[pronut-hiv] Coffee May Protect Against Alcoholic Cirrhosis

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Coffee May Protect Against Alcoholic Cirrhosis 

June 13, 2006 * Coffee may be protective of cirrhosis, particularly alcoholic cirrhosis, according to the results of a cohort study reported in the June 12 issue of the Archives of Internal Medicine.

"A minority of persons at risk develop liver cirrhosis, but knowledge of risk modulators is sparse," write Arthur L. Klatsky, MD, from the Kaiser Permanente Medical Care Program in Oakland, Calif, and colleagues. "Several reports suggest that coffee drinking is associated with lower cirrhosis risk."

In this study, 125,580 multiethnic members of a comprehensive prepaid healthcare plan who had no known liver disease supplied baseline data at voluntary health examinations from 1978 to 1985. Through 2001, 330 of these members were diagnosed as having liver cirrhosis, including 199 members with alcoholic cirrhosis and 131 subjects with nonalcoholic cirrhosis, confirmed by medical record review. The investigators used Cox proportional hazards models with 7 covariates to estimate the association of coffee drinking with cirrhosis, and they used logistic regression for cross-sectional analysis of baseline aspartate aminotransferase and alanine aminotransferase levels.

Relative risks for alcoholic cirrhosis for coffee drinking (vs none) were 0.7 for less than 1 cup per day (95% confidence interval [CI], 0.4 - 1.1); 0.6 for 1 to 3 cups, (95% CI, 0.4 - 0.8; P < .001); and 0.2 for 4 or more cups, (95% CI, 0.1 - 0.4; P < .001). For nonalcoholic cirrhosis, relative risks were 1.2 for less than 1 cup (95% CI, 0.6 - 2.2); 1.3 for 1 to 3 cups (95% CI, 0.8 - 2.1); and 0.7 for 4 or more cups (95% CI, 0.4 - 1.3).

These relative risks for coffee drinking were consistent in different subgroups. Tea drinking was not related to alcoholic or nonalcoholic cirrhosis. Cross-sectional analyses revealed that coffee drinking was related to lower prevalence of high aspartate aminotransferase and alanine aminotransferase levels. The odds ratio of 4 or more cups per day (vs none) for a high aspartate aminotransferase level was 0.5 (95% CI, 0.4 - 0.6; P < .001), and it was 0.6 for a high alanine aminotransferase level, (95% CI, 0.6 - 0.7; P < .001). Inverse relations were stronger in those who drank large quantities of alcohol.

"These data support the hypothesis that there is an ingredient in coffee that protects against cirrhosis, especially alcoholic cirrhosis," the authors write. "The absent relation of tea drinking to cirrhosis might mean that the relation is less likely due to caffeine than to some other coffee ingredient."

Study limitations include possible underreporting of intake by some heavy drinkers; substantial tea drinking relatively uncommon in the study population; ascertainment of habits only at baseline; lack of information about changes in coffee drinking habits before baseline evaluation; use of hospitalization and death as end points; incomplete follow-up of the cohort; inability to account for changes in alcohol drinking or inaccurate reporting of alcohol drinking; observational nature of the data; and the absence of an established mechanism.

"There are also no clear therapeutic implications; even if coffee is protective, the primary approach to reduction of alcoholic cirrhosis is avoidance or cessation of heavy alcohol drinking," the authors write. "Assuming causality, the data do suggest that coffee intake may partly explain the variability of cirrhosis risk in alcohol consumers. Basic research about hepatic coffee-ethanol interactions is warranted, but we should keep in mind that coffee might represent only one of a number of potential cirrhosis risk modulators."

The authors have disclosed no relevant financial relationships. The Kaiser Foundation Research Institute and the Alcoholic Beverage Medical Research Foundation supported this study.

Arch Intern Med. 2006;166:1190-1195