beyond those shared with these other externalizing disorders.18 In view of this, gene identification efforts for AAB are likely to be more successful in more severely affected samples or in samples where participants high in AAB also tend to have comorbid alcohol or substance-use disorders, such as the COGA sample. In contrast, for example, only 6% of the participants in the Tielbeek et al.13 community-based sample met their non-diagnostic AAB case criteria. This sample may also have had low rates of comorbid alcohol and other drug diagnoses, limiting the ability to find genome-wide significant effects. Second, we used a dimensional measure of AAB, which is more powerful than a binary diagnostic variable, and better represents the underlying dimensional structure of AAB.53 These differences may explain, in part, why we were able to detect a significant genetic association in the present sample.
