Liu Xiaojing, Jin Ming, Yang Zeping, Zhang Ziyi, Huang Ninghao, Huang Tao, Li Nan
Department of Epidemiology & Biostatistics, School of Public Health, Peking University, No. 38 Xueyuan Road, Haidian District, Beijing 100191, China.
Institute of Reproductive and Child Health, Peking University/Key Laboratory of Reproductive Health, National Health Commission of the People's Republic of China.
Age Ageing. 2024 Nov 28;53(12). doi: 10.1093/ageing/afae272.
Adverse early-life events influence the health with ageing throughout the life course. However, the effects of combined early-life risks on ageing acceleration in adults and the roles of social environment risks remain unknown.
To investigate associations of maternal smoking, breastfeeding and birth weight with accelerated biological age (BA), and to explore genetic-predicted effect and mediating effect of social environment risks.
Population-based prospective cohort.
UK Biobank.
151 773 participants.
We used Klemera-Doubal BA (KDM-BA), PhenoAge and leukocyte telomere length (LTL) as BA biomarkers. Associations of early-life risk factors and score with BA acceleration were estimated using linear regression models. Genetic risk score (GRS) was calculated based on genetic variations for maternal smoking and birth weight. Polysocial risk scores (PsRS) for each BA were calculated by summing the number of dichotomised social environment factors significantly associated with each of the three BA biomarkers.
Maternal smoking, non-breastfeeding and low birth weight were individually associated with BA acceleration. The early-life risk score was significantly associated with accelerated KDM-BA and PhenoAge and shorter LTL. The effects of GRS on accelerated BA were in the same direction. The BA-specific PsRS mediated the accelerated KDM-BA and PhenoAge and shorter LTL by 8.37%, 22.34% and 7.90%, respectively.
Our findings demonstrated a dose-dependent association of combined early-life risks with accelerated BA in middle-aged and older adults, partially mediated by social environment risks. The findings highlight the importance of early identification and surveillance of high-risk individuals for ageing acceleration during adulthood.
早年不良事件会影响一生的健康及衰老过程。然而，早年综合风险对成年人衰老加速的影响以及社会环境风险的作用尚不清楚。
研究母亲吸烟、母乳喂养和出生体重与生物年龄加速（BA）之间的关联，并探讨社会环境风险的遗传预测效应和中介效应。
基于人群的前瞻性队列研究。
英国生物银行。
151773名参与者。
我们使用克莱梅拉-杜巴尔生物年龄（KDM-BA）、表型年龄和白细胞端粒长度（LTL）作为生物年龄的生物标志物。使用线性回归模型估计早年风险因素及评分与生物年龄加速之间的关联。基于母亲吸烟和出生体重的基因变异计算遗传风险评分（GRS）。通过将与三种生物年龄生物标志物中每一种显著相关的二分社会环境因素数量相加，计算每种生物年龄的多社会风险评分（PsRS）。
母亲吸烟、非母乳喂养和低出生体重分别与生物年龄加速相关。早年风险评分与KDM-BA加速、表型年龄加速和较短的LTL显著相关。GRS对生物年龄加速的影响方向相同。特定生物年龄的PsRS分别介导了KDM-BA加速、表型年龄加速和较短LTL的8.37%、22.34%和7.90%。
我们的研究结果表明，早年综合风险与中老年成年人生物年龄加速之间存在剂量依赖性关联，部分由社会环境风险介导。这些发现凸显了成年期衰老加速高危个体早期识别和监测的重要性。
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