Both molecular and inferred genotype studies provide preliminary evidence that GxE differentially influence drinking over the course of development. Although the timing of age at first drink is largely influenced by environmental influences shared by siblings (Hopfer, Crowley, & Hewitt, 2003), genetic factors explain an increasingly greater proportion of individual differences in drinking as adolescents age (Bergen, Gardner, & Kendler, 2007; Rose & Dick, 2004). Some evidence using retrospective reports of adolescent environmental exposures indicates that alcohol-related GxE show stronger effects on drinking between ages 12–17, and more limited effects after age 17 (Kendler et al., in press). Likewise, studies of 5-HTTLPR genotype indicated that GxE effects were limited to adolescents and young adults, consistent with greater plasticity of genetic influences on drinking at earlier developmental stages (Table 4). Given evidence that early life stress can modulate the capacity to cope with later stress (e.g., by altering genetically influenced components of the HPA axis) and cause changes in the expression of genes that modulate the pleasurable effects of alcohol (Clarke et al., 2008; Enoch, 2011; Spanagel, 2009), it is possible
