Key Benefits

• Spot low-grade inflammation to refine your cardiovascular risk.
• Refine borderline heart risk; levels at or above 2 mg/L flag higher risk.
• Guide prevention plans; elevated results support statin discussions when risk is borderline.
• Drive lifestyle priorities; weight loss, exercise, and quitting smoking often lower hs-CRP.
• Flag hidden inflammation tied to diabetes, fatty liver, and high blood pressure risk.
• Track trends to gauge response to lifestyle, weight, and medication changes.
• Avoid misreads; don’t interpret during infections, flares, or soon after strenuous exercise.
• Best interpreted with a lipid panel, blood pressure, and ASCVD risk score.

What is High-Sensitivity C-Reactive Protein (hs-CRP)?

High-sensitivity C-reactive protein (hs‑CRP) is the same C-reactive protein measured at very low concentrations. CRP is a soluble protein made by the liver’s hepatocytes when inflammatory messengers (cytokines) such as interleukin‑6 (IL‑6), interleukin‑1β (IL‑1β), and tumor necrosis factor (TNF) trigger the acute‑phase response. It circulates in the blood and rises quickly when the body detects infection, tissue injury, or other stress.

CRP helps the innate immune system recognize and clear trouble. It binds to phosphocholine on microbes and damaged cells, activates the classical complement pathway via C1q, and flags targets for removal by phagocytes (opsonization). Because its production directly mirrors cytokine activity, the low levels captured by hs‑CRP reflect the background level of systemic inflammation, including in the vascular wall. In short, hs‑CRP provides an integrated snapshot of the body’s inflammatory tone and tissue injury signaling, changing rapidly as those signals wax and wane.

Why is High-Sensitivity C-Reactive Protein (hs-CRP) important?

High-sensitivity C-reactive protein (hs-CRP) is a liver-made “early-warning” protein that rises when the immune system is signaling inflammation. Because the high-sensitivity assay detects very small increases, it reflects low-grade, whole-body inflammation that touches blood vessels, metabolism, connective tissues, and even brain-immune crosstalk—key processes underlying cardiovascular health and recovery.

In most labs, values below about 1 are considered low, around 1–3 average, and above 3 elevated; optimal tends to sit at the low end. When hs-CRP is low, it usually means quiet cytokine activity, a calmer endothelium (the vessel lining), and less inflammatory “noise” affecting insulin signaling and coagulation. People typically feel well and recover predictably from day-to-day stresses. Exceptionally low results can appear in advanced liver dysfunction or certain immune deficiencies, where the signal may be muted despite illness. Women often run slightly higher than men, pregnancy raises baseline levels, and children usually have very low values except during infections.

When hs-CRP is high, it points to active innate-immune signaling. Persistent, modest elevation is linked to vascular inflammation, stiffer arteries, and insulin resistance, which can amplify fatigue, exercise intolerance, and aches even without overt symptoms. Markedly high spikes commonly accompany infections, flares of autoimmune disease, or tissue injury. Chronic kidney disease, obesity, and estrogen states can push levels upward; pregnancy has higher norms, but sustained high values can correlate with complications.

Big picture: hs-CRP integrates signals from immunity, metabolism, and the vasculature. Tracked alongside lipids, A1c, blood pressure, and kidney function, it helps map long-term risks for atherosclerosis, diabetes progression, and adverse outcomes—and how inflamed or resilient the system is over time.

What Insights Will I Get?

High-sensitivity C-reactive protein (hs-CRP) measures low concentrations of a liver-made acute-phase protein induced by interleukin-6. It tracks baseline innate immune activity. Because inflammation shapes energy use, vascular tone, coagulation, and repair, hs-CRP links to cardiometabolic health, cognition, and recovery from stressors.

Low values usually reflect quiet immune signaling and minimal inflammatory burden. Hepatic acute-phase synthesis is low, endothelial function is stable, and insulin signaling faces less interference. Very low levels occur in advanced liver dysfunction or rare CRP gene variants; in pregnancy, values are typically higher.

Being in range suggests balanced immune surveillance, steady endothelial function, and low background plaque activity. For cardiovascular risk, consensus places optimal toward the low end of the reference range when measured away from intercurrent illness.

High values usually reflect an IL-6–driven acute-phase response from infection, tissue injury, autoimmune disease, periodontal disease, visceral adiposity and insulin resistance, or active atherosclerotic inflammation. System effects include reduced nitric-oxide bioavailability, a prothrombotic tilt, catabolic signaling with fatigue, and worsened glycemic control. Levels rise with age, are higher in women, and increase with oral estrogen and during pregnancy.

Notes: Interpretation is context dependent. Acute illness, recent surgery, trauma, or hard exercise can transiently raise hs-CRP and may not reflect baseline. Statins and glucocorticoids lower it; estrogen therapy raises it. A high-sensitivity assay is required; severe liver failure may blunt responses.