By Dr Gavin McAuley | EmpowerVida
EmpowerVida | Long-form health feature — editorial review draft
Standfirst: Inflammation protects us from infection and helps injuries heal. But scientists are discovering that persistent inflammatory signalling can also contribute to disease. What does that mean for heart health, the ageing brain—and the supplements promising to put out the fire?
A splinter in your finger is a small biological emergency. Within minutes, blood vessels change, immune cells mobilise and chemical messengers coordinate a response. The skin becomes warm and tender. It isn't pleasant, but the machinery is doing precisely what it evolved to do.
Now imagine a quieter version of that signalling—less dramatic, more persistent, sometimes detectable only through changes in blood markers and immune-cell behaviour.
That is the idea behind chronic low-grade inflammation. It has become one of the most compelling themes in research on ageing and long-term disease.
It has also become a marketing opportunity. Scroll through the wellness industry and inflammation appears to explain almost everything: tiredness, abdominal fat, poor concentration, joint pain, heart disease, even cancer. The proposed solution is often an expensive supplement stack.
The science is more interesting—and less accommodating—than that.
How a protective response becomes a problem
Acute inflammation is a coordinated response to injury or infection. Blood vessels, white blood cells and signalling molecules help remove threats and begin repair. Resolution is part of a healthy response.
Chronic inflammation is different. It may occur when a trigger persists, as in some infections or autoimmune conditions. It can also accompany obesity, smoking, periodontal disease, chronic inflammatory disorders and aspects of ageing.
But 'inflammation' is not a single disease, nor is it always one measurable process. Rheumatoid arthritis, inflammatory bowel disease, atherosclerosis and age-associated low-grade inflammation involve different tissues, triggers and immune pathways. Their treatments are not interchangeable.
That distinction matters to someone living with fatigue or joint pain. Those symptoms can occur with inflammatory disease, but they can also arise from sleep disorders, anaemia, thyroid disease, medication effects, osteoarthritis, depression or many other conditions. Symptoms alone do not establish that the immune system is 'on fire'.
The paper that gave inflammaging a bigger stage
In 2019, an international group led by David Furman published Chronic inflammation in the etiology of disease across the life span in Nature Medicine.
It brought together evidence connecting persistent inflammatory activity with several conditions that become more common with age. The authors discussed infections, diet, the gut microbiome, cellular senescence and other potential contributors to chronic systemic inflammation.
It was an ambitious synthesis of a fast-moving field. It helped articulate why researchers increasingly view immune regulation as an important part of healthy ageing.
But there is a crucial caveat. The paper was a review of evidence, not a clinical trial proving that reducing a blood marker will prevent Alzheimer's disease or cancer. Nor did it establish that one inflammatory pathway is the master cause of every age-related illness.
The term inflammaging captures a useful hypothesis: ageing and persistent, low-grade inflammatory signalling may reinforce each other. Some senescent cells release inflammatory molecules. Changes in immune function may make inflammatory responses harder to resolve. Metabolic dysfunction and chronic disease can add to the picture.
Yet ageing is not reducible to inflammation. Genetics, exposures, cellular repair, vascular health and numerous other processes remain important.
What heart disease taught us about inflammation
For decades, cardiovascular disease was often described in mechanical terms: fatty deposits build up in arteries until blood flow is compromised.
That picture was incomplete. Atherosclerosis also involves immune cells and inflammatory signalling within the vessel wall. Lipoproteins, especially LDL-containing particles, play a causal role in initiating and sustaining plaque formation; inflammation helps shape how plaques develop and behave.
This is not an either-or choice between cholesterol and inflammation. Both matter.
One landmark experiment helped clarify the clinical relevance. In the CANTOS trial, published in 2017, researchers studied canakinumab, a drug targeting the inflammatory messenger interleukin-1 beta, in patients with previous myocardial infarction and elevated high-sensitivity C-reactive protein (hs-CRP). At one tested dose, treatment reduced recurrent cardiovascular events without lowering LDL cholesterol.
That result was striking: it supported the idea that targeting inflammation could reduce cardiovascular risk independently of cholesterol lowering.
It also came with trade-offs, including more fatal infections, and it did not turn canakinumab into a routine preventive treatment for the general population.
Other evidence has since strengthened the role of carefully selected anti-inflammatory treatments in certain cardiovascular settings. Low-dose colchicine, for example, has been studied and used in some patients with established coronary disease, subject to local approvals, contraindications and clinical guidance.
