ArticleGeroScience2026
Longitudinal changes in epigenetic measures over 2 years: methodological implications.
Article in GeroScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Phenotypic age metrics for risk stratification of chronic disease burden and all-cause mortality in adults.Cardiovascular diabetology. Endocrinology reports · 2026Article
- Epigenetic Signatures of Ageing in Asian Elephants Revealed by Reduced Representation Bisulphite Sequencing.Evolutionary applications · 2026Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.