transformations to our phenotypes, despite right-skew and zero-inflation in the distribution of adolescent alcohol use. This allows for intuitive interpretation of effect sizes in units of drinking days per year, but may have impacted results. Analysis with log transformed phenotypes (ln(phenotype+1)) produced negative heritability estimates in early adulthood (H2SNP =−0.0041 SE=0.0452), preventing complete assessment of this approach. The genetic correlations between the transformed and untransformed versions of adolescence (rG=1.00, SE=.21) and adulthood (rG=.96, SE=.16) suggest that the pattern of results would be similar with log transformed phenotypes. The genetic correlation between log transformed adolescence and log transformed adulthood was small and positive with a large standard error (rG=.14, SE=.71), suggesting that we do not have adequate power to determine the direction of this association. Fifth, our power analysis was not constructed to account for the phenotypic distribution of our data, instead focusing on the genetic correlations between phenotypes. Accuracy of our power estimates may vary as a function of phenotype distribution. Finally, these analyses model age as a series of ordinal developmental periods (adolescence age 12-17, early adulthood age 18-25, adulthood age 26+), rather than a continuum. This approach is not sensitive to differences in genetic liabilities that may exist
