The impact of stress on genetic risk for SUDs has not been as widely studied in the twin literature as mechanisms related to social control and opportunity; however, one study found that genetic influences on a composite of externalizing disorders (including substance use problems) increase as stressful life events increase22, an effect we have also found in adolescent Finnish twins (D.D. et al., unpublished data). This presumably would fall under a social triggering mechanism; however, the underlying mechanism for stress triggering a genetic predisposition toward alcohol use seems likely to be etiologically different than, for example, peer substance use triggering adolescent substance use. Further delineation of these risk pathways is clearly needed, and more work on the genetic epidemiology of the relationship between stress or adversity and genetic influences on substance use disorders is warranted. This seems especially relevant because most of the human studies testing for gene-environment interaction with specific risk genes in the area of substance use have focused on stress23–25, most having small sample sizes and thus far yielding mixed results. Greater integration of the literature on gene-environment interactions emerging from twin studies and tests of measured gene by environment interaction would benefit the field.
