Genetic influences on SUDs can operate via both shared genetic risk with other forms of externalizing as well as via substance specific pathways. Conventional analyses focused on a single phenotype, what we would term the “classical” GWAS approach, are unable to differentiate these pathways; newer multivariate approaches begin to make this possible. In the current analysis, we demonstrated the potential of disaggregating genetic variance in problematic alcohol use into risk shared with other externalizing behaviors/disorders versus risk that is specific to problematic alcohol use. We demonstrate that multivariate genomic analyses of correlated traits can increase the specificity for characterizing how genetic risk unfolds.
