Chronic low-grade inflammation: what it is and how to lower it
Chronic low-grade inflammation is a quiet, persistent activation of the immune system that runs in the background for years, without the redness, heat or pain of an ordinary injury. It is not the same as the helpful acute inflammation that heals a cut or clears an infection; it is that response stuck on a low simmer. It matters because it tracks with heart disease, type 2 diabetes and cognitive decline, and because the levers that genuinely lower it are mostly free: losing visceral fat, moving more, sleeping properly, not smoking, eating a sensible diet and looking after your gums. The supplement aisle is a much weaker lever than its marketing implies.
Key facts
- Acute inflammation is fast, local and self-limiting; chronic low-grade inflammation is systemic, persistent and below the threshold of symptoms.
- It is most often gauged by high-sensitivity C-reactive protein (hs-CRP): below 1 mg/L is lower cardiovascular risk, 1 to 3 average, above 3 higher, on the long-standing US CDC and American Heart Association bands.1
- In 54 prospective studies and 160,000 people, each rise in CRP tracked higher rates of heart disease, stroke and death, though genetic studies suggest CRP is a marker, not the cause.23
- The biggest modifiable drivers are visceral fat, inactivity, poor sleep, smoking, diet and untreated gum disease. Most anti-inflammatory supplements show small or inconsistent effects on hs-CRP.
Acute versus chronic: the same tool, two different jobs
Acute inflammation is one of the body's most useful responses. When tissue is injured or infected, immune cells flood the area, blood vessels widen, and you get the classic signs: redness, swelling, warmth and pain. It is intense, tightly targeted and, crucially, it switches off once the job is done. Without it, wounds would not heal and infections would not clear.
Chronic low-grade inflammation is that same machinery failing to stand down: a faint, body-wide hum of immune signalling driven by messengers such as interleukin-6 (IL-6), tumour necrosis factor alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta). It produces no obvious symptoms, which is exactly why it is dangerous. It does its damage silently, over decades, on blood vessel walls, in the pancreas and in the brain.
Inflammaging: why this rises with age
The term inflammaging was coined in 2000 by the Italian immunologist Claudio Franceschi and colleagues to describe the chronic, low-grade, sterile inflammation that increases with age even when no infection is present.4 It is now seen as one of the engines of biological ageing. Several things feed it: a gradual shift of the immune system toward a pro-inflammatory state, the buildup of worn-out senescent cells that leak inflammatory signals (the senescence-associated secretory phenotype), and the slow accumulation of cellular debris the body must keep clearing.
This sits alongside the wider biology of getting older, which we map in our guide to the hallmarks of ageing. Inflammaging is one of the threads tying many of them together, and partly why the same lifestyle levers help so many age-related conditions at once.
The disease links: strong, but read them honestly
Heart disease. This is the best-evidenced link. The Emerging Risk Factors Collaboration pooled 54 prospective studies and 160,309 people and found CRP rose in step with the risk of coronary heart disease, stroke and vascular death.2 The nuance is causality. Mendelian randomisation studies, which use genetic variants to test whether a marker actually drives disease, suggest genetically raised CRP does not itself cause coronary heart disease: CRP flags the fire, it is not the fire.3 The fire is real, though. In the CANTOS trial (Ridker and colleagues, New England Journal of Medicine, 2017), 10,061 people after a heart attack with hs-CRP at or above 2 mg/L were given canakinumab, a drug that blocks IL-1 beta. It cut recurrent cardiovascular events without lowering cholesterol at all, the first proof that targeting inflammation itself reduces risk.5 The LoDoCo2 trial later showed low-dose colchicine (0.5 mg daily) reduced events in chronic coronary disease.6
Canakinumab and colchicine are prescription anti-inflammatory drugs studied in people with established heart disease, not general anti-ageing tools. Colchicine is not licensed in the UK for routine cardiovascular prevention, and canakinumab was never marketed for it. Neither is a reason to self-medicate; the takeaway is mechanistic, not a prescription.
