The study of Monto et al. gives a sobering account of the effects of various amounts of alcohol intake on hepatitis C-related fibrosis. At issue is the compounding effect of alcohol and HCV and the practical concern of how much alcohol an HCV-infected patient can safely consume. The literature is replete with studies that uniformly show that high alcohol intake (ΟΎ50-80 g/day) greatly exacerbates fibrosis progression and cirrhosis development in patients with HCV infection. The net outcome has always been much more than additive. Few studies, however, have systematically examined the effects of lesser quantities of alcohol, and in those that have, the results have been conflicting. Monto et al. performed a careful estimation of lifetime alcohol intake and derived an average consumption in grams per day based on the calculation that one drink equals 10 grams of pure ethanol. The cohort was then divided into light (0-20 g/day), moderate (20-50 g/day) and heavy (ΟΎ50 g/day) consumption. The mean alcohol consumption in the cohort was 41.6 g/day, but it was not normally distributed so that the median was 17.4 g/d; 29% consumed ΟΎ50 g/day. Interestingly, alcohol intake did not correlate with the ALT or the inflammatory score on liver biopsy, suggesting that alcohol does not exert its fibrotic effects by enhancing inflammation. Alcohol intake was associated with a stepwise increase in mean fibrosis, and if alcohol use was dichotomized into Υ50g/day versus Ο½50 g/day, there was a significant difference (P Ο .01) between the groups. If dichotomized at Υ80 g/day, the difference was even greater ( P Ο .006), but no significant difference in fibrosis was found if dichotomization was performed at lower levels of intake. In a multivariate analysis, histologic inflammation, serum ALT, and patient age were independent predictors of fibrosis, but alcohol was not, though it was close (P Ο .06). Importantly, at every alcohol level, there was a broad range of fibrosis outcomes, and even among heavy drinkers, 47% had stage 0 or stage 1 fibrosis (Fig.). Just as in persons not infected with HCV, there appears to be a range of susceptibility to the fibrotic effects of alcohol.