It has become a cliché to say that individuals are predisposed to psychiatric illnesses by a gene × environment interaction, yet we cannot say with certainty which genes or environments account for illness risk. Although the 2 major psychiatric illnesses, schizophrenia and bipolar disorder, are familial (ie, they cluster within families), it has proven extremely difficult to dissect any clear genetic cause.1 Many potential reasons for this difficulty exist. One often cited is that the disorders are too heterogeneous because they are defined by symptom clusters, many of which overlap concurrently and longitudinally (ie, the phenotype problem). Although this factor likely contributes to the complexity of analysis, it is unlikely to be the major reason researchers are unable to find genetic loci because the diagnoses themselves are clearly familial and, therefore, affected individuals would be expected to share alleles. Another possible reason is that the clear familiality has led to an overestimate of the genetic, as opposed to the shared family environmental, risk. This could be a partial explanation because the precise quantification of genetic load is performed in twin and adoption studies, each of which has its own problems and biases.2 A third suggested reason for the lack of consistent observations is that to find and quantify the genetic risk loci, we need to factor in relevant environmental risk factors. This third approach is the topic of an article in this issue of the Archives.3
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