Moderation of the heritable component in individual differences in AD symptoms by age at 1st drink represents a G x E interaction. If earlier age at 1st drink is assumed to be representative of higher environmental risk, then our finding of increasing heritability with increasing environmental risk is consistent with prior studies which have shown that genetic influences on alcoholism risk tend to be manifest in the absence of protective environmental influences. For instance, Heath et al (Heath et al., 1989) found the heritability of alcohol consumption to be significantly higher in unmarried vs. married women and Koopmans and colleagues (Koopmans et al., 1999) found higher heritability of alcohol initiation in those with a non-religious upbringing. Our study suggests that, likewise, later age at 1st drink may serve to buffer against a genetic predisposition to AD symptoms. This finding has considerable implications. From a public health perspective, delaying the initiation of drinking in adolescents may dampen the influence of inherited and familial predisposition to AD, even though some of these predispositions are overlapping with the timing of 1st drink. Future
