Zhao Ying, Wang Yu, Chen Li, Chen Huimin, Tang Yuhan, He Yuefeng, Yao Ping
School of Public Health, Kunming Medical University, Kunming 650500, China.
Department of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, Ministry of Education Key Laboratory of Environment and Health and MOE Key Lab of Environment and Health, Key Laboratory of Environment and Health (Wuhan), Ministry of Environmental Protection, State Key Laboratory of Environment Health (Incubation), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Nutrients. 2025 May 8;17(10):1618. doi: 10.3390/nu17101618.
: 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. : 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. : 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. : 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.
生物衰老被认为是与年龄相关疾病的一个重要风险因素，但其在非酒精性脂肪性肝病（NAFLD）中的作用仍不确定。本研究旨在评估生物衰老与NAFLD的关联以及遗传易感性的修正作用。
本研究纳入了来自英国生物银行的329,040名参与者和来自中国东风-同济队列的6783名参与者。我们计算了按实足年龄调整的生物年龄，作为生物衰老的替代指标。加速衰老定义为生物年龄超过实足年龄。在这两个队列中评估了生物衰老与NAFLD风险之间的关联。在英国生物银行中，使用多基因风险评分（PRSs）来确定NAFLD的遗传易感性，并进一步分析其与生物衰老的相互作用。
在英国生物银行中，经年龄调整的生物年龄每增加一岁，NAFLD的患病风险增加6%。与未加速衰老相比，加速衰老导致NAFLD的风险比（HRs）及95%置信区间（95% CIs）分别为1.35（1.17, 1.56）和1.69（1.54, 1.85）。在东风-同济队列中，生物衰老与NAFLD呈前瞻性关联（加速衰老：优势比（OR）（95% CI） = 1.18（1.03, 1.36））。在英国生物银行中，与低遗传风险相比，高遗传风险与更高的NAFLD风险显著相关（HRs（95% CIs） = 1.65（1.40, 1.95））。联合效应分析显示，PRS高且加速衰老的参与者患NAFLD的风险最高[2.66（2.98, 3.57）和2.06（2.36, 3.96）]。然而，无论遗传风险如何，生物衰老与参与者中的NAFLD均呈前瞻性关联。遗传风险与生物衰老之间无显著相互作用。
加速生物衰老与更高的NAFLD风险相关，且独立于遗传易感性。通过使用替代指标识别具有加速生物衰老的人群并及时进行干预可能有助于预防NAFLD。
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