Type 2 diabetes. Visceral fat (the deep fat around the organs) behaves like an active inflammatory organ, releasing IL-6 and TNF-alpha that interfere with insulin signalling.7 Chronic inflammation and insulin resistance reinforce each other, which is why inflammation features in our piece on the early signs of insulin resistance.
Cognitive decline. Here the evidence is suggestive rather than settled. In the ARIC cohort, US adults with raised inflammatory markers in midlife showed a steeper 20-year decline in cognition.8 The association is consistent across several cohorts, but whether lowering inflammation protects the brain is not yet proven.
How it is measured: hs-CRP
The standard test is high-sensitivity C-reactive protein. CRP is made by the liver in response to IL-6; the high-sensitivity assay reads it down to about 0.3 mg/L, low enough to pick up the faint elevations ordinary CRP testing misses. Because a recent cold, an injury or hard exercise can all push it up temporarily, a single reading means little: it should be measured when you are well, ideally repeated, and read alongside everything else. We cover how to interpret it, and how it differs from ESR and ferritin, in our guide to inflammatory markers explained.
| hs-CRP level | Interpretation | Practical note |
|---|---|---|
| Below 1 mg/L | Lower cardiovascular risk | Reassuring in a well person |
| 1 to 3 mg/L | Average risk | Read in context of other risk factors |
| Above 3 mg/L | Higher risk | Recheck when well; if persistent, discuss with GP |
| Above 10 mg/L | Likely acute cause | Suggests infection or injury, not chronic risk |
In UK practice, hs-CRP is not a routine screening test. The NHS uses the QRISK calculator for cardiovascular risk, and inflammation is only one consideration among many. A raised hs-CRP is a prompt to look at the modifiable causes below, not a diagnosis in itself.
The honest hierarchy of levers
If you want to lower chronic inflammation, the evidence points clearly at lifestyle, not pills. The effects below are mostly measured as changes in hs-CRP or IL-6, and they overlap, so pursuing several at once usually beats obsessing over one.
| Lever | What the evidence shows | Strength |
|---|---|---|
| Reducing visceral fat | Visceral fat actively produces IL-6 and TNF-alpha; diet-induced weight loss lowers inflammatory cytokines.7 | Strong, mechanistic and clinical |
| Regular exercise | Pooled meta-analyses show exercise lowers CRP (mean effect roughly -0.38), with aerobic training most studied.9 | Strong (RCT meta-analyses) |
| Not smoking | Smoking raises CRP and fibrinogen dose-dependently; markers fall after quitting, normalising over about 5 years.10 | Strong (observational) |
| Mediterranean-style diet | In PREDIMED, the diet lowered hs-CRP, IL-6 and other markers over 3 to 5 years versus a low-fat diet.11 | Moderate to strong (RCT) |
| Sleep | Sleep disturbance and short sleep track higher CRP and IL-6 across 72 studies; effect sizes are modest.12 | Moderate (observational) |
| Treating gum disease | Periodontal treatment modestly lowers CRP and improves blood-vessel function within months.13 | Moderate (RCT, surrogate outcomes) |
A practical reading: visceral fat, exercise and not smoking do the heavy lifting; a Mediterranean-style pattern, good sleep and healthy gums add to it. If you are organising changes across diet, training and any supplements, our stack builder can help you avoid duplication.
The supplement market: where hype outruns evidence
"Anti-inflammatory" supplements are a large and confident market. The honest picture is more muted. Omega-3 fish oil shows no consistent effect on CRP in the general population, though it can lower it in specific groups such as people on dialysis.14 Curcumin (from turmeric) has more promising signals: several meta-analyses report reductions in hs-CRP, but the trials are often small, heterogeneous and of variable quality, and curcumin is poorly absorbed, so real-world results vary widely.15
Evidence read: no supplement comes close to the effect of losing visceral fat, exercising and not smoking. If a product helps you and is safe, that is fine, but it is a garnish, not the meal. Be wary of any supplement marketed as a complete inflammation fix, and treat large effect-size claims from small or industry-funded trials with caution.
- My hs-CRP is raised; could a recent infection or injury explain it, and should we recheck when I am well?
