Furthermore, previous studies have shown that alcohol exposure, genetic risk for alcoholism, and comorbid psychopathology may contribute independently to the P3b reduction seen in treatment-seeking populations (Hill et al., 1999a; Perlman et al., 2009). In treatment-naïve AUD samples such as the one studied here, levels of genetic risk for alcoholism and subdiagnostic psychopathology were probably lower than those in treatment-seeking AUD samples used elsewhere (Di Sclafani et al., 2008). Our eligibility criteria specified that those with diagnosable psychopathology were excluded from participation; hence, only those with subdiagnostic symptom counts were eligible, and the ceiling for comorbid psychopathology was set very low. As it turned out, most of our participants had no subdiagnostic psychopathology. Similarly, although we did not empirically evaluate genetic risk for alcoholism, our assessment of family history density of alcohol problems suggested that most had no known family history density of alcohol problems, and so again the ceiling for genetic risk for alcoholism was likely low.
