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High-sensitivity C-reactive protein (hs-CRP)

Updated October 31, 2026 · 37 sources · Written by the AumniVIDA team

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What is hs-CRP?

hs-CRP is a blood test that measures C-reactive protein, an inflammation protein made by the liver, at very low levels. For heart risk, CDC/AHA guidance treats under 1 mg/L (0.1 mg/dL) as lower risk, 1 to 3 mg/L as average and over 3 mg/L as higher. A result over 10 mg/L usually signals infection or injury and should be repeated.

Illustration of a ring-shaped protein made of five identical rounded subunits floating beside a cluster of liver cells that are releasing more of the same rings into a small blood vessel.
Liver cells release CRP as a ring of five identical subunits when the messenger IL-6 signals inflammation somewhere in the body.

Questions people ask about hs-CRP

  1. 01What does a high hs-CRP mean?A high hs-CRP means more inflammation than average. Between 3 and 10 mg/L (0.3 to 1.0 mg/dL) it marks higher relative heart risk, about twice the lowest group. Over 10 mg/L usually points to infection, injury or another inflammatory cause, so guidelines advise looking for it and repeating the test in about 2 weeks.Read the answer
  2. 02How to lower hs-CRPThe biggest lifestyle lever is weight loss: about 0.13 mg/L lower hs-CRP per kilogram lost, and 29% to 44% lower in intensive lifestyle programs. A Mediterranean diet lowers it by about 1 mg/L, regular exercise and not smoking help more slowly, and statins cut it by 17% to 37%.Read the answer
  3. 03What is a normal hs-CRP level?A normal hs-CRP for heart risk is under 3 mg/L (0.3 mg/dL), and under 1 mg/L (0.1 mg/dL) is the lowest-risk group.Read the answer
  4. 04hs-CRP vs CRP: what is the difference?hs-CRP and CRP measure the same protein.Read the answer
  5. 05hs-CRP test: fasting, timing and what affects itThe hs-CRP test is an ordinary blood draw and does not need fasting.Read the answer

Key takeaways

  1. 1

    hs-CRP and standard CRP measure the same protein; the hs test reads the low range (about 0.1 to 10 mg/L) that matters for heart risk [1].

  2. 2

    Under 1 mg/L is lower relative risk, 1 to 3 mg/L average and over 3 mg/L higher, with roughly twice the risk of the lowest group [2].

  3. 3

    In statin-treated patients, hs-CRP predicted future events more strongly than LDL cholesterol [3], and over 30 years in women it predicted as well as LDL and Lp(a) [4].

  4. 4

    One value is a noisy snapshot: results vary by about 42% within a person, so average two tests taken about 2 weeks apart [5] [2].

  5. 5

    Weight loss, a Mediterranean diet, regular exercise, not smoking and statins all lower hs-CRP; lifestyle programs with weight loss cut it by 29% to 44% [6] [7].

  6. 6

    Genetic studies suggest CRP itself does not cause heart disease; it reports on inflammation that does [8].

What is hs-CRP?

hs-CRP is a high-sensitivity test for C-reactive protein, a protein the liver releases when the body is inflamed. The high-sensitivity version reads the low range, under 10 mg/L, where small differences track long-term heart and stroke risk.

C-reactive protein (CRP) is one of the body's fastest alarm signals. In an infection or after an injury it can climb from under 0.05 mg/L to over 500 mg/L, a rise of about 10,000-fold [9]. Most healthy people sit far below that, with a median of about 0.6 to 0.8 mg/L [5] [9].

The "hs" stands for high sensitivity. It is not a different protein. It is a more precise way of measuring the same protein at the low concentrations that matter for cardiovascular risk. A conventional CRP test is designed for infection and inflammation and typically cannot detect values below about 3 mg/L; an hs test can read down to about 0.1 mg/L [1].

Doctors use the two tests for different questions:

  • Standard CRP: is there an active infection or inflammatory disease, and is it getting better?
  • hs-CRP: in a person who is well, how much low-grade inflammation is there, and what does it add to their heart risk?

The rest of this page covers the second question. For the details of the two assays, see hs-CRP vs CRP.