- Given my overall cardiovascular risk (for example my QRISK score), does this inflammation reading change anything?
- Could my waist measurement or visceral fat be driving this, and what would meaningful change look like?
- Are my gums, sleep or smoking worth addressing as part of the picture?
- Is there an underlying condition (such as an autoimmune problem) we should rule out behind a persistently high result?
References
- Pearson TA, Mensah GA, Alexander RW, et al. Markers of inflammation and cardiovascular disease: application to clinical and public health practice. A statement from the CDC and AHA. Circulation. 2003;107(3):499-511. ahajournals.org.
- Emerging Risk Factors Collaboration (Kaptoge S, et al). C-reactive protein concentration and risk of coronary heart disease, stroke, and mortality: an individual participant meta-analysis. Lancet. 2010;375(9709):132-140. thelancet.com.
- C Reactive Protein Coronary Heart Disease Genetics Collaboration. Association between C reactive protein and coronary heart disease: mendelian randomisation analysis based on individual participant data. BMJ. 2011;342:d548. PMC3039696.
- Franceschi C, Bonafe M, Valensin S, et al. Inflamm-aging: an evolutionary perspective on immunosenescence. Ann N Y Acad Sci. 2000;908:244-254. PMID 10911963.
- Ridker PM, Everett BM, Thuren T, et al. Antiinflammatory therapy with canakinumab for atherosclerotic disease (CANTOS). N Engl J Med. 2017;377(12):1119-1131. nejm.org.
- Nidorf SM, Fiolet ATL, Mosterd A, et al. Colchicine in patients with chronic coronary disease (LoDoCo2). N Engl J Med. 2020;383(19):1838-1847. nejm.org.
- Reilly SM, Saltiel AR (and related reviews). Adipose tissue inflammation and metabolic dysfunction in obesity. Nat Rev Endocrinol / PMC review. 2021. PMC8294624.
- Walker KA, Gottesman RF, Wu A, et al. Association of midlife inflammatory markers with cognitive performance at 10-year follow-up (ARIC). Neurology. 2022;99(20):e2294-e2304. PMC9694835.
- Khosravi N, et al (and Fedewa MV, et al). The effect of exercise on chronic systemic inflammation: meta-analyses of randomised trials. Sport Sci Health / J Sports Sci. PMID 33153926.
- Bakhru A, Erlinger TP. Smoking cessation and cardiovascular disease risk factors: results from the Third National Health and Nutrition Examination Survey. PLoS Med. 2005;2(6):e160. PMC1160573.
- Casas R, Sacanella E, Urpi-Sarda M, et al. Long-term immunomodulatory effects of a Mediterranean diet in adults at high cardiovascular risk (PREDIMED). J Nutr. 2016;146(9):1684-1693. PMID 27440261.
- Irwin MR, Olmstead R, Carroll JE. Sleep disturbance, sleep duration, and inflammation: a systematic review and meta-analysis of cohort studies and experimental sleep deprivation. Biol Psychiatry. 2016;80(1):40-52. PMC4666828.
- Tonetti MS, D'Aiuto F, Nibali L, et al. Treatment of periodontitis and endothelial function. N Engl J Med. 2007;356(9):911-920. nejm.org.
- Kavyani Z, et al. Efficacy of omega-3 fatty acid supplementation on inflammatory biomarkers: an umbrella meta-analysis. Int Immunopharmacol. 2022;111:109104. sciencedirect.com.
- Gorabi AM, et al. Effects of curcumin on inflammatory biomarkers: an umbrella meta-analysis of randomised clinical trials. Inflammopharmacology / PMC. 2023. PMC9870680.
This article is educational and does not constitute medical advice, diagnosis, or a treatment recommendation. Medication uses described as “off-label” are not licensed for that purpose in the UK and should only be considered under qualified clinical supervision. Always speak to your GP, pharmacist, or a registered specialist before starting, stopping, or changing any treatment. If you have severe or alarm symptoms - unintentional weight loss, blood in your stool, difficulty swallowing, persistent vomiting, a fever, or severe pain - seek urgent medical care.