limited (<0.30) genetic effects, particularly if the variance across the set of SNPs influencing each symptom is not constant. We have cautiously interpreted our study findings because of the limited power to detect modest SNP-heritability estimates and genetic correlations, especially in instances where the SNP-heritability of a pair of items was low and non-significant. As is the case with twin and family studies (Verhulst, 2017), cautious interpretation is warranted when estimating and interpreting genetic correlations between phenotypes when the magnitude of the genetic effect is limited. To aid in our interpretation of these data we modeled the raw genetic variance/covariance matrix to minimize bias. Similarly, we compared several multivariate factor models of the genetic covariance matrix and report bootstrapped confidence intervals of the loadings from the most parsimonious model. Altogether, when considering these factor, the pattern of results provide preliminary evidence to suggest that studying the shared liability across all of the DSM symptoms is a more genetically sensitive (i.e., evidencing a moderate heritability [0.30–0.60]) and parsimonious phenotype, since the loci likely reflects the lowest common denominator/factors for AUD.
