Laura Newman, MA
February 6, 2012 — Drinking caffeinated coffee protects against liver fibrosis in patients with nonalcoholic fatty liver disease, according to research published in the February issue of Hepatology.
In introducing the study, Jeffrey C. Molloy, MD, from the Division of Gastroenterology and Hepatology, Wilford Hall Medical Center, Lackland Air Force Base, Texas, and coauthors refer to previous research linking coffee with decreased progression of liver fibrosis in patients with alcoholic cirrhosis, cirrhosis in general, and elevated liver enzymes. "This news is significant," they write, "because any modality that decreases the progression of fibrosis in chronic liver disease, especially if it confers few adverse effects, has the potential to improve morbidity and mortality."
In summing up the import of their findings, they add: "Moderate coffee consumption may be a benign adjunct to the comprehensive management of patients with [nonalcoholic steatohepatitis (NASH)]."
However, Arthur L. Klatsky, MD, from the Kaiser Permanente Northern California Division of Research in Oakland, pins more benefit on "avoiding risk factors, such as obesity, high alcoholic intake, and viral hepatitis," he told Medscape Medical News. "In my opinion, these are much more important than suggesting that people drink moderate amounts of coffee."
He continued: "I don't think that the public should be advised to drink coffee." Dr. Klatsky was not involved in the present study, but he was the lead author of the first paper linking coffee intake to cirrhosis, published in 1992.
The new finding comes from a validated caffeine questionnaire administered to 4 patient groups at the Brooke Army Medical Center Hepatology Clinic in Fort Sam Houston, Texas: negative controls, bland steatosis/not-NASH, NASH stage 0 to 1, and NASH stage 2 to 4. Between March 2010 and March 2011, 306 patients completed the caffeine questionnaires, which also tabulated tea drinking. Overall, coffee drinking accounted for 71.5% of all caffeine consumed. Patients were also questioned about their intake of other caffeinated beverages, such as various teas, cocoa, caffeine-fortified drinks, chocolate, and caffeine pills. No other caffeinated beverages showed a correlation with any dimension of liver protection (eg, NASH, insulin resistance, diabetes, liver enzymes).
Patients with no to early fibrosis received 57.5% of their caffeine from regular coffee, in comparison with those with advanced fibrosis, who consumed only 35.9% of their caffeine from coffee (P = .041). Average caffeine intake varied significantly across the 4 groups on analysis of variance (P = .024). Coffee intake specifically varied between the 4 groups (P = .011).
The authors flagged the finding that patients with bland steatosis/not-NASH and control patients drank less coffee than those patients with NASH/steatosis. They speculate: "It may be that coffee is only beneficial to those [patients with nonalcoholic fatty liver disease] with a propensity for fibrosis (i.e., NASH patients)."
The authors acknowledge several limitations to their analysis; namely, that their study "was not prospective and thus did not follow the effects of differences in fibrosis on clinical outcomes over time," as well as a lack of blinding of the interviewers. They advise further study of the specific components of coffee and their effects on metabolic activities of the liver.
The study's senior author has disclosed that he consults for Amylin. Dr. Klatsky and the other authors have disclosed no relevant financial relationships.
Hepatology. 2012;55:429-436. Abstract
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