Assari Shervin, Zare Hossein
Department of Internal Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA, United States.
Department of Family Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA, United States.
Glob J Epidemol Infect Dis. 2024;4(1):8-19. doi: 10.31586/gjeid.2024.988. Epub 2024 Jul 12.
Epigenetic studies, which can reflect biological aging, have shown that measuring DNA methylation (DNAm) levels provides new insights into the biological effects of social environment and socioeconomic position (SEP). This study explores how race, family structure, and SEP (income to poverty ratio) at birth influence youth epigenetic aging at age 15. Data were obtained from the Future of Families and Child Wellbeing Study (FFCWS) cohort, with GrimAge used as a measure of DNAm levels and epigenetic aging. Our analysis included 854 racially and ethnically diverse participants followed from birth to age 15. Structural equation modeling (SEM) examined the relationships among race, SEP at birth, and epigenetic aging at age 15, controlling for sex, ethnicity, and family structure at birth. Findings indicate that race was associated with lower SEP at birth and faster epigenetic aging. Specifically, income to poverty ratio at birth partially mediated the effects of race on accelerated aging by age 15. The effect of income to poverty ratio at birth on DNAm was observed in male but not female youth at age 15. Thus, SEP partially mediated the effect of race on epigenetic aging in male but not female youth. These results suggest that income to poverty ratio at birth partially mediates the effects of race on biological aging into adolescence. These findings highlight the long-term biological impact of early-life poverty in explaining racial disparities in epigenetic aging and underscore the importance of addressing economic inequalities to mitigate these disparities. Policymakers should focus on poverty prevention in Black communities to prevent accelerated biological aging and associated health risks later in life. Interventions aimed at eliminating poverty and addressing racial inequities could have significant long-term benefits for public health. Future research should explore additional factors contributing to epigenetic aging and investigate potential interventions to slow down the aging process. Further studies are needed to understand the mechanisms underlying these associations and to identify effective strategies for mitigating the impact of SEP and racial disparities on biological aging.
表观遗传学研究能够反映生物衰老,该研究表明,测量DNA甲基化(DNAm)水平为了解社会环境和社会经济地位(SEP)的生物学效应提供了新的视角。本研究探讨了种族、家庭结构以及出生时的SEP(收入与贫困比率)如何影响15岁青少年的表观遗传衰老。数据来自家庭与儿童福祉未来研究(FFCWS)队列,使用GrimAge作为DNAm水平和表观遗传衰老的衡量指标。我们的分析纳入了854名从出生到15岁的不同种族和族裔的参与者。结构方程模型(SEM)研究了种族、出生时的SEP与15岁时的表观遗传衰老之间的关系,并对性别、种族和出生时的家庭结构进行了控制。研究结果表明,种族与出生时较低的SEP以及更快的表观遗传衰老相关。具体而言,出生时的收入与贫困比率部分介导了种族对15岁时加速衰老的影响。在15岁的男性青少年中观察到了出生时收入与贫困比率对DNAm的影响,而在女性青少年中未观察到。因此,SEP部分介导了种族对男性而非女性青少年表观遗传衰老的影响。这些结果表明,出生时的收入与贫困比率部分介导了种族对青春期生物衰老的影响。这些发现凸显了早期贫困在解释表观遗传衰老中的种族差异方面的长期生物学影响,并强调了解决经济不平等以减轻这些差异的重要性。政策制定者应关注黑人社区的贫困预防,以防止后期生活中生物衰老加速和相关健康风险。旨在消除贫困和解决种族不平等的干预措施可能会给公共卫生带来重大的长期益处。未来的研究应探索导致表观遗传衰老的其他因素,并研究减缓衰老过程的潜在干预措施。需要进一步的研究来了解这些关联背后的机制,并确定减轻SEP和种族差异对生物衰老影响的有效策略。