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If something in your body is inflamed, whether from an infection taking hold, a joint disease flaring, or damage you cannot feel yet, CRP (C-reactive protein) is one of the first numbers to move. It can surge a hundredfold or more within hours of a serious infection, and it can simmer at mildly elevated levels for years when chronic, low-grade inflammation is quietly raising your risk for heart disease, cancer, or organ damage.
That dual personality makes CRP one of the most widely ordered blood tests in medicine. A single reading can help your doctor decide whether you need antibiotics, flag a post-surgical complication, or signal that an autoimmune condition is worsening. And because your liver ramps up CRP production almost entirely in response to signals from your immune system, a rising or falling trend tells you, in near real time, whether inflammation in your body is getting better or worse.
CRP belongs to a family of ring-shaped proteins called pentraxins. Your liver cells crank out CRP when they receive chemical distress signals, mainly a molecule called IL-6 (interleukin-6), from immune cells responding to damage or infection anywhere in the body. Once released into your blood, CRP latches onto the surfaces of bacteria and damaged cells, tagging them for destruction by your immune system and activating a chain of defensive proteins called the complement system.
In healthy people with no active inflammation, CRP circulates at very low levels, typically well under 3 mg/L. When infection or injury strikes, it can rocket into the hundreds within 24 to 48 hours and fall just as quickly once the trigger resolves. That speed is what makes it so useful for tracking acute illness. But CRP also picks up slower, subtler signals: the persistent low-grade inflammation driven by excess body fat, vascular damage, or autoimmune conditions that keeps your level chronically elevated in the single digits.
Standard CRP and high-sensitivity CRP (hs-CRP) measure the same protein. The difference is the precision of the lab technique. Standard CRP assays are designed to detect the large swings seen in infection and acute illness, where levels often exceed 10 mg/L and can climb past 100 mg/L. hs-CRP uses a more sensitive method that can accurately resolve very small differences below 5 mg/L, which is the range that matters for cardiovascular risk stratification.
If you are ordering this test to investigate an active infection, monitor an autoimmune flare, or check for post-surgical complications, standard CRP is the right tool. If your main goal is to assess chronic, low-grade vascular inflammation as part of a heart disease risk workup, hs-CRP is the better choice. Both are inexpensive and widely available.
Chronic low-level CRP elevation is one of the most consistent predictors of future heart attacks and strokes. A major pooled analysis of over 160,000 people across 54 studies found that each roughly threefold increase in CRP was associated with about 37% higher risk of coronary heart disease and 27% higher risk of stroke from blocked arteries, even after adjusting for blood pressure, cholesterol, smoking, and diabetes.
The numbers hold up across different populations and study designs. In the ARIC study of nearly 10,000 adults without known heart disease, those whose hs-CRP was above the group's midpoint of 2.4 mg/L had higher rates of atherosclerotic cardiovascular events regardless of their lipid levels. A separate analysis of nearly 28,000 women followed for 30 years found that the highest fifth of hs-CRP had about 70% greater risk of major cardiovascular events compared to the lowest fifth, after accounting for standard risk factors.
One of the most striking findings is how CRP interacts with other risk markers. In the MESA study of about 4,700 adults and the ACCELERATE trial of over 10,500 high-risk patients, elevated Lp(a) (lipoprotein(a), a genetically driven cholesterol particle) only translated into clearly higher cardiovascular event rates and mortality when hs-CRP was also at or above 2 mg/L. When hs-CRP was low, high Lp(a) alone did not carry the same excess risk. This suggests inflammation may be a necessary accelerant for certain lipid-driven risks.
CRP does not just predict heart events. A meta-analysis of 14 cohorts totaling nearly 84,000 people found that those in the highest hs-CRP group had roughly 75% higher all-cause mortality compared to those in the lowest group. Cardiovascular deaths were about twice as common, and cancer deaths were about 25% more frequent. A community study of over 9,300 adults in Shanghai, followed for a median of 10.5 years, independently confirmed that higher baseline CRP predicted all-cause, cardiovascular, and cancer mortality with a dose-response pattern.
CRP's reach extends well beyond the heart. In chronic kidney disease (CKD), a meta-analysis of 81 studies found that higher CRP was associated with about 63% greater all-cause mortality. In chronic obstructive pulmonary disease (COPD), a 15-study meta-analysis linked the highest CRP levels to about 53% higher late mortality. In adults hospitalized with COVID-19, CRP above the median of 108 mg/L was associated with roughly 2.6 times higher odds of in-hospital death after extensive adjustment for other factors.
In cancer, elevated CRP tracks with worse prognosis across many solid tumor types. A meta-analysis of 35 studies in breast cancer found that high CRP in the metastatic setting was associated with about 87% higher risk of death. In people with stable coronary artery disease, the highest CRP category was associated with about 77% more major cardiovascular events and roughly 3.7 times higher all-cause mortality compared to the lowest category.
