Men With Heart and Metabolic Disease Show Faster Epigenetic Aging

This is an observational study in people. Researchers compared blood samples from 60 men with at least one cardiometabolic condition and 60 age-matched men without any. The men were aged 24 to 70. The conditions were hypertension, chronic ischemic heart disease, obesity and disorders of blood fats such as cholesterol (dyslipidemia). The design is a snapshot in time, so it shows an association, not a cause.

The team measured DNA methylation, chemical tags on DNA that change with age and health. Scientists feed these patterns into "epigenetic clocks" to estimate biological age, which can differ from the years on a birth certificate.

Men with cardiometabolic conditions showed significant age acceleration on several clocks. The effect was strongest for two second-generation clocks, GrimAge and GrimAge2, and for DunedinPACE, a measure of how fast a person is aging. The men with these conditions also had shorter estimated telomere length, based on a methylation estimate. Telomeres are protective caps on the ends of chromosomes.

One result may surprise. None of the 19 first-generation clocks detected a difference between the groups. Those older clocks were trained to predict chronological age. The authors say this suggests they have limited use in these conditions. The newer clocks were built with health and mortality information, and they picked up the signal.

The researchers also scanned the genome for single sites where methylation differed between the groups. Most of these sites were less methylated in the men with disease. Genes linked to these sites fell into nine groups of biological pathways. They include chronic inflammation, signaling through G protein-coupled receptors (a large family of cell surface sensors), metabolic disturbances, mitochondrial dysfunction, vascular remodeling and the regulation of salts and fluids in the kidney.

The team then tested whether the results held up elsewhere. They used an independent public dataset of men with generalized atherosclerosis: 138 cases and 122 controls. Four key findings were replicated: higher GrimAge acceleration, higher DunedinPACE, shorter estimated telomere length, and enrichment of inflammatory and GPCR pathways. The authors say this agreement across cohorts points to a fundamental pattern.

For you

What does this mean for personal health? The study did not test any treatment, and it did not show that controlling blood pressure, weight or cholesterol slows these clocks. It does show that these common conditions travel with a faster biological aging signature in men's blood. The authors suggest these measures could become candidate biomarkers, measurable in a minimally invasive blood sample, for early risk assessment and for monitoring disease progression.

There are limits. The groups were small, and the study included only men, so the results cannot be applied to women. The cases were grouped together, so the study does not separate the effect of one condition from another. The authors call for prospective studies before any clinical use.

The topic is different from our October 9 report on a gut bacteria molecule linked to Alzheimer's protein buildup. That study looked at a different disease. Both, however, point to blood-based markers that might one day flag risk earlier.

What to watch next

Prospective studies that follow men over time to see whether these clocks predict heart events, and whether they change when blood pressure, weight or cholesterol are brought under control.

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