It’s unclear how to interpret this result in terms of the context presented in the introduction (i.e., whether reduced P3b amplitude primarily reflects an endophenotypic marker for alcoholism and/or is a result of chronic alcohol abuse). We did not observe an association of P3b amplitude with the family history density of alcoholism or with alcohol use measures within TNAD; however, the much lower family history density in TNAD vs. LTAA, and the lower levels of alcohol use in TNAD vs. LTAA, are both associated with a much smaller decrease in P3b in TNAD vs. LTAA. The lower family history density in TNAD together with their having less of a reduction in P3b is consistent with family history density being an important determinant of the P3b reduction in alcoholics. The current study is consistent with the findings of an early COGA (Consortium on the Genetics of Alcoholism) study that compared P3 amplitudes in alcoholics (and their families) from a community sample with the P3s obtained from members of densely affected families ascertained through probands in treatment (Porjesz et al., 1998). In
