Accelerated Biological Aging, Genetic Susceptibility, and Non-Alcoholic Fatty Liver Disease: Two Prospective Cohort Studies
文献类型: 外文期刊
作者: Zhao, Ying 1 ; Wang, Yu 2 ; Chen, Li 4 ; Chen, Huimin 2 ; Tang, Yuhan 2 ; He, Yuefeng 1 ; Yao, Ping 2 ;
作者机构: 1.Kunming Med Univ, Sch Publ Hlth, Kunming 650500, Peoples R China
2.Huazhong Univ Sci & Technol, Key Lab Environm & Hlth Wuhan, State Key Lab Environm Hlth Incubat, Minist Educ,Minist Environm Protect,Dept Nutr & Fo, Wuhan 430030, Peoples R China
3.Huazhong Univ Sci & Technol, Tongji Med Coll, Sch Publ Hlth, MOE Key Lab Environm & Hlth, Wuhan 430030, Peoples R China
4.Chinese Acad Agr Sci, Hubei Key Lab Lipid Chem & Nutr, Oil Crops & Lipids Proc Technol Natl & Local Joint, Minist Agr,Oil Crops Res Inst, Wuhan 430062, Peoples R China
5.Chinese Acad Agr Sci, Oil Crops Res Inst, Key Lab Oilseeds Proc, Wuhan 430062, Peoples R China
关键词: biological aging; KDMAge; PhenoAge; non-alcoholic fatty liver disease; polygenic risk score; genetic susceptibility
期刊名称:NUTRIENTS ( 影响因子:5.0; 五年影响因子:6.0 )
ISSN:
年卷期: 2025 年 17 卷 10 期
页码:
收录情况: SCI
摘要: Background: Biological aging is considered a vital risk factor for age-related diseases, but its role in non-alcoholic fatty liver disease (NAFLD) remains uncertain. This study aimed to evaluate the associations of biological aging with NAFLD and the modified effect of genetic susceptibility. Methods: This study included 329,040 participants from the UK Biobank and 6783 participants from the Dongfeng-Tongji Cohort in China. We calculated the chronological age-adjusted biological age as a surrogate measure for biological aging. Accelerated aging was defined as biological age that exceeded chronological age. The association between biological aging and the risk of NAFLD was assessed in the two cohorts. Polygenic risk scores (PRSs) were used to determine genetic susceptibility for NAFLD in the UK Biobank and further analyze the interaction with biological aging. Results: In the UK Biobank, one year older in age-adjusted biological age increased prevalent NAFLD risk by 6%. The hazard ratios (HRs) and 95% confidence intervals (95% CIs) of NAFLD by accelerated aging were 1.35 (1.17, 1.56) and 1.69 (1.54, 1.85) compared to non-aging. In the Dongfeng-Tongji Cohort, biological aging was prospectively associated with NAFLD (accelerated aging: odds ratio (OR) (95% CI) = 1.18 (1.03, 1.36)). In the UK Biobank, high genetic risk was significantly associated with higher NAFLD risk compared to low genetic risk (HRs (95% CIs) = 1.65 (1.40, 1.95)). Analyses of joint effects showed that participants with high PRS and accelerated aging had the highest risk of NAFLD [2.66 (2.98, 3.57) and 2.06 (2.36, 3.96)]. However, biological aging was prospectively associated with NAFLD among participants regardless of genetic risk. There was no significant interaction between genetic risk and biological aging. Conclusions: Accelerated biological aging was associated with a higher risk of NAFLD independent of genetic susceptibility. Identifying populations with accelerated biological aging by the use of surrogate measures and timely intervention may be beneficial for the prevention of NAFLD.
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