Inflammation is a survival system. Acute inflammation is how the body contains infection, clears damaged tissue, and initiates repair. The problem, increasingly recognized across cardiology, oncology, neurology, and geriatrics, is that many people carry a low-grade version of this response for years, and that persistent background inflammation appears to accelerate several of the diseases that shorten healthy life.
Researchers coined the term inflammaging to describe the age-related rise in chronic low-grade inflammation observed across populations. The concept is not that inflammation is inherently bad, but that its persistent, unresolved form seems to nudge multiple aging pathways in the wrong direction.
What inflammaging looks like
In healthy young adults, inflammatory markers like C-reactive protein (CRP) and interleukin-6 (IL-6) are typically low at baseline and spike briefly during infection or injury. With age, average levels of these markers tend to drift upward, even in the absence of overt illness. Population studies have linked higher baseline IL-6 and CRP in older adults to increased risk of cardiovascular events, frailty, cognitive decline, and mortality.
Sources of chronic inflammatory signaling include:
- Visceral adipose tissue, which secretes inflammatory cytokines
- Senescent cells, which accumulate with age and release a proinflammatory secretome
- Gut barrier dysfunction, which can allow bacterial products to reach systemic circulation
- Chronic infections, including periodontal disease and some persistent viral infections
- Poor sleep and chronic psychological stress, both of which raise inflammatory markers in controlled studies
Where the causal evidence is strongest
The cleanest human causal evidence for inflammation as a driver of disease comes from cardiovascular medicine. The CANTOS trial, published in the New England Journal of Medicine in 2017, tested canakinumab, a monoclonal antibody against IL-1 beta, in patients with prior heart attack and elevated CRP. It reduced recurrent cardiovascular events without lowering LDL cholesterol, providing rare experimental support for the inflammation hypothesis in atherosclerosis. Serious infections were increased, and the drug did not reduce all-cause mortality.
Colchicine, a much older and cheaper anti-inflammatory drug, has since shown benefit in low doses for secondary prevention of cardiovascular events in trials such as LoDoCo2 and COLCOT, further supporting the idea that damping inflammation matters for vascular aging.
Evidence in other domains is more suggestive than definitive. Higher inflammatory markers correlate with dementia risk and with certain cancers, but disentangling cause from consequence in observational data is difficult.
What plausibly moves the needle
Most of the interventions that lower chronic inflammation are the same interventions that appear repeatedly in longevity research:
- Regular physical activity, which lowers CRP and IL-6 over months in randomized trials
- Weight loss when overweight, particularly loss of visceral fat
- Diets high in fiber, minimally processed plant foods, and fatty fish, which correlate with lower inflammatory markers in cohort studies
- Adequate sleep and treatment of sleep apnea
- Smoking cessation, one of the largest single reducers of systemic inflammation
- Treatment of periodontal disease and other chronic infections
Dietary supplements marketed as anti-inflammatory, including many botanicals and high-dose fish oil, have mixed evidence and should not be assumed equivalent to the interventions above.
The most reliable anti-inflammatory prescription in humans is still exercise, sleep, and not smoking, delivered consistently.
Measuring it responsibly
High-sensitivity CRP is the most commonly used clinical marker of chronic inflammation, though it is nonspecific and can be transiently elevated by infection, injury, or recent vigorous exercise. Repeat testing and clinical context matter. Panels of aging biomarkers are commercially available but their added value over conventional markers is not yet clearly established.
The bottom line
Chronic low-grade inflammation is one of the more credible unifying threads in aging biology, with strong causal evidence in cardiovascular disease and suggestive links elsewhere. The interventions with the best evidence to lower it are unglamorous but powerful: move regularly, sleep enough, do not smoke, and take chronic infections and visceral obesity seriously.