Chapter 3
“When Florida guard Canyon Barry began shooting free throws underhanded as a junior in high school, he knew he was inviting ridicule. His father, the basketball Hall of Famer Rick Barry, had perfected the form in the 1960s and 1970s…Still, despite his father’s success, and his years advocating the style, the technique dismissively known as ‘Granny style’ had all but disappeared. Canyon Barry knew all this when he made the switch. He knew the mockery he could expect….Barry took the ribbing in stride. In fact, he said, it motivated him to polish his technique, to prove that what his father had been preaching for so long actually worked.”
—February 8th, 2017 New York Times article on similar, yet unusual, father and son basketball free throw shooting styles125
If schizophrenia is a genetically transmitted disorder, it must be found in elevated numbers among the biological relatives of people carrying the diagnosis. To determine this, researchers first studied individual families and constructed pedigree charts, and then developed the family study method. This method identifies a group of people diagnosed with schizophrenia, and then determines whether their biological relatives are diagnosed at a significantly higher level versus the biological relatives of a control group, or versus the general population expectation. If a condition is found to cluster or “run” in families, the condition is familial. This is seen in the more methodologically sound schizophrenia family studies, where the first-degree biological relatives of people diagnosed with schizophrenia are diagnosed on average four times more often than the 1% rate in the general population.126
An example of a modern schizophrenia family study is a 1985 investigation by Kendler and his colleagues, who assessed the risk for psychiatric disorders among the 723 first-degree relatives of people diagnosed with schizophrenia at an Iowa psychiatric hospital, versus the risk among the 1,056 first-degree relatives of non-diagnosed matched surgical control patients. The researchers diagnosed patients and relatives blindly, using DSM-III criteria. They obtained information on relatives from personal interviews and/or hospital records. Kendler and colleagues calculated a schizophrenia “morbid risk” percentage (see below) that was significantly greater in the relatives of people diagnosed with schizophrenia (3.7%), versus the relatives of controls (0.2%). They concluded that this difference “provides strong evidence that schizophrenia, as defined by DSM-III, is a familial disorder.” 127
“Runs in the Family” ≠ Genetic
The key point, however, grudgingly acknowledged by the psychiatric genetics field over the decades, is that “familial” does not equal “genetic.” In reference to the story leading off this chapter, does Canyon Barry shoot free throws underhanded because he is genetically predisposed to do so, or because he learned this seldom-used technique from his father, and wanted to prove his father right?
In the same way, psychiatric disorders, medical conditions, and behavioral characteristics can run in families due solely to environmental factors such as exposure to common rearing patterns and abuse, trauma, learned behavior, diet, common exposure to pathogens, and many other aspects of the physical, social, and family environment. As a leading group of contemporary psychiatric genetic researchers recognized, “It is critical to understand…that familiality does not establish heritability. For example, religion and language are familial traits, as often all members of the same family practice the same religion and speak the same language. These facts are due not to the transmission of ‘religion genes’ or ‘language genes’ through the family, but rather to the common environment and upbringing that those family members share.”128 Plomin and colleagues also understood that while “many behaviors ‘run in families,’” this “family resemblance can be due to either nature or nurture.” This led them to conclude, correctly, that “family studies by themselves cannot disentangle genetic and environmental influences.”129
Most genetic researchers and their critics, therefore, are in agreement that potential genetic and environmental influences cannot be disentangled (separated) in a family study. This did not, however, prevent the author of a 2016 CNN report on schizophrenia and genetics from writing, “Importantly, schizophrenia often runs in families, so scientists have long believed it is a genetic disorder.”130 And yet, although modern researchers point to other types of evidence in support of genetic theories, this hasn’t always been the case.
Ernst Rüdin and the “Munich School” of Psychiatric Genetics
The first systematic schizophrenia family study was published in 1916 by Ernst Rüdin, the Swiss-German “father” of the psychiatric genetics field and co-founder of the German “racial hygiene” movement, and more than two dozen have been published since.131 Most of the earlier studies were carried out by strong supporters of the genetic position who did not diagnose/label blindly or use a control group, and who frequently diagnosed or labelled someone with schizophrenia on the basis of vague and differing definitions of schizophrenia, sometimes based on hearsay or sketchy information about unavailable or deceased relatives.
A major product of Rüdin’s founding “Munich School” of psychiatric genetics was the “empirical genetic prognosis” (empirische Erbprognose), which involved calculating the age-corrected probability that (presumably hereditary) psychiatric disorders would eventually appear in the biological relatives and descendants of people diagnosed with these disorders. These calculations, which were based mainly on family studies, produced “morbid risk” (MR) percentage figures for various groups of relatives biologically related to the diagnosed “proband.” (Proband is the psychiatric genetic term for a study’s first-identified relative.) In his 1916 investigation, Rüdin studied 2,732 siblings of 755 schizophrenia (dementia praecox) patients, and calculated narrowly and broadly defined MRs of 5.4% and 7.7% respectively.132 Rüdin’s colleagues and others subsequently confirmed that the age-corrected schizophrenia risks among the relatives of schizophrenia patients were higher than the rate expected in the general population, but mistakenly assumed that these elevated rates were caused by hereditary factors.
