What does the research show about high-sensitivity c-reactive protein (hs-crp)?

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

hs-CRP measures low levels of an inflammation protein. Bands attributed to the American Heart Association put below 1.0 mg/L at low, 1.0 to 3.0 at average and above 3.0 at high cardiovascular risk. Higher levels track with heart disease, diabetes and death, yet genetic studies suggest CRP itself is not a cause. Repeat results often change category.

Checked 2026-11-13

Status: A blood test ordered by a clinician and also sold direct to consumers by some US laboratories. FDA classifies C-reactive protein test systems as class II devices [1]. Its guidance separates three cleared types: conventional CRP, high-sensitivity CRP, and cardiac CRP, which is indicated as an aid in identifying and stratifying people at risk for future cardiovascular disease [2].
Measures: The concentration of C-reactive protein, an acute-phase protein that rises with infection and inflammation, using an assay whose range extends low enough to measure the levels found in apparently healthy people [2].
Also called: hs-CRP, hsCRP, high-sensitivity CRP, high sensitivity C-reactive protein, cardiac CRP, cCRP, CRP high sensitivity, C-reactive protein cardiac, ultra-sensitive CRP, CRP
Tested for: inflammation, heart attack risk, cardiovascular risk, chronic low-grade inflammation, deciding on statin therapy, general health check

Strong several reviews agree · Moderate one review or consistent trials · Limited one or a few small studies · Untested no study in people, listed with what it rests on

Linked in research6

StrongLinked to more coronary heart disease and stroke at higher levels, about 37% more coronary disease per threefold rise after adjusting for standard risk factors.
StrongLinked to more deaths at higher levels, about 75% more in the highest than the lowest category across pooled general population studies.
StrongShown in trials: a drug that lowered hs-CRP without changing cholesterol cut cardiovascular events 15%, while one that did not lower it made no difference.
StrongLinked to higher CRP in women with polycystic ovary syndrome, about twice the level of women without it, in two meta-analyses that held after accounting for obesity.
ModerateLinked to more type 2 diabetes at higher levels, with a 26% higher risk in a meta-analysis of 22 cohorts.
LimitedOne cohort of midlife women linked hs-CRP above 3 mg/L to more premenstrual mood symptoms, cramps or back pain, bloating and breast pain, but not headaches.

Reported risks0

No risks sourced yet.

Reference ranges

Each range is the one its source published, in mg/L. Also reported in mg/dL. Where sources differ, each is shown.

American Heart Association and Centers for Disease Control and Prevention cardiovascular risk categories, 2003

Adults being assessed for cardiovascular risk, tested when free of infection, systemic inflammation or trauma · [3], [2]

Range	What the source calls it
below 1 mg/L	"low risk"
1 to 3 mg/L	"average risk"
above 3 mg/L	"high risk"

Categories of cardiovascular risk, set for use alongside traditional risk factors and not as a substitute for them. The band wording is taken from the US National Library of Medicine, which attributes it to the American Heart Association [3]. FDA guidance names 1.0 mg/L as the AHA/CDC cutoff for the low risk category and lists limits it draws from the 2003 AHA/CDC statement: the average of two results taken about two weeks apart is used, persistently unexplained levels above 10 mg/L call for evaluation of non-cardiovascular causes, testing is not done during infection, inflammation or trauma, and screening the entire adult population is not advised [2]. A result above 10 mg/L therefore falls in the top band here without being a cardiovascular reading.

American Heart Association and American College of Cardiology cholesterol guideline, 2018

Adults aged 40 to 75 without cardiovascular disease, when hs-CRP has been measured · [4]

Range	What the source calls it
below 2 mg/L	No name given
2 or above mg/L	"elevated"

The guideline lists "elevated high-sensitivity C-reactive protein" of 2.0 mg/L or above as a risk-enhancing factor to weigh in a discussion about statin therapy for people at borderline or intermediate 10-year risk. It gives no term for results below 2.0 [4]. A 2026 guideline from the same bodies retires and replaces this one [5].