The lesson isn't 'everyone needs an anti-inflammatory'. It is that inflammation can be a treatable component of a particular disease when a treatment has demonstrated meaningful clinical benefits.
What about Alzheimer's disease?
The brain has immune cells of its own, including microglia. They help monitor the neural environment and respond to injury. Researchers are investigating how changes in microglial function and neuroinflammatory pathways interact with amyloid, tau, vascular disease and other processes implicated in Alzheimer's disease.
That research is important. It does not justify saying Alzheimer's is simply 'inflammation of the brain'.
You may also encounter the phrase 'type 3 diabetes'. Some researchers have used it informally to describe hypotheses about altered insulin signalling in Alzheimer's disease. It is not a standard clinical diagnosis, and it is not synonymous with neuroinflammation.
Most neuronal glucose uptake is not directly dependent on insulin in the same way as uptake in muscle or fat. The relationship between insulin signalling, brain metabolism and neurodegeneration is complex.
A supplement that changes an inflammatory marker in a cell experiment has not thereby been shown to prevent dementia in humans.
And cancer?
Chronic inflammation can contribute to cancer development in particular contexts. Long-standing inflammatory bowel disease, for example, can increase colorectal cancer risk. Certain chronic infections also raise the risk of specific cancers.
But cancer is not caused by inflammation alone. Mutations, inherited susceptibility, carcinogenic exposures, immune surveillance, tissue context and chance all play roles. Some inflammatory responses can even help the immune system recognise and attack tumours.
Calling inflammation 'the root cause of cancer' erases those distinctions. It may also encourage people to believe that antioxidants or dietary changes can replace established screening, vaccination or treatment. They cannot.
The blood test that became a wellness score
High-sensitivity C-reactive protein measures very low concentrations of CRP, a protein produced by the liver in response to inflammatory signalling. In cardiovascular medicine, hs-CRP can provide additional risk information in selected patients.
But it is not a universal 'biological ageing score'.
An elevated result is nonspecific. Infection, inflammatory illness, obesity and many other factors can raise it. A single measurement cannot diagnose a cause, prove that fatigue is inflammatory or predict someone's personal future with certainty.
In cardiovascular risk assessment, hs-CRP values around 2 mg/L or higher may be considered a risk-enhancing factor in certain guidelines and clinical contexts. That is different from claiming everyone should aim below 1 mg/L, that everyone over 35 needs screening or that a result above 3 mg/L proves accelerated ageing.
Testing should follow a clinical question. The result needs interpretation alongside symptoms, history, other risk factors and, where appropriate, repeat measurements.
A laboratory number is information. It isn't a verdict.
Does the modern diet 'cause inflammation'?
Diet can influence cardiometabolic health and inflammatory pathways. But sweeping statements about individual foods often go further than the evidence.
Take wheat. People with coeliac disease need to avoid gluten because it triggers an immune-mediated disorder. Wheat allergy and some other wheat-related conditions also deserve proper diagnosis and management.
That does not mean ordinary wheat consumption causes 'leaky gut', insulin resistance and systemic inflammation in everyone. Wholegrains are generally associated with favourable health outcomes in dietary research.
Seed oils are another popular target. They contain polyunsaturated fats, including omega-6 linoleic acid. The fact that omega-6 fatty acids participate in signalling pathways does not establish that eating commonly used seed oils causes chronic inflammation. Human trials and broader nutrition evidence are more nuanced, and replacing saturated fats with unsaturated fats can improve cardiovascular risk profiles.
A better question is not whether one ingredient is secretly poisoning our cells. It is what dietary patterns consistently support health.
Patterns rich in vegetables, fruit, legumes, wholegrains, nuts and unsaturated fats—such as Mediterranean-style eating—have a stronger evidence base than dramatic elimination lists. Minimising highly processed foods where they displace nutritious options can be sensible, without turning every packaged ingredient into a biological threat.
The antioxidant trap
Inflammation and oxidative stress are related, but they are not interchangeable. Reactive oxygen species can damage cells in some circumstances; they also participate in normal signalling and immune defence.
This is why the phrase 'more antioxidants' is not a treatment strategy.
Vitamin C is essential, but taking liposomal vitamin C has not been shown to prevent the broad range of inflammatory diseases sometimes claimed for it. N-acetylcysteine has established medical uses in specific circumstances, including paracetamol poisoning, but that does not make routine NAC supplementation a proven anti-ageing protocol.
