The science of healthy ageing
Why inflammation can linger as you get older.
The difference between a useful immune response and a signal that does not fully settle.
The short version
Inflammation helps protect and repair the body. With age, repeated cellular warning signs and slower clean-up can make some responses harder to resolve. But the human picture is more varied than a simple “more birthdays, more inflammation” story.
01 / A useful response
Inflammation is meant to have an ending.
Protection begins the response.
Resolution completes it.
A small cut gives you a familiar glimpse of inflammation at work. The surrounding skin may become warm, red or swollen as blood flow changes and immune cells arrive. What looks like irritation is part of an organised response: contain a problem, clear damaged material and make repair possible.
The important part is what happens next. Once the immediate threat is dealt with, the response needs to wind down. Cells that helped defend the tissue must be removed, inflammatory signals must ease, and the local environment must return towards normal. A good immune response is not simply a strong one. It is one that starts when needed and finishes appropriately.
When the timing changes.
With ageing, that timing can become less tidy. Researchers use the term inflammageing to describe the chronic, low-grade inflammatory activity often associated with older age. This is not necessarily the redness of an injury or the dramatic symptoms of an infection. It can be a quieter pattern of signals, detectable in research long before anyone could point to one obvious source.
So why might the response linger? One answer is that ageing tissues can generate more reasons to sound the alarm. Another is that the systems responsible for clearing up afterwards can become less effective. Understanding both sides gives us a more useful picture than the idea that inflammation is simply bad and should always be switched off.
Respond
Immune cells and signals help deal with a challenge.
Clear
Cells and material that are no longer needed must be removed.
Resolve
Signals ease and the local environment moves back towards normal.
02 / The alarm without an infection
Sometimes the trigger comes from within.
Our immune defences are built to recognise danger. Microbes are one source, but they are not the only one. Molecules released or displaced by stressed and damaged cells can also attract attention. Scientists call this sterile inflammation: an inflammatory response that does not require an invading pathogen.
This distinction matters because everyday maintenance becomes more demanding as tissues age. Cells accumulate damage, some enter a state called senescence, and the handling of cellular components can change. Senescent cells no longer divide, but they are not necessarily silent. Some release mixtures of signalling molecules that can influence nearby cells and immune activity.
DNA in the wrong place.
One particularly interesting alarm system is called cGAS–STING. DNA normally belongs in specific compartments within a cell. When DNA appears in the cell’s fluid interior, it can be a warning sign. The sensor cGAS detects it and sets off a signalling pathway involving STING, helping activate immune responses. That is useful during some infections. But misplaced DNA from our own cells can engage the same machinery.
From misplaced DNA to immune signalling.
- 01
Cellular stress
Material can leave its usual compartment.
- 02
cGAS detects DNA
The sensor recognises DNA in the cell’s fluid interior.
- 03
STING carries the signal
This pathway helps activate immune responses.
What the experiment showed.
A 2023 study connected this pathway with ageing-related inflammation in experimental systems. The researchers found that blocking STING reduced inflammatory features and improved certain functional measures in aged mice. The work helps explain how cellular damage might keep immune signals active even without an infection. It does not establish that people should take a STING-blocking treatment, or that an available supplement produces the same effects. [1]
Why a signal can keep finding a trigger.
Notice how this changes the usual picture of an immune threat. The relevant material does not have to be foreign, and there does not have to be a single dramatic event. Small disruptions in the way cells contain, recycle or dispose of their components can become part of the surrounding tissue’s conversation. The signals are real, even when there is no germ to remove.
The larger idea is straightforward: a danger detector can work as designed yet still contribute to a problem when warning material keeps appearing. An alarm does not have to be broken to ring too often.
03 / The overlooked half
Finishing the response takes work, too.
It is tempting to imagine inflammation ending when the original trigger disappears, like a light going out when you remove a battery. Biology is more active than that. Resolution involves coordinated changes in immune-cell behaviour, chemical signals and tissue repair.
Clearing cells is an active handover.
Consider the cells that arrive early during an inflammatory response. After doing their job, many die in a controlled way. Other immune cells, including macrophages, recognise and engulf these dead cells. This process has an awkward name, efferocytosis, but an important purpose: tidy removal before the contents of dead cells create further trouble.
That clean-up can also help redirect the response towards resolution. A macrophage is not just a rubbish collector. What it encounters and takes up can influence the signals it sends next. If dead cells accumulate or clearance is inefficient, a tissue may remain in an environment that encourages continued inflammatory activity.
