relatives manifest low P3 amplitude, particularly in multiplex AUD families compared to individuals with and without AUD from non-AUD families (Porjesz and Begleiter, 1996a; Porjesz et al., 1998; Begleiter et al., 1984; Berman et al., 1993; Hill and Steinhauer, 1993; Hill et al., 1999; Hesselbrock et al., 2001). 2) Reduced P3 is heritable and can be a familial risk. Indeed, evidence shows that P3 amplitude recorded during a visual oddball paradigm is directly related to the number of first-degree alcoholic relatives and not the drinking history of an alcoholic or high-risk individual (Pfefferbaum et al., 1991; Cohen et al., 1994; Benegal et al., 1995; Porjesz et al., 2005). Moreover, supporting the notion that P3 is heritable, twin studies have shown that identical twins manifest more similar P3 amplitudes than unrelated individuals, with a meta-heritability (via aggregating twin correlations across five studies) of 60% (Steinhauer et al., 1987; O’Connor et al., 1994; van Beijsterveldt and van Baal, 2002). Additionally, Carlson et al. (2004) have shown that P3 amplitude in nonalcoholic adolescent twin pairs who become discordant for AUD as adults also present reduced P3 amplitude, supporting the notion that this risk is familial. Further, Perlman, Johnson, and Iacono (2009) have showed
