Effects of race and socioeconomic status on the epigenetic aging clock

National Institute On Aging

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Abstract

We have continued our work examining the biology of health disparities because it is through biological mechanisms that social determinants of health result in disparate health outcomes. We have continued to focus on the role of DNA methylation as a possible mechanism through which the environmental stresses associated with health disparities among minoritized population result in poor health outcomes. We focused on understand the influence of poverty on biologic aging and age acceleration in African Americans and Whites living above and Below poverty in Baltimore using a new measure of biological aging. The Dunedin Pace of Aging Calculated From the Epigenome (DunedinPACE) measure is a newly constructed DNA methylation (DNAm) biomarker associated with morbidity, mortality, and adverse childhood experiences in several cohorts of European ancestry. However, there are few studies of the DunedinPACE measure among socioeconomically and racially diverse cohorts with longitudinal assessments. To investigate the association of race and poverty status with DunedinPACE scores in a socioeconomically diverse middle-aged cohort of African American and White participants. This longitudinal cohort study used data from the Healthy Aging in Neighborhoods of Diversity Across the Life Span (HANDLS) study. Among 470 participants, the mean (SD) chronological age at visit 1 was 48.7 (8.7) years. Participants were balanced by sex (238 50.6% were men and 232 49.4% were women), race (237 50.4% African American and 233 49.6% White), and poverty status (236 50.2% living below poverty level and 234 49.8% living above poverty level). The mean (SD) time between visits was 5.1 (1.5) years. Overall, the mean (SD) DunedinPACE score was 1.07 (0.14), representing a 7% faster pace of biological aging than chronological aging. Linear mixed-effects regression analysis revealed an association between the 2-way interaction between race and poverty status (White race and household income below poverty level: = 0.0665; 95% CI, 0.0298-0.1031; P < .001) and significantly higher DunedinPACE scores and an association between quadratic age (age squared: = -0.0113; 95% CI, -0.0212 to -0.0013; P = .03) and significantly higher DunedinPACE scores. In this cohort study, household income below poverty level and African American race were associated with higher DunedinPACE scores. These findings suggest that the DunedinPACE biomarker varies with race and poverty status as adverse social determinants of health. Consequently, measures of accelerated aging should be based on representative samples. Our findings suggest that while poverty status is associated with rates of biological aging, DunedinPACE values are inextricably confounded by social class. In this study, both poverty status and race as a social construct were associated with accelerated biological aging. Although this biomarker is sensitive to adverse life experience, it cannot disentangle the consequences of race from those of SES, highlighting the fact that race is not a biological construct. If measures of biological aging are proposed as end points in blinded randomized clinical trials of senolytics or other antiaging therapies, then it is important to base these measures on heterogeneous and representative population cohorts in which genetic variation and ancestry are considered. Otherwise, it may be difficult to prove that a clinical benefit for proposed therapies to enhance health span exists for all groups. However, this algorithm is useful in targeting possible points of intervention in the population overall. In a cohort of African American and White adults living above or below poverty, we found that lower diet quality was associated with a faster pace of aging. We also utilized longitudinal nutritional and epigenetic data. These data build upon earlier studies that focused on specific dietary components and first- or second-generation epigenetic measures [12, 13, 23, 33]. These studies found that specific dietary components, those considered healthy food options including fruits/vegetables and fish intake, are associated with lower epigenetic age whereas red meat intake accelerates epigenetic age. Our data support these findings. In this longitudinal cohort study, our findings revealed that lower dietary quality was associated with a higher DundinPACE score. These results support that eating a low-quality diet may accelerate the biological pace of aging as measured using the DunedinPACE DNAm biomarker. Consequently, these data indicate that eating a healthy, anti-inflammatory diet can promote healthy aging. This may provide important foundational information for future interventions.