Epigenetic aging and methylation in men with cardiometabolic conditions
In an abstract, men with cardiometabolic disturbances showed epigenetic age acceleration on second-generation clocks and pace-of-aging measures, plus differential methylation; key findings replicated in a separate cohort of men with atherosclerosis. [1]
Automatic summary · not editorially reviewed
The key findings
New DNA methylation profiles came from whole blood of men with cardiometabolic disturbances and age-matched healthy controls. [1]
Cases showed epigenetic age acceleration, most pronounced for GrimAge, GrimAge2 and DunedinPACE, with shortened DNAmTL. [1]
GrimAge acceleration, DunedinPACE elevation, DNAmTL shortening and inflammatory and GPCR pathway enrichment replicated in an independent cohort of men with atherosclerosis. [1]
The source at a glance
- Study type / format
- Abstract of a cohort study with an independent replication cohort
- Population / context
- Men with cardiometabolic disturbances (hypertension, ischemic heart disease, obesity, dyslipidemia) and age-matched healthy men; a separate replication cohort of men with atherosclerosis.
- Summary based on
- Study abstract
- Original publication
- July 6, 2026
Men with cardiometabolic burden versus healthy controls
The abstract describes a cohort composed exclusively of men. New DNA methylation profiles were generated from whole blood of men with cardiometabolic disturbances (hypertension, ischemic heart disease, obesity, dyslipidemia) and from age-matched healthy controls. The comparison was therefore between men with these conditions and healthy men of matched age, not a test of any treatment.
Supporting source [1]
Accelerated epigenetic age and hypomethylated positions in cases
Cases showed significant epigenetic age acceleration, most pronounced for second-generation clocks (GrimAge, GrimAge2) and pace-of-aging measures (DunedinPACE), with shortened epigenetic telomere length (DNAmTL). None of the 19 evaluated first-generation clocks was sensitive to the studied diseases. Differentially methylated positions were predominantly hypomethylated in cases; pathway clusters included chronic inflammation, GPCR signaling dysregulation, metabolic disturbances, mitochondrial dysfunction, vascular remodeling and renal electrolyte regulation.
Supporting source [1]
Replication in men with atherosclerosis and abstract-only scope
GrimAge acceleration, DunedinPACE elevation, DNAmTL shortening and enrichment of inflammatory and GPCR pathways were replicated in an independent cohort of men with atherosclerosis. The authors describe these as candidate biomarkers measurable in minimally invasive blood samples that may assist early risk stratification, and call for further prospective evaluation. These are associations, not proof of cause; the abstract does not report sample sizes, follow-up or effect estimates.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. The abstract does not report sample sizes, follow-up, effect estimates or adjustment details, and the described biomarkers are associations requiring prospective evaluation, not established clinical tools.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Kalyakulina A, Yusipov I, Botasheva F, Bujlova N, Zagaynova E, Franceschi C, Ivanchenko M. · europepmc.org · July 6, 2026