientific Racism, Urbana, IL/Chicago: University of Illinois Press (originally published in 1977).

[←12]

International Schizophrenia Consortium, (2009), Common Polygenic Variation Contributes to Risk of Schizophrenia and Bipolar Disorder, Nature, 460, 748-752, p. 748; Sekar et al., (2016), Schizophrenia Risk from Complex Variation of Complement Component 4, Nature, 530, 177-183. See also Rees, E., O’Donovan, M. C., & Owen, M. J., (2015), Genetics of Schizophrenia, Current Opinion in Behavioral Sciences, 2, 8-14

[←13]

MacDonald, A. W., & Schulz, S. C., (2009), What We Know: Findings That Every Theory of Schizophrenia Should Explain, Schizophrenia Bulletin, 35, 493-508.

[←14]

Read, J., (2013d), “The Invention of Schizophrenia,” in J. Read & J. Dillon (Eds.), Models of Madness: Psychological, Social and Biological Approaches to Psychosis (2nd ed.; pp. 20-33), London: Routledge, p. 32.

[←15]

Szasz, 1976, p. xiv.

[←16]

Moncrieff, J., & Middleton, H., (2015), Schizophrenia: A Critical Psychiatry Perspective, Current Opinion in Psychiatry, 28, 264-268.

[←17]

Barondes, S. H., (1999), Molecules and Mental Illness, New York: Scientific American Library, p. 154.

[←18]

Read, J., Mosher, L., & Bentall, R., (2013), “‘Schizophrenia’ Is not an Illness,” in J. Read & J. Dillon (Eds.), Models of Madness: Psychological, Social and Biological Approaches to Psychosis, (2nd ed.; pp. 3-8), London: Routledge, p. 4.

[←19]

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

[←20]

Boyle, M., (2007), The Problem with Diagnosis, The Psychologist, 20, 290-292, p. 291.

[←21]

Rees et al., 2015, p. 8. Although in the first few decades of the 20^th century pellagra was seen as a strongly genetic disorder, once it was shown to be caused by a vitamin deficiency, a possible genetic vulnerability to pellagra became largely irrelevant. For more on the history of pellagra and genetic research, see Joseph, J., (2006), The Missing Gene: Psychiatry, Heredity, and the Fruitless Search for Genes, New York: Algora, Chapter 4; Chase, A., (1975, February), The Great Pellagra Cover-Up, Psychology Today, 8 (9), pp. 82-86; Chase, 1980, Chapter 9.

[←22]

Read, J., (2013b), “Childhood Adversity and Psychosis,” in J. Read & J. Dillon (Eds.), Models of Madness: Psychological, Social and Biological Approaches to Psychosis, (2nd ed.; pp. 249-275), London: Routledge; Read, J. Johnstone, L., & Taitimu, M., (2013), “Psychosis, Poverty and Ethnicity,” in J. Read & J. Dillon (Eds.), Models of Madness: Psychological, Social and Biological Approaches to Psychosis, (2nd ed.; pp. 191-209), London: Routledge.

[←23]

Read, 2013e, p. 205.

[←24]

Read et al., (2014), The Traumagenic Neurodevelopmental Model of Psychosis Revisited, Neuropsychiatry, 4, 65-79, p. 66.

[←25]

Read et al., 2014.

[←26]

Read, 2013b, p. 253.

[←27]

Kessler et al., (2005), Lifetime Prevalence and Age-of-Onset Distributions of DSM-IV Disorders in the National Comorbidity Survey Replication, Archives of General Psychiatry, 62, 593-602, p. 601.

[←28]

Lewontin, R. C., (1991), Biology as Ideology, New York: Harper Perennial, p. 16.

[←29]

American Psychiatric Association, (2013), Diagnostic and Statistical Manual of Mental Disorders (5^th ed.), Arlington, VA: Author [DSM-5], p. 103.

[←30]

Lichtenstein et al., (2006), Recurrence Risks for Schizophrenia in a Swedish National Cohort, Psychological Medicine, 36, 1417-1425. I thank M. C. Jones for bringing this study and its family recurrence rate to my attention.

[←31]

Gottesman, I. I., (1991), Schizophrenia Genesis: The Origins of Madness, New York: W. H. Freeman & Company, pp. 102-103.

[←32]

Torrey, E. F., (1995), Surviving Schizophrenia (3^rd ed.), New York: Harper Perennial, p. 157.

[←33]

Andreasen, N. C., (2000), Schizophrenia: The Fundamental Questions, Brain Research Reviews, 31, 106-112, p. 109.

[←34]

Torrey, E. F., & Yolken, R. H., (2010), Psychiatric Genocide: Nazi Attempts to Eradicate Schizophrenia, Schizophrenia Bulletin, 36, 26-32. See also Joseph, J., & Wetzel, N., (2013), Ernst Rüdin: Hitler’s Racial Hygiene Mastermind, Journal of the History of Biology, 46, 1-30; Lifton, R. J., (1986), The Nazi Doctors, New York: Basic Books; Müller-Hill, B., (1998), Murderous Science, Plainview, NY: Cold Spring Harbor Laboratory Press (original English version published in 1988); Proctor, R. N., (1988), Racial Hygiene: Medicine Under the Nazis, Cambridge, MA: Harvard University Press; Weiss, S. F., (2010), The Nazi Symbiosis: Human Genetics and Politics in the Third Reich, Chicago: University of Chicago Press.

[←35]

Longden, E., & Read, J., (2016), Social Adversity in the Etiology of Psychosis: A Review of the Evidence, American Journal of Psychotherapy, 70, 5-33.

[←36]

Gottesman, 1991, p. 80.

[←37]

Read, J., (2013a), “Biological Psychiatry’s Lost Cause,” in J. Read & J. Dillon (Eds.), Models of Madness: Psychological, Social and Biological Approaches to Psychosis, (2nd ed.; pp. 62-71), London: Routledge, pp. 62-63.

[←38]

Read, J., (2013c), “Does ‘Schizophrenia’ Exist? Reliability and Validity,” in J. Read & J. Dillon (Eds.), Models of Madness: Psychological, Social and Biological Approaches to Psychosis (2nd ed.; pp. 47-61), London: Routledge, p. 51.

[←39]

Kirk, S. A., Gomory, T., & Cohen, D., (2013), Mad Science: Psychiatric Coercion, Diagnosis, and Drugs, New Brunswick, NJ: Transaction, pp. 164-166.

[←40]

Murray, R. M., (2017), Mistakes I Have Made in My Research Career, Schizophrenia Bulletin, 43, 253-256.

[←41]

Hill, D., (1983), The Politics of Schizophrenia: Psychiatric Oppression in the United States, Lanham, MD: University Press of America.

[←42]

Penrose, L., (1968), “A Critical Survey of Schizophrenia Genetics,” in G. Howells (Ed.), Modern Perspectives in World Psychiatry (pp. 3-19), Edinburgh and London: Oliver & Boyd, p. 4.

[←43]

Professional Staff of the United States-United Kingdom Cross National Project, (1974), The Diagnosis and Psychopathology of Schizophrenia in New York and London, Schizophrenia Bulletin, 11, 80-102, p. 85.

[←44]

Professional Staff of the United States-United Kingdom Cross National Project, 1974, p. 95.

[←45]

Rosenhan, D. L., (1973), On Being Sane in Insane Places, Science, 179, 250-258.

[←46]

Kirk et al., 2013; Kirk, S. A., & Kutchins, H., (1992), The Selling of DSM: The Rhetoric of Science in Psychiatry New York: Aldine De Gruyter.

[←47]

Read, 2013c.

[←48]

Read, 2013a, p. 63.

[←49]

Frances, A., (2011, July 27), The British Psychological Society Condemns DSM 5 [Web log post, Psychology Today “DSM5 in Distress”].

[←50]

Rutter, M., (2006), Genes and Behavior: Nature-Nurture Interplay Explained, Malden, MA: Blackwell, p. 52.

[←51]

Andreasen, N. C., (1998), Understanding Schizophrenia: A Silent Spring?, American Journal of Psychiatry, 155, 1657-1659, p. 1659.

[←52]

Andreasen, N. C., (2001), Brave New Brain: Conquering Mental Illness in the Era of the Genome, Oxford: Oxford University Press, pp. 197, 209.

[←53]

Frances, A., (2013), Saving Normal: An Insider’s Revolt Against Out-of-Control Psychiatric Diagnosis, DSM-5, Big Pharma, and the Medicalization of Ordinary Life, New York: William Morrow, p. 10.

[←54]

Moncrieff & Middleton, 2009, p. 2015.

[←55]

Torrey, 1995, p. 87.

[←56]

Read, 2013a.

[←57]

Read et al., 2001, The Contribution of Early Traumatic Events to Schizophrenia in Some Patients: A Traumagenic Neurodevelopmental Model, Psychiatry, 64, 319-345; Read et al., 2014.

[←58]

Ho et al., (2011), Long-term Antipsychotic Treatment and Brain Volumes, Archives of General Psychiatry, 68, 128-137.

[←59]

Bentall, R. P., (2009), Doctoring the Mind: Is Our Current Treatment of Mental Illness Really Any Good?, New York: New York University Press, p. 152.

[←60]

Read, 2013a, p. 64.

[←61]

Edwards et al., (2016), Evaluating the Dopamine Hypothesis of Schizophrenia in a Large-Scale Genome-Wide Association Study, Schizophrenia Research, 176, 136-140; Moncrieff, J., (2009), A Critique of the Dopamine Hypothesis of Schizophrenia and Psychosis, Harvard Review of Psychiatry, 17, 214-225.

[←62]

Boyle, 2002a.

[←63]

Read, 2013d, p. 23.

[←64]

Laing, R. D., (1981), “A Critique of Kallmann’s and Slater’s Genetic Theory of Schizophrenia,” in R. Evans, Dialogue with R. D. Laing (pp. 97-156), New York: Praeger, p. 97.

[←65]

Turkheimer, E., (2015), Arsonists at the Cathedral, PsycCRITIQUES, 60 (40), 1-4. DOI: http://dx.doi.org/10.1037/a0039763. For a response to Turkheimer, see Joseph, J., (2015c, November 2), Twin Studies are Still in Trouble: A Reply to Turkheimer, [Web log post, Mad in America “The Gene Illusion”].

[←66]

Conrad, P., (2002), “Genetics and Behavior in the News: Dilemmas of a Rising Paradigm,” in J. Alper et al., (Eds.), The Double-Edged Helix: Social Implications of Genetics in a Diverse Society (pp. 58-79), Baltimore: Johns Hopkins University Press.

[←67]

A 1958 French schizophrenia molecular genetic study by J. K. Constantinidis was cited in McGuffin, P., & Sturt, E., (1986), Genetic Markers in Schizophrenia, Human Heredity, 36, 65-88, p. 80.

[←68]

Elston et al., (1973), Possible Linkage Relationships Between Certain Blood Groups and Schizophrenia or Other Psychoses, Behavior Genetics, 3, 101-106, p. 105.

[←69]

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

[←70]

Plomin et al., (2013), Behavioral Genetics (6th ed.), New York: Worth Publishers, p. 240.

[←71]

Faraone, S. V., (2013), Real Progress in Molecular Psychiatric Genetics, Journal of the American Academy of Child and Adolescent Psychiatry, 52, 1006-1008, p. 1006.

[←72]

Faraone et al., 1999, p. 198.

[←73]

Merikangas, K. R., & Risch, N., (2003), Will the Genomics Revolution Revolutionize Psychiatry?, American Journal of Psychiatry, 160, 625-635, p. 626.

[←74]

Faraone, 2013, p. 1007.

[←75]

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

[←76]

Shorter, E., (1997), A History of Psychiatry, New York: Wiley, p. 246.

[←77]

Tsuang, M. T., & Faraone, S. V., (1997), Schizophrenia: The Facts (2^nd ed.), Oxford: Oxford University Press, pp. 52-53.

[←78]

Cloninger, C. R., (2002), The Discovery of Susceptibility Genes for Mental Disorders, Proceedings of the National Academy of Sciences, 99, 13365-13367.

[←79]

Anonymous, (2003), Scientific Breakthrough of the Year: The Runners-Up, Science, 302, 2039-2045, p. 2039.

