According to the non-causal/common vulnerability hypothesis, age at 1st drink and subsequent AD symptomatology are both influenced by overlapping genetic and environmental factors. These factors may predispose individuals to initiation of alcohol use at a young age and to later development of AD symptomatology (and potentially, to a host of other problem behaviors) (Jessor, 1987; Jessor and Jessor, 1977; Kendler et al., 2003; Krueger et al., 2002; McGue et al., 2006; McGue and Iacono, 2005; Young et al., 2006). If there was evidence for the common vulnerability hypothesis, we would, first, identify significant correlations between the genetic and environmental influences on age at 1st drink and AD symptoms and, second, after accounting for these shared predispositions, there would be no additional relationship between age at 1st drink and AD symptoms. As shown in our study (and in prior work by Prescott & Kendler (1999)), there is considerable evidence for this. Particularly in our study, we found that significant proportions of the genetic influences on age at 1st drink and AD symptoms were shared, particularly in men. Work by Sartor and
