In all models, paternal history of DD/AD was predictive of increased risk for all alcohol outcomes. Risk associated with paternal DD/AD was modest for age at first use and transition from first use to AD symptom (a 19–29% increased hazard). A much stronger effect of paternal history was observed for the transition from first use to AD diagnosis (a 58–62% increased hazard), consistent with findings by Jacob et al. (2003) and Sartor et al. (2007). Additionally, there was some evidence of genetic influence on the transition to AD diagnosis: risk among offspring with an affected MZ uncle was increased, with effect sizes (HR range: 1.54–1.79) comparable to those observed for offspring of affected fathers. In contrast, offspring with an affected DZ uncle were comparable to control offspring in their risk of developing AD (HR range: 0.92 – 1.04), with one exception (for age at first use, the offspring with an AD DZ uncle had a 36% increased hazard, which was greater than those with a DD DZ uncle and the control offspring). There was little evidence that mother’s AD or heavy cannabis use provided additional predictive utility above and beyond father’s DD/AD history. (see Supplemental Tables 1–3)
