Researchers report an association between alcohol use and liver fat—even after heavy users of alcohol were excluded from the analysis. Finding from the study, published in Clinical Gastroenterology and Hepatology, indicate that alcohol use is a risk factor for nonalcoholic fatty liver disease (NAFLD).
Many individuals presumed to have NAFLD consume moderate amounts of alcohol. However, little is known about patterns of alcohol use in patients with NAFLD or how drinking behaviors affect liver fat.
Some studies found excessive alcohol consumption to be a risk factor for fatty liver, steatohepatitis, and cirrhosis. Other studies, however, reported beneficial effects from moderate alcohol consumption in individuals NAFLD, no protection, or detrimental effects on liver fat. These discrepancies might be attributed to different alcohol consumption patterns in different study populations.
Michele T Long et al performed a cross-sectional study of 3180 participants in the Framingham Heart Study with hepatic steatosis. They examined the association between different alcohol drinking patterns and liver fat, determined by multidetector computed tomography, after adjusting for covariates. The authors excluded heavy alcohol users and aimed to determine whether associations between alcohol use pattern and liver fat differ by type of alcohol consumed.
Long et al found that risky weekly drinking occurred at a relatively low frequency and was equally common among women and men. However, binge drinking was common, particularly among men, and drinking in excess of dietary guideline limits was common among women and men. The prevalence of hepatic steatosis increased from 15.3% to 54.3% among increasing categories of alcohol use as measured by participant-reported alcoholic drinks per week (see figure).
In adjusted models, the odds of hepatic steatosis increased by 15% for each standard deviation increase in the number of alcoholic drinks consumed per week.
Long et al found associations between the frequency of alcohol use and hepatic steatosis and binge drinking and hepatic steatosis (adjusted odds ratio, 1.45; 95% CI, 1.06–1.98) among drinkers in adjusted models.
More than half of the participants reported either primary beer drinking (n = 575) or primary wine drinking (n = 809). Beer drinkers consumed more alcoholic drinks per week, had higher maximum consumption, and had a greater likelihood of binge drinking (49.6% vs 17.3% for wine drinkers).
Among beer drinkers, there was an association between alcohol drinks per week, maximum drinks in 24 hours, and binge drinking behavior and hepatic steatosis. In multivariable-adjusted models, for beer drinkers, the odds of hepatic steatosis increased by 28% per standard deviation increase in the number of beer drinks per week and by 44% per standard deviation increase in the maximum number of drinks consumed. Beer drinkers who reported binge drinking had 2.52-fold the adjusted odds of hepatic steatosis compared with beer drinkers who did not report binge drinking.
For liquor or spirit drinkers (n = 249) the odds of hepatic steatosis increased by 24% per standard deviation increase in the frequency of alcohol consumed or by 50% per standard deviation increase in the maximum number of drinks consumed. No associations were observed between wine use patterns and hepatic steatosis.
Long et al conclude that even after they exclude participants with alcohol consumption exceeding current criteria for NAFLD, there is a substantial prevalence of binge drinking and consumption in excess of the US dietary guideline limits. Similarly, the Coronary Artery Risk Development in Young Adults Study found that binge drinking behavior occurred in 27.7% participants with NAFLD who consumed alcohol. Binge drinking was associated with hepatic steatosis, even after Long et al accounted for metabolic syndrome components.
Why have observational studies found protective effects of light or moderate alcohol use on hepatic steatosis or more advanced NAFLD histology? Alcohol use often is self-reported and former or infrequent drinkers may be misclassified as nondrinkers, and used as the reference group. In addition, confounding from sociodemographic differences between nondrinkers or moderate alcohol drinkers can account partially or completely for the beneficial effects of alcohol. More stringent alcohol use thresholds or criteria for defining binge drinking should be used for trials of NAFLD.
Prospective studies are needed to validate the findings of Long et al and determine if more comprehensive alcohol use screening tools should be used in practice or clinical trial settings. Alcohol use might be a focus for research, prevention, and treatment of presumed NAFLD.