Results from mean level prediction analyses demonstrated that all four PGSs harbor genetic variants relevant to AUBs, but the growth model results indicated that these may not be the same genes shaping dynamic changes in drinking. Some evidence suggests that, despite the relatively high heritability of AUBs, the genetic influences on trajectories of heavy (episodic) drinking are quite low (17). If so, this may reflect genetic equifinality – high genetic risk leads to high AUB manifestation at some point in life, although the specific timing is shaped by the environment or stochastic effects. Other studies, however, have demonstrated that the heritability of latent growth factors for alcohol frequency and quantity is similar to that of cross-sectional measures of AUBs, ~30–50% (39, 48). Further research is needed to resolve this question, and it may be necessary to incorporate longitudinal phenotypes into gene discovery efforts to determine whether the same (or any) genes are associated with dynamic versus static AUB measures (49). The continued low variance in mean AUB levels explained by PGSs suggests that other avenues are worth pursuing in an
