superior (Davies et al., 1997; Vandeleur et al., 2008), thereby ensuring reliability of our findings. Third, the density measures accounted for two variations in the inclusion of affected family members—in one variation, primary and secondary non-descendants were included and in another, the entire extended family (all available relatives) was included. This allowed for encapsulating more familial information and allowed for testing if the predictive validity of FH increased/decreased when considering all available versus only the first- and second-degree relatives. The findings suggest that inclusion of all relatives does not improve the predictive value of the FH measure. Indeed, the density measure–FHDrPSND–AUDMaxSxCnt–based on primary and secondary non-descendants emerged as most consistently robust across alcohol outcomes and social groups. Fourth, contrary to existing studies (Stoltenberg et al., 1998; Milne et al., 2013) that have compared associations of different FH measures with alcohol and substance use symptoms and diagnoses (e.g., alcohol dependence), we examined associations of FH measures with important risk factors for the development of AUD. Importantly, ample evidence shows that age of onset of regular drinking is associated with increased alcohol problems during adult life and that parietal P3 amplitude is a biomarker for AUD-risk. Given that FH is an index
