hsCRP
High-sensitivity C-reactive protein — a liver-produced marker of systemic inflammation.
Optimal Range
< 1.0 mg/L (optimal) · > 3.0 mg/L (high risk)
Risk-Stratified Targets
| Population / Context | Target |
|---|---|
| Optimal (longevity) | < 0.5 mg/L |
| Low cardiovascular risk | < 1.0 mg/L |
| Moderate risk | 1.0–3.0 mg/L |
| High cardiovascular risk | > 3.0 mg/L |
| Acute inflammation (not CV risk)Likely infection or acute injury; recheck after resolution | > 10 mg/L |
Why It Matters
Chronic low-grade inflammation is a central driver of aging ('inflammaging') and disease. hsCRP is one of the most validated inflammatory biomarkers for predicting cardiovascular events and all-cause mortality.
Understanding hsCRP
High-sensitivity C-reactive protein (hsCRP) is an acute-phase protein produced by the liver in response to inflammatory signals, particularly interleukin-6 (IL-6). While standard CRP testing detects the dramatic elevations seen in acute infections and autoimmune flares, the high-sensitivity assay detects the subtle, chronic low-grade inflammation that drives atherosclerosis, cancer, neurodegeneration, and accelerated aging — a process increasingly referred to as 'inflammaging.'
The landmark JUPITER trial (2008) demonstrated that individuals with elevated hsCRP (>2.0 mg/L) but normal LDL-C benefited significantly from statin therapy, reducing cardiovascular events by 44%. This was pivotal in establishing that inflammation, independent of cholesterol levels, drives cardiovascular events. The CANTOS trial (2017) then showed that targeting inflammation directly with canakinumab (an IL-1β antibody) reduced cardiovascular events independent of any lipid lowering — providing causal proof that inflammation itself causes cardiovascular disease.
When interpreting hsCRP, context matters. Acute infections, injuries, vigorous exercise, and chronic conditions like obesity or autoimmune disease will elevate hsCRP independently of cardiovascular risk. A single elevated reading should be confirmed with a repeat test 2–4 weeks later. Persistent elevation above 3.0 mg/L confers significantly increased cardiovascular risk and warrants investigation of the underlying inflammatory source.
Key Research
Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein (JUPITER trial)
Ridker PM et al. · N Engl J Med (2008)
Key finding: Statin therapy reduced cardiovascular events by 44% in patients with elevated hsCRP but normal LDL-C, establishing inflammation as an independent cardiovascular risk factor.
Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease (CANTOS trial)
Ridker PM et al. · N Engl J Med (2017)
Key finding: Targeting IL-1β inflammation directly reduced cardiovascular events without lowering lipids — providing causal proof that inflammation drives cardiovascular disease.