[←80]

Elkin et al., (2004), Have Schizophrenia Genes Been Found?, Current Opinion in Psychiatry, 17, 107-113, p. 107.

[←81]

Fanous, A. H., & Kendler, K. S., (2005), Genetic Heterogeneity, Modifier Genes, and Quantitative Phenotypes for Psychiatric Illness: Searching for a Framework, Molecular Psychiatry, 10, 6-13, pp. 10-11.

[←82]

David Goldstein, director of Columbia University’s Institute for Genomic Medicine, quoted in Balter, M., (2017, May), Schizophrenia’s Unyielding Mysteries, Scientific American, 56-61, p. 58.

[←83]

Charney, E., (2012), Behavior Genetics and Postgenomics, Behavioral and Brain Sciences, 35, 331-358; Charney, E., & English, W., (2012), Candidate Genes and Political Behavior, American Political Science Review, 106, 1-34.

[←84]

Crow, T. J., (2008), The Emperors of the Schizophrenia Polygene Have No Clothes, Psychological Medicine, 38, 1681-1685, p. 1682.

[←85]

Former American Psychiatric Association (APA) President Jeffrey Lieberman fittingly called past false positive gene discovery claims “fool’s gold.” See Lieberman, J., & Ogas, O., (2016, March 3rd), Genetics and Mental Illness—Let’s Not Get Carried Away, Wall Street Journal.

[←86]

Balter, 2017, p. 56.

[←87]

Richardson, K., (2017), Genes, Brains, and Human Potential: The Science and Ideology of Intelligence, New York: Columbia University Press.

[←88]

Cross-Disorder Group of the Psychiatric Genomics Consortium, (2013), Identification of Risk Loci with Shared Effects on Five Major Psychiatric Disorders: A Genome-Wide Analysis, Lancet, 381, 1371-1379.

[←89]

Balter, 2017, p. 56.

[←90]

Schizophrenia Working Group of the Psychiatric Genomics Consortium, (2014), Biological Insights from 108 Schizophrenia-Associated Genetic Loci, Nature, 511, 421-427.

[←91]

Sekar et al., (2016), Schizophrenia Risk from Complex Variation of Complement Component 4, Nature, 530, 177-183.

[←92]

Jia et al., 2017, SZGR 2.0: A One-Stop Shop of Schizophrenia Candidate Genes, Nucleic Acids Research, 45, D915-D924.

[←93]

Balter, 2017, p. 56.

[←94]

Bachner-Melman et al., (2005), AVPR1a and SLC6A4 Gene Polymorphisms Are Associated with Creative Dance Performance, PLoS Genetics; Beaver et al., (2010), Monoamine Oxidase A Genotype is Associated with Gang Membership and Weapon Use, Comprehensive Psychiatry, 51, 130-134; Boomsma et al., (2006), Genetic Linkage and Association Analysis for Loneliness in Dutch Twin and Sibling Pairs Points to a Region on Chromosome 12q23-24, Behavior Genetics, 36, 137-146; Fowler, J. H., & Dawes, C. T., (2008), Two Genes Predict Voter Turnout, Journal of Politics, 70, 579-594; De Neve, J., & Fowler, J. H., (2014), Credit Card Borrowing and the Monoamine Oxidase A (MAOA) Gene, Journal of Economic Behavior and Organization (published online).

[←95]

Hewitt, J. K., (2012), Editorial Policy on Candidate Gene Association and Candidate Gene-by-Environment Interaction Studies of Complex Traits, Behavior Genetics, 42, 1-2, p. 1.

[←96]

American Psychiatric Association (2013a, May 3rd), Chair of DSM-5 Task Force Discusses Future of Mental Health Research; Statement by David Kupfer, M.D., American Psychiatric Association [Press release].

[←97]

American Psychiatric Association, 2013b, p. 103.

[←98]

See D. Charney et al., (2002), “Neuroscience Research Agenda to Guide Development of a Pathophysiologically Based Classification System,” in Kupfer et al. (Eds.), A Research Agenda for DSM-V (pp. 31-83), Washington, DC: American Psychiatric Association; Joseph, J., (2013a, October 27), DSM-5’s “Speculative” 2002 Diagnostic System Based On Expected Gene Findings, [Web log post, Mad in America “The Gene Illusion”].

[←99]

Panofsky, A., (2014), Misbehaving Science: Controversy and the Development of Behavior Genetics, Chicago: University of Chicago Press, Chapter 6.

[←100]

For a critique of the GCTA method, see Charney, E., (2013, September 19th), Still Chasing Ghosts: A New Genetic Methodology Will Not Find the “Missing Heritability,” Independent Science News; Kumar et al., 2016, Limitations of GCTA as a Solution to the Missing Heritability Problem, PNAS, 113, E61-E70. See also Joseph, J., (2013d, October 21), Twin Studies and the “Nonreplication Curse” in Psychiatric Molecular Genetic Research, [Web log post, Mad in America “The Gene Illusion”].

[←101]

Jones et al., (2016), Phenotypic Manifestation of Genetic Risk for Schizophrenia During Adolescence in the General Population, JAMA Psychiatry, 73, 221-228; Kendler, K., (2016), The Schizophrenia Polygenic Risk Score: To What Does It Predispose in Adolescence?, JAMA Psychiatry, 73, 193-194.

[←102]

Crow, T. J., (2011), The Missing Genes: What Happened to the Heritability of Psychiatric Disorders?, Molecular Psychiatry, 16, 362-364, p. 362.

[←103]

Moncrieff, J., (2014, September 1), A Critique of Genetic Research on Schizophrenia – Expensive Castles in the Air, [Web log post].

[←104]

As might be expected, there exist studies whose authors claimed that genes may render some people more susceptible to concussions than others.

[←105]

For the first major mainstream academic publication on the “missing heritability” problem, see Manolio et al., (2009), Finding the Missing Heritability of Complex Diseases, Nature, 461, 747-753. Critiques of the concept can be found in Joseph, J., (2012), The “Missing Heritability” of Psychiatric Disorders: Elusive Genes or Non-Existent Genes?, Applied Developmental Science, 16, 65-83; Latham, J., & Wilson, A., (2010), The Great DNA Data Deficit: Are Genes for Disease a Mirage?, The Bioscience Research Project; and Chaufan, C., & Joseph, J., (2013), The Heritability of Common Disorders is “Missing”: Should Health Researchers Care?, International Journal of Health Services, 43, 281-303.

[←106]

Joseph, 2006.

[←107]

Zuk et al., (2012), The Mystery of Missing Heritability: Genetic Interactions Create Phantom Heritability, PNAS, 109, 1193-1198.

[←108]

Insel, T. R, & Collins, F. S., (2003), Psychiatry in the Genomics Era, American Journal of Psychiatry, 160, 616-620.

[←109]

Lush, J. L., (1949), Heritability of Quantitative Characteristics in Farm Animals, Hereditas (Suppl.), G. Bonnier & R. Larsson (Eds.).

[←110]

There are several problems with model fitting procedures, which include the many questionable assumptions they are based upon. See Goldberger, A. S., (1979), Heritability, Economica, 46, 327-347; Joseph, J., (2015b), The Trouble with Twin Studies: A Reassessment of Twin Research in the Social and Behavioral Sciences, New York: Routledge, Chapters 4 and 5; Richardson, 2017, Chapter 2; Taylor, H. F., (1980), The IQ Game: A Methodological Inquiry into the Heredity-Environment Controversy, New Brunswick, NJ: Rutgers University Press.

[←111]

Plomin et al. 2013, p. 419.

[←112]

Plomin et al., 2013, p. 87.

[←113]

Faraone, S. V., Tsuang, M. T., & Tsuang, D. W., (1999), Genetics of Mental Disorders, New York: Guilford, p. 32; Gottesman, I. I., & Shields, J., (1967), A Polygenic Theory of Schizophrenia, Proceedings of the National Academy of Sciences of the United States of America, 58, 199-205, p. 201.

[←114]

Sullivan et al., (2003), Schizophrenia as a Complex Trait: Evidence from a Meta-Analysis of Twin Studies, Archives of General Psychiatry, 60, 1187-1192.

[←115]

Moore, D. S., (2013), “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.

[←116]

Burt, C. H., & Simons, R. L., (2014), Pulling Back the Curtain on Heritability Studies: Biosocial Criminology in the Postgenomic Era, Criminology, 52, 223-262; Burt, C. H., & Simons, R. L., (2015), Heritability Studies in the Postgenomic Era: The Fatal Flaw is Conceptual, Criminology, 53, 103-112; Charney, 2012; Joseph, 2015b, Chapter 4; Keller, E. F., (2010), The Mirage of a Space Between Nature and Nurture, Durham, NC: Duke University Press; Richardson, K. & Norgate, S., (2006), A Critical Analysis of IQ Studies of Adopted Children, Human Development, 49, 319-335.

[←117]

Lewontin, R. C., (1974), The Analysis of Variance and the Analysis of Causes, American Journal of Human Genetics, 26, 400–411, p. 402; Meaney, M. J., (2010), Epigenetics and the Biological Definition of Gene x Environment Interactions, Child Development, 81, 41-79, p. 42.

[←118]

Moore, D. S., & Shenk, D., (2016), The Heritability Fallacy, WIREs Cognitive Science, 1-8, DOI: 10.1002/wcs.1400

[←119]

Wahlsten, D., (1990), Insensitivity of the Analysis of Variance to Heredity-Environment Interaction, Behavioral and Brain Sciences, 13, 109-120.

[←120]

Moore & Shenk, 2016, p. 1.

[←121]

For more on problems with the use of heritability estimates in the social and behavior sciences, see 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; Joseph, J., (2004), The Gene Illusion: Genetic Research in Psychiatry and Psychology Under the Microscope, New York: Algora, Chapter 5; Joseph, J., 2015b, Chapter 4, and the references therein. See also Joseph, J., (2015a, June 24), Are DSM Psychiatric Disorders “Heritable”?, [Web log post, Mad in America “The Gene Illusion”]; Moore & Shenk, 2016.

[←122]

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.

[←123]

Moore, 2013, 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.

[←124]

Panofsky, 2014, p. 190.

[←125]

Casey, T., (2017, February 8th), Like Father, Like Son, Like Granny? A Case for Underhand Free Throws, New York Times.

[←126]

For more on modern schizophrenia family studies, see Joseph, J., & Leo, J., (2006), Genetic Relatedness and the Lifetime Risk for Being Diagnosed with Schizophrenia: Gottesman’s 1991 Figure 10 Reconsidered, Journal of Mind and Behavior, 27, 73-89.

[←127]

Kendler, K. S., Gruenberg, A. M., & Tsuang, M. T., (1985), Psychiatric Illness in First-Degree Relatives of Schizophrenic and Surgical Control Patients, Archives of General Psychiatry, 42, 770-779, p. 775.

[←128]

Glatt, S. J., Faraone, S. V., & Tsuang, M. T., (2008), “Psychiatric Genetics: A Primer,” in J. Smoller et al., (Eds.), Psychiatric Genetics: Applications in Clinical Practice (pp. 3-26), Washington, DC: American Psychiatric Publishing, pp. 6-7.

[←129]

Plomin et al., (2008), Behavioral Genetics (5th ed.), New York: Worth Publishers, p. 70, 151.

[←130]

Scutti, S., (2016, October 19^th), Scientists Confirm Genetics of Schizophrenia, CNN.

[←131]

Rüdin, E., (1916), Zur Vererbung und Neuentstehung der Dementia Praecox [On the Heredity and New Development of Dementia Praecox], Berlin: Springer Verlag OHG. David Rosenthal called Rüdin the “father of psychiatric genetics”; see Rosenthal, D., (1981), “Genetic Transmission in Schizophrenia,” in S. Matthysse (Ed.), Psychiatry and the Biology of the Human Brain: A Symposium Dedicated to Seymour S. Kety (pp. 227-238), Elsevier, p. 227.

