COGA has tested the extent to which PGS index some of these familial environmental pathways of risk and resilience. Analyzing the extent to which aggregate genetic risk from a PGS contributes to trait variance in a family‐based study necessitates distinctions between PGS and measures of family history, as the latter are also indices of aggregate and latent genetic liability and family environmental influences. COGA's family‐based design has been instrumental in showing that PGS and family history independently contribute to the genetics of AUD, with PGS providing further risk resolution within family history positive persons, 121 a finding that has since been mirrored for other noncommunicable diseases in other cohorts (e.g., Reference [122]). Furthermore, COGA's refined family density measures, which quantify family history across the many first‐ and second‐degree relatives within the pedigree, have been found to be better predictors of AUD and correlates (including EEG data) compared to other, less refined FH measures. 123 COGA's densely affected pedigrees have shown that family history represents an amalgam of genetic liability, such as that indexed by a PGS, as well as familial environment, cultural transmission, genetic nurture and gene–environment correlation. 124 , 125 , 126