Where does CRP come from and why does it rise?

Liver cells make CRP, mainly when the messenger molecule interleukin-6 (IL-6) tells them to. CRP has a fixed half-life of about 19 hours, so its blood level is a direct readout of how hard the liver is being pushed to make it.

CRP is a ring of five identical subunits, each 206 amino acids long [9]. It binds to damaged cells and some bacteria and helps the immune system clear them. It was the first acute-phase protein described, found in 1930 in the blood of people with pneumonia because it reacted with the "C" fraction of the pneumococcus [10].

Three facts explain how to read the number:

  1. IL-6 drives it. Hepatocytes in the liver make CRP mainly under the control of IL-6 [9]. Fat tissue releases IL-6, which is one reason body fat raises CRP [11].
  2. It responds fast. After a single trigger, CRP passes 5 mg/L within about 6 hours and peaks at about 48 hours [9].
  3. It clears at a steady rate. The half-life is about 19 hours in health and disease, so the only thing that sets the level is how fast it is made [9]. Once a trigger ends, the level falls within days.

Part of a person's baseline CRP is inherited: twin studies show a significant genetic component that is independent of age and body weight [9]. CRP shows little daily or seasonal rhythm and is not affected by meals [2] [12].

Illustration of a ring-shaped protein made of five identical rounded subunits floating beside a cluster of liver cells that are releasing more of the same rings into a small blood vessel.
Liver cells release CRP as a ring of five identical subunits when the messenger IL-6 signals inflammation somewhere in the body.

Why does hs-CRP matter for heart disease?

Atherosclerosis is partly an inflammatory disease, and hs-CRP tracks that inflammation. People with higher hs-CRP have more heart attacks and strokes even when their LDL cholesterol is normal, and trials such as JUPITER, CANTOS, COLCOT and LoDoCo2 showed that treating this risk lowers events.

The link was first shown in healthy men in 1997: the top quarter of CRP carried about three times the risk of heart attack of the bottom quarter (relative risk 2.9) [13]. In women, hs-CRP was the strongest of 12 markers tested, with a relative risk of 4.4 between the top and bottom quarters [14]. In 27,939 women, CRP and LDL cholesterol were almost unrelated (r = 0.08), so each picked out a different group at risk [15].

Pooled data from 160,309 people in 54 studies put the size of the effect in context: each threefold higher CRP carried a 37% higher coronary risk after adjusting for standard risk factors [16].

Residual inflammatory risk

Cardiologists now talk about two kinds of leftover risk in treated patients: residual cholesterol risk and residual inflammatory risk. In 31,245 patients already on statins, the top quarter of hs-CRP predicted major cardiovascular events (hazard ratio 1.31), cardiovascular death (2.68) and death from any cause (2.42). LDL cholesterol was neutral for major events in the same patients (1.07) [3].

Over 30 years in 27,939 initially healthy women, the top fifth of hs-CRP carried a hazard ratio of 1.70 for a first major event, against 1.36 for LDL cholesterol and 1.33 for lipoprotein(a). Each added independent information, and the three together separated risk best [4].

What the trials showed

  • JUPITER (2008): in 17,802 healthy people with LDL under 130 mg/dL (3.4 mmol/L)3.4 mmol/L (130 mg/dL) but hs-CRP of 2 mg/L or more, rosuvastatin lowered hs-CRP by 37% and major events by 44% [17].
  • CANTOS (2017): canakinumab, an antibody against the inflammatory signal IL-1 beta, lowered hs-CRP without changing lipids and cut recurrent events by 15% at the 150 mg dose, at the cost of more fatal infections [18].
  • COLCOT (2019): low-dose colchicine started within 30 days of a heart attack lowered events from 7.1% to 5.5% [19].
  • LoDoCo2 (2020): in chronic coronary disease, colchicine lowered events from 9.6% to 6.8% [20].
  • CLEAR SYNERGY (2025): colchicine started right after a heart attack lowered CRP by 1.28 mg/L but did not reduce events over 3 years [21].

The 2025 ACC scientific statement concluded that the case linking inflammation with atherosclerosis is now clinically actionable, while cautioning that not every anti-inflammatory trial has succeeded [22].

