Abstract
Differences in health status by socioeconomic position (SEP) tend to be more evident at older ages, suggesting the involvement of a biological mechanism responsive to the accumulation of deleterious exposures across the lifespan. DNA methylation (DNAm) has been proposed as a biomarker of biological aging that conserves memory of endogenous and exogenous stress during life.We examined the association of education level, as an indicator of SEP, and lifestyle-related variables with four biomarkers of age-dependent DNAm dysregulation: the total number of stochastic epigenetic mutations (SEMs) and three epigenetic clocks (Horvath, Hannum and Levine), in 18 cohorts spanning 12 countries.The four biological aging biomarkers were associated with education and different sets of risk factors independently, and the magnitude of the effects differed depending on the biomarker and the predictor. On average, the effect of low education on epigenetic aging was comparable with those of other lifestyle-related risk factors (obesity, alcohol intake), with the exception of smoking, which had a significantly stronger effect.Our study shows that low education is an independent predictor of accelerated biological (epigenetic) aging and that epigenetic clocks appear to be good candidates for disentangling the biological pathways underlying social inequalities in healthy aging and longevity.
Highlights
Aging is characterized by a gradual and constant increase in health inequalities across socioeconomic groups [1, 2], an association based on strong epidemiological evidence known as the ‘social gradient in health’
The estimated effects of risk factors on stochastic epigenetic mutations (SEMs) were re-scaled to be expressed in years as for the three epigenetic clocks using a two-step approach based on the Cohen’s D statistic, described in the supplementary text
Considering the categories defined by the Encyclopedia of DNA Elements (ENCODE) project with Chromatin ImmunoPrecipitation Sequencing (ChIP-Seq) experiments on human embryonic stem cells, we found enrichment of SEMs in ‘inactive/poised promoters’ (p
Summary
Aging is characterized by a gradual and constant increase in health inequalities across socioeconomic groups [1, 2], an association based on strong epidemiological evidence known as the ‘social gradient in health’. The role of epigenetic mechanisms in response to trauma, and evidence for their involvement in intergenerational transmission of biological impacts of traumatic stress have been proposed to explain how social adversity gets biologically embedded [4], leading to differences in biological functionalities among individuals in different social conditions, especially at older ages. Two different mechanisms have been proposed to contribute to age-related DNAm changes: ‘epigenetic drift’ and the ‘epigenetic clock’ that sometimes are used as synonyms even though describe different molecular mechanisms [8,9,10]. Both are related to aging, epigenetic drift represents the trend of increasing DNAm variability over time across the whole genome. Levine EAA was found to outperform other measures with regard to the prediction of a variety of aging outcomes, including all-cause mortality, the incidence of and survival from cancer, and physical functioning [15]
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