To exclude age effects as possible confounders, we calculated a simple regression (V3″ over age) in each group (alcoholic patients and control subjects) and an analysis of covariance, with diagnosis being the only categorical factor: in all investigated ROIs, the slope of the regression line did not differ significantly from zero. Age effects estimated with analysis of covariance were negligible (age-associated loss of V3″ in the ventral striatum, −0.015 per decade). In the striatal ROI (average of left and right), V3″ did not differ significantly between alcoholic patients with a family history positive (n = 10, 2.67 ± 0.46) or negative (n = 10, 2.66 ± 0.31, t = 0.06, descriptive P = .95) for alcoholism, with early (type 2, n = 7, 2.76 ± 0.39) vs late (type 1, n = 13) age of onset of alcoholism (2.62 ± 0.38, t = 0.76, descriptive P = .46), or who were nonsmoking (n = 5, 2.57 ± 0.25) or smoking (n = 15, 2.70 ± 0.41, t = 0.67, descriptive P = .51). All (alcoholic and nonalcoholic) smokers (n = 16, 2.65 ± 0.45) did not differ significantly from nonsmokers (n = 13, 2.37 ± 0.41, t = 1.72, descriptive P = .10); the number of cigarettes smoked per day was only weakly correlated with the V3″ in the ventral striatum (r = 0.21, descriptive P = .32). Among the 20 alcoholic patients, the V3″ in the ventral striatum was only weakly correlated with the number of cigarettes smoked (r = −0.13, descriptive P = .65), age of onset (r = −0.34, P = .19), the severity of alcohol dependence (Severity of Alcohol Dependence Questionnaire score: r = 0.22, descriptive P = .40), or the severity of liver dysfunction (eg, γ-glutamyltranspeptidase: r = 0.18, descriptive P = .51).