From pneumonia serum to anti-inflammatory heart trials

  1. 1930

    Tillett and Francis find a protein in pneumonia serum that reacts with pneumococcal C fraction

  2. 1997

    CRP predicts heart attack in healthy men (Physicians' Health Study)

  3. 2002

    CRP outpredicts LDL cholesterol for first events in 27,939 women

  4. 2003

    CDC/AHA set the under 1, 1 to 3 and over 3 mg/L categories

  5. 2008

    JUPITER: rosuvastatin cuts events in people with hsCRP 2 mg/L or more and normal LDL

  6. 2011

    Genetic study: CRP itself is unlikely to cause heart disease

  7. 2017

    CANTOS: lowering inflammation without touching lipids cuts recurrent events

  8. 2019

    COLCOT: low-dose colchicine after a heart attack lowers events

  9. 2020

    LoDoCo2: colchicine lowers events in chronic coronary disease

  10. 2023

    hsCRP beats LDL as a predictor in 31,245 statin-treated patients

  11. 2024

    30-year data in women: hsCRP, LDL and Lp(a) each predict risk

  12. 2025

    CLEAR SYNERGY neutral; ACC statement calls inflammation clinically actionable

CRP went from a curiosity in pneumonia serum in 1930 to a tested treatment target for heart disease within a century.

How is hs-CRP measured?

hs-CRP is measured on an ordinary blood sample with an antibody-based assay that is precise at low concentrations. Good hs assays keep their error under 10% from 0.3 to 10 mg/L, and you do not need to fast.

Laboratories measure hs-CRP with immunoturbidimetric, immunonephelometric or ELISA methods that can detect CRP from about 0.01 to 10 mg/L [12]. The CDC/AHA statement noted that hs-CRP assays generally keep their coefficient of variation under 10% across the 0.3 to 10 mg/L range [2].

The same statement set the ground rules that most labs still follow [2]:

  • Report results in mg/L only. Some labs still print mg/dL; divide mg/L by 10 to get mg/dL.
  • Test in a metabolically stable person, not during an infection, flare or recovery from injury.
  • Fasting or nonfasting results are both fine.
  • Average two measurements, ideally about 2 weeks apart, because a single value varies.

That variation is large. In healthy people, CRP varied by about 42% from one measurement to the next, and two results had to differ by 118% before the change was likely to be real [5]. More on timing and preparation is on the hs-CRP test page.

How do you read an hs-CRP result?

Under 1 mg/L (0.1 mg/dL) is lower relative heart risk, 1 to 3 mg/L (0.1 to 0.3 mg/dL) average and over 3 mg/L (0.3 mg/dL) higher. US guidelines also treat 2 mg/L or more as a risk-enhancing factor, and a value over 10 mg/L should be repeated.

The CDC/AHA categories were set as approximate thirds of the adult population, pooled from more than 15 populations and 40,000 people. People in the top third had about twice the relative risk of those in the bottom third [2]. They describe relative risk, which means they only make sense alongside the rest of a person's risk profile: age, blood pressure, smoking, diabetes, LDL cholesterol or ApoB, and lipoprotein(a).

Major guidelines use hs-CRP differently. The table puts them side by side. For what counts as normal, average values and differences by sex, see normal hs-CRP levels.

How major guidelines and trials use hs-CRP, in mg/L and mg/dL
SourceThreshold in mg/LSame in mg/dLHow it is used
CDC/AHA statement, 2003Under 1.0 / 1.0 to 3.0 / over 3.0Under 0.1 / 0.1 to 0.3 / over 0.3Lower, average and higher relative risk; optional for people at intermediate risk (10% to 20% over 10 years); not for screening everyone
CDC/AHA statement, 2003Over 10Over 1.0Repeat the test and look for infection or inflammation; persistent unexplained values need evaluation for other causes
AHA/ACC cholesterol guideline, 20182.0 or more0.2 or moreRisk-enhancing factor that can favor a statin at borderline or intermediate risk
JUPITER trial entry, 20082.0 or more0.2 or moreHealthy people with LDL under 130 mg/dL who benefited from rosuvastatin
CANTOS trial entry, 20172 or more0.2 or morePeople after a heart attack with residual inflammatory risk
ESC prevention guideline, 2021None setNone setCRP adds limited value to risk prediction; routine biomarker testing not advised
ACC scientific statement, 2025Not reproduced hereNot reproduced hereCalls for broad hs-CRP screening together with LDL cholesterol in primary and secondary prevention

