Klopack Eric T, Crimmins Eileen M, Cole Steve W, Seeman Teresa E, Carroll Judith E
University of Southern California, United States.
University of California, Los Angeles, United States.
SSM Popul Health. 2022 Mar 16;17:101071. doi: 10.1016/j.ssmph.2022.101071. eCollection 2022 Mar.
Adverse childhood experiences (ACEs) increase risk for depression at subsequent ages and have been linked to accelerated biological aging. We hypothesize that accelerated epigenetic aging may partially mediate the link between ACEs and depression. This study examines 3 three second-generation epigenetic aging measures (viz., GrimAge, PhenoAge, and DunedinPoAm38) as mediators of the link between ACEs and depressive symptoms in older adulthood. We utilize structural equation modeling to assess mediation in the Health and Retirement Study (N = 2672). Experiencing ACEs is significantly associated with an older GrimAge and a faster pace of aging via the DunedinPoAm38. Having an older GrimAge and faster DunedinPoAm38 pace of aging were also significantly associated with more depressive symptoms. PhenoAge was not significantly associated with depressive symptoms and was only associated with experiencing three ACEs. These associations were reduced by socioeconomic and lifestyle factors, including obesity and substance use. GrimAge explained between 9 and 14% of the association between ACEs and adult depressive symptoms, and DunedinPoAm38 explained between 2 and 7% of the association between ACEs and adult depressive symptoms. Findings indicate accelerated aging, as measured by GrimAge and DunedinPoAm38, is associated with ACEs and with depressive symptoms in older Americans. Findings also show these epigenetic aging measures mediate a portion of the association between ACEs and adult depressive symptoms. Epigenetic aging may represent a physiological mechanism underlying the link between early life adversity and adult depression. Weight maintenance and substance use are potentially important areas for intervention.
童年不良经历(ACEs)会增加后续年龄段患抑郁症的风险,并与生物衰老加速有关。我们假设,表观遗传衰老加速可能部分介导了ACEs与抑郁症之间的联系。本研究考察了三种第二代表观遗传衰老指标(即GrimAge、PhenoAge和DunedinPoAm38),作为ACEs与老年抑郁症状之间联系的中介因素。我们利用结构方程模型在健康与退休研究(样本量N = 2672)中评估中介效应。经历ACEs与更高的GrimAge以及通过DunedinPoAm38衡量的更快衰老速度显著相关。GrimAge更高以及DunedinPoAm38衰老速度更快也与更多的抑郁症状显著相关。PhenoAge与抑郁症状无显著关联,仅与经历三种ACEs有关。这些关联因社会经济和生活方式因素而减弱,包括肥胖和物质使用。GrimAge解释了ACEs与成人抑郁症状之间9%至14%的关联,DunedinPoAm38解释了ACEs与成人抑郁症状之间2%至7%的关联。研究结果表明,以GrimAge和DunedinPoAm38衡量的衰老加速与美国老年人的ACEs和抑郁症状有关。研究结果还表明,这些表观遗传衰老指标介导了ACEs与成人抑郁症状之间部分关联。表观遗传衰老可能代表了早期生活逆境与成人抑郁症之间联系的一种生理机制。体重维持和物质使用可能是重要的干预领域。