Early responders finish
After doing their job, many immune cells die in a controlled way.
Macrophages clear them
Other immune cells recognise and engulf these dying cells.
The signals can change
What macrophages take up can help redirect the response towards resolution.
A clean-up pathway in ageing mice.
In a mouse study published in 2020, researchers examined how ageing affected this process in a model of injury following interrupted and restored blood flow. Older mice showed impaired resolution, with changes involving a molecule called MerTK that helps macrophages clear dying cells. The study offers a concrete example of a clean-up pathway becoming less effective with age. It is mechanistic animal evidence, not proof that this exact pathway explains every person’s inflammatory profile. [2]
Explore the idea
A response can be useful.
Persistence changes the picture.
Compare a response that resolves with one that persists.
The duration matters, too.
Together, the trigger and clean-up stories explain why simply asking “How much inflammation is there?” can miss something. The duration of the response, the source of the signals and the quality of resolution also matter. An immune system needs both a reliable accelerator and a reliable way to come back to rest.
04 / The human picture
Ageing does not follow one inflammatory script.
Mechanisms explain what can happen. They do not tell us how consistently it happens across different lives. That is an important distinction, because much of what we know about human ageing comes from populations living in industrialised settings.
A 2025 study in Nature Aging challenged the idea that a familiar inflammageing pattern is universal. Researchers examined inflammatory cytokine patterns in four populations: cohorts in Italy and Singapore, the Tsimane in Bolivia and the Orang Asli in Malaysia. The age-related inflammatory structure seen in the industrialised cohorts did not generalise in the same way to the two Indigenous populations. [3]
A pattern is different from a ranking.
This was not a simple contest over which population had the lowest inflammation. The assays and available markers differed, limiting direct comparisons of absolute cytokine levels. The useful finding concerned patterns and their relationships with age and health. It suggests that the environment in which people live may shape what we recognise as inflammageing.
It also does not identify one food, habit or supplement that explains the difference. Infection exposure, lifestyle and other conditions are intertwined, and an observational comparison cannot neatly separate them. What it does provide is a valuable correction: persistent inflammation is associated with ageing in many settings, but it should not be presented as an identical, unavoidable trajectory for everyone.
05 / Reading the evidence
A marker is a clue, not the whole story.
Research often measures inflammation through substances in the blood. C-reactive protein, or CRP, is one familiar example. Cytokines such as interleukin-6, usually written as IL-6, are another. These measurements make it possible to study associations and compare changes over time, but they are not interchangeable descriptions of the entire immune system.
How might it work?
Cell and animal experiments can reveal pathways and test biological explanations.
What changed in people?
A trial can measure a specific blood marker without establishing a long-term health benefit.
Did people fare better?
Evidence of fewer illnesses or better function answers a different, more direct question.
What a blood marker can tell us.
A blood marker cannot, by itself, tell us which tissue started a signal, whether local repair is proceeding well or whether all inflammatory pathways have changed together. A lower result for one marker is therefore narrower evidence than the phrase “reduces inflammation” might imply.
A change in a marker is one kind of result.
There is a second distinction worth keeping in view: changing a marker is not the same as demonstrating a meaningful health outcome. A study may show an effect on CRP without testing whether people live longer, remain independent for longer or develop fewer diseases. Those outcomes require their own evidence, usually from larger or longer studies.
Why studies can appear to disagree.
It also helps explain why studies can appear to disagree. One may examine a short-term change in a single cytokine; another may assess a panel of markers or follow a different group for much longer. Similar language in the headlines can hide quite different scientific questions. Looking at the actual measurement is more informative than counting how many studies use the word inflammation.
Read the actual question.
This does not make biomarkers unhelpful. It makes them useful within their limits. The clearest reading asks three questions: what was measured, in whom, and what actually changed? Those questions are especially valuable when a headline moves quickly from a promising biological mechanism to a claim about healthy ageing.
06 / From mechanism to intervention
Human trials are where the claims get narrower.
Can inflammatory markers change in response to an intervention? Yes. But the details matter more than a broad promise to “fight inflammageing”.
