The results in our article and the Grant and colleagues (2009) study have both pragmatic and theoretical implications. Practically, our results suggest that for both genetic epidemiologic and molecular genetic investigations into alcohol use disorders, it would be feasible to closely index the genetic risk for AD by collecting relatively simple quantitative data on the frequency and quantity of AC during periods of maximum drinking. Such information can be collected quickly and potentially by self-report questionnaire (although in our study these measures were obtained at personal interview). Furthermore, these measures would yield a quantitative phenotype that may be more informative and provide greater statistical power than the dichotomous diagnosis of AD or even the semi-continuous scale of number of AD criteria. Whether measures of AC would be judged to have sufficient face validity to replace traditional measures of AD is another question that cannot be addressed by this research design. Furthermore, it is clear from our results (depicted in Figs. 2 and 3) that genetic influences on AC include factors unrelated to AD. While measures for AC may capture most
