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. 2020 Jul;18(8):1831-1841.e5.
doi: 10.1016/j.cgh.2019.11.022. Epub 2019 Nov 14.

Alcohol Use Is Associated With Hepatic Steatosis Among Persons With Presumed Nonalcoholic Fatty Liver Disease

Affiliations

Alcohol Use Is Associated With Hepatic Steatosis Among Persons With Presumed Nonalcoholic Fatty Liver Disease

Michelle T Long et al. Clin Gastroenterol Hepatol. 2020 Jul.

Abstract

Background & aims: Many individuals presumed to have nonalcoholic fatty liver disease (NAFLD) consume moderate amounts of alcohol. Little is known about patterns of alcohol use in patients with NAFLD or how drinking behaviors affect liver fat.

Methods: We conducted a cross-sectional study of 2475 participants of the Framingham Heart Study with hepatic steatosis, as determined by computed tomography. We performed multivariable-adjusted logistic regression models to evaluate the association between alcohol drinking patterns and hepatic steatosis. Models were adjusted for sociodemographic factors, diet, and the components of the metabolic syndrome. We excluded heavy alcohol users, defined as women who consume more than 14 alcohol drinks per week and men who consume more than 21 alcohol drinks per week.

Results: In our sample (mean age, 49.8 ± 10.2 y; 50.3% women), the prevalence of hepatic steatosis was 17.5%. The total number of alcohol drinks per week and the maximum drinks consumed per drinking day each were associated with hepatic steatosis (adjusted odds ratio [aOR], 1.15; 95% CI, 1.02-1.29 and aOR 1.15; 95% CI, 1.02-1.30). Binge drinking occurred in 25.4% of individuals with presumed NAFLD and was associated with an increased odds of hepatic steatosis (aOR, 1.45; 95% CI, 1.06-1.98) among alcohol users. In a beverage-specific analysis, alcohol use patterns were associated with hepatic steatosis among beer drinkers, but not among wine drinkers.

Conclusions: In a cross-sectional study of participants of the Framingham Heart Study with hepatic steatosis, we observed an association between alcohol use and liver fat, even after excluding heavy alcohol users from our analysis. Alcohol use therefore appears to be a risk factor for NAFLD. Prospective studies are needed to validate these findings and determine if alcohol use should be a focus for research, prevention, and treatment of presumed NAFLD.

Keywords: CT; Epidemiology; Lifestyle Factor; Social.

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Conflict of interest statement

Conflicts of interest

The authors disclose no conflicts.

Figures

Figure 1.
Figure 1.
Prevalence of alcohol consumption patterns among participants with presumed NAFLD (n = 433) and the entire cohort (n = 2475). Risky weekly drinking was defined as 8 or more drinks per week for women and 15 or more drinks per week for men. Usual consumption above US dietary guidelines was defined as 2 or more drinks for women or 3 or more drinks for men. Binge drinking was defined as 4 or more drinks for women or 5 or more drinks for men in 24 hours.
Figure 2.
Figure 2.
Prevalence of hepatic steatosis by alcoholic drink per week category. The unadjusted prevalence of hepatic steatosis increased from 15.3% (n = 159 of 1037) to 16.3% (n = 73 of 447) to 25.0% (n = 36 of 144) to 54.3% (n = 6 of 11; men only) across increasing categories of alcohol use as measured by reported drinks per week. We excluded women who drink more than 14 drinks per week and men who drink more than 21 drinks per week from the analysis. LPR, liver phantom ratio.

Comment in

  • Alcohol Use Patterns and Liver Outcomes: Is There Really a Difference Between Drinking Beer and Drinking Wine?
    Marcellin F, Beo VD, Carrieri P. Marcellin F, et al. Clin Gastroenterol Hepatol. 2020 Jun;18(7):1650-1651. doi: 10.1016/j.cgh.2019.12.018. Epub 2019 Dec 27. Clin Gastroenterol Hepatol. 2020. PMID: 31887441 No abstract available.
  • Reply.
    Long MT, Naimi TS. Long MT, et al. Clin Gastroenterol Hepatol. 2020 Jun;18(7):1651-1652. doi: 10.1016/j.cgh.2020.01.001. Epub 2020 Jan 8. Clin Gastroenterol Hepatol. 2020. PMID: 31926338 Free PMC article. No abstract available.
  • Alcohol Use in Patients With NAFLD.
    Bonacini M. Bonacini M. Clin Gastroenterol Hepatol. 2021 Jul;19(7):1506. doi: 10.1016/j.cgh.2020.08.004. Epub 2020 Nov 26. Clin Gastroenterol Hepatol. 2021. PMID: 33248071 No abstract available.
  • Reply.
    Long MT, Naimi TS. Long MT, et al. Clin Gastroenterol Hepatol. 2021 Jul;19(7):1506-1507. doi: 10.1016/j.cgh.2020.08.058. Epub 2020 Nov 26. Clin Gastroenterol Hepatol. 2021. PMID: 33248106 No abstract available.

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