Department of Psychology and
Population Research Center, The University of Texas at Austin, Austin, Texas.
Pediatrics. 2021 Jun;147(6). doi: 10.1542/peds.2020-024406. Epub 2021 May 17.
Children who grow up in socioeconomic disadvantage face increased burden of disease and disability throughout their lives. One hypothesized mechanism for this increased burden is that early-life disadvantage accelerates biological processes of aging, increasing vulnerability to subsequent disease. To evaluate this hypothesis and the potential impact of preventive interventions, measures are needed that can quantify early acceleration of biological aging in childhood.
Saliva DNA methylation and socioeconomic circumstances were measured in = 600 children and adolescents aged 8 to 18 years (48% female) participating in the Texas Twin Project. We measured pace of biological aging using the DunedinPoAm DNA methylation algorithm, developed to quantify the pace-of-aging-related decline in system integrity. We tested if children in more disadvantaged families and neighborhoods exhibited a faster pace of aging as compared with children in more affluent contexts.
Children living in more disadvantaged families and neighborhoods exhibited a faster DunedinPoAm-measured pace of aging ( = 0.18; = .001 for both). Latinx-identifying children exhibited a faster DunedinPoAm-measured pace of aging compared with both White- and Latinx White-identifying children, consistent with higher levels of disadvantage in this group. Children with more advanced pubertal development, higher BMI, and more tobacco exposure exhibited faster a faster DunedinPoAm-measured pace of aging. However, DunedinPoAm-measured pace of aging associations with socioeconomic disadvantage were robust to control for these factors.
Children growing up under conditions of socioeconomic disadvantage exhibit a faster pace of biological aging. DNA methylation pace of aging might be useful as a surrogate end point in evaluation of programs and policies to address the childhood social determinants of lifelong health disparities.
在社会经济劣势中成长的儿童在其一生中面临着更多的疾病和残疾负担。这种负担增加的一个假设机制是,早期生活劣势加速了衰老的生物学过程,增加了随后患病的脆弱性。为了评估这一假设以及预防干预的潜在影响,需要有能够量化儿童期生物衰老早期加速的措施。
在德克萨斯州双胞胎项目中,我们测量了 600 名 8 至 18 岁(48%为女性)的儿童和青少年的唾液 DNA 甲基化和社会经济状况。我们使用 DunedinPoAm DNA 甲基化算法测量生物衰老的速度,该算法用于量化与系统完整性相关的衰老速度下降。我们测试了生活在较贫困家庭和社区的儿童是否比生活在较富裕环境中的儿童表现出更快的衰老速度。
生活在较贫困家庭和社区的儿童表现出更快的 DunedinPoAm 测量的衰老速度( = 0.18;两者均为 =.001)。与白人及白人和拉丁裔混合身份的儿童相比,拉丁裔身份的儿童表现出更快的 DunedinPoAm 测量的衰老速度,这与该群体中较高的劣势水平一致。青春期发育较早、BMI 较高和吸烟较多的儿童表现出更快的 DunedinPoAm 测量的衰老速度。然而,控制这些因素后,DunedinPoAm 测量的与社会经济劣势相关的衰老速度仍然存在。
在社会经济劣势中成长的儿童表现出更快的生物衰老速度。DNA 甲基化衰老速度可能是评估解决儿童期终身健康差异的社会决定因素的计划和政策的替代终点。