These studies provided evidence of the mechanism of the relationship between smoking and the prevalence of NAFLD. Other studies have shown that the activation of sterol regulatory element-binding proteins (SREBPs), which stimulate the synthesis of fatty acids in the liver, is associated with NAFLD ( 27). Furthermore, a study conducted in mice without apolipoprotein E, a condition wherein fatty liver is easily occurs, found that nicotine in electronic cigarettes (e-cigarettes) causes genetic mutations and promotes NAFLD outbreaks ( 26). An experimental study suggested cigarettes accelerated the progression of NAFLD in obese mice-fed diets ( 25). In particular, it has been reported to be an independent risk factor for the progression of advanced fibrosis in patients with primary biliary cirrhosis ( 23) and chronic hepatitis C ( 24).Ī positive association between smoking and NAFLD has been continuously reported ( 25– 27). Previous studies have suggested smoking is associated with increased prevalence and incidence of liver diseases ( 23, 24). Smoking is closely related to chronic diseases, such as cardiovascular diseases, cancer, and type 2 diabetes ( 16– 19), which are also related to NAFLD ( 20– 22). Tobacco smoke contains more than 7,000 chemicals, of which at least 250 are known to be harmful, such as ammonia and hydrogen cyanide ( 14, 15). Therefore, NAFLD must be managed immediately due to its expected serious public health burden and significant social costs ( 12, 13). Furthermore, patients with NAFLD have a higher mortality rate than healthy controls, and the mortality rate related to liver disease is also high ( 8– 11). In addition, between 10 and 29% of patients with nonalcoholic fatty hepatitis develop cirrhosis within 10 years and between 4 and 27% of patients develop liver cancer ( 6, 7). The prevalence of NAFLD is rapidly increasing in Asian countries due to the increase in Westernized eating habits, obesity, and the diabetic population ( 4, 5). Although there are some differences in its frequency from country to country, it has been reported that 6.3 to 33% and an average of approximately 20% of patients worldwide have been affected by the disease ( 3). It is a condition in which neutral fat accumulates excessively in the liver ( 1, 2). Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease. Our study suggests cessation of smoking may help management of NAFLD. Furthermore, NAFLD had a dose-dependent positive effect on pack-years, which was 10 to 20 (OR: 1.39, 95% CI: 1.04–1.86) and over 20 (OR: 1.51, 95% CI: 1.14–2.00).Ĭonclusion: This study found that smoking may contribute to NAFLD. Ex-smokers who ceased smoking for <10 years (OR: 1.33, 95% CI: 1.00–1.77) were more likely to have a strong correlation with NAFLD. The OR increased in magnitude with smoking status. The odds ratio (OR) for having NAFLD in ex-smokers and current smokers in males was 1.12 (95% confidence interval : 0.90–1.41) and 1.38 (95% CI: 1.08–1.76) compared to that in nonsmokers, respectively. Results: In total, 9,603 participants were enrolled in this study. Multiple logistic regression analysis was conducted to examine the association between smoking history and NAFLD in the South Korean population. Smoking status was classified as into nonsmokers, ex-smokers, and current smokers. NAFLD was diagnosed according to an NAFLD liver fat score of >-0.640. Methods: Data from the Korea National Health and Nutrition Examination Survey 2019-2020 were used for the analysis. Therefore, this study aimed to investigate the association between smoking history and nonalcoholic fatty liver disease (NAFLD). However, the impact of smoking on developing nonalcoholic fatty liver disease remains controversial, and clinical data on this is limited. 3Department of Preventive Medicine, Yonsei University College of Medicine, Seoul, Republic of Koreaīackground: Smoking is well known to be associated with a higher prevalence and incidence of liver diseases such as advanced fibrosis. 2Institute of Health Services Research, Yonsei University, Seoul, Republic of Korea.1Department of Public Health, Graduate School, Yonsei University, Seoul, Republic of Korea.Yun Seo Jang 1,2 Hye Jin Joo 1,2 Yu Shin Park 1,2 Eun-Cheol Park 2,3 Sung-In Jang 2,3 *
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