Some limitations of our study are noteworthy: First, our sample consisted of Caucasian young adult Australians. To the extent that heritability of age at 1st drink and AD symptomatology vary by race or ethnicity, our results may not extrapolate to populations with other demographic characteristics. Second, our results from secondary analyses examining the effect of age at 1st drink and models examining the moderation of common and specific genetic influences on AD symptoms (e.g. bivariate moderation) may have been somewhat limited by power. As a result, we restricted ourselves to only testing for moderation of genetic influences in our secondary analyses of bivariate moderation (i.e. C and E were modeled as unmoderated variables). The models for these analyses are fairly complex, and as a consequence, we also did not include the modeling of opposite sex pairs for these models. Finally, while the normality of the distribution of AD symptoms improved upon log-transformation, there was some skewness in the measure when conduct disorder was not regressed out. We reran our analyses with the raw log-transformed AD symptoms measure and while the overall findings of significant moderation remained unchanged, we view those results (not shown) with some caution.
