Longitudinal changes in epigenetic measures over 2 years: methodological implications.

Rikuta Hamaya, Sidong Li, Brian H Chen, Alexandre C Pereira, Nichole Rigby, Haidong Zhu, Kerry L Ivey, Pamela M Rist, JoAnn E Manson, Yanbin Dong, Howard D Sesso

Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, 900 Commonwealth Ave, Boston, MA, USA. [email protected]. · pubmed

Paper

Abstract

Epigenetic clocks are increasingly proposed as surrogate endpoints in aging trials, yet their short-term behavior in healthy older adults is not well characterized. We analyzed DNA methylation at baseline, year 1, and year 2 in 899 COSMOS-Blood participants (mean age 70.0; 50% women), deriving Horvath, Hannum, PhenoAge, and GrimAge clocks (original and principal component [PC] versions) and DunedinPACE. Epigenetic age acceleration was computed by regressing each clock on chronological age. Chronological age was independent of epigenetic age acceleration and DunedinPACE. PC clocks exhibited substantially smaller 2-year change variance than original clocks, indicating greater measurement stability. Linear mixed-effects models showed statistically detectable but numerically small annual epigenetic age acceleration increases for several PC clocks (e.g., PC Horvath + 0.14 year/year; PC GrimAge + 0.16 year/year), whereas DunedinPACE did not change significantly. Baseline values strongly predicted the same measure at years 1 and 2 (R

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Research summary

The paper claims that epigenetic clocks exhibit varying stability and changes over a two-year period in healthy older adults. This research is relevant as it explores the stability and predictive power of epigenetic measures, which are increasingly considered in the context of aging and longevity research.

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