Finally, this study does not provide insight into the psychophysiological mechanisms underlying P3AR. P300 amplitude has been proposed as an index of the neuroelectrical activity underlying “context updating” (Donchin, 1981), but it is unclear how a specific deficit in context updating translates to risk for AAU. This may not be correct level of analysis needed to relate P300 amplitude to AAU. Polich (2007) hypothesized that P300 amplitude indexes neuronal inhibition associated with attention allocation and memory updating, a function attributed to working memory. No study to our knowledge has examined whether working memory deficits mediate the association between P300 amplitude and risk for AAU. Others have proposed that P3AR reflects a disinhibitory process in the brain associated with excess central nervous system excitability that is alleviated by the ingestion of alcohol (Begleiter & Porjesz, 1999). Although behavior genetic research has the potential to provide leads regarding the underpinnings of P3AR, additional research is required to characterize the specific (or global) psychophysiological deficits associated with reduced P300 amplitude, and why these deficits relate to AAU.