hs-CRP categories in mg/L

AverageHigher relative riskLower relative risk: 0 to 1 mg/LLower relative risk: 0 to 1 mg/LLower relative risk: 0 to 1 mg/LLower relative risk: 0 to 1 mg/LAverage: 1 to 3 mg/LAverage: 1 to 3 mg/LAverage: 1 to 3 mg/LAverage: 1 to 3 mg/LAverage: 1 to 3 mg/LAverage: 1 to 3 mg/LAverage: 1 to 3 mg/LAverage: 1 to 3 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LRepeat and look for another cause: 10 to 12 mg/LRepeat and look for another cause: 10 to 12 mg/LRepeat and look for another cause: 10 to 12 mg/LRepeat and look for another cause: 10 to 12 mg/LRepeat and look for another cause: 10 to 12 mg/LRepeat and look for another cause: 10 to 12 mg/LRepeat and look for another cause: 10 to 12 mg/LRepeat and look for another cause: 10 to 12 mg/LLower relative risk: 0 to 1 mg/LLower relative risk: 0 to 1 mg/LLower relative risk: 0 to 1 mg/LLower relative risk: 0 to 1 mg/LAverage: 1 to 3 mg/LAverage: 1 to 3 mg/LAverage: 1 to 3 mg/LAverage: 1 to 3 mg/LAverage: 1 to 3 mg/LAverage: 1 to 3 mg/LAverage: 1 to 3 mg/LAverage: 1 to 3 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LHigher relative risk: 3 to 10 mg/LRepeat and look for another cause: 10 to 12 mg/LRepeat and look for another cause: 10 to 12 mg/LRepeat and look for another cause: 10 to 12 mg/LRepeat and look for another cause: 10 to 12 mg/LRepeat and look for another cause: 10 to 12 mg/LRepeat and look for another cause: 10 to 12 mg/LRepeat and look for another cause: 10 to 12 mg/LRepeat and look for another cause: 10 to 12 mg/L01CDC/AHA low cut point: 1 mg/L2Risk-enhancing factor; JUPITER and CANTOS entry: 2 mg/L3CDC/AHA high cut point: 3 mg/L10Repeat in about 2 weeks: 10 mg/L12 mg/L
Lower relative risk
0 to 1
Average
1 to 3
Higher relative risk
3 to 10
Repeat and look for another cause
10 to 12
  • 1 mg/L: CDC/AHA low cut point
  • 2 mg/L: Risk-enhancing factor; JUPITER and CANTOS entry
  • 3 mg/L: CDC/AHA high cut point
  • 10 mg/L: Repeat in about 2 weeks
Under 1 mg/L is lower relative risk, 1 to 3 mg/L average and over 3 mg/L higher; a result over 10 mg/L usually means something else is going on and should be repeated.

What raises hs-CRP besides heart risk?

Infection, injury and surgery raise CRP the most, often well over 10 mg/L. Excess body fat, smoking, chronic inflammatory disease, hormone therapy, a very hard endurance effort and disturbed sleep raise it less, by fractions of a mg/L to a few mg/L.

Because CRP responds to inflammation anywhere in the body, an hs-CRP result is only a heart-risk number when nothing else is going on. The CDC/AHA statement lists elevated blood pressure, body mass index, smoking, metabolic syndrome and diabetes, low HDL with high triglycerides, estrogen or progestogen use, chronic infections such as gum disease or bronchitis, and chronic inflammation such as rheumatoid arthritis as conditions linked to higher levels [2].

We have not found the typical size of each effect gathered in one place, so the table below compiles it from the original studies. Several of these causes overlap: smokers and people with diabetes are often also heavier, for example. When a result is over 10 mg/L, read what a high hs-CRP means.

