Genetic modeling revealed that just under half of the variance in AD symptoms and over 60% of variance in the other three phenotypes could be accounted for by heritable sources of influence. Our estimated heritability of 46.8% for AD symptoms is slightly lower but within the expected range for dependence symptomatology; the majority of studies in this area have examined AD as a dichotomous outcome, producing heritability estimates of 50-60% (Heath et al., 1997; Knopik et al., 2004; Reed et al., 1996; True et al., 1996; van den Bree et al., 1998). Far fewer genetically-informative investigations have focused on heaviness of alcohol consumption and results have varied widely. Compared with the few published studies, our results fall at the high end of the range (Heath et al., 1991; King et al., 2005; Whitfield et al., 2004). By contrast, our findings for cannabis use and dependence symptoms closely match those from prior studies, which have estimated heritability at 45-85%, with little distinction between estimates for use and dependence phenotypes (Agrawal and Lynskey, 2006; Kendler et al., 2000; Kendler and Prescott, 1998;