US Food and Drug Administration guidance on CRP assays, 2005, conventional CRP

Results read as a conventional CRP test for infection, tissue injury and inflammatory disorders · [2]

Range	What the source calls it
5 or below mg/L	"apparently healthy individuals"
5.1 to 10 mg/L	No name given
above 10 mg/L	"clinically significant"

This is how FDA describes conventional CRP assays, not the cardiovascular use. The guidance states that apparently healthy people have levels of 5 mg/L or below, that values are typically considered clinically significant above about 10 mg/L, and that levels reach roughly 20 to 500 mg/L within hours of an acute inflammatory event. It does not characterize results between 5 and 10 mg/L, and it stresses that a rise in CRP is non-specific [2]. Another federal source gives conventional CRP in mg/dL and notes that normal values vary from laboratory to laboratory [3].

What has been shown to move it

Shown to lower it20

Thunder god vineCautionStrong

Rheumatoid arthritis

Shown to improve joint swelling, stiffness and grip in adults with rheumatoid arthritis, matching or beating standard drugs, in trials mostly from China.

Against DMARDs, grip strength, morning stiffness, CRP and tender joint count differed (P < 0.05), and ESR and swollen joint count did not.

The numbers and sources

Effect: Across 14 RCTs, TwHF extracts improved grip strength, swollen joint count and morning stiffness against placebo (P < 0.001). Against DMARDs, grip strength, morning stiffness, CRP and tender joint count differed (P < 0.05), and ESR and swollen joint count did not [1]. Across 40 RCTs (3,092 patients), tripterygium glycosides added to DMARDs lowered morning stiffness, tender and swollen joint counts, pain scores, CRP, ESR and rheumatoid factor against DMARDs alone (all p < .001) [2]. A network meta-analysis of 21 trials (5,039 participants) ranked TwHF with methotrexate first and TwHF alone second for ACR20 response among the conventional DMARDs compared [3]. In 207 patients, ACR50 response at 24 weeks was 46.4% on methotrexate, 55.1% on TwHF (p 0.014) and 76.8% on both (p < 0.001) [4]. In 121 US patients, 65.0% on TwHF extract and 32.8% on sulfasalazine met ACR20 at 24 weeks (P 0.001) [5].
Population: Adults with active rheumatoid arthritis, mostly in China [1][2][3][4]. 121 patients at US centers [5].
Sources: [1], [2], [3], [4], [5]
Caveats: The methotrexate trial was open label, with blinded assessors [4]. In the sulfasalazine trial only 62 patients had outcome data at 24 weeks, and 62% and 41% stayed on treatment [5]. Most pooled trials were small and Chinese.

TurmericStrong

C-reactive protein and other inflammation markers

Shown to lower CRP and some other inflammation markers in adults with inflammatory conditions or diabetes. These are blood markers, not clinical outcomes.

The numbers and sources

Effect: In 9 studies, curcumin lowered CRP by 3.67 mg/L (95% CI -6.96 to -0.38). In 23 studies hs-CRP was lower than placebo, with stronger effects below 2,000 mg a day [14]. In 28 RCTs in prediabetes and type 2 diabetes, curcumin or turmeric lowered CRP (SMD -0.50), TNF-alpha (SMD -1.70) and IL-6 (SMD -2.97) [15]. In 6 RCTs (472 adults with type 2 diabetes), hs-CRP was 1.06 mg/L lower (95% CI -1.97 to -0.16, I² 17.3%) [16]. In 21 knee osteoarthritis studies (1,705 patients), CRP (SMD -0.906, 95% CI -1.543 to -0.269) and TNF-alpha were lower than placebo, while ESR, IL-1beta, IL-6 and PGE-2 did not differ [17]. With piperine added, 18 RCTs showed lower IL-6, while CRP and TNF-alpha did not change significantly [18].
Population: People with proinflammatory or autoinflammatory conditions [14]; adults with prediabetes or type 2 diabetes [15][16]; adults with knee osteoarthritis [17]; adults in curcumin with piperine trials [18].
Sources: [14], [15], [16], [17], [18]
Caveats: Blood markers, not clinical outcomes. Certainty was low for every marker in the 28-trial review, which also found publication bias for CRP [15]. The curcumin with piperine review found no significant CRP change [18].

TurmericStrong

Rheumatoid arthritis

Shown to lower disease activity, joint counts and inflammation markers in adults with rheumatoid arthritis, in few small trials with very low certainty.

Across 7 RCTs, DAS28 fell by 1.47 (95% CI -1.68 to -1.26), with lower rheumatoid factor, ESR and CRP.