CRP interpretation depends heavily on context. A level of 15 mg/L means something very different in a person with a sore throat than in someone who feels perfectly fine. The ranges below reflect published clinical thresholds and large population data. Because CRP varies by age, sex, ethnicity, and body weight, these should be treated as orientation, not rigid boundaries. Always compare your results within the same lab over time.
| Range (mg/L) | Interpretation |
|---|---|
| Below 1 | Low inflammation. Associated with the lowest observed long-term cardiovascular risk in large cohorts. |
| 1 to 3 | Average range in Western adult populations. Moderate cardiovascular risk tier per AHA guidelines. |
| 3 to 10 | Mildly elevated. In an otherwise healthy person, suggests chronic low-grade inflammation, often linked to excess weight, metabolic stress, or early vascular disease. Warrants investigation and repeat testing. |
| 10 to 50 | Moderately elevated. Common in active autoimmune flares, significant infections, or substantial tissue injury. |
| Above 50 | Strongly elevated. Typical of serious bacterial infection, major trauma, or post-surgical inflammation. Values above 100 mg/L are common in sepsis. |
A classic study of healthy blood donors found that the middle 95% of CRP values fell between 0.08 and 3.11 mg/L, with a median of 0.64 mg/L. No significant sex difference was found in that carefully screened group. However, large population studies show meaningful ethnic variation: median CRP in midlife women was about 3.2 mg/L in African-American women, 2.3 mg/L in Hispanic women, 1.5 mg/L in white women, 0.7 mg/L in Chinese women, and 0.5 mg/L in Japanese women. Much of this difference is explained by differences in body weight, but African-American women remained more likely to have CRP above 3 mg/L even after adjusting for BMI.
Obesity is one of the strongest drivers of baseline CRP. A meta-analysis of 51 studies found a correlation of about 0.36 to 0.37 between BMI and log-transformed CRP, meaning that a large portion of "elevated" CRP in the general population traces back to excess body fat and the low-grade inflammation it produces. The association is stronger in women and in North American and European populations compared to Asian populations.
CRP is nonspecific by design. It rises whenever inflammation is present, regardless of the cause. That sensitivity is a strength when you want a fast signal that something is wrong, but it means a single elevated reading can be misleading without context.
Within-person variability is the biggest practical challenge. A systematic review of 60 studies found a median within-subject coefficient of variation of about 41% for CRP and 44% for hs-CRP. In a controlled study of coronary artery disease patients measured at 21 time points over a year, 46% of subjects crossed the clinically important 2 mg/L threshold at least once. In the MESA study, nearly 70% of people who initially tested above 3 mg/L fell into a lower risk category on repeat testing.
Because of that variability, a single CRP reading is a snapshot with a lot of noise. Two readings taken weeks apart give you a much clearer picture. Three readings establish a trend you can act on with confidence.
AHA and Canadian cardiovascular guidelines recommend at least two hs-CRP measurements, taken several weeks apart and free of acute illness, before using the result to guide treatment decisions. For standard CRP used in disease monitoring (autoimmune conditions, infection recovery, cancer prognosis), serial trending is even more valuable. A reading that starts at 45 mg/L and drops to 8 mg/L over two weeks tells you the infection or flare is resolving. A reading that starts at 5 mg/L and climbs to 12 mg/L over three months tells you something is getting worse.
A practical cadence: get a baseline when you are feeling well, with no recent illness, surgery, or injury. If the result is elevated and you are making changes (weight loss, dietary shifts, starting a medication), retest in 8 to 12 weeks. Once you have a stable baseline, annual testing is reasonable for ongoing monitoring. If you are tracking an acute condition, your clinician may want readings every few days.
An elevated CRP without an obvious cause (you are not sick, have not had surgery, and are not in an autoimmune flare) should prompt two questions: is this a fluke, and what is driving it?
First, retest in two to three weeks. If the second result is also elevated, the signal is real. Next, look at the pattern. If your CRP is in the 3 to 10 mg/L range with no acute symptoms, the most likely drivers are excess body fat, metabolic syndrome, early vascular inflammation, or a low-grade autoimmune or infectious process. Companion tests that help narrow the cause include a complete blood count with differential (to check for infection or blood disorders), a metabolic panel (kidney and liver function), hs-CRP (if your standard CRP is in the single digits and you want finer cardiovascular risk resolution), fasting insulin and HbA1c (to assess metabolic health), and an ESR (erythrocyte sedimentation rate, another inflammation marker that moves on a different timescale and can help distinguish acute from chronic processes).
If your CRP is above 10 mg/L without a clear explanation, your clinician will typically want imaging or further labs to look for infection, autoimmune disease, or malignancy. Persistent elevation above 3 mg/L in the setting of known cardiovascular risk is itself a treatment target: the CANTOS trial showed that directly blocking IL-1 beta (the upstream signal that drives CRP production) reduced major cardiovascular events in post-heart attack patients whose hs-CRP remained at or above 2 mg/L despite statin therapy.
The bottom line: CRP is not a diagnosis. It is a flare gun. When it goes off, your job is to find out what lit the fuse and whether it is still burning.
Evidence-backed interventions that affect your CRP level
CRP is best interpreted alongside these tests.