distribution, and it is thought to be associated with redirection of attention monitoring (Polich, 2007; Polich and Criado, 2006). Consistent with previous studies in chronic alcoholics (Hada et al., 2000;Rodriguez Holguin et al., 1999a), subjects with more severe drinking histories than our twin subjects, our results thus suggest that long-term neuronal effects of alcohol abuse are reflected by reduced amplitude of P3 to novel sounds. This result may seem to contradict a previous interpretation that novel P3 amplitude is a genetic marker of vulnerability to, rather than consequence of, alcohol abuse (Hada et al., 2001; Porjesz and Begleiter, 1997; Rodriguez Holguin et al., 1999b). It is, therefore, important to note that the clearest associations with genetic predisposition to alcoholism have been found in the visual modality, specifically associated with target P3s, instead of novelty detection (Polich et al., 1994). Our analyses also suggest, albeit tentatively, that genetic factors influence the association between adolescent alcohol abuse and diminished P3 to novel sounds. Stated differently, the detrimental neuronal effects reflected by the novel P3 diminution might be most severe in individuals with an inherited dispositional sensitivity to ethanol. At the same time, there are essential methodological differences between the above-mentioned studies (Hada