[←132]

Kendler, K. S., & Zerbin-Rüdin, E., (1996), Abstract and Review of “Studien Über Vererbung und Entstehung Geistiger Storungen. I. Zur Vererbung und Neuentstehung der Dementia praecox,” (Studies on the Inheritance and Origin of Mental Illness: I. To the Problem of the Inheritance and Primary Origin of Dementia Praecox), American Journal of Medical Genetics (Neuropsychiatric Genetics), 67, 338-342.

[←133]

Gütt, A., Rüdin, E., & Ruttke, F., (1934), Gesetz zur Verhütung Erbkranken Nachwuchses [Law for the Prevention of Genetically Diseased Offspring], Munich: J. F. Lehmanns.

[←134]

Schneider, F., (2011), Psychiatry Under National Socialism: Remembrance and Responsibility, European Archives of Psychiatry and Clinical Neuroscience, 261, Supplement 2, S111-118.

[←135]

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; Schulze, T. G., Fangerau, H., & Propping, P., (2004), From Degeneration to Genetic Susceptibility, from Eugenics to Genetics, from Bezugsziffer to LOD Score: The History of Psychiatric Genetics, International Review of Psychiatry, 16, 260-283; Weindling, P., (1989), Health, Race, and German Politics Between National Unification and Nazism, 1870-1945, Cambridge: Cambridge University Press.

[←136]

Joseph & Wetzel, 2013; Luxenburger, H., (1934), “Rassenhygienisch Wichtige Probleme und Ergebnisse der Zwillingspathologie” [Racial Hygienic Important Problems and Results of Twin Pathology], in E. Rüdin (Ed.), Erblehre und Rassenhygiene im Völkischen Staat [Genetics and Racial Hygiene in the Völkish State] (pp. 303-316), Munich: Lehmanns; Schulz, B., (1934), Rassenhygienische Eheberatung [Racial Hygienic Marriage Counseling], Volk und Rasse, 9, 138-143. See Weiss, 2010, Chapter 3 for a detailed description of the work of Rüdin, Luxenburger, and Schulz in the Nazi era.

[←137]

Lifton, 1986; Proctor, 1988. The German “euthanasia” program led to the killing of approximately 70,000 people by gas, lethal injection, starvation, and other methods in the first phase between 1939 and 1941 under the direction of the government and doctors and psychiatrists. Many thousands more people were killed between 1939 and 1945 in further actions both in Germany and the occupied territories. Although there is no evidence that Rüdin played a role in initiating the “euthanasia” program, the evidence suggests that he helped implement and justify it, and that he participated in aspects of it. For evidence showing Rüdin’s involvement in the T4 “euthanasia” program, see Joseph & Wetzel, 2013; Roelcke, V., (2000), “Psychiatrische Wissenschaft im Kontext Nationalsozialistischer Politik und ‘Euthanasie’: Zur Rolle von Ernst Rüdin und der Deutschen Forschungsanstalt/Kaiser-Wilhelm-Institut für Psychiatrie” [Psychiatric Science in the Context of National Socialist Politics and “Euthanasia”: On the Role of Ernst Rüdin and the German Research Institute/Kaiser-Wilhelm Institute for Psychiatry], in D. Kaufmann (Ed.), Die Kaiser-Wilhelm-Gesellschaft im Nationalsozialismus [The Kaiser-Wilhelm Society Under National Socialism] (pp. 112-150), Göttingen, Germany: Wallstein; Roelcke, V., (2012), Ernst Rüdin – Renommierter Wissenschaftler, Radikaler Rassenhygieniker [Ernst Rüdin – Distinguished Scientist, Radical Racial Hygienist], Der Nervenarzt, 83, 303-310 [English language abstract]; Weiss, 2010.

[←138]

Kösters et al., (2015), Ernst Rüdin’s Unpublished 1922-1925 Study “Inheritance of Manic-Depressive Insanity”: Genetic Research Findings Subordinated to Eugenic Ideology, PLoS Genetics, 11(11): e1005524. doi:10.1371/journal.pgen.1005524

[←139]

Slater, E., (1936), The Inheritance of Manic-Depressive Insanity, Proceedings of the Royal Society of Medicine, 29, 981-990, p. 982.

[←140]

Kösters et al., 2015, p. 5.

[←141]

As I showed in Chapter 10 of The Missing Gene, the widespread claim that bipolar disorder is “highly heritable” is based on a body of weak evidence, based mainly on very problematic twin and adoption studies.

[←142]

Kallmann, F. J., (1938a), The Genetics of Schizophrenia: A Study of Heredity and Reproduction in the Families of 1,087 Schizophrenics, New York: J. J. Augustin, p. xiv.

[←143]

Black, E., (2003), War Against the Weak: Eugenics and America’s Campaign to Create a Master Race, New York: Four Walls Eight Windows; Chase, 1980; Reilly, P. R., (1991), The Surgical Solution: A History of Involuntary Sterilization in the United States, Baltimore: Johns Hopkins University Press.

[←144]

Kallmann, 1938a, p. 3.

[←145]

Kallmann, 1938a, p. 47. Before he was forced to leave Germany due to his partial Jewish ancestry, at a 1935 meeting Kallmann called for the compulsory sterilization of people diagnosed with schizophrenia and their non-diagnosed “heterozygous” relatives as well. According to Kallmann, “It is desirable to extend prevention of reproduction to relatives of schizophrenics who stand out because of minor anomalies, and, above all, to define each of them as being undesirable from the eugenic point of view at the beginning of their reproductive years.” Quoted in Müller-Hill, 1998, p. 11.

[←146]

Baron, M., (1998), Psychiatric Genetics and Prejudice: Can the Science be Separated from the Scientist?, Molecular Psychiatry, 3, 96-100; Gershon, E. S., (1981), The Historical Context of Franz Kallmann and Psychiatric Genetics, Archives of Psychiatry and Neurological Sciences, 229, 273-276.

[←147]

Erlenmeyer-Kimling, E., (1972), Comments on Past and Present in Genetic Research on Schizophrenia, Psychiatric Quarterly, 46, 363-370, p. 363.

[←148]

Kallmann, F. J., (1938b), Heredity, Reproduction, and Eugenic Procedure in the Field of Schizophrenia, Eugenical News, 13, 105-113, p. 105.

[←149]

Boyle, M., (2002b), Schizophrenia: A Scientific Delusion? (2nd ed.), Hove, UK: Routledge, pp. 69-76, 172-173. For an early critique of Kallmann’s 1938 family study, see Pastore, N., (1949), The Genetics of Schizophrenia: A Special Review, Psychological Bulletin, 46, 285-302.

[←150]

For schizophrenia family studies finding no significant elevation of schizophrenia among first-degree biological relatives, see Abrams, R., & Taylor, M. A., (1983), The Genetics of Schizophrenia: A Reassessment Using Modern Criteria, American Journal of Psychiatry, 140, 171-175; Coryell, W., & Zimmerman, M., (1988), The Heritability of Schizophrenia and Schizoaffective Disorders, Archives of General Psychiatry, 45, 323-327; Pope et al., (1982), Failure to Find Evidence of Schizophrenia in First-Degree Relatives of Schizophrenic Probands, American Journal of Psychiatry, 139, 826-828.

[←151]

Slater, E., (1953), Psychotic and Neurotic Illnesses in Twins, Medical Research Council Special Report Series No. 278, London: Her Majesty’s Stationary Office, pp. 166-168.

[←152]

Plomin et al., 2013, p. 82.

[←153]

Grove et al., (1990), Heritability of Substance Abuse and Antisocial Behavior: A Study of Monozygotic Twins Reared Apart, Biological Psychiatry, 27, 1293-1304. For a critique of media reports on individual MISTRA “reared-apart” MZ pairs, see Joseph, J., (2016a, March 6), “Bewitching Science” Revisited: Tales of Reunited Twins and the Genetics of Behavior, [Web log post, Mad in America “The Gene Illusion ”].

[←154]

Alford et al., 2005, Are Political Orientations Genetically Transmitted?, American Political Science Review, 99, 153-167, p. 155.

[←155]

Luxenburger, H., (1928), Vorläufiger Bericht über Psychiatrische Serienuntersuchungen an Zwillingen [Provisional Report on a Series of Psychiatric Investigations of Twins], Zeitschrift fur die Gesamte Neurologie und Psychiatrie, 116, 297-347.

[←156]

Rosanoff et al., (1934), The Etiology of So-Called Schizophrenic Psychoses, American Journal of Psychiatry, 91, 247-286.

[←157]

Joseph, J., (2013c), “‘Schizophrenia’ and Heredity: Why the Emperor (Still) Has No Genes,” in J. Read & J. Dillon (Eds.), Models of Madness: Psychological, Social and Biological Approaches to Psychosis (2nd ed.; pp. 72-89), London: Routledge, p. 74. A list of published schizophrenia twin studies, and accompanying concordance rates, can be found in this publication.

[←158]

Kallmann, F. J., (1946), The Genetic Theory of Schizophrenia: An Analysis of 691 Schizophrenic Twin Index Families, American Journal of Psychiatry, 103, 309-322, p. 321.

[←159]

Koskenvuo et al., (1984), Psychiatric Hospitalization in Twins, Acta Geneticae Medicae et Gemellologiae, 33, 321-332.

[←160]

Neel, J. V., & Schull, W. J., (1954), Human Heredity, Chicago: University of Chicago Press, p. 280. For more examples of the traditional definition of the twin method’s equal environment assumption, see Joseph, 2015b, pp. 155-156.

[←161]

See also Fosse, R., Joseph, J., & Jones, M., (2015), Schizophrenia: A Critical View on Genetic Effects, Psychosis (published online September 14th, DOI: 10.1080/17522439.2015.1081269)

[←162]

Joseph, 2015b. See also Jackson, D. D., (1960), “A Critique of the Literature on the Genetics of Schizophrenia,” in D. Jackson (Ed.), The Etiology of Schizophrenia (pp. 37-87), New York: Basic Books; Joseph, J., (2013e), The Use of the Classical Twin Method in the Social and Behavioral Sciences: The Fallacy Continues, Journal of Mind and Behavior, 34, 1-39.

[←163]

See Joseph, 2015b, Table 7.1.

[←164]

Kringlen, E., (1967), Heredity and Environment in the Functional Psychoses: An Epidemiological-Clinical Study, Oslo: Universitetsforlaget, p. 115.

[←165]

Segal, N. L., & Johnson, W., (2009), “Twin Studies of General Mental Ability,” in Y. Kim (Ed.), Handbook of Behavior Genetics (pp. 81-99), New York: Springer, p. 82. For a list of quotations by researchers using the “twin create their more similar environments” Argument A over a 50 year span, see Joseph, 2015b, Appendix C.

[←166]

Kendler et al., (1993), A Test of the Equal-Environment Assumption in Twin Studies of Psychiatric Illness, Behavior Genetics, 23, 21-27, p. 21. Kendler’s original detailed justification for supporting Argument A is found in Kendler, K. S., (1983), Overview: A Current Perspective on Twin Studies of Schizophrenia, American Journal of Psychiatry, 140, 1413-1425.

[←167]

Joseph, J., Chaufan, C., Richardson, K., Shultziner, D., Fosse, R., James, O., Latham, J., & Read, J., (2015), The Twin Research Debate in American Criminology, Logos, 14 (Nos. 2-3) (published online 8/9/2015).

[←168]

Turkheimer, 2015.

[←169]

Kendler, K. S., (2000), “Schizophrenia: Genetics,” in B. Sadock & V. Sadock (Eds.), Kaplan & Sadock’s Comprehensive Textbook of Psychiatry (7th ed., Vol. 1, pp. 1147-1158), Philadelphia: Lippincott, Williams, & Wilkins, p. 1149.

[←170]

Lyons, M. J., Kendler, K. S., Provet, A. G., & Tsuang, M. T., (1991), “The Genetics of Schizophrenia,” in Tsuang et al., (Eds.), Genetic Issues in Psychosocial Epidemiology (pp. 119-152), New Brunswick, NJ: Rutgers University Press, p. 126.

[←171]

Lilienfeld, S. O., Lynn, S. J., & Lohr, J. M., (2003), “Science and Pseudoscience in Clinical Psychology: Initial Thoughts, Reflections, and Considerations,” in S. Lilienfeld et al., (Eds.), Science and Pseudoscience in Clinical Psychology (pp. 1-14), New York: Guilford, p. 7.

