Inflammation and biological age are intertwined — but which one drives the other?
Two of the most discussed processes in aging science — chronic low-grade inflammation and epigenetic changes in DNA — turn out to be closely connected.
Epigenetic aging is a way of measuring biological age. The principle is straightforward: as we grow older, chemical ‘tags’ on our DNA change in predictable patterns. By analysing these patterns, researchers can estimate how old someone’s cells are biologically — regardless of what their birth certificate says. The so-called epigenetic clocks, of which four established versions now exist (Horvath, Hannum, PhenoAge and GrimAge), have become a standard measurement in aging research over the past decade.
Inflammaging — the slow-burning, low-grade inflammation that accumulates with age — has long been associated with cardiovascular disease, dementia, type 2 diabetes, and a range of other age-related conditions. But whether inflammaging causes epigenetic aging, whether epigenetic aging drives inflammaging, or whether both are pushed along by some shared upstream process, had not been clearly established.
Four clocks, one consistent pattern
A study published in Cell Genomics examined the relationship between markers of systemic inflammation and scores on all four major epigenetic clocks. The finding: the association exists, and it holds across all four clocks. People with higher levels of inflammatory markers — such as C-reactive protein (CRP) and interleukin-6 (IL-6), substances produced by the immune system during inflammation — also show higher epigenetic age. In other words, their biological clocks run faster.
The research gives stronger empirical grounding to something scientists had long suspected: inflammaging and epigenetic aging are not parallel but intertwined processes. The potential clinical implication is considerable. If reducing chronic inflammation — through lifestyle changes, medication, or other interventions — also slows epigenetic aging, that would represent a direct route to delaying multiple age-related diseases simultaneously.
Causality remains the hard question
But here is the problem. An association is not proof of cause and effect. It is entirely possible that both processes are driven by a third factor — damaged mitochondria, for instance, or the accumulation of senescent cells, which have stopped dividing but continue to secrete inflammatory substances. Those cells have already been under scrutiny as potential drivers of aging. Whether suppressing inflammaging through targeted interventions actually resets the epigenetic clock still needs to be demonstrated in prospective studies. That is a fundamentally different question from establishing a correlation — and the answer is unlikely to come quickly.