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 colleagues (in press), using dichotomous measures of early-onset drinking and DSM-IV AD in the same sample have found no evidence for sex differences but reported genetic overlap across the measures – differences across that study and the present may be attributable to our use of quantitative indices (and exclusion of the effects of conduct disorder). The public health implication of these common etiologic underpinnings is that initiatives targeted at increasing the age at 1st drink may not have a direct causal impact on reduced AD symptoms as individuals already bear the predisposing influences for AD symptoms. However, we do not find support for the second assumption of the correlated vulnerabilities model – in our study, even after controlling for shared predispositions, there continues to be a moderating influence of age at 1st drink on AD symptoms.
