hs-CRP: The Inflammation Marker Worth Tracking

Across 160,309 adults in 54 prospective studies, a three-fold higher C-reactive protein came with 63% more coronary events. Adjust for smoking, blood pressure, lipids and diabetes, and that falls to 37%. Still there. Much smaller.

That is the Emerging Risk Factors Collaboration, published in the Lancet in 2010. It is still the best observational estimate anyone has. A second collaboration, pooling 47 studies, put the same figure at 33%.

So the signal is real, and it is modest. A three-fold gap in CRP is a wide gap. It buys about a third more risk on top of what your other numbers already told you.

What the test actually is

hs-CRP is the same protein your GP measures when they suspect an infection. The difference is the assay, not the molecule.

A standard CRP test reports reliably down to about 5 mg/L. That is fine for spotting pneumonia. It is useless for cardiovascular risk, where the whole interesting range sits below 5.

A high-sensitivity assay reads to roughly 0.1 mg/L. Same blood, same protein, finer ruler. When a private panel lists "hs-CRP", that is all it means.

CRP itself is made in the liver in response to interleukin-6. It is downstream of whatever is driving the inflammation, which turns out to matter a great deal later in this article.

The three bands, and what they are worth

The CDC and the American Heart Association drew the lines in 2003. Under 1 mg/L is low risk. Between 1 and 3 is average. Above 3 is high.

Those thresholds are tertiles of a healthy American population. They are not a diagnosis and they are not a cliff edge. A reading of 3.1 tells you nothing meaningfully different from 2.9.

Above 10 mg/L, the number has usually stopped talking about your arteries. It is reporting an infection, an injury, a dental problem or a flare of something autoimmune. The standard response is to discard the reading and repeat it later.

For a 55-year-old who trains five times a week, the useful question is not which band you land in. It is whether your average sits nearer 0.6 or nearer 2.5, and which direction it has moved over two years.

Why a single reading is close to useless

This is the part most private testing companies skip. hs-CRP is a very noisy measurement within the same person.

A 2024 systematic review pooled 60 studies of biological variation. The median within-subject coefficient of variation for hs-CRP was 0.44, with a range from 0.27 to 0.76.

Put plainly: retest the same unchanged person and the second result can land 40% or more away from the first. Nothing has happened. That is just the marker breathing.

Clinical practice handles it bluntly. Take two readings about two weeks apart and average them. If the first came back above 2 mg/L, the repeat is not optional.

Training adds a second layer of noise. CRP climbs after hard eccentric work, peaks 24 to 72 hours after a marathon, and stays above baseline for two or three days. One marathon cohort recorded a 266% rise at 24 hours.

So: book bloods on a rest day, at least 72 hours after your hardest session, and not within a fortnight of a cold, a vaccination or dental work. Do that and the number is worth reading. Skip it and you are measuring last Sunday's long run.

The awkward finding about causation

If CRP drove atherosclerosis, people born with genes for higher CRP should have more heart attacks. They do not.

The C Reactive Protein Coronary Heart Disease Genetics Collaboration pooled individual data from 47 studies across 15 countries. It used four common variants in the CRP gene as a natural randomisation — you inherit them at conception, so they are not confounded by lifestyle.

Carriers had reliably higher circulating CRP. Their coronary risk was not raised to match. The authors concluded that CRP is unlikely to be even a modest causal factor.

That reframes what the test is for. CRP is the thermometer, not the fire. Pushing the thermometer down for its own sake achieves nothing. Changing what the thermometer is reading is a different matter.

Does lowering inflammation change outcomes?

Two large trials have tried, and their answers differ in an instructive way.

JUPITER randomised 17,802 adults with LDL under 3.4 mmol/L but hs-CRP at or above 2 mg/L to rosuvastatin 20 mg or placebo. The primary endpoint fell from 1.36 to 0.77 events per 100 person-years, a hazard ratio of 0.56. Median hs-CRP at four years was 1.8 versus 3.3 mg/L.

The trouble is that LDL fell too, by roughly half. You cannot separate the two effects from that design. Physician-reported diabetes was also higher on rosuvastatin, 3.0% against 2.4%.

CANTOS was cleaner. It gave canakinumab — an antibody against interleukin-1 beta — to 10,061 people with a previous heart attack and hs-CRP of at least 2 mg/L. The drug lowers inflammation without touching LDL at all.

Both trials ran in high-risk patients under close medical supervision, using prescription drugs. Neither says anything about supplements. What they do establish is that inflammation is a legitimate target, which is why the marker is worth watching at all.

What actually moves the number

Three levers have decent controlled evidence behind them, and they are the unglamorous ones.

Body weight is the strongest. A systematic review of diet, exercise and surgical weight-loss studies found each kilogram lost tracked with a 0.13 mg/L fall in CRP, a near-linear relationship across the whole range.

Training works, including without weight change. A 2017 meta-analysis of 3,769 participants reported an effect size of 0.38 when BMI fell alongside the training, and 0.19 when it did not. Roughly half the benefit survives without any change on the scales.

In people with type 2 diabetes, 14 randomised trials in 824 patients found exercise lowered CRP by 0.66 mg/L, about 14% from baseline. That is a real shift for a group with plenty of room to move.

