4.5 Article

The Socioeconomic Gradient in Epigenetic Ageing Clocks: Evidence from the Multi-Ethnic Study of Atherosclerosis and the Health and Retirement Study

Journal

EPIGENETICS
Volume -, Issue -, Pages -

Publisher

TAYLOR & FRANCIS INC
DOI: 10.1080/15592294.2021.1939479

Keywords

DNA methylation age; epigenetic clock; socioeconomic status; polygenic score

Funding

  1. National Heart, Lung, and Blood Institute (NHLBI)
  2. MESA [HHSN268201500003I, N01-HC-95159, N01-HC-95160, N01-HC-95161, -95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168, N01-HC -95169, UL1-TR-000040, UL1-TR-001079, UL1-TR-001420, UL1-TR-001881, DK063491]
  3. NHLBI [N02-HL-64278]
  4. NIH [R01HL101250, R01HL119962, R01DK101921, R01HL135009, 1RF1AG054474]
  5. National Institute on Aging (NIA) [U01AG009740]
  6. University of Michigan
  7. National Institute on Aging [R21 AG045625, P30 AG017625]
  8. [HL071759-01]

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Studies have shown robust associations between socioeconomic status and epigenetic clocks, partially mediated by health behaviors. In older adults, socioeconomic status and genetic risk may contribute additively to faster biological aging.
Epigenetic clocks have been widely used to predict disease risk in multiple tissues or cells. Their success as a measure of biological ageing has prompted research on the connection between epigenetic pathways of ageing and the socioeconomic gradient in health and mortality. However, studies examining social correlates of epigenetic ageing have yielded inconsistent results. We conducted a comprehensive, comparative analysis of associations between various dimensions of socioeconomic status (SES) (education, income, wealth, occupation, neighbourhood environment, and childhood SES) and eight epigenetic clocks in two well-powered US ageing studies: The Multi-Ethnic Study of Atherosclerosis (MESA) (n = 1,211) and the Health and Retirement Study (HRS) (n = 4,018). In both studies, we found robust associations between SES measures in adulthood and the GrimAge and DunedinPoAm clocks (Bonferroni-corrected p-value < 0.01). In the HRS, significant associations with the Levine and Yang clocks were also evident. These associations were only partially mediated by smoking, alcohol consumption, and obesity, which suggests that differences in health behaviours alone cannot explain the SES gradient in epigenetic ageing in older adults. Further analyses revealed concurrent associations between polygenic risk for accelerated intrinsic epigenetic ageing, SES, and the Levine clock, indicating that genetic risk and social disadvantage may contribute additively to faster biological aging.

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