The current analyses assessed the impact of parental EB on young adult AUD as a function of timing and accumulation of exposure. We found that any exposure to parental EB increased risk of young adult AUD, but there was no evidence that any of the time periods examined represented a particularly sensitive period: all were similarly pathogenic. We further found that cumulative exposure to parental EB in the form of sustained exposure across multiple developmental periods significantly increased AUD risk. However, while having two affected parents conferred greater risk than having a single affected parent, the effect of the second parent was lower than that of the first. These findings suggest that parental EB acts as a risk factor for offspring AUD regardless of the stage of social and cognitive development of the child during the period of exposure. The effects of sustained exposure may be indexing parental EB severity, which could increase risk via both biological (genetic) and environmental mechanisms.