[←172]

Fosse R., Joseph J., & Richardson, K., (2015), A Critical Assessment of the Equal Environment Assumption of the Twin Method for Schizophrenia, Frontiers in Psychiatry, 6:62, DOI: 10.3389/fpsyt.2015.00062

[←173]

Joseph, 2004.

[←174]

Kringlen, E., (1976), Twins—Still Our Best Method, Schizophrenia Bulletin, 2, 429-433, p. 431.

[←175]

Fuller, J. L., & Thompson, W. R., (1960), Behavior Genetics, New York: John Wiley & Sons, p. 113.

[←176]

Critical analyses of the EEA-test literature include Felson, J., (2014), What Can We Learn from Twin Studies? A Comprehensive Evaluation of the Equal Environments Assumption, Social Science Research, 43, 184-199; Joseph, 2004; Joseph 2006, Chapter 9; Pam et al., (1996), The “Equal Environment Assumption” in MZ-DZ Comparisons: An Untenable Premise of Psychiatric Genetics?, Acta Geneticae Medicae et Gemellologiae, 45, 349-360; Richardson, K. & Norgate, S., (2005), The Equal Environment Assumption of Classical Twin Studies May Not Hold, British Journal of Educational Psychology, 75, 339-350.

[←177]

See Joseph, 2006, p. 129. Pooled DZ schizophrenia concordance rates are same-sex 59/523 (11.3%), and opposite-sex 20/422 (4.7%). An additional 2007 study of 29,602 Swedish twin pairs, which recorded hospitalization rates for psychosis and other psychiatric disorders, revealed that same-sex DZ psychosis correlations again were 2-3 times higher than the opposite-sex DZ correlations; see Prescott et al., (2007), Twin Pair Resemblance for Psychiatric Hospitalization in the Swedish Twin Registry: A 32-Year Follow-Up Study of 29,602 Twin Pairs, Behavior Genetics, 37, 547-558, p. 553.

[←178]

See Joseph, 2004, pp. 176-178.

[←179]

Gottesman, 1991, p. 96. For a critical analysis of this publication’s “Table 10,” cited in countless textbooks in support of genetic theories, see Joseph & Leo, 2006.

[←180]

Slater, 1953, pp. 34-35. The sibling rates are found on page 56.

[←181]

Jackson, 1960, p. 60.

[←182]

Lewontin. R. C., Rose, S., & Kamin, L. J., (1984), Not in Our Genes, New York: Pantheon, p. 218.

[←183]

Keefe, R. S. E., & Harvey, P. D., (1994), Understanding Schizophrenia: A Guide to the New Research on Causes and Treatment, New York: The Free Press, pp. 82-83.

[←184]

Keefe & Harvey, 1994, p. 82.

[←185]

Keefe & Harvey, 1994, p. 81, Table 5-1.

[←186]

Polderman et al., (2015), Meta-Analysis of the Heritability of Human Traits Based on Fifty Years of Twin Studies, Nature Genetics, 47, 702-709.

[←187]

Turkheimer, 2015.

[←188]

Hogben, L., (1933), Nature and Nurture, London: George Allen & Unwin, p. 121.

[←189]

Mukherjee, S., (2016), The Gene: An Intimate History, New York, Scribner.

[←190]

Mukherjee, 2016, p. 300.

[←191]

Mukherjee, 2016, p. 442.

[←192]

The autism twin study cited by Mukherjee was Folstein, S. E., & Rutter, M., (1977), Infantile Autism: A Genetic Study of 21 Twin Pairs, Journal of Child Psychology and Psychiatry, 18, 297-321.

[←193]

Fischer, M., (1973), Genetic and Environmental Factors in Schizophrenia, Copenhagen: Munksgaard; Fischer, M., Harvald, B., & Hauge, M., (1969), A Danish Twin Study of Schizophrenia, British Journal of Psychiatry, 115, 981-990; Gottesman, I. I., & Shields, J., (1966), Schizophrenia in Twins: 16 Years’ Consecutive Admissions to a Psychiatric Clinic, British Journal of Psychiatry, 112, 809-818; Gottesman, I. I., & Shields, J., (1972), Schizophrenia and Genetics: A Twin Study Vantage Point, New York: Academic Press; Tienari, P., (1963), Psychiatric Illnesses in Identical Twins, Copenhagen: Munksgaard; Tienari, P., (1975), Schizophrenia in Finnish Male Twins, British Journal of Psychiatry Special Publication, No. 10, M. Lader (Ed.), pp. 29-35.

[←194]

Mukherjee, 2016, pp. 442-443.

[←195]

Sullivan et al., 2003, p. 1188.

[←196]

Mukherjee, 2016, p. 298.

[←197]

The original study was Pollin et al., (1969), Psychopathology in 15,909 Pairs of Veteran Twins: Evidence for a Genetic Factor in the Pathogenesis of Schizophrenia and its Relative Absence in Psychoneurosis, American Journal of Psychiatry, 126, 597-610. The results were also published in Hoffer, A., & Pollin, W., (1970), Schizophrenia in the NAS-NRC Panel of 15,909 Veteran Twin Pairs, Archives of General Psychiatry, 23, 469-477.

[←198]

Pollin et al., 1969, p. 608.

[←199]

Pollin et al., 1969, p. 599.

[←200]

Hoffer & Pollin, 1970, p. 475.

[←201]

Kendler, K. S., & Robinette, C. D., (1983), Schizophrenia in the National Academy of Sciences-National Research Council Twin Registry: A 16-year Update, American Journal of Psychiatry, 140, 1551-1563, p. 1551.

[←202]

Mukherjee, 2016, p. 380.

[←203]

Mukherjee, 2016, p. 380.

[←204]

Fischer, M., (1971), Psychoses in the Offspring of Schizophrenic Monozygotic Twins and their Normal Co-Twins, British Journal of Psychiatry, 118, 43-51; Gottesman, I. I., & Bertelsen, A., (1989), Confirming Unexpressed Genotypes for Schizophrenia, Archives of General Psychiatry, 46, 867-872.

[←205]

Kringlen, E., & Cramer, G., (1989), Offspring of Monozygotic Twins Discordant for Schizophrenia, Archives of General Psychiatry, 46, 873-877.

[←206]

For a critical analysis of research on the offspring of discordant MZ pairs, see Joseph, 2004, pp. 187-193; Torrey, E. F., (1990), Offspring of Twins with Schizophrenia [Letter to the Editor], Archives of General Psychiatry, 47, 976-977.

[←207]

Farber, S. L., (1981), Identical Twins Reared Apart: A Reanalysis, New York: Basic Books, p. 156. For the original publication, see Craike, W. H., & Slater, E., (1945), Folie a Deux in Uniovular Twins Reared Apart, Brain, 68, Part III, 213-221. For more on this pair, see Joseph, 2004, pp. 185-186.

[←208]

Gottesman, I. I., (1982), [Review of the Book Identical Twins Reared Apart: A Reanalysis, by S. Farber], American Journal of Psychology, 95, 350-352, p. 351.

[←209]

Boomsma et al., (2005), Genetic and Environmental Contributions to Loneliness in Adults: The Netherlands Twin Register Study, Behavior Genetics, 35, 745-752; Bradshaw, M., & Ellison, C. G., (2008), Do Genetic Factors Influence Religious Life? Findings from a Behavior Genetic Analysis of Twin Siblings, Journal for the Scientific Study of Religion, 47, 529–544; Dawood et al., (2005), Genetic and Environmental Influences on the Frequency of Orgasm in Women, Twin Research and Human Genetics, 8, 27-33; Långström et al., 2002, Genetic and Environmental Influences on Problematic Masturbatory Behavior in Children: A Study of Same-Sex Twins, Archives of Sexual Behavior, 31, 343-350; Luciano et al., (2005), The Genetics of Tea and Coffee Drinking and Preference for Source of Caffeine in a Large Community Sample of Australian Twins, Addiction, 100, 1510-1517.

[←210]

Rosenthal, D., (1979), “Genetic Factors in Behavioural Disorders,” in M. Roth & V. Cowie (Eds.), Psychiatry, Genetics and Pathography: A Tribute to Eliot Slater (pp. 22-33), London: Oxford University Press, p. 25.

[←211]

Rosenthal, D., (1971b), A Program of Research on Heredity in Schizophrenia, Behavioral Science, 16, 191-201, p. 192.

[←212]

Kendler, 1983; Kendler, K. S., & Prescott, C. A., (2006), Genes, Environment, and Psychopathology: Understanding the Causes of Psychiatric and Substance Abuse Disorders, New York: Guilford.

[←213]

Kendler, K. S., (1993), Twin Studies of Psychiatric Illness: Current Status and Future Directions, Archives of General Psychiatry, 50, 905-915, p. 907.

[←214]

Burt & Simons, 2014. The response to Burt and Simons was Barnes et al., (2014), Demonstrating the Validity of Twin Research in Criminology, Criminology, 52, 588-626. This article was accompanied by 23 pages of online supporting material. The 24 collaborators included the seven co-authors, five “anonymous reviewers,” and twelve other (some prominent) researchers acknowledged by the authors for their help; see Barnes et al., 2014, p. 588.

[←215]

DeLisi, L. E., (2017), 100 Questions & Answers About Schizophrenia: Painful Minds (3^rd ed.), Burlington, MA: Jones & Bartlett, pp. 94-95.

[←216]

Rosenthal, D., (1970), Genetic Theory and Abnormal Behavior, New York: McGraw-Hill, p. 56.

[←217]

Tsuang et al., (1991), The Genetics of Schizophrenia: Current Knowledge and Future Directions, Schizophrenia Research, 4, 157-171, p. 160.

[←218]

For my previous analyses of schizophrenia adoption research, see Joseph, 2004, Chapter 7; Joseph 2006, Chapters 3, 5, and 6.

[←219]

Cassou et al., (1980), Génétique et Schizophrénie: Réévaluation d’un Consensus [Genetics and Schizophrenia: Reevaluation of a Consensus], Psychiatrie de l’Enfant, 23, 87-201.

[←220]

Shore, A. N., (2001), Effects of a Secure Attachment Relationship on Right Brain Development, Affect Regulation, and Infant Mental Health, Infant Mental Health Journal, 22, 7-66; Siegel, D. J., (1999), The Developing Mind: Toward a Neurobiology of Interpersonal Experience, New York: Guilford.

[←221]

Newman et al., (2015), Attachment and Early Brain Development—Neuroprotective Interventions in Infant-Caregiver Therapy, Translational Developmental Psychiatry, 3: 28647- http://dx.doi.org/10.3402/tdp.v3.28647

[←222]

Maté, G., (2010), In the Realm of the Hungry Ghosts: Close Encounters with Addiction, Berkeley: North Atlantic Books, p. 217.

[←223]

Maté, 2010, p. 433.

[←224]

Gabor Maté, personal communication via e-mail, 10/19/2016.

[←225]

Ken Richardson, personal communication via e-mail, 10/12/2016.

[←226]

Stoolmiller, M., (1999), Implications of the Restricted Range of Family Environments for Estimates of Heritability and Nonshared Environment in Behavior-Genetic Adoption Studies, Psychological Bulletin, 125, 392-409.

[←227]

Rosenthal, D., (1971a), Genetics of Psychopathology, New York: McGraw-Hill, p. 194.

[←228]

Sham, P. C., & Kendler, K. S., (2008), “Genetic Etiology,” in R. Murray et al., (Eds.), Essential Psychiatry (4^th ed., pp. 80-94), Cambridge: Cambridge University Press, p. 85.

[←229]

Plomin et al., 2013, p. 78. The term “generalizability” refers to whether a study’s findings can be transferred to situations or people other than those originally studied. In this case it refers to the question of whether findings from schizophrenia studies using adopted (abandoned) children apply to the general non-adopted population.

[←230]

Mendlewicz, J., & Rainer, J. D., (1977), Adoption Study Supporting Genetic Transmission in Manic-Depressive Illness, Nature, 268, 327-329. For a critical analysis of this study, see Joseph, 2006, Chapter 10.

[←231]

Sham & Kendler, 2008, p. 85.

