college attendance, suggesting that our findings were not driven by individuals’ college student status. Next, we reran our analyses controlling for gene-by-covariate and covariate-by-environment interactions to address any concerns that our gene-by-environment effects were confounded (Keller, 2014). When controlling for these interaction terms, we found a pattern of results that was consistent with those observed in the primary polygenic risk score analyses. Finally, after controlling for family ascertainment status, we observed the same pattern of effects as in our primary polygenic risk score analyses. This suggests that group-level differences between the clinically ascertained and unascertained community comparison families did not influence our results.
