The idea that genetic or biological predispositions are likely to interact with environmental factors to contribute to psychiatric and substance use disorders has been entertained for quite some time (Whytt, 1765). Long before it was feasible and cost-efficient to measure specific genes, twin studies documented that the importance of overall genetic influences (i.e., heritability) could vary considerably as a function of measured environmental factors (K. S. Kendler & Eaves, 1986). For instance, Kendler and colleagues found that people at highest genetic risk for depression (i.e., individuals with an identical twin with a history of depression) were significantly more likely than individuals not carrying a genetic predisposition to have an onset of the disorder in the presence of exposure to a severe stressful life event, suggesting that genetic factors influence the risk for major depression in part by altering individual sensitivity to the depression-inducing effects of stressful life events (K. S. Kendler et al., 1995). With methodological advances that allowed twin researchers to model how genetic influences change as a function of the environment (Button et al., 2009), studying gene-environment interaction
