C-Reactive Protein (CRP)

C-reactive protein is a pentameric plasma protein that binds phosphocholine exposed on damaged membranes and some bacteria, opsonising them and activating the classical complement pathway through C1q. Hepatocytes synthesise it under interleukin-6 signalling, amplified by interleukin-1. Its half-life is roughly nineteen hours and does not change with disease, which is why plasma concentration tracks the current rate of production almost directly and moves quickly in both directions.

Concentrations rise within about six hours of a stimulus and peak near forty-eight hours, spanning under 1 mg/L in health to above 300 mg/L in serious bacterial infection. The high-sensitivity assay measures the same protein with a lower detection limit, and the cardiovascular risk tiers conventionally used are below 1, 1 to 3, and above 3 mg/L. JUPITER randomised people with LDL under 130 mg/dL and hs-CRP at or above 2 mg/L to rosuvastatin and stopped early for benefit; CANTOS later showed that blocking interleukin-1 beta cut recurrent cardiovascular events without touching lipids.

Fast kinetics make CRP useful for following a trajectory and poor for diagnosis, since it cannot separate infection from trauma, malignancy or an autoimmune flare. Assay choice is not cosmetic: a standard CRP reports everything below roughly 5 mg/L as normal, so ordering it for cardiovascular risk stratification discards the entire range of interest.

A single hs-CRP is close to worthless as a risk estimate. Any intercurrent infection moves it, and a value above 10 mg/L should be repeated. Before-and-after CRP readings are the commonest self-experiment evidence circulated for peptides, and the most fragile: an elevated starting value tends to fall on repeat measurement whatever is done, so regression to the mean and resolution of the original cause explain most reported improvements.