Caffeine Linked to Reduced Liver Fibrosis

Caffeine Linked to Reduced Liver Fibrosis

By Todd Neale, Staff Writer, MedPage Today
Published: January 05, 2010
Reviewed by Zalman S. Agus, MD; Emeritus Professor
University of Pennsylvania School of Medicine and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner Earn CME/CE credit
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Caffeine may help reduce hepatic fibrosis in patients with chronic liver disease, a cross-sectional study showed.

Those who consumed more than 308 mg of caffeine a day -- equal to about 2.25 cups of coffee -- were 75% less likely to have advanced fibrosis than those who consumed less (P=0.006), according to Jay Hoofnagle, MD, of the National Institutes of Diabetes and Digestive and Kidney Diseases in Bethesda, Md., and colleagues.

The two-cups-plus appeared to be a threshold, the researchers reported in the January issue of Hepatology.

"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," they wrote.

Drinking coffee has been associated with slower progression of liver disease, but Hoofnagle and his colleagues noted that no one is sure whether the coffee or caffeine is the primary driver of the relationship, or whether hepatic fibrosis specifically is affected. (See Coffee Could Stall Liver Disease Progression)

To explore the issue, the researchers surveyed 177 patients who were undergoing a liver biopsy to determine their caffeine consumption from food and beverages using a specially designed food frequency questionnaire.

About two-thirds (68%) of the patients had chronic hepatitis C virus (HCV) infection.

The biopsies revealed that 69% had no or mild fibrosis and the rest had bridging fibrosis or cirrhosis.

The surveys revealed that overall, 71% of the caffeine consumed came from regular coffee.

Daily caffeine consumption ranged from 0 to 1,028 mg (average 195 mg, equal to about 1.4 cups of coffee), and was significantly greater in patients with less severe fibrosis scores (212 versus 154 mg, P=0.043).

After adjustment for factors known to affect fibrosis, including age, sex, race, liver disease, body mass index, and alcohol intake, daily caffeine consumption above the 75th percentile (308 mg) was associated with a reduced risk of advanced fibrosis (OR 0.25, 95% CI 0.09 to 0.67).

The apparent protective effect was even stronger among patients with HCV infection (OR 0.19, 95% CI 0.05 to 0.66).

Caffeine from coffee appeared to be the primary driver of the relationship, with no significant association between fibrosis and consumption of caffeine from other sources.

Patients with greater caffeine consumption also had improvements on other measures, including lower aspartate aminotransferase, alkaline phosphatase, and direct bilirubin, and higher levels of serum albumin (P<0.05 for all).

Although it's unclear how caffeine might work in this regard, the researchers cited evidence that it might be through a direct antifibrogenic mechanism.

Animal studies and investigations on human hepatoma cell lines have shown that coffee and some its major components, including caffeine, can alter the expression and activity of enzymes involved in xenobiotic metabolisms, they said.

Caffeine has also been reported to inhibit the transforming growth factor beta pathway, they noted, which "is an attractive explanation for antifibrogenic effects attributed to caffeine."

The authors noted that as this was a cross-sectional study, causality could not be determined and unaccounted-for confounding factors could play a role.

As an example, they noted, "patients with more advanced liver fibrosis may have reduced their caffeine intake because of a presumption that caffeine may not be good for their health. "

In addition, they wrote, "caffeine is metabolized by the liver, and therefore it is also possible that as hepatic function deteriorated, patients may have required less caffeine to achieve the same physiological effects, leading them to reduce their intake over time."

They also pointed out that the study didn't take into account "other factors that may affect caffeine consumption such as socioeconomic status, education level, and recreational drug use."

The authors reported no conflicts of interest.

Primary source: Hepatology
Source reference:
Modi A, et al "Increased caffeine consumption is associated with reduced hepatic fibrosis" Hepatology 2010; 51: 201-09.