Coffee May Decrease Fibrosis Severity in Patients With Chronic Liver Disease
Nancy Fowler Larson
January 6, 2010 — Drinking 2.25 cups of regular coffee each day results in milder liver fibrosis in patients with chronic liver disease, but additional caffeine does not boost the benefit, according to a study published in the January 2010 issue of Hepatology.
"Coffee consumption appears to lower liver enzymes and has a protective effect against complications in patients with advanced disease," write Apurva Modi, MD, from the Liver Diseases Branch, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, and colleagues. "However, the relationship between coffee and progression of fibrosis has not been examined, and it is also unclear whether coffee itself or caffeine provides the beneficial effect."
Researchers studied the results of questionnaires completed between January 2006 and November 2008 by 177 patients who were undergoing liver biopsy. A majority of respondents (68%) were infected with hepatitis C virus (HCV). Participants reported the quantity of their daily caffeine intake and its sources, including coffee, soft drinks, tea, chocolate, and medications. Each patient took the questionnaire 3 times during a period of 6 months and was asked whether their caffeine consumption had changed in the previous 6 months or 5 years.
The results showed that participants who ingested an average of 308 mg, or approximately 2.25 cups, of regular coffee every day had milder hepatic fibrosis (odds ratio [OR], 0.33; 95% confidence interval [CI], 0.14 - 0.80; P = .015) than others, as measured by the Ishak fibrosis score.
"Patients with Ishak fibrosis less than 3 had a mean caffeine intake of 212 ± 21 mg/day compared with 154 ± 19 mg/day in those with advanced fibrosis (P = 0.043). In patients with HCV infection, this difference was more pronounced (241 ± 28 mg/day versus 146 ± 19 mg/day; P = 0.033)," the authors write.
Participants took in 71% of their caffeine from regular coffee. Researchers found that other sources of caffeine were not related to milder liver fibrosis in the entire study population (OR per 67 mg of caffeine, 0.84; 95% CI, 0.60 - 1.17; P = .30) or in the group with HCV (OR per 67 mg of caffeine, 0.78; 95% CI, 0.52 - 1.16; P = .21).
The positive effect of coffee remained constant after adjusting for age, sex, race, liver disease, body mass index, and alcohol intake in all participants. Ingestion of coffee in excess of 380 mg a day did not appear to provide any significant additional benefit.
The authors stated 2 limitations to their study:
* Participants with advanced disease may have reduced their caffeine consumption because their altered liver function caused them to require less to produce the same effect, or they believed caffeine to be harmful because of their condition.
* Other factors affecting caffeine intake, including socioeconomic status, education level, and recreational drug use, were not considered.
Because the study was cross-sectional, causality was not determined. The authors noted that recent in vitro data demonstrate that the caffeine, cafestol, and kahweol in coffee may change the expression and activity of enzymes involved in xenobiotic metabolisms. They posited that caffeine's influence may result from a direct antifibrogenic mechanism, citing evidence that there is no association between caffeine intake and liver inflammation, and concluded that long-term studies are needed to reinforce or refute their findings.
"Although it is tempting to conclude that caffeine has a protective effect on fibrogenesis, other explanations are also possible," the authors write. "With accumulating data on the beneficial role of coffee and caffeine in liver disease, as well as the supporting in vitro data, it may now be time to consider a prospective study of coffee or caffeine on hepatic fibrogenesis."