[←232]

Lilienfeld et al., 2003, p. 9. For more on the problematic “converging evidence” argument, see Joseph, 2006, Chapter 1.

[←233]

Chambers, 2017.

[←234]

Chambers, 2017, p. 25.

[←235]

Head et al., (2015), The Extent and Consequences of P-Hacking in Science, PLoS Biology, 13(3): e1002106. doi:10.1371/journal.pbio.1002106

[←236]

Head et al., 2015.

[←237]

Chambers, 2017, p. 25.

[←238]

John, L. K., Loewenstein, G., & Prelec, D., (2012), Measuring the Prevalence of Questionable Research Practices with Incentives for Truth Telling, Psychological Science, 23, 524-532.

[←239]

Kerr, N. L., (1998), HARKing: Hypothesizing After the Results Are Known, Personality and Social Psychology Review, 2, 196-217.

[←240]

Kerr, 1998, p. 197.

[←241]

Chambers, 2017, pp. 18-19.

[←242]

Jekel et al., (2007), Epidemiology, Biostatistics, and Preventive Medicine (3^rd ed.), Philadelphia: Saunders-Elsevier, p. 206.

[←243]

Joseph, J., & Baldwin, S., (2000), Four Editorial Proposals to Improve Social Sciences Research and Publication, International Journal of Risk and Safety in Medicine, 13, 117-127.

[←244]

Chambers, 2017, p. 21.

[←245]

Gershon et al., (1994), “Detecting Discrete Genes for Susceptibility to Bipolar Disorder or Schizophrenia,” in E. Gershon & C. R. Cloninger (Eds.), Genetic Approaches to Mental Disorders (pp. 205-230), Washington, DC: American Psychiatric Press, p. 208.

[←246]

Gottesman, I. I., & Shields, J., (1976), A Critical Review of Recent Adoption, Twin, and Family Studies of Schizophrenia: Behavioral Genetics Perspectives, Schizophrenia Bulletin, 2, 360-401, p. 364.

[←247]

Kety, S. S., (1959), Biochemical Theories of Schizophrenia, Part II, Science, 129, 1590-1596.

[←248]

For examples of David Rosenthal’s praise of Rüdin and the work of his German psychiatric genetic colleagues, see Rosenthal, 1970, 1971a.

[←249]

Rosenthal, D., (1963), The Genain Quadruplets: A Study of Heredity and Environment in Schizophrenia, New York: Basic Books.

[←250]

Kety et al., (1978a), “The Biologic and Adoptive Families of Adopted Individuals Who Became Schizophrenic: Prevalence of Mental Illness and Other Characteristics,” in L. Wynne et al., (Eds.), The Nature of Schizophrenia: New Approaches to Research and Treatment (pp. 25-37), New York: John Wiley & Sons.

[←251]

Heston, L. L., (1966), Psychiatric Disorders in Foster Home Reared Children of Schizophrenic Mothers, British Journal of Psychiatry, 112, 819-825.

[←252]

Heston, 1966, p. 823.

[←253]

Heston, L. L., & Denny, D. D., (1968), “Interactions Between Early Life Experience and Biological Factors in Schizophrenia,” in D. Rosenthal & S. Kety (Eds.), The Transmission of Schizophrenia (pp. 363-376), New York: Pergamon Press, p. 369; Heston, 1966, p. 822.

[←254]

Heston & Denny, 1968, p. 374.

[←255]

For a critical analysis of Heston’s study, see Joseph, 2004, pp. 204-212.

[←256]

Kety et al., (1968), “The Types and Prevalence of Mental Illness in the Biological and Adoptive Families of Adopted Schizophrenics,” in D. Rosenthal & S. Kety (Eds.), The Transmission of Schizophrenia (pp. 345-362), New York: Pergamon Press.

[←257]

There were actually 34 index adoptees. One consisted of the members of an MZ twin pair adopted by the same parents, who were counted as one adoptee by the researchers.

[←258]

Kety et al. 1968, p. 361.

[←259]

Kety et al., (1975), “Mental Illness in the Biological and Adoptive Families of Adopted Individuals who Have Become Schizophrenic: A Preliminary Report Based on Psychiatric Interviews,” in R. Fieve et al., (Eds.), Genetic Research in Psychiatry (pp. 147-165), Baltimore: The Johns Hopkins Press.

[←260]

One control adoptee was added to the 1975 study, because the researchers decided to count both control adoptees matched to the index adoptee MZ twin pair. This index twin pair was still counted as one index adoptee in the 1975 study.

[←261]

Kety et al., 1975, p. 151.

[←262]

Kety et al., 1975, p. 163.

[←263]

Kety et al., (1978b), “Genetic Relationships within the Schizophrenia Spectrum: Evidence from Adoption Studies,” in R. Spitzer & D. Klein (Eds.), Critical Issues in Psychiatric Diagnosis (pp. 213-223), New York: Raven Press; Kety et al., (1994), Mental Illness in the Biological and Adoptive Relatives of Schizophrenic Adoptees: Replication of the Copenhagen Study to the Rest of Denmark, Archives of General Psychiatry, 51, 442-455.

[←264]

Kety et al., 1994, p. 442.

[←265]

Rosenthal et al., (1968), “Schizophrenics’ Offspring Reared in Adoptive Homes,” in D. Rosenthal & S. Kety (Eds.), The Transmission of Schizophrenia (pp. 377-391), New York: Pergamon Press; Rosenthal et al., (1971), The Adopted-Away Offspring of Schizophrenics, American Journal of Psychiatry, 128, 307-311.

[←266]

Rosenthal et al., 1971, p. 308.

[←267]

Rosenthal et al., 1968, p. 386.

[←268]

Rosenthal et al., 1971, p. 307.

[←269]

Wender et al., (1974), Crossfostering: A Research Strategy for Clarifying the Role of Genetic and Experiential Factors in the Etiology of Schizophrenia, Archives of General Psychiatry, 30, 121-128.

[←270]

Wender et al., 1974, p. 122.

[←271]

Wender et al., 1974, p. 121.

[←272]

Wender et al., 1974, p. 121.

[←273]

Tienari, Sorri, et al., (1987), Genetic and Psychosocial Factors in Schizophrenia: The Finnish Adoptive Family Study, Schizophrenia Bulletin, 13, 477-484; Tienari et al., (2003), Genetic Boundaries of the Schizophrenia Spectrum: Evidence from the Finnish Adoptive Family Study, American Journal of Psychiatry, 160, 1587-1594.

[←274]

Based on figures from Tienari et al., 2003. In this 2003 publication (p. 1590), Tienari and colleagues diagnosed DSM-III-R schizophrenia in 7 out of 137 index adoptees whose biological mothers were also diagnosed with DSM-III-R schizophrenia (5.1%). DSM-III-R schizophrenia was diagnosed in 3 of the 192 control adoptees (1.6%). Using Fisher’s Exact Test, one-tailed, the probability value for this difference = .065, which is not statistically significant at the conventional .05 level of significance. See the VassarStats website to calculate.

[←275]

Tienari et al., (2004), Genotype-Environment Interaction in Schizophrenia-Spectrum Disorders, British Journal of Psychiatry, 184, 216-222, p. 216.

[←276]

Documentation of problem areas 2-4 can be found in Joseph, 2004, pp. 261-271, and in the references therein.

[←277]

For critical analyses of Tienari’s study, see Boyle, M., 2002b, pp. 194-199; Jackson, G. E., (2003), Rethinking the Finnish Adoption Studies of Schizophrenia: A Challenge to Genetic Determinism, Journal of Critical Psychology, Counselling and Psychotherapy, 3, 129-138; Joseph, J., (1999), A Critique of the Finnish Adoptive Family Study of Schizophrenia, Journal of Mind and Behavior, 20, 133-154; Joseph, 2004, Chapter 7, pp. 261-271.

[←278]

Lichtenstein et al., (2009), Common Genetic Determinants of Schizophrenia and Bipolar Disorder in Swedish Families: A Population-Based Study, Lancet, 373, 234–239.

[←279]

Kety et al., (1976b), Studies Based on a Total Sample of Adopted Individuals and their Relatives: Why They Were Necessary, What They Demonstrated and Failed to Demonstrate, Schizophrenia Bulletin, 2, 413-428, p. 427.

[←280]

Wender et al., (1977), Schizophrenics’ Adopting Parents, Archives of General Psychiatry, 34, 777-784, p. 777.

[←281]

Critical analyses of the Danish-American schizophrenia adoption studies include: Benjamin, L. S., (1976), A Reconsideration of the Kety and Associates Study of Genetic Factors in the Transmission of Schizophrenia, American Journal of Psychiatry, 133, 1129-1133; Boyle, 2002b, Chapter 6; Cassou et al., 1980; Joseph, 2004, 2006, 2013c; Lewontin et al., 1984, Chapter 8; Lidz, T., (1976), Commentary on a Critical Review of Recent Adoption, Twin, and Family Studies of Schizophrenia: Behavioral Genetics Perspectives, Schizophrenia Bulletin, 2, 402-412; Lidz, T., & Blatt, S., (1983), Critique of the Danish-American Studies of the Biological and Adoptive Relatives of Adoptees who Became Schizophrenic, American Journal of Psychiatry, 140, 426-435; Lidz, T., Blatt, S., & Cook, B., (1981), Critique of the Danish-American Studies of the Adopted-Away Offspring of Schizophrenic Parents, American Journal of Psychiatry, 138, 1063-1068; Marshall, R., (1990), “The Genetics of Schizophrenia: Axiom or Hypothesis?,” in R. Bentall (Ed.), Reconstructing Schizophrenia (pp. 89-117), London: Routledge; Pam, A., (1995), “Biological Psychiatry: Science or Pseudoscience?,” in C. Ross & A. Pam (Eds.), Pseudoscience in Biological Psychiatry: Blaming the Body (pp. 7-84), New York: John Wiley & Sons; Sarbin, T. R., & Mancuso, J. C., (1980), Schizophrenia: Medical Diagnosis or Moral Verdict?, New York: Pergamon Press; Sedarati, J., (2016), Schizophrenia’s Etiology: Behavioural Geneticists’ Research and the Research They Ignore, Journal of Critical Psychology, Counselling and Psychotherapy, 16, 257-266.

[←282]

Examples of “independent” analyses of the Danish-American studies based on DSM-III diagnostic criteria include Lowing, P. A., Mirsky, A. F., & Pereira, R., (1983), The Inheritance of Schizophrenia Spectrum Disorders: A Reanalysis of the Danish Adoptee Study Data, American Journal of Psychiatry, 140, 1167-117; Kendler, K. S., & Gruenberg, A. M., (1984), An Independent Analysis of the Danish Adoption Study of Schizophrenia, Archives of General Psychiatry, 41, 555-564; Kendler, K. S., Gruenberg, A. M., & Kinney, D. K., (1994), Independent Diagnoses of Adoptees and Relatives as Defined by DSM-III in the Provincial and National Samples of the Danish Adoption Study of Schizophrenia, Archives of General Psychiatry, 51, 456-468.

[←283]

In a 1975 publication, Rosenthal described how he and his colleagues searched through the “APA Diagnostic and Statistical Manual, second edition” (DSM-II) to select the spectrum disorders they used in their studies. See Rosenthal, D., (1975b), “The Spectrum Concept in Schizophrenic and Manic-Depressive Disorders,” in D. Freedman (Ed.), Biology of the Major Psychoses (pp. 19-25), New York: Raven Press, pp. 19-20. In February of 1967, a pre-publication draft of the DSM-II was distributed to psychiatrists. See American Psychiatric Association, (1968), Diagnostic and Statistical Manual of Mental Disorders (2nd ed. [DSM-II]), Washington, DC: Author, p. ix.

[←284]

Kety et al., 1968, pp. 351-352.

[←285]

Kety, S. S., (1974), From Rationalization to Reason, American Journal of Psychiatry, 131, 957-963, p. 960.

[←286]

Kety, S. S., (1987), The Significance of Genetic Factors in the Etiology of Schizophrenia: Results from the National Study of Adoptees in Denmark, Journal of Psychiatric Research, 21, 423-429, p. 424.