Common causes of a raised hs-CRP and their typical size, compiled from the cited studies
CauseTypical effect on CRPHow long it lastsSource
Bacterial infection, injury, surgeryOften over 10 mg/L; can exceed 500 mg/LRises within 6 hours, peaks near 48 hours, falls with a 19 hour half-life once the trigger ends
Marathon or other very hard endurance effortSignificant short-term risePeaks the next day, still raised after 3 days
ObesityOdds of CRP 2.2 mg/L or more about 2 times higher in obese men and 6 times in obese womenPersists while excess fat persists
SmokingHigher with more pack-years; 41.1% of current versus 35.8% of former heavy smokers had 2 mg/L or moreStill raised up to 5 years after quitting
Chronic inflammatory disease or chronic infectionRaised; size depends on disease activityPersists while the disease is active
Estrogen or progestogen hormone useRaisedWhile taking it
Metabolic syndrome, diabetes, high blood pressureRaisedPersists
Disturbed or very long sleepSmall rise (effect size 0.12 to 0.17)Habitual pattern
Female sexMedian 3.3 mg/L in women versus 1.8 mg/L in menLifelong difference
Inherited baselineSignificant heritable componentLifelong

What raises hs-CRP, and by how much

Acute: often over 10 mg/L

Rises within hours, settles within days.

  • Bacterial infection
  • Injury or surgery
  • Severe cases can exceed 500 mg/L

Short-term rise

A significant rise for a few days.

  • Marathon or very hard endurance effort: still raised after 3 days

Chronic: shifts the baseline

Fractions of a mg/L to a few mg/L.

  • Obesity: about 6 times the odds of 2.2 mg/L or more in women, 2 times in men
  • Smoking: dose related, raised up to 5 years after quitting
  • Chronic inflammatory disease or chronic infection, such as gum disease
  • Estrogen or progestogen use
  • Metabolic syndrome, diabetes, high blood pressure
  • Disturbed or very long sleep: small effect
  • Female sex: median 3.3 versus 1.8 mg/L

What lowers it

Slower changes in the baseline.

  • Weight loss
  • Mediterranean diet
  • Regular exercise
  • Not smoking
  • Statins

Causes overlap: smokers and people with diabetes are often also heavier. A heart-risk reading only counts when nothing acute is going on.

Infection and injury push CRP into the tens or hundreds of mg/L; body fat, smoking, chronic inflammatory disease and hormones shift the baseline by a few mg/L.

What lowers hs-CRP?

Weight loss has the largest lifestyle effect, about 0.13 mg/L per kilogram lost. A Mediterranean diet lowers hs-CRP by about 1 mg/L, regular exercise and quitting smoking lower it more slowly, and statins cut it by 17% to 37%.

Each kilogram of weight lost lowered CRP by about 0.13 mg/L across 33 studies [23]. Intensive lifestyle programs that combined diet, activity and weight loss cut median CRP by 29% to 33% in the Diabetes Prevention Program [6] and by 43.6% in Look AHEAD [7].

  • Diet: a Mediterranean pattern lowered hs-CRP by 0.98 mg/L across 17 trials [24]. See the Mediterranean diet and anti-inflammatory diet protocols.
  • Exercise: training lowered CRP across 83 trials, most when it also reduced body fat [25]. See Zone 2 training.
  • Smoking: CRP falls after quitting, but slowly, over years [26].
  • Sleep: disturbed sleep is linked to higher CRP, a small effect [27]. See sleep consistency.
  • Medicines: statins lowered CRP by 16.9% (pravastatin) to 37% (rosuvastatin) [28] [17]; anti-inflammatory drugs such as colchicine lower it too [21]. These are decisions for a clinician.

The full ranking, with how fast each works, is on how to lower hs-CRP.

