Inflammaging is the chronic, low-grade inflammation that tends to build up with age. It is linked to heart disease, diabetes, frailty and other conditions of later life, and one major trial suggests lowering inflammation can reduce repeat heart events in some people.
Inflammaging is the slow, low-grade, body-wide inflammation that tends to develop as people get older, even without an infection or injury. The term was coined in 2000, and researchers now see it as one of the shared threads running through many conditions of later life, including heart disease, diabetes, frailty and dementia. The link with heart disease is the best supported: a large randomized trial showed that blocking one inflammatory pathway lowered repeat cardiovascular events in people with high inflammation markers. For most other conditions, whether reducing inflammation changes outcomes is still an open question.
Inflammation is part of the immune system's normal response. A 2019 perspective in Nature Medicine by Furman and colleagues explains that intermittent increases in inflammation are critical for survival during injury and infection. The concern is a different pattern the authors call systemic chronic inflammation, which certain social, environmental and lifestyle factors can promote and which can in turn contribute to many of the leading causes of disability and death worldwide.
Inflammaging is the age-related form of this pattern. In the original 2000 paper, Franceschi and colleagues described a progressive increase in pro-inflammatory status as a major characteristic of the aging process, driven by a lifetime of antigenic load and stress. They framed it in evolutionary terms: inflammation that protects us early in life may become harmful late in life, a period largely not foreseen by evolution.
A 2018 review in Nature Reviews Cardiology by Ferrucci and Fabbri lists several potential mechanisms:
A companion 2018 review in Nature Reviews Endocrinology by Franceschi and colleagues groups the triggers more simply, as signals from pathogens, from the body's own cell debris and misplaced molecules, and from nutrients and gut bacteria. It also describes "metaflammation," the chronic inflammation driven by nutrient excess, as sharing the same mechanisms as inflammaging.
According to Ferrucci and Fabbri, high levels of inflammatory markers are common in older people and predict risk of cardiovascular disease, frailty, multiple chronic conditions, and decline in physical and cognitive function. Inflammaging is also a risk factor for chronic kidney disease, diabetes, cancer, depression, dementia and sarcopenia (age-related muscle loss).
Aging clocks show a similar pattern from another angle. In the 2018 study that introduced the DNAm PhenoAge clock, Levine and colleagues found that people whose epigenetic age ran ahead of their actual age showed increased activation of pro-inflammatory and interferon pathways. You can read more about these tools in biological age vs. chronological age.
Being linked to a disease is not the same as causing it. Ferrucci and Fabbri write that whether modulating inflammation benefits the course of non-cardiovascular health problems is controversial.
The clearest test of whether inflammation causes harm came from cardiology. In the CANTOS trial, published in the New England Journal of Medicine in 2017, Ridker and colleagues enrolled 10,061 people who had previously had a heart attack and had a high-sensitivity C-reactive protein (an inflammation marker) of 2 mg or more per liter. Participants received canakinumab, an antibody that blocks the inflammatory signal interleukin-1 beta, or placebo, and were followed for a median of 3.7 years.
| Finding | Result |
|---|---|
| Effect on inflammation marker | Lowered C-reactive protein compared with placebo |
| Effect on cholesterol | No reduction in lipid levels |
| Repeat heart attack, stroke or cardiovascular death | Significantly lower with the middle dose tested (hazard ratio 0.85) |
| Fatal infections | More common than with placebo |
| Deaths from any cause | No significant difference |
The trial supported the idea that inflammation itself contributes to heart disease, independent of cholesterol. It also showed the trade-off: suppressing part of the immune system raised the risk of fatal infection. Canakinumab was tested in a specific high-risk group, and these results are averages that do not apply to everyone.
Researchers are still working on ways to detect and track chronic inflammation early, and Furman and colleagues propose strategies for advancing diagnosis, prevention and treatment. In the research reviewed here, no single test or product has been shown to measure or reverse "inflammaging" as a whole.
What the research does highlight is a set of risk factors that promote chronic inflammation, several of which are within reach of everyday choices. Furman and colleagues name infections, physical inactivity, poor diet, environmental and industrial toxicants, and psychological stress. Ferrucci and Fabbri point to central obesity and visceral fat. These overlap with familiar advice for heart and metabolic health, which is a practical reason to focus on physical activity, food quality, stress and staying current on preventive care. For how inflammation fits with other aging processes, see why we age: the hallmarks of aging.
No. It describes a gradual biological state rather than a diagnosis. Researchers consider it a risk factor that contributes to several age-related diseases, and there is no single clinical test that diagnoses it.
Blood tests can measure markers such as high-sensitivity C-reactive protein, which the CANTOS trial used to select participants. No single marker captures inflammaging as a whole, so a licensed provider should interpret any result in context.
Not without medical guidance. The best evidence comes from one targeted drug in people with prior heart attacks, and it raised the risk of fatal infections. Evidence that suppressing inflammation helps other age-related conditions is limited and debated.
Not necessarily. The original 2000 paper on inflamm-aging described the paradox that healthy centenarians can show increased blood levels of inflammatory cytokines and related proteins. The authors proposed that the capacity to cope with and adapt to stressors varies between people and has a genetic component.
If you are concerned about inflammation, a licensed provider can review your health history, decide whether any testing makes sense, and focus on the risk factors that matter most for you. This article is educational and does not determine eligibility for any treatment.
Written by the NewDay Wellness editorial team from the sources above and checked against them before publication, and medically reviewed by Dr. Sean Arora and Dr. Shannon Arora of Arora Health & Aesthetics; see our editorial standards. This article is educational and does not diagnose conditions, establish eligibility for any medication, or replace care from a licensed provider. Compounded medications are not FDA-approved.
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