There is now overwhelming evidence suggesting that heritable influences play a substantial role in AD diagnoses and symptomatology (Heath, 2007; Kendler et al., 1992; McGue, 1999; Prescott et al., 1994). Additionally, there is support for familial influences on age at 1st drink (McGue et al., 2001a) and, as described above, there appears to be considerable genetic overlap between age at 1st drink and AD (Grant et al., 2005; Prescott and Kendler, 1999). However, age at 1st alcohol use can also be viewed as an environmental measure. In fact, neither Prescott and Kendler (1999) nor Grant et al. (2005) could unequivocally rule out the environmental impact of age at 1st (or regular) drink on AD. If early exposure to alcoholic beverages is an environmental measure, then it can be related to the highly heritable AD phenotypes (i.e., diagnosis and symptomatology) in multiple ways. First, its relationship with AD may be viewed in the context of unmeasured gene-measured environment correlation (or rGE) where the same latent/unmeasured genetic factors that induce individual differences in AD phenotypes also increase the likelihood of exposure to