Rüdin played a major role in creating and implementing the 1933 German “Law for the Prevention of Genetically Diseased Offspring” (Gesetz zur Verhütung erbkranken Nachwuchses). This law provided for the compulsory surgical sterilization of people diagnosed/labelled with schizophrenia, “manic-depressive insanity,” “feeble-mindedness,” and several non-psychiatric conditions. Approximately 400,000 Germans were forcibly sterilized under the law between 1934 and 1939, largely on the basis of being labeled “feeble-minded” or “schizophrenic.” Rüdin was one of three co-authors of a commentary summarizing the alleged scientific justification for the law.133 About 6,000 people died as a direct result of the surgical procedure.134
German psychiatric geneticists of the 1930s and 1940s strongly supported compulsory sterilization and other racial hygienic (eugenic) measures because they believed that societal and racial “degeneration” would eventually result without the implementation of such measures.135 In collaboration with his Munich colleagues Hans Luxenburger and Bruno Schulz, much of Rüdin’s Nazi era (1933-1945) work involved calculating psychiatric disorder morbidity risks in the service of the regime’s sterilization law and other racial hygienic measures.136 Hitler’s regime moved beyond compulsory eugenic sterilization in the late 1930s and instituted a secret plan to kill mental patients and others in a program named “T4,” euphemistically referred to by the authorities as “euthanasia.”137
Gundula Kösters and colleagues published a 2015 article on Rüdin’s 1920s-era family study of “manic-depressive insanity” (now called bipolar disorder)—a study that Rüdin never published.138 They described Rüdin’s unpublished manic-depression family study as consisting of “approximately 160 pages of unbound typescript, each chapter paginated separately, with Rüdin’s hand-written corrections, and numerous large-format, hand-written charts.” The study was referenced in a 1936 article by the Munich-trained British psychiatric genetic twin researcher Eliot Slater, who wrote that “the investigations of Rüdin have never been published, and [therefore] cannot be criticized.”139
Rüdin’s manic-depression sample consisted of 661 German probands from 650 families, and included 4,351 siblings in total. In 566 families both parents were “healthy,” and in 84 families one parent had an affective disorder. Rüdin compared the morbid risks he calculated in these families against “the proportions expected from a Mendelian crossing in order to prove Mendelian inheritance and thereby the inheritance of affective disorders.”140 Kösters and colleagues concluded that Rüdin decided against publishing this study because the results did not fit his theories of single-gene Mendelian inheritance or his advocacy of eugenic policies.141
Kallmann’s Study
A major early schizophrenia family study was the massive 1938 investigation of 1,087 German schizophrenia patients and their 13,851 relatives. It was performed by Rüdin’s psychiatric genetic colleague Franz Kallmann, who claimed that his results provided “conclusive proof of the inheritance of schizophrenia.”142 This study was published in English after Kallmann immigrated to the United States in 1936—a country where many states had already passed laws (some well before 1933) permitting the compulsory eugenic sterilization of people labelled “insane” or “schizophrenic.”143 Kallmann called for directing eugenic measures not only at people diagnosed/labelled with schizophrenia, but at their non-diagnosed “heterozygotic taint-carrier” biological relatives as well.144 For Kallmann, these relatives were “eugenically undesirable” people whose numbers should be “kept at the lowest possible number” by sterilization and other means.145 Like Rüdin, Luxenburger, Schulz and others, Kallmann believed that the reproduction of “schizophrenics” posed a danger to society. A founder of American psychiatric genetics,146 Kallmann played a major role in bringing the Munich School message to the English-speaking world. As an admiring American colleague wrote of his work, “Out of Rüdin’s laboratory came Kallmann and many of the other workers who developed psychiatric genetics and introduced it internationally.”147 Upon arriving in the United States, Kallmann wrote in a 1938 edition of Eugenical News:
“From a eugenic point of view, it is particularly disastrous that these [schizophrenia] patients not only continue to crowd mental hospitals all over the world, but also afford, to society as a whole, an unceasing source of maladjusted cranks, asocial eccentrics and the lowest types of criminal offenders. Even the faithful believer in the predominance of individual liberty will admit that mankind would be much happier without those numerous adventurers, fanatics, and pseudo-saviors of the world who are found again and again to come from the schizophrenic genotype.”148
Because Kallmann viewed his “schizophrenia probands” and their relatives as the dangerous carriers of the “hereditary taint of schizophrenia,” and because he did not diagnose/label people blindly, his objectivity has been called into question by several authors. Amazingly, Kallmann failed to adequately describe how he defined “schizophrenia” in his 1938 family study. In addition, as Boyle has argued, some people labelled with schizophrenia in the early European studies may actually have suffered from the viral infection encephalitis lethargica.149
Conclusion
Similar to the above-mentioned Kendler study, several schizophrenia family studies published after 1980 used control groups, and made diagnoses blindly on the basis of structured interviews. Most found lower first-degree relative rates than the older studies, and at least three studies found no significant difference between the first-degree relatives of people diagnosed with schizophrenia versus the expected population rate, or versus the rate among the first-degree relatives of controls.150
Because it is now widely understood that the results of family studies can be explained entirely by non-genetic (environmental) factors, authoritative genetic researchers and textbook authors usually cite twin studies and adoption studies in support of genetic theories of schizophrenia. While conceding that genetic interpretations of family study results are confounded by environmental factors, they argue that genetic interpretations of twin study and adoption study results, for the most part, are not. In the next two chapters I will attempt to show that, in addition to major methodological issues and biases, twin studies and adoption studies are also subject to major environmental confounds. This calls into question psychiatry’s claim that these studies show convincingly that genetic factors strongly influence schizophrenia and other psychiatric disorders.