Impact of Psychosocial Stress in Early Life on Pace of Aging in Young Adulthood.

Shaoyong Su, Tené T Lewis, Daniel W Belsky, Yutao Liu, Kai Zhang, Harold Snieder, Xiaoling Wang
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Abstract

Background: Early-life psychosocial stress is increasingly recognized as a contributor to accelerated biological aging and health disparities, yet its impact during young adulthood remains underexplored.​ Existing studies often focus on one or two dimensions of stress exposure and rely on retrospective assessments. Utilizing data from a longitudinal cohort initiated in 1989, we aim to examine the impact of early life psychosocial stress on accelerated aging in young adulthood, as well as its potential contribution to health disparities between Black and White Americans. Participants included 470 individuals (223 Black and 247 White Americans) with DNA samples collected at age > 20 years.​ Psychosocial stress exposures in the first 20 years of life were assessed prospectively using validated instruments across individual, family, and neighborhood domains. DunedinPACE, a novel biomarker of the pace of aging, was calculated from DNA methylation data generated from peripheral blood using the Illumina 450K array. The joint effect of early life psychosocial factors on DunedinPACE and the relative importance of each stressor were estimated using the Weighted Quantile Sum (WQS) approach. Mediation analysis was conducted to evaluate the contribution of early life stress to racial disparities in aging.

Results: Compared to White Americans, Black Americans reported higher overall levels of early life stress (mean = 1.54 vs. 1.40, adjusted p = 0.003) and exhibited a faster pace of aging in young adulthood (DunedinPACE z-score mean = 0.21 vs. -0.19, adjusted p < 0.001). WQS analysis revealed a positive joint effect of early life psychosocial stress on DunedinPACE (β = 0.26, 95% CI: 0.167-0.353), with the top four contributors being parental socioeconomic status, peer pressure, family emotional expression, and neighborhood safety conditions. Mediation analysis indicated that early-life stress accounted for 22% of the racial disparity in biological aging (p = .01).​ Conclusion: Our findings suggest that exposure to disadvantaged psychosocial environments in early life is associated with accelerated biological aging in young adulthood. Racial differences in stress exposure partially explain disparities in aging, underscoring the importance of early interventions to reduce health disparities across the life course.

早期社会心理压力对青年期衰老速度的影响
背景:早期生活的社会心理压力越来越被认为是加速生物衰老和健康差距的一个因素,但其在青年成年期的影响仍未得到充分探讨。现有的研究往往侧重于压力暴露的一个或两个维度,并依赖于回顾性评估。利用1989年开始的纵向队列数据,我们旨在研究早期生活心理社会压力对青年期加速衰老的影响,以及它对美国黑人和白人之间健康差异的潜在贡献。参与者包括470名美国人(223名黑人和247名白人),他们的DNA样本采集于20岁至20岁之间。使用经过验证的工具,在个人、家庭和社区领域对生命前20年的社会心理压力暴露进行前瞻性评估。DunedinPACE是一种新的衰老速度生物标志物,使用Illumina 450K阵列从外周血中产生的DNA甲基化数据计算得出。采用加权分位数和(WQS)方法评估早期生活心理社会因素对DunedinPACE的共同影响以及各应激源的相对重要性。本研究采用中介分析来评估早期生活压力对老龄化种族差异的影响。结果:与美国白人相比,美国黑人报告的早期生活压力总体水平更高(平均= 1.54比1.40,校正p = 0.003),并且在青年期表现出更快的衰老速度(DunedinPACE z-score平均= 0.21比-0.19,校正p
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