[←287]

Rosenthal, D., (1968), “The Heredity-Environment Issue in Schizophrenia: Summary of the Conference and Present Status of Our Knowledge,” in D. Rosenthal & S. Kety (Eds.), The Transmission of Schizophrenia (pp. 413-427), New York: Pergamon Press.

[←288]

Kety et al., 1976b, p. 420.

[←289]

Kety, 1974, p. 960.

[←290]

Rosenthal et al., (1975), Assessing Degree of Psychopathology from Diagnostic Statements, Canadian Psychiatric Association Journal, 20, 35-45, p. 44.

[←291]

Boyle, 2002b, p. 179.

[←292]

Lidz, 1976, p. 407.

[←293]

Kety et al., 1968, p. 352.

[←294]

Kety et al., 1975, p. 163.

[←295]

Ingraham, L. J., & Kety, S. S., (1988), “Schizophrenia Spectrum Disorders,” in M. Tsuang & J. Simpson (Eds.), Handbook of Schizophrenia, Vol. 3: Nosology, Epidemiology and Genetics (pp. 117-137), New York: Elsevier Science Publishers, p. 121.

[←296]

Kety, S. S., (1983b), Mental Illness in the Biological and Adoptive Relatives of Schizophrenia Adoptees: Findings Relevant to Genetic and Environmental Factors in Etiology, American Journal of Psychiatry, 140, 720-727, p. 724.

[←297]

Boyle, M., (1990), Schizophrenia: A Scientific Delusion? (1^st ed.), New York: Routledge, p. 141.

[←298]

Boyle, 1990, p. 144.

[←299]

Rosenthal, D., (1974b), “The Genetics of Schizophrenia,” in S. Arieti & E. Brody (Eds.), American Handbook of Psychiatry (2nd ed., pp. 588-600), New York: Basic Books, p. 589.

[←300]

American Psychiatric Association, 1968, p. 44.

[←301]

American Psychiatric Association, (1980), Diagnostic and Statistical Manual of Mental Disorders (3rd ed.), Washington, DC: Author; Spitzer, R. L., & Endicott, J., (1979), Justification for Separating Schizotypal and Borderline Personality Disorders, Schizophrenia Bulletin, 6, 95-104.

[←302]

Kety, S. S., & Ingraham, L. J., (1992), Genetic Transmission and Improved Diagnosis of Schizophrenia from Pedigrees of Adoptees, Journal of Psychiatric Research, 26, 247-255, p. 250.

[←303]

Spitzer & Endicott, 1979, p. 98.

[←304]

APA, 1980, p. 310.

[←305]

Kety et al., 1978b, p. 220.

[←306]

Kety, 1987, p. 424.

[←307]

Kety et al., 1975, p. 154.

[←308]

Rosenthal, 1979, p. 23.

[←309]

Rosenthal et al., 1968, p. 387. This index adoptee’s complete “schizophrenia spectrum diagnosis” was listed as “border-line schizophrenia or pervert.”

[←310]

Rosenthal et al., 1975, p. 40; Wender et al., 1974, p. 124, Table 2.

[←311]

Kety et al., 1968, p. 252, Table 3.

[←312]

American Psychiatric Association, 1968, pp. 33-35.

[←313]

Wender, P. H., & Klein, D. F., (1981), Mind, Mood, and Medicine, New York: Farrar, Straus, & Giroux, p. 127.

[←314]

Jones et al., 2016, p. 222.

[←315]

For example, Kety, Rosenthal, and Wender wrote that chronic schizophrenia “is the only syndrome which merits the designation of schizophrenia in Denmark”; see Kety et al., 1978b, p. 214.

[←316]

Rosenthal, D., (1972), Three Adoption Studies of Heredity in the Schizophrenic Disorders, International Journal of Mental Health, 1, 63-75, pp. 73-74.

[←317]

Kendler & Gruenberg, 1984, p. 556.

[←318]

Lewontin et al., 1984, p. 224.

[←319]

Jacobs, D., (1994), Environmental Failure—Oppression Is the Only Cause of Psychopathology, Journal of Mind and Behavior, 15, 1-18, p. 8.

[←320]

Paikin et al., (1974), “Characteristics of People Who Refused to Participate in a Social and Psychopathological Study,” in S. Mednick et al., (Eds.), Genetics, Environment and Psychopathology (pp. 293-322), New York: American Elsevier, pp. 308-310. See Boyle, 2002b, Chapter 6 for more on problems and inconsistencies in the Danish-American interviewing and diagnostic process.

[←321]

The original B1 diagnosis for the biological parent of control adoptee C9 is found in Kety et al., 1968, p. 355, Table 4b. In Kety et al., 1975, p. 159, Table 4b he was listed as a biological father, along with his 1968 B1 diagnosis and a notation that he had subsequently died.

[←322]

See Kety et al. 1975, p. 160.

[←323]

B1 rates of 5/173 index versus 1/174 control produce a probability value of .11 (Fisher’s Exact Test, one-tailed), which is not statistically significant at the conventional .05 level of statistical significance used by the Danish-American researchers. See the VassarStats website to calculate. For more on the C9 biological father and how he was counted, see Joseph, 2004, pp. 238-239. In 1988 Kety again counted this long-dead relative as B1, but by then his diagnosis could be added to the Provincial Study totals, and the B1 comparison remained statistically significant; see Ingraham & Kety, 1988, p. 122, Table 1.

[←324]

Rosenthal, 1971b, p. 194.

[←325]

Rosenthal, 1975b, p. 19.

[←326]

Rosenthal, 1970, p. 158.

[←327]

Kendler, K., (2016), Phenomenology of Schizophrenia and the Representativeness of Modern Diagnostic Criteria, JAMA Psychiatry, 73, 1082-1092.

[←328]

For more details, see Joseph, 2006, Chapter 3.

[←329]

Rosenthal, 1972, p. 65.

[←330]

Rosenthal, 1971b, p. 194.

[←331]

Kendler & Gruenberg, 1984, p. 556.

[←332]

Kety et al., 1994, p. 452.

[←333]

Sarbin & Mancuso, 1980, p. 138.

[←334]

In a 1971 discussion of the origins of the Kety-led studies, Kety and colleagues wrote, “For the purpose of this study we agreed that we would include as ‘schizophrenic’ those individuals whose psychiatric history was characteristic of ‘chronic schizophrenia,’ ‘acute schizophrenia reaction,’ or ‘borderline schizophrenia’ as these terms are commonly used in the United States.” They claimed that they “postulated in advance” that the spectrum would include these three categories, as well as the “uncertain” versions of each diagnosis. See Kety, et al., (1971), Mental Illness in the Biological and Adoptive Families of Adopted Schizophrenics, American Journal of Psychiatry, 128, 302-306, p. 303. In this publication Kety and colleagues implied, but did not specifically state, that the spectrum was developed well before 1968. Rosenthal later claimed that the spectrum hypothesis had been worked out by the researchers in 1962. See Rosenthal, 1981, p. 229.

[←335]

Kety, 1983b, p. 724.

[←336]

Kety, S. S., (1983a), Dr. Kety Responds [Letter to the Editor], American Journal of Psychiatry, 140, 964, p. 964.

[←337]

Bleuler, 1950, p. 294. For a discussion of E. Bleuler’s views on schizophrenia and latent schizophrenia, versus the Danish-American researchers’ accounts of his views, see Joseph, 2006, Chapter 3, pp. 74-77.

[←338]

Bleuler, 1950, p. 239.

[←339]

Kety, S. S., (1980), The Syndrome of Schizophrenia: Unresolved Questions and Opportunities for Research, British Journal of Psychiatry, 136, 421-436, p. 423.

[←340]

For a detailed explanation of how the researchers incorrectly counted “borderline schizophrenia” and other spectrum diagnoses, and how they determined whether these diagnoses were “genetically related to chronic schizophrenia,” see Joseph, 2006, Chapter 3. See also Joseph, 2004, Chapter 7.

[←341]

Index B3 biological relatives 6/173 (3.4%), versus control B3 biological relatives 3/174 (1.7%), probability = .25, not statistically significant. These figures were reported in Kety et al., 1975, p. 154, Table 3.

[←342]

Kendler & Gruenberg, 1984, p. 557, Table 2.

[←343]

Ingraham & Kety, 1988, pp. 121-123.

[←344]

Kety et al., 1978b, p. 217.

[←345]

Kety, S. S., (1985), “The Concept of Schizophrenia,” in M. Alpert (Ed.), Controversies in Schizophrenia: Changes and Constancies, (pp. 3-11), New York: Guilford Press, p. 6. Although Kety gave the reference for Bleuler’s quotation on acute schizophrenia as “Bleuler, 1911/1950, p. 204,” Bleuler did not mention acute schizophrenia on page 204, and I was not able to find this quotation elsewhere in Bleuler’s 1911 book.

[←346]

Kety et al., 1975, p. 154.

[←347]

The mid-20^th century chronic schizophrenia rate in the Danish population has been given as 0.69%. See Slater, E., & Cowie, V., (1971), The Genetics of Mental Disorders, London: Oxford University Press, p. 13.

[←348]

Haier, R. J., Rosenthal, D., & Wender, P. H., (1978), MMPI Assessment of Psychopathology in the Adopted-Away Offspring of Schizophrenics, Archives of General Psychiatry, 35, 171-175, p. 174, Table 3.

[←349]

Faraone, S. V., Tsuang, D., & Tsuang, M. T., (2002), “Methods in Psychiatric Genetics,” in M. Tsuang & M. Tohen, Textbook in Psychiatric Epidemiology (2^nd ed., pp. 65-130), Hoboken, NJ: John Wiley & Sons, p. 77.

[←350]

Kety et al., 1968, p. 349.

[←351]

Rosenthal et al., 1971, p. 308.

[←352]

Kety et al., 1968, p. 356.

[←353]

Plomin, R., & DeFries, J. C., (1985), Origins of Individual Differences in Infancy: The Colorado Adoption Project, Orlando, FL: Academic Press.

[←354]

For problem areas in the Colorado Adoption Project, see Joseph, J., (2013b), “The Lost Study: A 1998 Adoption Study of Personality that Found No Genetic Relationship Between Birthparents and Their 240 Adopted-Away Biological Offspring,” in R. Lerner & J. Benson (Eds.), Advances in Child Development and Behavior, 45, 93-124, San Diego: Elsevier; Richardson & Norgate, 2006; Stoolmiller, 1999.

[←355]

Heston, L. L., & Denny, D. D., (1968), “Interactions Between Early Life Experience and Biological Factors in Schizophrenia,” in D. Rosenthal & S. Kety (Eds.), The Transmission of Schizophrenia (pp. 363-376), New York: Pergamon Press, p. 366.

[←356]

Benjamin 1976, p. 1130.

[←357]

Mosher, L. R., (1975), unpublished letter to Gottesman, dated 10/14/75.

[←358]

Kety et al., 1975, p. 163, Table 6.

[←359]

Boyle, 2002b, pp. 186-187. Family diagnostic counts are based on data in Kety et al., 1975, pp. 158-161 (Tables 4a and 4b).

[←360]

After correcting for the errors found in the Kety et al. 1975 publication’s Table 6 (p. 163), there are 8 index biological families out of 33 with at least one B1, B2, or B3 diagnosis, versus 3 control biological families out of 34 with at least one B1, B2, or B3 diagnosis (see pp. 158-161). This comparison is not statistically significant at the conventional .05 level (index families 8/33 vs. control families 3/34, Fisher’s Exact Test, one-tailed, p = .084). For the B and D diagnoses combined, the comparison remains statistically non-significant (index families 11/33 vs. control families 5/34, Fisher’s Exact Test, one-tailed, p = .066). See the VassarStats website to calculate.

[←361]

Boyle, 2002b, p. 186.

[←362]

Kety et al., 1978a, p. 30.

[←363]

See Rosenthal et al., 1971, p. 309.

[←364]

Rosenthal, 1971a, p. 124.

[←365]

Rosenthal et al., 1971. For more on this point, see Joseph 2004; Lidz et al., 1981.

[←366]

Rosenthal et al., 1971, p. 309.

[←367]

Kety et al., 1976b, p. 417.

[←368]

Rosenthal et al., 1971, p. 309.

