for alcohol problems. This suggests that individuals with a higher genetic loading may need only minimal familial stress to experience an increased risk for alcohol problems. In contrast, individuals with a lower genetic loading may need higher levels of familial stress to develop alcohol problems. This pattern of effects is consistent with the additive model of gene-environment interaction diathesis-stress perspective (Karg & Sen, 2011; Monroe & Simons, 1991). Although prior studies of gene-environment interactions have typically focused on multiplicative gene-environment interactions (Nederhof et al., 2012; Thompson et al., 2008; Waldron et al., 2014), our findings highlight the importance of also considering additive gene-environment interactive effects. This is especially true from a public health perspective, as our findings indicate that the relative risk of developing AUD increases as a function of both children’s polygenic predispositions, as well as their exposure to familial stressors.
