Studies of families, adoptees, and twins have been widely used to attempt to understand the relative contributions of genetic and environmental effects upon risk for schizophrenia. These “old genetics” approaches use phenotypic resemblance of relatives as an indirect means by which to infer the roles of genes and environment. There are many important assumptions and methodological issues with these studies [8]; however, genetic epidemiological studies of schizophrenia have yielded a remarkably consistent set of findings, as summarized in Table 1 [9, 10].
To summarize this literature briefly, schizophrenia is familial, or “runs” in families. Both adoption and twin studies indicate that the familiality of schizophrenia is due mainly to genetic effects. Twin studies suggest the relevance of small but significant shared environmental influences that are likely prenatal in origin. Thus, schizophrenia is best viewed as a complex trait resulting from both genetic and environmental etiological influences. These results are only broadly informative, as they provide no information about the location of the genes or the identity of the environmental factors that predispose or protect against schizophrenia. Searching for genetic influences that mediate vulnerability to schizophrenia is rational, given the larger overall effect size and lesser error of measurement in comparison to typical assessments of environmental effects. Note that high heritability is no guarantee of success in efforts to identify candidate genes.
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