[←369]

Rosenthal et al., 1968, p. 382.

[←370]

Pam, 1995, p. 31.

[←371]

Lidz et al., 1981, p. 1064.

[←372]

Kety, 1959, p. 1594.

[←373]

Rosenthal, D., (1967), “An Historical and Methodological Review of Genetic Studies of Schizophrenia,” in J. Romano (Ed.), The Origins of Schizophrenia: Proceedings of the First Rochester International Conference on Schizophrenia, March 29-31, 1967 (pp. 15-26), New York: Excerpta Medica Foundation, p. 25.

[←374]

Kety et al., 1968, p. 346.

[←375]

Kety et al., 1968, p. 353.

[←376]

Kety et al., 1968, p. 353.

[←377]

Kety et al., 1968, p. 358, Table 5.

[←378]

Lidz & Blatt, 1983, pp. 426-427.

[←379]

Lidz, T., (1967), “The Family, Personality Development, and Schizophrenia,” in J. Romano (Ed.), The Origins of Schizophrenia: Proceedings of the First Rochester International Conference on Schizophrenia, March 29-31, 1967 (pp. 131-138), New York: Excerpta Medica Foundation. There is a photograph of Lidz and other Rochester conference attendees, including David Rosenthal, on page viii of this book.

[←380]

Rosenthal, 1970, p. 57.

[←381]

Kety, 1974, p. 961.

[←382]

Kety et al., (1976c), Mental Illness in the Biological and Adoptive Families of Adopted Individuals Who Have Become Schizophrenic, Behavior Genetics, 6, 219-225, p. 222. This article was based on a speech Kety gave in October, 1974.

[←383]

Kety et al., 1975, p. 153. In the mid-1970s Kety sometimes reported a 13.9% IB spectrum rate, and at other times he reported a 21% IB rate. The difference is based on whether he decided to include spectrum Category C (schizoid or inadequate personality), or whether he counted only “definite schizophrenia” B1, B2, and B3 relatives.

[←384]

Kety et al., 1976b, p. 420.

[←385]

Kety et al., 1978a.

[←386]

Kety et al., 1978b, p. 218.

[←387]

Kety, S. S., (1978a), “Genetic and Biochemical Aspects of Schizophrenia,” in A. Nicholi (Ed.), The Harvard Guide to Modern Psychiatry (pp. 93-102), Cambridge, MA: Harvard University Press, p. 97.

[←388]

Kety, S. S., (1978b), “Heredity and Environment,” in J. Shershow (Ed.), Schizophrenia: Science and Practice (pp. 47-68), Cambridge, MA: Harvard University Press, p. 52.

[←389]

Kety, 1983b, p. 721.

[←390]

Kety, 1983a, p. 964.

[←391]

Andreasen, N. C., (1984), The Broken Brain: The Biological Revolution in Psychiatry, New York: Harper & Row, pp. 29-30. On page 426 of Lidz and Blatt’s critique, published in the April, 1983 edition of the American Journal of Psychiatry, it was stated that the article was first received by the editor on November 1^st, 1978. After four revisions, it was finally accepted for publication on March 15^th, 1982, and appeared in print 13 months later. In contrast, Kety’s response to Lidz and Blatt was accepted for publication (after one revision) two months after it was received, and was published four months later. See Kety, 1983b, p. 720.

[←392]

Walster, G. W., & Cleary, T. A., (1970), A Proposal for a New Editorial Policy in the Social Sciences, The American Statistician, 24, 16-19, p. 18.

[←393]

Rosenthal et al., 1968, pp. 390-391.

[←394]

Rosenthal et al., 1968, p. 389.

[←395]

Rosenthal, 1971a, p. 81.

[←396]

Chambers, 2017, pp. 26-27.

[←397]

Rosenthal et al., 1968, p. 380.

[←398]

Rosenthal et al., 1971, p. 310.

[←399]

Rosenthal et al., 1968, p. 388.

[←400]

Albee, G. W., (1982), The Politics of Nature and Nurture, American Journal of Community Psychology, 10, 4-36, p. 5.

[←401]

Savan, B., (1988), Science Under Siege: The Myth of Objectivity in Scientific Research, Montreal: CBC Enterprises, p. 51.

[←402]

Chambers, 2017, p. 174.

[←403]

Kety et al., 1976, p. 418, Table 2a.

[←404]

Gottesman & Shields, 1976, p. 370.

[←405]

Benjamin, 1976, p. 1131.

[←406]

Rosenthal, 1974b, p. 589.

[←407]

Lidz & Blatt, 1983; Kety, 1983b, p. 722.

[←408]

Rosenthal, 1972, p. 67.

[←409]

Wender et al., (1986), Psychiatric Disorders in the Biological and Adoptive Families of Adopted Individuals with Affective Disorders, Archives of General Psychiatry, 43, 923-929, p. 925.

[←410]

Kety et al., 1975, p. 156.

[←411]

Kety et al., 1975, p. 156.

[←412]

Kety repeated this statement in the following publications: Kety, S. S., (1976a), Studies Designed to Disentangle Genetic and Environmental Variables in Schizophrenia: Some Epistemological Questions and Answers, American Journal of Psychiatry, 133, 1134-1137, p. 1134; Kety, S. S. (1976b), Genetics Aspects of Schizophrenia, Psychiatric Annals, 6, 6-15, p. 13; Kety, 1978b, p. 58; Kety, S. S., & Matthysse, S., (1988), “Genetic and Biological Aspects of Schizophrenia,” in A. Nicholi (Ed.), The New Harvard Guide to Psychiatry (3^rd ed., pp. 139-151), Cambridge, MA: Harvard University Press, p. 142.

[←413]

Kety et al., 1975, p. 156.

[←414]

Kety et al., 1975, p. 156.

[←415]

Kringlen, 1976, p. 430.

[←416]

Joseph, 2004; Lidz & Blatt, 1983. Kety and colleagues continued to count Category C “schizoid or inadequate personality” as a schizophrenia spectrum disorder in the 1975 Kety-led study. In Table 3 of the Kety et al. 1975 publication (p. 154), Category C was located under the “Schizophrenia spectrum” heading, and the 26 Category C index and control biological relative diagnoses were included among the 56 index and control biological relative diagnoses falling into the clearly marked “Total in schizophrenia spectrum” category. On page 155 they wrote, “We are not prepared to dismiss the possibility that there is a schizoid or inadequate personality which is genetically related to schizophrenia.” In a different 1975 publication (found in the same edited book), Rosenthal defended the retention of Category C in the spectrum. See Rosenthal, D., (1975a), “Discussion: The Concept of Schizophrenic Disorders,” in R. Fieve et al., (Eds.), Genetic Research in Psychiatry (pp. 199-208), Baltimore: The Johns Hopkins Press.

[←417]

Kety et al., 1976b, p. 418, Table 2a. Schizophrenia spectrum disorders, including the “Category C” schizoid/inadequate diagnosis, as were listed in this publication’s Table 2a as 18/63 index, versus 11/64 control, with the probability given as .094. This comparison is not statistically significant below the conventional .05 level.

[←418]

See Joseph, 2006, pp. 110-112.

[←419]

Rosenthal, 1975a, p. 201.

[←420]

Kety et al., 1978a, p. 30.

[←421]

Kety et al., 1994, p. 448, Figure 1.

[←422]

Kety et al., 1976b, p. 417.

[←423]

Lewontin et al., 1984, p. 226.

[←424]

Haier et al., 1978, p. 174. The Haier et al. 1978 investigator-defined schizophrenia spectrum consisted of chronic schizophrenia, borderline schizophrenia, and “schizophrenic personality.” The results, as seen in Table 3 of this publication, showed 21/60 (35%) index adoptees with a spectrum disorder diagnosis, versus a control adoptee spectrum disorder diagnostic rate of 16/62 (26%). This comparison produces a probability value of .18 (Fisher’s Exact Test, one-tailed), which is not statistically significant at the conventional .05 level of statistical significance used by the Danish-American researchers. See the VassarStats website to calculate.

[←425]

A 1983 reanalysis of the Rosenthal-led study by Patricia Lowing and colleagues, who used DSM-III diagnostic criteria, provided no valid evidence in support of the original researchers’ (mistaken) conclusions in favor of genetics. In addition, Lowing et al. did not mention or reference the 1978 Haier et al. article or its authors’ publication of the Adoptees Study consensus spectrum diagnoses. See Joseph, 2004, pp. 259-262; Lowing et al., 1983.

[←426]

Lewontin et al., 1984, p. 226.

[←427]

Joseph, 2006, pp. 104-107.

[←428]

Kety, 1983b, p. 724.

[←429]

Kety & Matthysse, 1988; Rosenthal, D., (1980), “Genetic Aspects of Schizophrenia,” in H. van Praag, et al., (Eds.), Handbook of Biological Psychiatry (Part 3, pp. 3-34), New York: Marcel Dekker; Wender & Klein, 1981.

[←430]

Wender & Klein, 1981, p. 174.

[←431]

Boyle, 2002b; Joseph, 2004; Lewontin et al., 1984; Lidz & Blatt, 1983.

[←432]

Lewontin et al., 1984, p. 224.

[←433]

Further analysis of the Danish-American Crossfostering Study can be found in Boyle, 2002b, pp. 192-194; Joseph, J., (1998), A Critical Analysis of the Genetic Theory of Schizophrenia, unpublished doctoral dissertation, California School of Professional Psychology, Alameda, pp. 286-292; Lewontin et al., 1984, pp. 226-227.

[←434]

Paikin et al., 1974, p. 313, Table 14.

[←435]

Wender et al., 1974, p. 126.

[←436]

Wender et al., 1974, p. 127.

[←437]

Van Dyke, J. L., Rosenthal, D., & Rasmussen, P. V., (1975), Schizophrenia: Effects of Inheritance and Rearing on Reaction Time, Canadian Journal of Behavioural Science, 7, 223-236, p. 227, Table 2.

[←438]

Wender & Klein, 1981, p. 175.

[←439]

Kety et al., 1978b, p. 217.

[←440]

Kety, 1983b, p. 723.

[←441]

Kety, S. S., (1985), “The Adoption Strategy for Examining Genetic and Environmental Factors in Mental Disorder,” in T. Sakai & T. Tsuboi (Eds.), Genetic Aspects of Human Behavior (pp. 157-164). New York: Igaku-Shoin, p. 160.

[←442]

Ingraham & Kety, 1988, p. 122.

[←443]

Kety & Ingraham, 1992, p. 248.

[←444]

Kety & Ingraham, 1992, p. 249.

[←445]

Kety et al., 1994, p. 450.

[←446]

Kendler, K. S., & Diehl, S. R., (1993), The Genetics of Schizophrenia: A Current, Genetic-Epidemiologic Perspective, Schizophrenia Bulletin, 19, 261-285, p. 265.

[←447]

Kety, S. S., (1983c), “Observations on Genetic and Environmental Influences in the Etiology of Mental Disorder from Studies on Adoptees and their Relatives,” in S. Kety et al., (Eds.), Genetics of Neurological and Psychiatric Disorders (pp. 105-114), New York: Raven Press, p. 109.

[←448]

Kety et al., 1994, p. 446.

[←449]

For more on the reduction of the Provincial Study control group, see Joseph, 2004, pp. 243-245.

[←450]

Kendler et al., 1994, p. 459, Table 2.

[←451]

Kendler et al., 1994, p. 460, Table 3.

[←452]

Joseph, 2004, p. 243; Kety et al., 1994, p. 448.

[←453]

The family of chronic schizophrenia index adoptee “069.” See Kety et al., 1994, p. 448, Figure 1.

[←454]

Rosenthal, D., (1974a), “The Concept of Subschizophrenic Disorders,” in S. Mednick, et al., (Eds.), Genetics, Environment, & Psychopathology (pp. 167-176), New York: American Elsevier, p. 167. Rosenthal’s use of the term “Pandora’s box” in reference to creating the schizophrenia spectrum is taken directly from this publication.

[←455]

Bentall, 2009, p. 124.