Sleep debt, smoking, heavy alcohol and untreated gum disease all push the number the other way. None of them are news, and all of them are larger levers than anything in a capsule.

Where omega-3 actually sits

Here the honest answer is narrower than the marketing. A 2025 dose-response meta-analysis pooled 40 randomised trials of EPA and DHA.

It found a non-linear reduction in CRP up to about 1,200 mg/day of combined EPA and DHA in people with cardiovascular disease, metabolic syndrome or hypertension. In people with dyslipidaemia, the fall was linear with dose.

In overweight and obese participants it found nothing. No significant reduction, and no dose-response relationship at any intake tested.

That null result deserves more attention than the positive ones. The trials that moved CRP were run in people who were already metabolically unwell. If your hs-CRP averages 1.2 and you train four times a week, you are not the population that was studied.

We sell algal omega-3, so treat this as the disclosure it is: the only claim the GB register permits us is that EPA and DHA contribute to the normal function of the heart, at 250 mg combined per day. That claim says nothing about CRP, and we are not going to imply otherwise. If you want the mechanistic split between the two fatty acids, we covered it in DHA vs EPA.

Getting tested in the UK

NHS CRP testing is generally ordered to investigate infection or inflammation, using the standard assay. Asking for it as a cardiovascular check will usually get a polite no, and QRISK3 — the calculator UK primary care actually uses — does not take CRP as an input.

That leaves private panels, where hs-CRP is rarely sold alone and usually bundled with lipids, HbA1c and liver function. Bundling is fine, because a lone CRP number is the least useful way to read it.

Interpret it alongside the rest. A CRP of 2.4 with an HbA1c of 41 mmol/mol, central fat and a poor sleep record is a coherent picture. The same 2.4 in a lean, well-slept 58-year-old is probably noise, or a cold you shrugged off three weeks ago.

Take anything persistently above 3 mg/L to a GP as a question about your overall risk profile, not as a result to be fixed on its own.

What to do with it

Test twice, two weeks apart, both on rest days, and average the two. Repeat annually alongside lipids, HbA1c and blood pressure. One reading in isolation is not worth the venepuncture.

Judge the trend rather than the band. Moving from an average of 2.8 to 1.6 over eighteen months while your waist and your dietary pattern both improved is a meaningful signal. Crossing from 3.1 to 2.9 is not.

And keep the causal picture straight. The genetics say CRP is a readout, not a cause. Chasing the number with anything that lowers it cosmetically misses the point entirely. Chasing what raises it — visceral fat, poor sleep, sedentary weeks, untreated dental problems — is the whole of the useful work.

References

1. Emerging Risk Factors Collaboration (2010). "C-reactive protein concentration and risk of coronary heart disease, stroke, and mortality: an individual participant meta-analysis." The Lancet, 375(9709), 132-140. PMID 20031199.
2. C Reactive Protein Coronary Heart Disease Genetics Collaboration (2011). "Association between C reactive protein and coronary heart disease: mendelian randomisation analysis based on individual participant data." BMJ, 342, d548. PMID 21325005.
3. Pearson TA, Mensah GA, Alexander RW, et al. (2003). "Markers of inflammation and cardiovascular disease: application to clinical and public health practice. A statement for healthcare professionals from the CDC and the American Heart Association." Circulation, 107(3), 499-511.
4. Ridker PM, Danielson E, Fonseca FAH, et al. (2008). "Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein (JUPITER)." New England Journal of Medicine, 359(21), 2195-2207.
5. Ridker PM, Everett BM, Thuren T, et al. (2017). "Antiinflammatory therapy with canakinumab for atherosclerotic disease (CANTOS)." New England Journal of Medicine, 377(12), 1119-1131.
6. Selvin E, Paynter NP, Erlinger TP (2007). "The effect of weight loss on C-reactive protein: a systematic review." Archives of Internal Medicine, 167(1), 31-39. PMID 17210875.
7. Fedewa MV, Hathaway ED, Ward-Ritacco CL (2017). "Effect of exercise training on C reactive protein: a systematic review and meta-analysis of randomised and non-randomised controlled trials." British Journal of Sports Medicine, 51(8), 670-676. PMID 27445361.
8. Hayashino Y, Jackson JL, Hirata T, et al. (2014). "Effects of exercise on C-reactive protein, inflammatory cytokine and adipokine in patients with type 2 diabetes: a meta-analysis of randomized controlled trials." Metabolism, 63(3), 431-440.
9. Rahimlou M, et al. (2025). "Dose-dependent effects of omega-3 polyunsaturated fatty acids on C-reactive protein concentrations in cardiometabolic disorders: a dose-response meta-analysis of randomized clinical trials." Inflammopharmacology. PMID 40263171.
10. Pieters Z, et al. (2024). "Within-subject variation of C-reactive protein and high-sensitivity C-reactive protein: a systematic review and meta-analysis." PLOS ONE, 19(10), e0304961. PMID 39485740.
11. Nowakowska A, et al. (2025). "Inflammatory response to ultramarathon running: a review of IL-6, CRP and TNF-alpha." International Journal of Molecular Sciences, 26(13), 6317.

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