How much each lever lowered hs-CRP in trials

Show the data
How much each lever lowered hs-CRP in trials
ItemValue (% lower hs-CRP)LowHighNote
Intensive lifestyle, weight loss (Look AHEAD)43.6Median change at 1 year; usual care fell 16.7%
Rosuvastatin 20 mg (JUPITER)37Versus placebo, healthy people with hsCRP 2 mg/L or more
Canakinumab, IL-1 beta antibody (CANTOS)372641Percentage points beyond placebo, by dose; after a heart attack
Intensive lifestyle (Diabetes Prevention Program)33293333% in men, 29% in women at 1 year
Pravastatin 40 mg (PRINCE)16.9Versus placebo at 24 weeks
Intensive lifestyle programs that produce weight loss lowered hs-CRP about as much as a high-intensity statin; each bar comes from a different trial and population, so compare the order of size, not exact values.

What does the evidence not show?

The evidence does not show that CRP itself causes heart disease, that lowering hs-CRP alone prevents heart attacks, or that testing everyone improves outcomes. hs-CRP is a marker of inflammatory risk, and its added value over standard risk factors is modest.

  • CRP is probably a messenger, not a cause. Gene variants that raise CRP by up to 30% per allele did not raise coronary risk in 194,418 people [8]. The inflammation upstream, such as the IL-1 and IL-6 pathway targeted in CANTOS, is the likely culprit [18].
  • Added prediction is small on average. Adding CRP to standard risk factors raised the C-index by only 0.0039; targeted testing of intermediate-risk adults might prevent one extra event for every 400 to 500 people screened over 10 years [29]. The 2021 ESC guideline concluded that CRP adds limited value [30].
  • CRP is not specific to the heart. Higher CRP also predicts death from several cancers and lung disease, with associations of similar size [16].
  • Lowering CRP is not the same as lowering risk. CLEAR SYNERGY lowered CRP with colchicine but did not reduce events [21], and statins lower both LDL and CRP, so JUPITER cannot separate the two effects [17].
  • No screening trial exists. No trial has randomized people to hs-CRP screening versus none, which is why the 2003 statement advised against screening the whole adult population [2]. The 2025 ACC statement now argues for broad screening; others, including the CLEAR SYNERGY lead investigator, want more data first [31].
  • Thresholds may not fit everyone. Median CRP differs by sex and race, and the 2003 statement noted that data for racial and ethnic groups were limited when the uniform cut points were set [32] [2].

The research

Foundational studies

The work that established what this marker means.

Guidelines and reviews

Where expert bodies and systematic reviews have landed.

Recent research

Notable work from the last three years.

What well-known voices say about hs-CRP

Their positions, summarized in our words. Follow each link for the full context.

  • Paul RidkerCardiologist at Brigham and Women's Hospital, lead investigator of JUPITER and CANTOS, co-author of the 2025 ACC statement

    Argues that inflammation matters at least as much as cholesterol for heart risk, that current guidelines treat hs-CRP as little more than a tiebreaker, and that routine measurement is the first step because clinicians do not treat what they do not measure.

    TCTMD, ACC: It's time for clinicians to address inflammation in CVD (2025)

  • Sanjit JollyCardiologist and lead investigator of the CLEAR SYNERGY colchicine trial

    Accepts that inflammation predicts risk but is not convinced it is yet actionable for most patients, opposes widespread hs-CRP screening for now and wants further trial data first.

    TCTMD, ACC: It's time for clinicians to address inflammation in CVD (2025)

  • John DaneshEpidemiologist at the University of Cambridge who led large pooled analyses of CRP and heart disease

    After a large British study found CRP to be only a moderate predictor that adds little to cholesterol, blood pressure and smoking, argued that there was no good scientific reason to use it as a predictive test and called its rapid adoption a cautionary tale.

    NBC News / Associated Press, Latest heart disease test may not be helpful (2004)

Watch

Talks and explainers worth your time. Nothing loads from YouTube until you press play.

  • Universal Screening for hsCRP commentary by Dr. Paul Ridker, MD, MPH

    ASPCOpen on YouTube

    The researcher behind JUPITER and CANTOS makes the case for routine hs-CRP testing to a preventive cardiology society.

  • Inflammation and Coronary Artery Disease with Dr Paul Ridker

    Future Pulse CardiologyOpen on YouTube

    A longer conversation on residual inflammatory risk and how it differs from residual cholesterol risk.

