种族、出生时的贫困状况与 15 岁青少年的 DNA 甲基化。

Shervin Assari, Hossein Zare
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摘要

表观遗传学研究可反映生物衰老,研究表明,测量 DNA 甲基化(DNAm)水平可为了解社会环境和社会经济地位(SEP)对生物的影响提供新的视角。本研究探讨了出生时的种族、家庭结构和社会经济地位(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 "未来家庭与儿童福祉研究"(FFCWS)队列,GrimAge 用作 DNAm 水平和表观遗传老化的测量指标。我们的分析包括 854 名从出生到 15 岁的不同种族和民族的参与者。结构方程建模(SEM)检验了种族、出生时的SEP和15岁时的表观遗传衰老之间的关系,并控制了出生时的性别、种族和家庭结构。研究结果表明,种族与较低的出生时 SEP 和较快的表观遗传衰老有关。具体来说,出生时的收入与贫困比率部分地调节了种族对 15 岁时加速衰老的影响。出生时的收入与贫困比率对 DNAm 的影响在 15 岁的男性青年中可以观察到,而在女性青年中则观察不到。因此,在男性青少年中,SEP 部分介导了种族对表观遗传衰老的影响,而在女性青少年中则没有。这些结果表明,出生时的收入与贫困率在一定程度上介导了种族对青春期生物衰老的影响。这些研究结果凸显了早年贫困在解释表观遗传衰老的种族差异方面所产生的长期生物学影响,并强调了解决经济不平等问题以缓解这些差异的重要性。政策制定者应重点关注黑人社区的贫困预防工作,以防止生物老化加速和日后相关的健康风险。旨在消除贫困和解决种族不平等的干预措施可为公共健康带来重大的长期利益。未来的研究应探索导致表观遗传衰老的其他因素,并调查减缓衰老过程的潜在干预措施。还需要进一步的研究来了解这些关联的内在机制,并确定有效的策略来减轻社会经济政策和种族差异对生物衰老的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Race, Poverty Status at Birth, and DNA Methylation of Youth at Age 15.

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.

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