In the AA sample, we did not find evidence that polygenic loading for problematic alcohol use was associated with the longitudinal course of HED or modified the effects of familial stressors on the longitudinal course of HED. These null effects likely reflect reduced statistical power due to smaller sample size and the limited predictive power of polygenic scores in African-like populations, stemming from the historic exclusion of diverse populations in genome-wide association studies.49 This highlights the need for well-powered genetic risk scores in diverse populations to advance research on genetic and familial influences on alcohol misuse trajectories and to ensure that gains from research are shared equitably across all groups. To address the issue of predictive power of polygenic scores in the AA sample, we conducted post hoc sensitivity analyses by using parental history of AUD to index genetic risk. Contrary to our expectation, parental history of AUD was also not associated with the longitudinal course of HED at a statistically significant level. We note that in the context of our high-risk sample, the majority of the AA sample had
