- Category: Fibrosis & Cirrhosis
- Published on Tuesday, 07 February 2012 00:00
- Written by Liz Highleyman
A new study published in the February 2012 issue of Hepatology adds to the evidence that drinking caffeinated coffee may help slow or prevent progression of liver damage, this time in people with nonalcoholic fatty liver disease (NAFLD).
Fat accumulation in the liver, or steatosis, is a growing concern as rates of obesity, diabetes, and metabolic syndrome increase in the U.S. Fatty liver disease may also develop in people with viral hepatitis -- especially hepatitis C virus (HCV) genotype 3 -- exposure to hepatotoxic drugs, or other causes of liver injury. A subset of people with NAFLD will develop nonalcoholic steatohepatitis, or NASH, characterized by fat accumulation resulting in liver inflammation and fibrosis, or build-up of scar tissue
Several prior studies have shown that consumption of coffee -- or in some cases caffeine more generally -- is associated with reduced liver fibrosis in people hepatitis C and other chronic liver diseases. The present analysis looked at the association between caffeinated coffee and NAFLD, which has not yet been established.
Stephen Harrison and colleagues asked more than 300 people to complete a questionnaire about their coffee and caffeine consumption. Some were participants in a previously published NAFLD prevalence study and others were patients with non-alcoholic steatohepatitis (NASH) identified at the Brooke Army Medical Center hepatology clinic in Fort Sam Houston, TX.
The researchers determined the association between coffee consumption and extent of NASH, categorized into 4 groups: ultrasound negative for steatosis (control patients), "bland steatosis"/not NASH, NASH stage 0-1 (mild fibrosis), and NASH stage 2-4 (moderate to severe fibrosis).
- Average milligrams of total and coffee caffeine consumed per day in the 4 groups was as follows:
o No steatosis: 307 mg total caffeine and 228 mg coffee caffeine;
o Bland steatosis/not NASH: 229 mg and 160 mg, respectively;
o NASH stage 0-1: 351 mg and 255 mg, respectively;
o NASH stage 2-4: 252 mg and 152 mg, respectively.
- Patients with bland steatosis/not NASH reported significantly lower coffee caffeine consumption than those with NASH stage 0-1 (P = 0.005).
- Patients with NASH stage 0-1 likewise reported significantly less coffee caffeine consumption than those with NASH stage 2-4 (P = 0.016).
- People with NASH stage 0-1 derived 58% of their caffeine intake from coffee, compared with 36% for those with NASH stage 2-4.
- Total caffeine consumption did not have a significant correlation with extent of NASH fibrosis in a multivariate analysis.
- No significant relationship was observed between diabetes/insulin resistance and either extent of NASH fibrosis, or caffeine or coffee consumption.
Based on these findings, the study authors concluded, "Coffee caffeine consumption is associated with a significant reduction in risk of fibrosis among NASH patients."
"In this cross-sectional study of patients with NAFLD, an inverse relationship between regular coffee caffeine consumption and hepatic fibrosis was observed," with a statistically significant difference in caffeine and coffee intake observed between control patients and those with bland steatosis/not NASH, NASH stage 0-1 fibrosis, and NASH stage 2-4 fibrosis," they elaborated in their discussion.
"It is not clear, from our data, what amount of coffee confers the greatest decreased risk of fibrosis," they continued. "It is interesting that patients with bland steatosis/not NASH, as well as the control group, drank less coffee than those patients with NASH stage 0-1 fibrosis. It may be that coffee is only beneficial to those NAFLD patients with a propensity for fibrosis (i.e., NASH patients)."
Further review of the data showed that total caffeine consumption was not significantly correlated with risk of NASH versus not NASH, they noted, adding that "[t]his would suggest that other properties of coffee beyond caffeine may affect disease progression in NASH patients," for example its antioxidant effect.
They acknowledged, however, that this cross-sectional study did not allow analysis of changes in NASH fibrosis over time, and further research is needed to determine if greater coffee or caffeine consumption can help reduce fibrosis progression in people with fatty liver disease.
Investigator affiliations: Divison of Gastroenterology and Hepatology, Wilford Hall Medical Center, Lackland Air Force Base, TX; Department of Medicine, Division of Gastroenterology and Hepatology, Brooke Army Medical Center, Fort Sam Houston, TX; Divison of Gastroenterology and Hepatology, Walter Reed Army Medical Center, Bethesda, MD
JW Molloy, CJ Calcagno, CD Wiliams, SA Harrison, et al. Associationof coffee and caffeine consumption with fatty liver disease, nonalcoholic steatohepatitis, and degree of hepatic fibrosis. Hepatology 55(2):429-436. February 2012.
Wiley-Blackwell. Coffee consumption reduces fibrosis risk in those with fatty liver disease. Press release. February 2, 2012.