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 genomic efforts targeted at identifying genes for AD symptomatology may also wish to consider their findings in the context of age at 1st drink. First, our findings suggest that individuals with adult onset of drinking may not be genetically informative in the study of AD symptomatology as variation in their AD symptoms is largely non-genetic in origin. Second, gene expression for AD symptoms is maximal in those with earlier age at 1st drink. When power permits, this G x E interaction should be modeled as it may increase our ability to isolate genes for AD. Third, our study underscores the importance of genetic influences on a putative environmental measure. As reviewed by Kendler and Baker (Kendler and Baker, 2007), a majority of known environmental factors have been found to have a heritable component – and these genetic underpinnings, when shared with the outcome of interest, may represent gene-environment correlations (rGE) (Plomin et al., 1977; Rutter et al., 2006; Scarr and