  • Targeting inflammation in cardiovascular disease: From canakinumab to colchicine

    University of Ottawa Heart InstituteOpen on YouTube

    A heart institute lecture that walks through the anti-inflammatory trials from CANTOS to the colchicine studies.

  • Changes in C-Reactive Protein With Risk of CVD, Cancer, and Mortality

    Mayo ProceedingsOpen on YouTube

    A journal summary showing that CRP tracks risk well beyond the heart, a useful reminder that it is not heart-specific.

  • C-Reactive Protein (CRP) - Inflammation - Acute phase reactant (APR) - Labs

    Medicosis PerfectionalisOpen on YouTube

    A clear medical-school explanation of CRP as an acute-phase protein and how the lab test behaves.

Protocols that act on hs-CRP

Common questions

What does hs-CRP measure?

It measures C-reactive protein, a protein the liver makes when the body is inflamed, at low concentrations from about 0.1 to 10 mg/L. In a person who is otherwise well, it reflects low-grade inflammation linked to heart and stroke risk [1] [2].

Does hs-CRP increase with age?

Only slightly. In healthy blood donors, the link between CRP and age was weak [5]. Body fat, smoking and chronic disease, which become more common with age, explain much more of the difference between people [11] [2].

Can hs-CRP be too low?

No guideline sets a lower limit. Under 1 mg/L is the lowest-risk category [2], and a result below the assay's detection limit, often reported as under 0.1 mg/L or similar, simply means very little inflammation was found [1].

Does a high hs-CRP cause symptoms?

Low-grade elevations between 1 and 10 mg/L cause no symptoms by themselves. Symptoms come from whatever is driving the inflammation, such as an infection or a joint disease, which is why very high values call for a look for a cause [2].

What is the link between hs-CRP and homocysteine?

Both have been studied as extra heart-risk markers. In postmenopausal women, the top quarter of hs-CRP carried a relative risk of 4.4 versus 2.0 for homocysteine [14]. They measure different things, inflammation and amino acid metabolism, so one does not replace the other.

Is hs-CRP related to lipoprotein(a)?

They are separate risk signals. Over 30 years in women, hs-CRP, LDL cholesterol and lipoprotein(a) each predicted events on their own, and risk was clearest when all three were measured [4].

Can hs-CRP detect cancer?

No. Higher CRP is linked to death from several cancers in large cohorts [16], but it rises with so many conditions that it cannot diagnose or rule out cancer.

What does hs-CRP mean in rheumatoid arthritis?

Chronic inflammatory diseases such as rheumatoid arthritis raise CRP [2], so in someone with an active autoimmune disease an hs-CRP result mostly reflects disease activity and is hard to read as a heart-risk number. A rheumatologist interprets CRP in that setting.

Is hs-CRP the same as ESR?

No. ESR (erythrocyte sedimentation rate) is a different, indirect test of inflammation. CRP responds within hours and settles within days because of its 19 hour half-life [9], and only hs-CRP has validated cut points for heart risk [2].

Sources

  1. 1.Grootendorst DC, de Jager DJ, Brandenburg VM, et al. Excellent agreement between C-reactive protein measurement methods in end-stage renal disease patients--no additional power for mortality prediction with high-sensitivity CRP. Nephrology Dialysis Transplantation, 2007. doi:10.1093/ndt/gfm381
  2. 2.Pearson TA, Mensah GA, Alexander RW, et al. Markers of inflammation and cardiovascular disease: application to clinical and public health practice: A statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association. Circulation, 2003. doi:10.1161/01.cir.0000052939.59093.45
  3. 3.Ridker PM, Bhatt DL, Pradhan AD, et al. Inflammation and cholesterol as predictors of cardiovascular events among patients receiving statin therapy: a collaborative analysis of three randomised trials. Lancet, 2023. doi:10.1016/S0140-6736(23)00215-5
  4. 4.Ridker PM, Moorthy MV, Cook NR, Rifai N, Lee IM, Buring JE. Inflammation, Cholesterol, Lipoprotein(a), and 30-Year Cardiovascular Outcomes in Women. New England Journal of Medicine, 2024. doi:10.1056/NEJMoa2405182
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