[←456]

Mednick, S. A., & Hutchings, B., (1977), “Some Considerations in the Interpretation of the Danish Adoption Studies in Relation to Asocial Behavior,” in S. Mednick & K. Christiansen (Eds.), Biosocial Bases of Criminal Behavior (pp. 159-164), New York: Gardner Press, p. 160. See Joseph, 2004, Chapter 8 for a critical review of Mednick’s adoption studies of criminal and antisocial behavior.

[←457]

Clerget-Darpoux et al., (1986), Clinical Methods in Psychiatric Genetics, III, Environmental Stratification May Simulate a Genetic Effect in Adoption Studies, Acta Psychiatrica Scandinavica, 74, 305-311, p. 305.

[←458]

Bleuler, M, (1978), The Schizophrenic Disorders: Long-Term Patient and Family Disorders, New Haven, CT: Yale University Press, p. 473.

[←459]

Hansen, B. S., (1996), “Something Rotten in the State of Denmark: Eugenics and the Ascent of the Welfare State,” in G. Broberg & N. Roll-Hansen (Eds.), Eugenics and the Welfare State: Sterilization Policy in Denmark, Sweden, Norway, and Finland (pp. 9-76), East Lansing, MI: Michigan State University Press; Kemp, T., (1957), Genetic-Hygienic Experiences in Denmark in Recent Years, Eugenics Review, 49, 11-18.

[←460]

Hansen, 1996.

[←461]

Mother’s Aid Organization for Copenhagen, Copenhagen County and Frederiksborg County, Annual Report for 1946-47. Quoted in Mednick & Hutchings, 1977, p. 163.

[←462]

Häfner, H., & der Heiden, W., (1986), The Contribution of European Case Registers to Research on Schizophrenia, Schizophrenia Bulletin, 12, 26-51.

[←463]

Kemp, 1957.

[←464]

Mednick, S. A., (1996), “General Discussion III,” in G. Bock & J. Goode (Eds.), Genetics of Criminal and Antisocial Behavior (pp. 129-137), New York: John Wiley and Sons, p. 134.

[←465]

Kety et al., 1994.

[←466]

Lewontin et al., 1984, p. 223.

[←467]

Olson, C. P., (Ed.), (1920), Oregon Laws: Showing All the Laws of a General Nature in Force in the State of Oregon (Vol. 2), San Francisco: The Bancroft-Whitney Company. See also Joseph, 2004, pp. 204-212.

[←468]

Olson, 1920, p. 3176.

[←469]

Anonymous, (1925), Galton Society, Eugenical News, 10, 69-71, p. 71.

[←470]

Kitzhaber, J., (2002), Proclamation of Human Rights Day, and Apology for Oregon’s Forced Sterilization of Institutionalized Patients, December 3rd, 2002.

[←471]

Heston & Denny, 1968, p. 365.

[←472]

Popenoe, P., (1929, September), The Foster Child, Scientific Monthly, 29, 243-248.

[←473]

Kringlen, E., (1987), “Contributions of Genetic Studies on Schizophrenia,” in H. Häfner & W. Gattaz (Eds.), Search for the Causes of Schizophrenia (pp. 123-142), New York: Springer Verlag, pp. 132-133.

[←474]

Hemminki et al., (1997), Sterilization in Finland: From Eugenics to Contraception, Social Science and Medicine, 45, 1875-1884; Hietala, M., (1996), “From Race Hygiene to Sterilization: The Eugenics Movement in Finland,” in G. Broberg & N. Roll-Hansen (Eds.), Eugenics and the Welfare State (pp. 195-258), East Lansing, MI: Michigan State University Press.

[←475]

Tienari, Lahti, et al., (1987), “The Finnish Adoptive Family Study of Schizophrenia: Possible Joint Effects of Genetic Vulnerability and Family Interaction,” in K. Halweg & M. Goldstein (Eds.), Understanding Major Mental Disorder: The Contribution of Family Interaction Research (pp. 33-54), New York: Family Process Press, pp. 44-45.

[←476]

Broberg, G., & Tydén, M., (1996), “Eugenics in Sweden: Efficient Care,” in G. Broberg & N. Roll-Hansen (Eds.), Eugenics and the Welfare State (pp. 77-149), East Lansing, MI: Michigan State University Press.

[←477]

McClearn, G. E., (1964), “The Inheritance of Behavior,” in L. Postman (Ed.), Psychology in the Making (pp. 144-252), New York: Alfred A. Knopf, p. 204.

[←478]

Leo, J., & Joseph, J., (2002), Schizophrenia: Medical Students Are Taught It’s All in the Genes, But Are They Hearing the Whole Story?, Ethical Human Sciences and Services, 4, 17-30.

[←479]

Joseph, 2006, Chapter 10.

[←480]

Kaplan, H. I., & Sadock, B. J., (1996), Concise Textbook of Clinical Psychiatry (1^st ed.), Baltimore: Williams & Wilkins, p. 127.

[←481]

Kaplan, H. I., & Sadock, B. J., (2004), Concise Textbook of Clinical Psychiatry (2^nd ed.), Philadelphia: Lippincott, Williams & Wilkins, p. 139; Kaplan, H. I., & Sadock, B. J., (1998), Kaplan & Sadock’s Synopsis of Psychiatry: Behavioral Sciences/Clinical Psychiatry (8^th ed.), Baltimore: Williams & Wilkins, p. 465; Sadock, B. J., & Sadock, V. A., (2003), Kaplan & Sadock’s Synopsis of Psychiatry: Behavioral Sciences/Clinical Psychiatry (9^th ed.), Philadelphia: Lippincott, Williams & Wilkins, p. 482.

[←482]

Choudary, P. V., & Knowles, J. A., (2008), “Genetics,” in R. Hales et al. (Eds.), The American Psychiatric Publishing Textbook of Psychiatry (5^th ed.; pp. 191-243), Washington DC: American Psychiatric Publications, p. 210; Knowles, J. A., (2003), “Genetics,” in R. Hales et al. (Eds.), The American Psychiatric Publishing Textbook of Clinical Psychiatry (4^th ed.; pp. 3-65), Washington DC: American Psychiatric Publications, p. 20.

[←483]

Gottesman, I. I., & Shields, J., (1982), Schizophrenia: The Epigenetic Puzzle, New York: Cambridge University Press, pp. 123-126.

[←484]

See Joseph, 2004, 2006; Joseph & Leo, 2006; Joseph & Wetzel, 2013.

[←485]

Minzenberg et al., (2011), “Schizophrenia,” in R. E. Hales et al., (Eds.), Essentials of Psychiatry (3^rd ed.; pp. 111-150), Washington, DC: American Psychiatric Publishing, p. 126.

[←486]

Surgeon General, (1999), Mental Health: A Report of the Surgeon General, Chapter 4, p. 256. The two bipolar adoption studies cited in this report were Mendlewicz & Rainer, 1977, and Wender et al., 1986.

[←487]

Kety et al., 1994, p. 442.

[←488]

Egan, M. F., & Hyde, T. M., (2000), “Schizophrenia: Neurobiology,” in B. Sadock & V. Sadock (Eds.), Kaplan & Sadock’s Comprehensive Textbook of Psychiatry (7th ed., Vol. 1; pp. 1129-1147), Philadelphia: Lippincott, Williams, & Wilkins, p. 1130.

[←489]

Ridley, M., (2004), The Agile Gene: How Nature Turns on Nurture [Originally published as Nature via Nurture], New York: Perennial, pp. 105-106.

[←490]

Sadock, B. J., & Sadock, V. A., (2008), Concise Textbook of Clinical Psychiatry (3^rd ed.), Philadelphia: Lippincott, Williams & Wilkins, p. 158.

[←491]

Lyons et al., 1991, p. 125; Cardno, A. & McGuffin, P., (2003), “Quantitative Genetics,” in P. McGuffin et al. (Eds.), Psychiatric Genetics and Genomics (pp. 35-53), Oxford: Oxford University Press, p. 35; Maxmen, J. S., & Ward, N. G., (1995), Essential Psychopathology and Its Treatment (2^nd ed., revised for DSM-IV), New York: W. W. Norton, pp. 70-71; Owen, M. J., O’Donovan, M. C., & Gottesman, I. I., (2003), “Schizophrenia,” in P. McGuffin et al. (Eds.), Psychiatric Genetics and Genomics (pp. 247-266), Oxford: Oxford University Press, p. 249; Riley, B., Asherson, P., & McGuffin, P., (2003), “Genetics and Schizophrenia,” in S. Hirsch & D. Weinberger (Eds.), Schizophrenia (pp. 251-276), Malden, MA: Blackwell, p. 255; Sullivan, P. F., (2005), The Genetics of Schizophrenia, PLOS Medicine, July, 2(7), 0614-0618 (see Table 1 of this publication); Tsuang, M. T., & Vandermey, R., (1980), Genes and the Mind: Inheritance of Mental Illness, Oxford: Oxford University Press, p. 59.

[←492]

DeLisi, 2017, p. 95.

[←493]

Paris, J., (1999), Nature and Nurture in Psychiatry: A Predisposition-Stress Model of Mental Disorders, Washington, DC: American Psychiatric Press, p. 97.

[←494]

Kety et al., 1975, p. 158.

[←495]

Andreasen, 2001, p. 199.

[←496]

Lieberman & Ogas, 2016. See also Joseph, J., (2016b, March 21), Comments on Jeffrey Lieberman and Ogi Ogas’ Wall Street Journal Article on the Genetics of Psychiatric Disorders, [Web log post, Mad in America “The Gene Illusion”].

[←497]

Lieberman et al., (Eds.), (2006), The American Psychiatric Publishing Textbook of Schizophrenia, Washington, DC: American Psychiatric Publishing.

[←498]

Joseph, 2006, Chapter 7, pp., 125-127.

[←499]

Lieberman, J., & Ogas, O., (2015), Shrinks: The Untold Story of Psychiatry, New York, NY: Little Brown, p. 231.

[←500]

Kety et al., 1968, p. 356.

[←501]

See Joseph, J., (2000), Inaccuracy and Bias in Textbooks Reporting Psychiatric Research: The Case of the Schizophrenia Adoption Studies, Politics and the Life Sciences, 19, 89-99; Joseph, 2006, Chapter 5.

[←502]

Joseph, 2006, p. 113.

[←503]

Thomas Kuhn observed in his classic The Structure of Scientific Revolutions that textbooks and popular works can be “systematically misleading” when recording “the stable outcome of past [scientific] revolutions and thus display the bases of the current normal-scientific tradition.” Kuhn, T. S., (1996), The Structure of Scientific Revolutions (3^rd ed.), Chicago: The University of Chicago Press (originally published in 1962), p. 137.

[←504]

Gould, S. J., (1981), The Mismeasure of Man, New York: W. W. Norton, pp. 89, 102.

[←505]

Read J., & Dillon, J., (Eds.), (2013), Models of Madness (2nd ed.), London: Routledge.

[←506]

Read, Johnstone, & Taitimu, 2013, p. 205. See also Hill, 1983.

[←507]

Watson, J. D., (2005), “The Double Helix 50 Years Later: Implications for Psychiatry,” in N. Andreasen (Ed.), Research Advances in Genetics and Genomics: Implications for Psychiatry (pp. xi-xii), Washington, DC: American Psychiatric Publishing, p. xii.

[←508]

Kety, 1974, p. 961.

[←509]

For a list of previous APA Task Forces, see https://psychiatry.org/psychiatrists/search-directories-databases/library-and-archive/task-force-reports?_ga=1.213846679.2004961364.1483043075

[←510]

See Ioannidis, J. P. A., (2016a), Evidence-Based Medicine Has Been Hijacked: A Report to David Sackett, Journal of Clinical Epidemiology, 73, 82-86; Ioannidis, J., (2016b), The Mass Production of Redundant, Misleading, and Conflicted Systematic Reviews and Meta-Analyses, PLoS Medicine, 2, 696-701.

[←511]

Joseph, J., (1999), The Genetic Theory of Schizophrenia: A Critical Overview, Ethical Human Sciences and Services, 1, 119-145, p. 137.

[←512]

Tandon et al., (2008), Schizophrenia “Just the Facts”: What We Know in 2008, 2, Epidemiology and Etiology, Schizophrenia Research, 102, 1–18, p. 12.