Zhenqiu Liu1, Chen Suo2, Renjia Zhao3, Huangbo Yuan1, Li Jin1, Tiejun Zhang3, Xingdong Chen4. 1. State Key Laboratory of Genetic Engineering, Human Phenome Institute, and School of Life Sciences, Fudan University, Shanghai, China; Fudan University Taizhou Institute of Health Sciences, Taizhou, China. 2. Fudan University Taizhou Institute of Health Sciences, Taizhou, China; Key Laboratory of Public Health Safety, Fudan University, Ministry of Education, Shanghai, China; Department of Epidemiology, School of Public Health, Fudan University, Shanghai, China. 3. Key Laboratory of Public Health Safety, Fudan University, Ministry of Education, Shanghai, China; Department of Epidemiology, School of Public Health, Fudan University, Shanghai, China. 4. State Key Laboratory of Genetic Engineering, Human Phenome Institute, and School of Life Sciences, Fudan University, Shanghai, China; Fudan University Taizhou Institute of Health Sciences, Taizhou, China. Electronic address: xingdongchen@fudan.edu.cn.
Abstract
BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is prevalent worldwide. We aim to identify the factors promoting NAFLD progression. METHODS: UK Biobank study participants were diagnosed for whether NAFLD presented at baseline. Cox regression model was used to examine the association of risk factors with incident diseases (significant liver diseases [SLDs], type 2 diabetes [T2D], cardiovascular diseases [CVDs], chronic kidney diseases [CKDs], and cancers) among NAFLD cases. RESULTS: Of 78 283 individuals, 35 159 (44.9%) were females, and the mean (SD) age was 57.56 (7.90) years. Compared with participants had both low genetic and lifestyle risk, individuals with both high genetic and lifestyle risk had a hazard ratio of 1.64 (95% CI 1.32-2.03) for SLDs, 1.16 (1.08-1.24) for T2D, 1.25 (1.13-1.37) for CVDs, 1.33 (1.18-1.49) for CKDs, and 1.13 (1.05-1.22) for cancers. Compared with participants who were non-obese and had low genetic risk, those with obesity and high genetic risk had an 75% (95% CI 38-123%), 147% (128-167%), 46% (33-61%), and 76% (56-99%) increased risk for developing SLDs, T2D, CVDs, and CKDs, respectively. The population-attributable fractions suggested that lifestyle risk and obesity contributed more to the progression of NAFLD than genetic risk. CONCLUSION: Adhering to a healthy lifestyle and avoiding obesity are important to prevent NAFLD progression.
BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is prevalent worldwide. We aim to identify the factors promoting NAFLD progression. METHODS: UK Biobank study participants were diagnosed for whether NAFLD presented at baseline. Cox regression model was used to examine the association of risk factors with incident diseases (significant liver diseases [SLDs], type 2 diabetes [T2D], cardiovascular diseases [CVDs], chronic kidney diseases [CKDs], and cancers) among NAFLD cases. RESULTS: Of 78 283 individuals, 35 159 (44.9%) were females, and the mean (SD) age was 57.56 (7.90) years. Compared with participants had both low genetic and lifestyle risk, individuals with both high genetic and lifestyle risk had a hazard ratio of 1.64 (95% CI 1.32-2.03) for SLDs, 1.16 (1.08-1.24) for T2D, 1.25 (1.13-1.37) for CVDs, 1.33 (1.18-1.49) for CKDs, and 1.13 (1.05-1.22) for cancers. Compared with participants who were non-obese and had low genetic risk, those with obesity and high genetic risk had an 75% (95% CI 38-123%), 147% (128-167%), 46% (33-61%), and 76% (56-99%) increased risk for developing SLDs, T2D, CVDs, and CKDs, respectively. The population-attributable fractions suggested that lifestyle risk and obesity contributed more to the progression of NAFLD than genetic risk. CONCLUSION: Adhering to a healthy lifestyle and avoiding obesity are important to prevent NAFLD progression.