Finally, we evaluated polygenic scores in Add Health and COGA [14]. The PGS for ALCP-specific were almost exclusively related to alcohol phenotypes, indicating that the model successfully differentiates shared and specific risk. While there were differences in the magnitudes in effect sizes across COGA and Add Health, which could reflect differences in how the samples were ascertained (nationally representative sample vs clinically ascertained), the overall patterns were similar. In longitudinal models, EXT was associated with higher mean-levels of AUI while ALCP-specific was associated with increased growth in AUI. Notably, these results illustrate that externalizing genetic risk is associated with differences in AUI early in development. In contrast, during emerging adulthood, when alcohol use becomes legal and more readily accessible, there is further differentiation by alcohol-specific genetic risk. Therefore, alcohol-specific risk does not lead to alcohol problems without exposure to drinking, while broader externalizing risk captures propensity to drinking exposure across the life course. This longitudinal model reiterates the developmentally contextual nature of risk [13, 14]. Overall, the PGS results support the notion of a shared externalizing risk pathway and an alcohol-specific risk pathway.
