© Monstera Production
September 11, 2026
Marianne Waldenfels
Why do some people stay healthy longer than others? One possible explanation is the phenomenon known as inflammaging. New research is shedding light on the processes behind it – and on the role that exercise, diet, and lifestyle can play.
Inflammation serves an important purpose: it helps the body fight off infections and heal injuries. But as we age, this protective mechanism can shift. The immune system may remain subtly active even in the absence of any infection or injury. Researchers call this phenomenon "inflammaging." Over time, this persistent low-level inflammatory activity can stress tissues and organs and contribute to age-related diseases.
How pronounced this effect is, however, varies considerably from person to person. And that is precisely what makes inflammaging so compelling for longevity research: alongside genetic predispositions, environment and lifestyle also appear to play a significant role.
The term itself is a portmanteau of "inflammation" and "aging," coined by Italian immunologist Claudio Franceschi in 2000. More than 25 years later, inflammaging has become an important area of research in geriatric medicine.
A recent review in the European Journal of Immunology highlights just how complex the process really is: cellular senescence, changes in immune cells, mitochondrial dysfunction, and disrupted regulation of inflammatory responses all appear to interact with one another.
Unlike acute inflammation, inflammaging typically goes unnoticed. It does not hurt, there is no visible swelling, and there is no single identifiable trigger. Instead, inflammatory activity quietly continues running in the background.
One contributing factor is so-called senescent cells. These cells no longer divide, but they do not necessarily disappear from the tissue either. Instead, they can release a cocktail of pro-inflammatory signaling molecules known as the senescence-associated secretory phenotype, or SASP, which can amplify the body's inflammatory "background noise."
But senescent cells are only part of the picture. More recent research suggests that immune cells also change with age, mitochondria become less reliable, and inflammatory responses are less effectively switched off. Inflammaging is therefore less a single process than the result of multiple interacting changes.
Think of it like a smoke detector that no longer turns off properly: it does not blare an alarm, but it is never quite silent either. Over the course of years, this chronic activation can contribute to tissue strain and the progression of age-related diseases.
Inflammatory markers such as CRP, interleukin-6, and TNF-α can be measured in the blood, among others. However, no single laboratory value currently allows inflammaging to be reliably diagnosed. An elevated CRP alone therefore cannot tell us how quickly someone is aging.
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How strongly chronic inflammatory activity increases over a lifetime depends on many factors. Genetics play a role, as do past infections, environmental exposures, and changes within the immune system itself.
There are also factors that are at least partially within our control. Smoking, physical inactivity, chronic stress, sleep problems, and significant excess weight have all been linked to chronic inflammatory processes.
Particularly noteworthy is the fat stored in the abdominal cavity. Visceral fat is not simply an energy reserve; it is metabolically active tissue that can release pro-inflammatory signaling molecules, among other things. A current review in Nature Aging concludes that the accumulation of visceral fat is likely not merely a sign of metabolic aging, but can itself contribute to metabolic disorders and age-related changes.
Researchers are therefore increasingly working to measure the changes of the aging immune system more precisely. Even so, an established "inflammaging test" that would allow a physician to determine a person's individual inflammatory age does not yet exist.
Chronic low-grade inflammatory processes are now linked to a broad range of diseases that become more common in older age. These include, among others:
● Cardiovascular diseases
● Type 2 diabetes
● Neurodegenerative diseases such as Alzheimer's
● Muscle loss and frailty in old age
● Certain cancers
It is important to distinguish between association and causation. Inflammaging does not necessarily cause these diseases. Rather, chronic inflammatory activity appears to be one of several factors that can influence their development and progression.
There is currently no therapy that simply "switches off" inflammaging. The more pressing question, therefore, is whether chronic inflammatory activity can be influenced through lifestyle choices. For some factors, the evidence is now fairly strong.
Physical activity is among the most thoroughly studied factors. A systematic review and meta-analysis from 2025 compared people who had trained regularly over many years with untrained adults of the same age. Those who had been consistently active showed lower CRP levels and higher levels of the anti-inflammatory signaling molecule IL-10. For other inflammatory markers, the results were less clear-cut.
The flip side of these findings is also worth noting: even lifelong training apparently could not completely prevent age-related changes in the immune system. Compared with young adults, older athletes also showed differences in certain inflammatory markers.
Exercise therefore appears capable of mitigating inflammaging, but according to current research it cannot fully halt the process.
The evidence on diet is also becoming more concrete. A meta-analysis published in 2026 of 33 randomized controlled trials with a total of 3,476 participants examined the effects of a Mediterranean diet on inflammatory markers.
In people following a Mediterranean diet, hs-CRP, interleukin-6, and interleukin-17, among others, decreased significantly more than in the control groups. However, not all of the inflammatory markers studied changed. The results therefore do not support a single "anti-inflammaging diet," but they do add to the growing body of evidence that dietary patterns can influence chronic inflammatory processes.
A Mediterranean diet is typically characterized by an abundance of vegetables and fruit, legumes and whole grains, nuts, olive oil, and regular fish consumption.
Sleep deprivation, chronic stress, and excess weight can also burden the body and drive inflammatory processes. Excess weight is particularly well studied in this context: visceral fat in particular is metabolically active and can release signaling molecules that promote inflammation. Losing significant excess weight can therefore also reduce inflammatory activity in the body.
The same applies to sleep and stress. Too little sleep, chronically poor sleep quality, and persistent psychological stress are all associated with elevated inflammatory markers in studies. In addition to exercise and diet, getting adequate sleep, not smoking, and maintaining a healthy body weight can therefore also help keep chronic inflammatory processes as low as possible.
This is precisely the question that longevity research is now actively pursuing. One approach involves so-called senolytics: compounds designed to selectively eliminate senescent cells. Senomorphics take a somewhat different approach, aiming to reduce the harmful signals from these cells without destroying them.
The current inflammaging review from 2026 also describes further potential approaches, ranging from metabolic agents such as metformin and rapamycin to therapies targeting the immune system or the gut microbiome. Early clinical investigations are yielding interesting signals, but the evidence is not yet sufficient to support an established anti-inflammaging therapy in humans.
Considerable attention was already drawn in 2024 to a study in Nature in which researchers blocked the signaling pathway of the inflammatory molecule interleukin-11 (IL-11) in mice. The animals were less frail in old age and showed improved metabolism and muscle function, among other benefits. In older mice, the treatment also significantly extended remaining lifespan.
Whether such results can be translated to humans, however, remains to be seen.
Inflammaging illustrates that aging is accompanied by meaningful changes in our immune system. How strongly chronic inflammatory activity increases over time appears to differ considerably from person to person.
Research is now attempting to target individual mechanisms with medications. However, before any anti-aging therapies actually emerge from this work, a great deal of further research will be needed. Exercise and diet are less dramatic by comparison, but they hold one decisive advantage: evidence for their influence on chronic inflammatory processes in humans already exists.
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