Alcohol consumption produced no apparent cardiovascular benefits among individuals with nonalcoholic fatty liver disease, according to a study of 570 white and black adults from the Coronary Artery Risk Development in Young Adults (CARDIA) longitudinal cohort.

After researchers controlled for multiple demographic and clinical confounders, alcohol use was not associated with cardiovascular risk factors such as diabetes, hypertension, or hyperlipidemia, nor with homeostatic model assessment of insulin resistance, C-reactive protein level, total cholesterol, systolic or diastolic blood pressure, coronary artery calcification, E/A ratio, or global longitudinal strain among individuals with nonalcoholic fatty liver disease (NAFLD), reported Lisa B. VanWagner, MD, of Northwestern University, Chicago, and her associates. “[A] recommendation of cardiovascular disease risk benefit of alcohol use in persons with NAFLD cannot be made based on the current findings,” they wrote. They advocated for prospective, long-term studies to better understand how various types and doses of alcohol affect hard cardiovascular endpoints in patients with NAFLD. Their study was published in Gastroenterology.

CARDIA enrolled 5,115 black and white adults aged 18-30 years from four cities in the United States, and followed them long term. Participants were asked about alcohol consumption at study entry and again at 15, 20, and 25 years of follow-up. At year 25, participants underwent computed tomography (CT) examinations of the thorax and abdomen and tissue Doppler echocardiography with myocardial strain measured by speckle tracking (Gastroenterology. 2017 Aug 9. doi: 10.1053/j.gastro.2017.08.012 ).

The 570 participants with NAFLD averaged 50 years of age, 54% were black, 46% were female, and 58% consumed at least one alcoholic drink per week, said the researchers. Compared with nondrinkers, drinkers had attained significantly higher education levels, were significantly more likely to be white and male, and had a significantly lower average body mass index (34.4 kg/m2 vs. 37.3 kg/m2) and C-reactive protein level (4.2 vs. 6.1 mg per L), and a significantly lower prevalence of diabetes (23% vs. 37%), impaired glucose tolerance (42% vs. 49%), obesity (75% vs. 83%) and metabolic syndrome (55% vs. 66%) (P less than .05 for all comparisons). Drinkers and nondrinkers resembled each other in terms of lipid profiles, use of lipid-lowering medications, liver attenuation scores, and systolic and diastolic blood pressures, although significantly more nondrinkers used antihypertensive medications (46% vs.35%; P = .005).

Drinkers had a higher prevalence of coronary artery calcification, defined as Agatston score above 0 (42% vs. 34%), and the difference approached statistical significance (P = .05). However, after they adjusted for multiple potential confounders, the researchers found no link between alcohol consumption and risk factors for cardiovascular disease or between alcohol consumption and measures of subclinical cardiovascular disease. This finding persisted in sensitivity analyses that examined alcohol dose, binge drinking, history of cardiovascular events, and former heavy alcohol use.

Taken together, the findings “challenge the belief that alcohol use may reduce cardiovascular disease risk in persons with nonalcoholic fatty liver disease,” the investigators concluded. Clinical heart failure was too rare to reliably assess, but “we failed to observe an association between alcohol use and multiple markers of subclinical changes in cardiac structure and function that may be precursors of incident heart failure in NAFLD,” they wrote. More longitudinal studies would be needed to clarify how moderate alcohol use in NAFLD affects coronary artery calcification or changes in myocardial structure and function, they cautioned.

The National Institutes of Health supported the work. The investigators reported having no relevant conflicts of interest.