Why we measure it

Chronic low-grade inflammation is not a side effect of cardiovascular disease — it is a central mechanism in its development. CRP is produced by the liver in direct response to inflammatory cytokines, primarily IL-6, making it a downstream readout of the same inflammatory process that destabilises arterial plaques. Studies involving over 150,000 patients have demonstrated that elevated hsCRP independently predicts myocardial infarction, stroke, and cardiovascular mortality — even in individuals with normal LDL cholesterol. The JUPITER trial, which enrolled 17,802 healthy adults with elevated hsCRP but normal LDL, showed that statin therapy significantly reduced cardiovascular events in this group, establishing that CRP-defined inflammatory risk is not merely a bystander but a clinically actionable target. Beyond cardiovascular disease, elevated hsCRP is associated with insulin resistance, type 2 diabetes, non-alcoholic fatty liver disease, and several cancers — making it one of the most broadly informative single biomarkers available.

Why every 3 months

CRP responds to lifestyle, diet, sleep, stress, and subclinical infection on a timescale of days to weeks — it rises fast and, with appropriate change, falls fast. This responsiveness is exactly what makes it useful for tracking, and what makes annual testing almost useless for this purpose. A single annual reading tells you where you were on one morning. It cannot tell you whether your hsCRP has been elevated for six months and recently normalised, or whether a dietary change you made three months ago actually shifted your inflammatory baseline. Quarterly resolution gives you the minimum data density to see direction — whether you are improving, stable, or drifting — and to attribute that movement to something you changed. An annual hsCRP misses flares that start and resolve entirely between measurements.

What movement means

In a 2003 joint scientific statement, the American Heart Association and Centers for Disease Control and Prevention classified cardiovascular risk from hsCRP into three bands: below 1.0 mg/L (low), 1.0–3.0 mg/L (intermediate), and above 3.0 mg/L (high). A reading above 10 mg/L is generally considered to reflect acute infection, injury, or active inflammatory disease rather than chronic low-grade inflammation; clinical practice guidance recommends retesting once the acute cause has resolved. These classifications are from external bodies — not Nexuses. What the data shows over time is the trend: the direction and magnitude of change across draws.

In the protocol