et al 2011; Bidaut-Russell et al 1994) or on either affected mothers or fathers (Chassin et al 1993; Lieb et al 2002), evidence suggested relationships of maternal AUD with offspring AUD involvement, but often was not definitive owing to small numbers of affected mothers. Our data provided evidence for influences of maternal-only (versus paternal-only) AUD across early and late AUD transitions, with estimated hazard ratios for maternal-only AUD that were similar in magnitude to those for 2 AUD parents. Our findings contrast with a report where maternal AUD influences were limited to initiation (Sartor et al., 2007). Potential explanations for our results are that maternal AUD may reflect a higher genetic loading, or may be linked to greater disruption in the offspring's rearing environment, thus contributing as both a genetic and an environmental risk factor, lines of inquiry that can be investigated in future analyses. We did not observe gender interactions with parental AUD, unlike others who have reported that mothers’ AUD may be particularly influential for their daughters’ substance involvement (Bohman et al 1983). We did not consider either severity or persistence of AUD, which might have altered our results, nor did we consider outcomes other than alcohol involvement,
