Health Sciences North Research Institute, Sudbury, ON, Canada.
Department of Epidemiology, Columbia University Mailman School of Public Health, NY, United States; Robert N. Butler Columbia Aging Center, Columbia University, NY, United States.
Psychoneuroendocrinology. 2022 Aug;142:105821. doi: 10.1016/j.psyneuen.2022.105821. Epub 2022 Jun 3.
People exposed to adverse childhood experiences (ACEs) suffer from an increased risk of chronic disease and shorter lifespan. These individuals also tend to exhibit accelerated reproductive development and show signs of advanced cellular aging as early as childhood. These observations suggest that ACEs may accelerate biological processes of aging through direct or indirect mechanisms; however, few population-based studies have data to test this hypothesis. We analysed ACEs and biological aging data from the Canadian Longitudinal Study on Aging (CLSA; n = 23,354 adults aged 45-85) and used the BioAge R package to compute three indices of biological aging from blood-chemistry and organ-function data: Klemera-Doubal method (KDM) biological age, phenotypic age (PA), and homeostatic dysregulation (HD). Adults with ACEs tended to be biologically older than those with no ACEs, although the observed effect-sizes were small (Cohen's d<0.15), with the exception of neglect (d=0.35 for KDM and PA). Associations were similar for men and women and tended to be smaller for older as compared to midlife participants. Subtypes of ACEs perceived as being more severe (e.g., being pushed or kicked, experiencing forced sexual activity, witnessing physical violence) and more frequent and diverse exposures were associated with relatively larger effect-sizes. These findings support the hypothesis that ACEs contribute to accelerated biological aging, although replication is needed in studies with access to prospective records of ACEs and cellular-level measurements of biological aging. Furthermore, future work to better understand the degree to which associations between ACEs and biological aging are moderated by specific life-course pathways, and mediated by lifestyle and socioeconomic factors is warranted.
经历过不良儿童经历（ACEs）的人患慢性病和寿命缩短的风险增加。这些人还倾向于表现出加速的生殖发育，并早在童年就表现出先进的细胞衰老迹象。这些观察结果表明，ACEs 可能通过直接或间接机制加速衰老的生物学过程；然而，很少有基于人群的研究有数据来检验这一假设。我们分析了加拿大老龄化纵向研究（CLSA；n=23354 名 45-85 岁的成年人）中的 ACEs 和生物衰老数据，并使用 BioAge R 包从血液化学和器官功能数据中计算了三种生物衰老指数：Klemera-Doubal 方法（KDM）生物年龄、表型年龄（PA）和体内平衡失调（HD）。有 ACEs 的成年人往往比没有 ACEs 的成年人更显老，尽管观察到的效应大小很小（Cohen's d<0.15），但忽视除外（KDM 和 PA 的 d=0.35）。这些关联在男性和女性中相似，并且在与中年参与者相比，年龄较大的参与者中往往更小。被认为更严重的 ACEs 亚型（例如，被推或踢，经历强迫性行为，目睹身体暴力）以及更频繁和多样化的暴露与相对较大的效应大小相关。这些发现支持 ACEs 导致加速生物衰老的假设，尽管需要在有机会获得 ACEs 的前瞻性记录和生物衰老的细胞水平测量的研究中进行复制。此外，有必要进一步研究 ACEs 和生物衰老之间的关联在多大程度上受到特定生命历程途径的调节，以及受生活方式和社会经济因素的影响。
