GxE studies of specific environments and genetic markers focus on exposure to stress, either as stressful life events or traumatic stress exposure (Dick & Kendler, 2012b). Stressful environmental exposures during childhood increase risk for alcohol dependence. The hypothalamic-pituitary-adrenal (HPA) axis increases glucocorticoid and cortisol production in order to maintain biological homeostasis during exposure to stress, and it is thought that exposure to early stressors has a long-lasting impact on development via the mesolimbic dopamine pathway (Enoch, 2012). Consequently, GxE studies testing the role of specific genetic influences have focused on the evaluation of genes whose products modulate HPA function in response to stressful environments; e.g., CRHR1 (Blomeyer et al., 2008; Ducci et al., 2008b; Nelson et al., 2010; Ray et al., 2013) or with genes possessing a glucocorticoid response element in their promoter regions, (i.e., MAOA, COMT, and SLC6A4; Ducci et al., 2008a; Enoch, 2013). For example, the short allele of the polymorphic promoter region of the serotonin transporter gene (5-HTTLPR) was associated with more frequent drinking as well as heavy drinking and drug use in college students if they