Astaxanthin has interesting laboratory properties. Claims that it protects the human brain from degeneration or functions as an 'internal sunscreen' require much stronger clinical evidence.
Methylene blue deserves particular caution. It is a drug with legitimate medical indications, not an established supplement for mitochondrial rejuvenation. It can interact dangerously with serotonergic medicines, potentially causing serotonin toxicity, and may cause haemolysis in people with G6PD deficiency. It should not be presented as an at-home anti-inflammatory or longevity treatment.
Laboratory antioxidant rankings—'thousands of times stronger than vitamin C'—do not tell us whether a product prevents disease in people. Clinical outcomes, safety and study quality matter far more.
What genuinely deserves attention?
The strongest approach is often less glamorous than the supplement advertising.
Don't smoke. Smoking drives cardiovascular and cancer risk through multiple pathways, including inflammation. Stopping has benefits far beyond changes in a biomarker.
Move regularly. Physical activity improves cardiometabolic health and can influence inflammatory markers. Resistance training also helps preserve strength and function with age.
Pay attention to sleep. Chronic sleep disruption can affect immune and metabolic regulation. Persistent sleepiness, loud snoring or unrefreshing sleep may warrant assessment rather than another supplement.
Treat the conditions you actually have. Managing hypertension, diabetes, dyslipidaemia, periodontal disease and established inflammatory disorders has a far clearer rationale than chasing a vague 'inflammation detox'.
Eat for the long term. A balanced dietary pattern is more defensible than eliminating whole food categories based on isolated mechanistic studies.
Keep perspective. If joint pain, unexplained fatigue, weight loss, fevers or persistent symptoms are affecting your life, seek a clinical assessment. These symptoms need a differential diagnosis, not an automatic label of chronic inflammation.
None of this is a claim that lifestyle can cure autoimmune disease or replace medication. Modern anti-inflammatory and immune-modulating treatments have transformed outcomes for many people with conditions such as rheumatoid arthritis and inflammatory bowel disease. Dismissing them as 'mere symptom management' would be profoundly unfair to patients—and scientifically wrong.
Why this research gives us reason to be optimistic
The most exciting part of the inflammation story is not the prospect of a universal anti-inflammatory pill. It is the growing ability to identify specific immune pathways and test whether changing them improves outcomes that matter to patients.
The CANTOS trial offered a powerful proof of principle in a carefully selected cardiovascular population: targeting an inflammatory pathway changed clinical events without lowering LDL cholesterol. That did not settle the question for every disease, and the safety trade-offs were real. But it opened an important door.
Meanwhile, researchers are studying how immune ageing, senescent cells, metabolic health and tissue repair interact. Some ideas will fail when tested in people. Others may eventually reshape prevention or treatment. Both outcomes move the field forward.
For anyone interested in living longer and living better, that's an energising prospect: a deeper understanding of biology could lead to more targeted care.
What you can do with this knowledge today
Protect the fundamentals. Regular physical activity, not smoking, adequate sleep and a balanced dietary pattern support health through multiple pathways. You do not need to prove that each habit 'switches off inflammation' for it to be worth doing.
Treat real risk factors. Blood pressure, LDL cholesterol, diabetes risk and established inflammatory conditions deserve attention because there are interventions with meaningful clinical evidence behind them.
Be curious, not alarmed, about biomarkers. If hs-CRP is appropriate to a cardiovascular risk discussion, it can add context. It should not become a score you chase with supplements.
Investigate symptoms properly. Persistent fatigue, joint pain or unexplained systemic symptoms are reasons for thoughtful clinical assessment, not a self-diagnosis of inflammaging.
Keep experimental treatments in their lane. Methylene blue, antioxidant stacks and other fashionable interventions should not be promoted as established longevity therapies simply because their mechanisms sound promising.
The discoveries worth watching
Three areas deserve particular attention: trials of targeted immune therapies in defined diseases; research on how cellular senescence interacts with inflammatory signalling; and better ways to distinguish harmful chronic inflammation from the immune responses we need.
The goal is not to suppress the immune system indiscriminately. It is to understand when, where and for whom an intervention changes health outcomes.
That is a far more hopeful future than a shelf full of 'fire extinguishers'.
Inflammation is not the explanation for every illness. But learning to understand it—and, in the right circumstances, treat it more precisely—could be one of the important chapters in the story of healthier ageing.