hs-CRP

High-sensitivity C-reactive protein (hs-CRP) is a cheap blood test for the low-grade, long-running inflammation that comes with ageing, and in a 30-year study of women it predicted heart attacks and strokes well. It is a strong risk marker; whether acting on the number itself, beyond the cholesterol and metabolic levers that drive it, changes outcomes is less certain.

Have hs-CRP measured with your yearly bloods, not while you have, or are recovering from, an infection or injury, nor within 48 hours of a hard workout, and repeat any high value several weeks later before acting on it. If it is raised, fix the metabolic picture first (weight, activity, diet), then recheck.

What it measures

hs-CRP is the most validated blood marker of chronic, low-grade inflammation ("inflammaging"), which underlies hardened arteries (atherosclerosis), neurodegeneration and several cancers.

It is also an acute-phase reactant: it jumps with short-term stress on the body. A fresh viral infection, a hard workout in the last 24–48 hours or a recent injury will all push it up for a while, so a single high reading means little on its own.

A 30-year signal

The long-horizon evidence is unusually clean. In 27,939 initially healthy women followed for 30 years in a large US cohort (the Women's Health Study), those in the top fifth for hs-CRP at the start had about a 70% higher risk of a major cardiovascular event than those in the bottom fifth. That was a stronger and more durable signal than LDL cholesterol gave over the same period (about 36% higher), and independent of it: hazard ratio 1.70 (95% CI 1.52–1.90) for hs-CRP, against 1.36 (1.23–1.52) for LDL cholesterol.^[1] The confidence interval (CI) in brackets is the range in which the true effect most plausibly lies; when it sits entirely above 1.0, as both do here, the link is unlikely to be chance. This was an observational study in women, so it shows hs-CRP predicts risk, not that lowering it prevents events.

Where guidelines use it

The 2026 US cholesterol guideline (from the American College of Cardiology and American Heart Association) counts hs-CRP as a risk-enhancing factor. For adults without cardiovascular disease whose estimated 10-year risk is borderline (3% to under 5%), an hs-CRP of 2 mg/L or more on two successive occasions, with no other explanation, means a high-intensity statin can be useful.^[2]

A large statin trial (JUPITER) selected apparently healthy adults on an hs-CRP of 2.0 mg/L or more and still cut cardiovascular events sharply. How to act on lipids is covered in Lipid management.

Reading the number

hs-CRP	What it usually means
Under 1.0 mg/L	Lowest-risk range; no target below the guideline line (2 mg/L twice) has been tested against outcomes
1.0–3.0 mg/L	Raised background inflammation; look for metabolic and lifestyle drivers
3.0 mg/L or more, twice, weeks apart	High risk; consider tighter lipid and metabolic control

Inflammation also raises ferritin, so a high ferritin is read alongside hs-CRP and transferrin saturation before anyone calls it iron overload; see Iron and aging.

Insulin resistance and inflammation travel together

In a cross-sectional study of 2,588 untreated Korean adults, those with a fasting insulin above 90 pmol/L (15 μIU/mL) had nearly five times the odds of an hs-CRP above 2 mg/L compared with those below 30 pmol/L (5 μIU/mL), although the comparison did not account for body weight.^[3] A snapshot like this can't say which drives which, but it is why improving the metabolic picture (weight, activity, diet) is a sensible first step: recheck hs-CRP afterwards before adding anything aimed at inflammation itself. See HOMA-IR and fasting insulin.

Is CRP itself the culprit?

Probably not. Among 113,491 white Danish adults, the fifth with the highest CRP had about 70% higher risk of dying over follow-up than the lowest fifth, yet in genetic analyses (which used only a few gene variants), people carrying variants that raise their CRP did not die earlier.^[4] That pattern suggests CRP is a bystander that reflects whatever is driving the inflammation, not a cause of harm itself. Trials in heart patients are mixed: some anti-inflammatory drugs have cut heart attacks and strokes, but in the largest colchicine trial, started soon after a heart attack, the drug lowered CRP by about 1.3 mg/L without reducing further heart attacks, strokes or cardiovascular deaths.^[5] So treat a raised hs-CRP as a reason to look for its drivers, not as a number to push down for its own sake.

What to do

Test once a year as part of the midlife lab panel, not while you have, or are recovering from, an infection or injury, nor within 48 hours of a hard workout.
Repeat any raised value (2 mg/L or more) several weeks later before acting on it.
If it stays high, start with the metabolic levers, then recheck. With a borderline 10-year risk, a level of 2 mg/L or more on two occasions is a reason to discuss a statin.
Don't chase a number below 1 mg/L. It is the lowest-risk range, not an outcome-tested target.