The CALERIE trial provides one example. It studied a sustained calorie-restriction intervention in healthy adults aged 21 to 50 who were not obese. Over two years, participants in the intervention group achieved an average reduction in calorie intake of about 12%, less than the intended 25%. An analysis reported improvements in several cardiometabolic risk measures, including high-sensitivity CRP. [4]
What this human result establishes.
That is evidence that a structured intervention can change particular risk markers in a defined group. It is not evidence that calorie restriction extends human lifespan, and the participants were not a representative sample of older adults. Nor does a supervised research programme translate into a blanket instruction to eat less. The study belongs in this story because it shows the difference between a measured human result and a much larger longevity claim.
From a pathway to a person.
The same discipline applies to compounds studied for their effects on inflammatory pathways. An ingredient can have interesting activity in cells, produce an effect in an animal model and still deliver an uncertain or modest result in people. Human biology introduces absorption, metabolism, dose, baseline health and many other variables that a laboratory experiment cannot fully reproduce.
That gap is not a reason to dismiss research. It is the reason to keep asking for the next layer of evidence rather than treating the first layer as the final answer.
07 / A familiar ingredient, a careful distinction
Where does quercetin fit?
Quercetin is a plant compound often discussed in relation to inflammation and healthy ageing. Its laboratory biology is interesting, but the human evidence should not be condensed into a promise that taking it will switch off inflammageing.
A human trial gives a reality check.
A large 12-week randomised trial gives a useful reality check. Of 1,023 people recruited, 1,002 completed the study. Participants received placebo or one of two supplements providing 500mg or 1,000mg of quercetin daily, alongside vitamin C and niacin. The study did not find a broad improvement across the inflammatory measures assessed, although there was a small IL-6 difference with the higher-dose supplement. [5]
Reading the trial
What the combination can establish.
Two details stop this becoming a misleading headline in either direction. First, the supplement contained more than quercetin, so its effects cannot be attributed to quercetin alone. Second, a result in this particular population, at these doses and over this period, does not settle every possible use. It does, however, argue against presenting quercetin as a proven general solution for chronic age-related inflammation.
Reading the product
Why the formulation matters.
It is also important not to transfer findings between formulations. A study using one combination does not validate a different product merely because both contain quercetin. Ingredient amounts help you understand what is in a bottle; they do not establish what that bottle will do for ageing or disease.
The takeaway
The goal is not silence.
It is a well-timed response.
Inflammation is part of how the body protects and repairs itself. The ageing question is not why that system exists, but why some signals continue after their useful moment has passed. Repeated cellular warning signs and less effective clean-up offer two connected explanations.
Human research adds a necessary layer of perspective. Inflammatory ageing patterns are not identical across populations, blood markers reveal only part of the process, and interventions need to be judged by what they actually demonstrate in people.
That leaves a more interesting idea than “all inflammation is bad”. Healthy immune function depends on context and timing: recognising a problem, mounting an appropriate response, clearing what is no longer needed and making room for repair. The science of inflammageing is, in large part, the science of how that ending can become harder to reach.
Read the research
Sources & further reading.
- Gulen et al. (2023). cGAS–STING drives ageing-related inflammation and neurodegeneration. Nature.Experimental cell and mouse evidence; not a clinical treatment trial.
- Rymut et al. (2020). Resolvin D1 promotes efferocytosis in aging by limiting senescent cell-induced MerTK cleavage. FASEB Journal.Published online in 2019; experimental ageing and injury models.
- Franck et al. (2025). Nonuniversality of inflammaging across human populations. Nature Aging.Four-population observational analysis; cytokine patterns and associations, not directly comparable absolute levels across all assays.
- Kraus et al. (2019). 2 years of calorie restriction and cardiometabolic risk (CALERIE): exploratory outcomes of a multicentre, phase 2, randomised controlled trial. The Lancet Diabetes & Endocrinology.Exploratory outcomes of a randomised trial; risk markers rather than lifespan.
- Knab et al. (2011). Influence of quercetin supplementation on disease risk factors in community-dwelling adults. Journal of the American Dietetic Association.Quercetin combined with vitamin C and niacin; 12-week trial.
- Arnardottir et al. (2014). Aging delays resolution of acute inflammation in mice: reprogramming the host response with novel nanoproresolving medicines. Journal of Immunology.Further mechanistic reading on active resolution, not evidence for a consumer supplement.
- Eternum Labs: Quercetin with Bromelain.Source for current formulation and bottle image only, checked 27 October 2026. Product marketing claims are not used as clinical evidence.
