Thoetchai Bee Peeraphatdit1, Joseph C Ahn2, Dae Hee Choi2, Alina M Allen2, Douglas A Simonetto2, Patrick S Kamath2, Vijay H Shah3. 1. Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN; Center for Liver Diseases, University of Chicago Medicine, Chicago, IL. 2. Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN. 3. Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN. Electronic address: shah.vijay@mayo.edu.
Abstract
OBJECTIVE: To study the interaction of alcohol consumption with body mass index (BMI) in the development of hepatic steatosis and mortality. PARTICIPANTS AND METHODS: We conducted a retrospective cohort study of 18,506 participants without fatty liver disease or cirrhosis at enrollment in the Mayo Clinic Biobank from April 9, 2009, through March 31, 2016. Participants were classified by self-reported alcohol consumption status (nondrinkers, moderate drinkers [0 to 2 drinks per day], and heavy drinkers [>2 drinks per day]). The primary outcome of interest was the incidence of hepatic steatosis, identified by International Classification of Diseases, Ninth Revision code and confirmed with imaging. The secondary outcome of interest was all-cause mortality. Multivariate Cox regression analysis determined the impact of alcohol consumption stratified by BMI on outcomes compared with nondrinkers. RESULTS: The cohort (mean ± SD age, 55.8±16.9 years; 63.8% female; mean ± SD BMI, 28.8±6.1 kg/m2) of 18,506 participants included 3657 (19.8%) nondrinkers, 14,236 (76.9%) moderate drinkers, and 613 (3.3%) heavy drinkers at enrollment. After a median follow-up of 5.8 years (interquartile range, 3.8 to 7.2 years), 684 participants had development of hepatic steatosis and 968 died. In moderate drinkers, the risk of hepatic steatosis development was high in the obese group (adjusted hazard ratio [AHR], 1.31; 95% CI, 1.03 to 1.67), insignificant in the overweight group (AHR, 0.86; 95% CI, 0.58 to 1.26), and decreased in the normal-BMI group (AHR, 0.48; 95% CI, 0.26 to 0.90). Heavy drinkers had an increased risk of hepatic steatosis irrespective of BMI. Moderate alcohol use was associated with decreased mortality in the normal-weight (AHR, 0.44; 95% CI, 0.34 to 0.58) and overweight (AHR, 0.70; 95% CI, 0.56 to 0.88) groups but not in the obese group (AHR, 0.80; 95% CI, 0.64 to 1.00). CONCLUSION: In obese individuals, even moderate alcohol use is associated with the development of hepatic steatosis. Moderate alcohol consumption is associated with lower mortality in normal-BMI and overweight individuals but not in those who are obese.
OBJECTIVE: To study the interaction of alcohol consumption with body mass index (BMI) in the development of hepatic steatosis and mortality. PARTICIPANTS AND METHODS: We conducted a retrospective cohort study of 18,506 participants without fatty liver disease or cirrhosis at enrollment in the Mayo Clinic Biobank from April 9, 2009, through March 31, 2016. Participants were classified by self-reported alcohol consumption status (nondrinkers, moderate drinkers [0 to 2 drinks per day], and heavy drinkers [>2 drinks per day]). The primary outcome of interest was the incidence of hepatic steatosis, identified by International Classification of Diseases, Ninth Revision code and confirmed with imaging. The secondary outcome of interest was all-cause mortality. Multivariate Cox regression analysis determined the impact of alcohol consumption stratified by BMI on outcomes compared with nondrinkers. RESULTS: The cohort (mean ± SD age, 55.8±16.9 years; 63.8% female; mean ± SD BMI, 28.8±6.1 kg/m2) of 18,506 participants included 3657 (19.8%) nondrinkers, 14,236 (76.9%) moderate drinkers, and 613 (3.3%) heavy drinkers at enrollment. After a median follow-up of 5.8 years (interquartile range, 3.8 to 7.2 years), 684 participants had development of hepatic steatosis and 968 died. In moderate drinkers, the risk of hepatic steatosis development was high in the obese group (adjusted hazard ratio [AHR], 1.31; 95% CI, 1.03 to 1.67), insignificant in the overweight group (AHR, 0.86; 95% CI, 0.58 to 1.26), and decreased in the normal-BMI group (AHR, 0.48; 95% CI, 0.26 to 0.90). Heavy drinkers had an increased risk of hepatic steatosis irrespective of BMI. Moderate alcohol use was associated with decreased mortality in the normal-weight (AHR, 0.44; 95% CI, 0.34 to 0.58) and overweight (AHR, 0.70; 95% CI, 0.56 to 0.88) groups but not in the obese group (AHR, 0.80; 95% CI, 0.64 to 1.00). CONCLUSION: In obese individuals, even moderate alcohol use is associated with the development of hepatic steatosis. Moderate alcohol consumption is associated with lower mortality in normal-BMI and overweight individuals but not in those who are obese.