OR24-06 The Role Of Oxidative Stress In The Association Of Smoking And Alcohol Consumption With Hepatic Steatosis

Disclosure: M. Shaheen: None. K. Schrode: None. D. Pan: None. S.M. Najjar: None. T.C. Friedman: None. Hepatic steatosis (HS) is the most prevalent chronic liver disease in the United States. While heavy alcohol consumption is known to be a risk factor for HS, the effect of moderate consumption is still debated. Similarly, while smoking is a known risk factor for many chronic conditions, its contribution to HS is still in question. A potential mechanism by which these factors could increase risk for HS is through oxidative stress. Oxidative stress is an imbalance between free radicals and antioxidants in the body that causes inflammation and cellular damage. Behaviors such as smoking and alcohol consumption are thought to increase oxidative stress. This study aims to determine the role of oxidative stress in the relationship between smoking and moderate alcohol consumption with HS among the adult population of the United States. We analyzed data for 3444 participants from the National Health and Nutrition Examination Survey 2017-2018. Hepatic steatosis was measured by FibroScan® using controlled attenuation parameter (CAP) values, and we used levels of γ-glutamyltransferase (GGT) as a biomarker for oxidative stress. We categorized alcohol consumption and smoking as none, former (for smoking), light, and moderate-heavy following the National Center for Health Statistics. We used bivariate chi square analysis and multivariable logistic regression adjusting for the demographics, laboratory, and co-morbidity and consider the design and weight. We developed two models with and without oxidative stress. In bivariate analyses, oxidative stress was significantly associated with heavier smoking and alcohol consumption, and with HS (all p<0.05). A multivariable model without oxidative stress showed that light drinking alone, light smoking alone, and combination of light smoking and light drinking were not associated with HS (p>0.05), but moderate-heavy smoking combined with light drinking or moderate-heavy drinking increased the odds of HS compared to abstinence from both smoking and drinking (Adjusted Odds Ratio [AOR]=3.9, 95% Confidence Interval [95% CI]= 1.5 - 10.2, p=0.006; AOR=6.2, 95% CI= 1.4 - 26.9, p= 0.014, respectively). When we included oxidative stress in the model, oxidative stress was independently associated with HS (AOR=1.1, 95% Ci=1.0-1.1, p=0.011) and the odds ratios for the interaction of smoking and alcohol did not change, indicating that oxidative stress was not a mediator of these relationships. Our findings indicated that smoking and alcohol consumption can interact to increase the odds of HS in the US population independent of oxidative stress. Further research is needed to identify the underlying mechanisms.Grants: R01MD012579, R24DA017298, U54MD007598, S21MD000103, UL1TR001881 Presentation: Saturday, June 17, 2023