The numbers and sources

Effect: Across 6 publications (539 patients), curcumin lowered DAS28 (MD -1.20, 95% CI -1.85 to -0.55), ESR (MD -29.47), swollen joint count (MD -5.33) and tender joint count (MD -6.33) against controls [19]. Across 7 RCTs, DAS28 fell by 1.47 (95% CI -1.68 to -1.26), with lower rheumatoid factor, ESR and CRP [20]. Across 6 placebo-controlled trials (244 participants), ACR20 response, DAS28, ESR, CRP, pain and joint counts all improved, with very low certainty for most outcomes [21].
Population: Adults with rheumatoid arthritis [19][20][21].
Sources: [19], [20], [21]
Caveats: The trials were few and small, heterogeneity was substantial [20], and the certainty of evidence was very low [21].

Beta-sitosterolModerate

Blood pressure and other heart risk markers

Shown to lower systolic blood pressure by about 1.6 mmHg for plant sterols and stanols as a class. HDL, blood sugar and weight did not change.

The numbers and sources

Effect: Plant sterols and stanols lowered systolic blood pressure by 1.55 mmHg (95% CI 0.42 to 2.67), diastolic by 0.84 mmHg, apoB by 0.06 g/L and hs-CRP by 0.25 mg/L. HDL cholesterol, fasting glucose, HbA1c, body weight, waist and fat mass did not change [5].
Population: Adults of mixed health status in trials pooled across 14 meta-analyses. Blood pressure came from one of them [5].
Sources: [5]
Caveats: Class-level evidence, not beta-sitosterol alone. These are risk markers, not heart attacks or strokes. Certainty was moderate to high for most outcomes, downgraded for inconsistency, imprecision or publication bias [5].

Fisetin and quercetin (senolytics)Moderate

Liver enzymes and lipids in fatty liver disease (quercetin alone)

Shown to lower liver enzymes, LDL and triglycerides with quercetin alone in people with fatty liver disease, at very low to moderate certainty.

The numbers and sources

Effect: A 2025 meta-analysis of 7 RCTs (540 patients) with metabolic dysfunction-associated steatotic liver disease found that quercetin lowered ALT, AST, GGT, direct bilirubin and C-reactive protein, lowered total cholesterol, LDL and triglycerides, and raised HDL. BMI, body fat, kidney function and TNF-α did not change [10].
Population: 540 patients with fatty liver disease in 7 RCTs [10].
Sources: [10]
Caveats: GRADE certainty ranged from very low to moderate. Dose, baseline BMI and age may explain heterogeneity. The abstract gives no pooled effect sizes [10]. None of the trials measured senescent cells.

GarlicModerate

Inflammation markers

Shown to lower CRP by about 0.6 mg/L and lower TNF in adults. These are blood markers, and the reviews disagree on IL-6.

The numbers and sources

Effect: In 16 RCTs, garlic lowered CRP by 0.61 mg/L (95% CI -1.12 to -0.11, I² 76.9%, 13 trials), IL-6 by 0.73 ng/L (5 trials) and TNF by 0.26 ng/L (7 trials). Adiponectin and leptin did not change significantly [8].
Population: Adults in 16 RCTs lasting 2 to 52 weeks [8].
Sources: [4], [8]
Caveats: Blood markers, not clinical outcomes. Heterogeneity for CRP was high [8]. The 108-trial review found CRP 1.6 mg/L and TNF 3.94 pg/mL lower, effects several times larger than [8], and found no change in IL-6 [4].

GingerModerate

Inflammation markers

Shown to lower CRP, TNF-α and IL-6 in adults, more in people with health conditions. These are blood markers, not clinical outcomes.

The numbers and sources

Effect: In a 2025 GRADE-assessed meta-analysis of 29 RCTs, ginger lowered CRP by 0.86 mg/L (95% CI -1.10 to -0.62), TNF-α by 1.90 pg/mL (95% CI -2.61 to -1.18) and IL-6 by 1.15 pg/mL (95% CI -1.90 to -0.41). Malondialdehyde fell, and total antioxidant capacity and superoxide dismutase rose [8].
Population: Adults in 29 RCTs [8].
Sources: [8]
Caveats: Blood markers, not clinical outcomes. The authors report high heterogeneity among trials and larger effects in people with underlying health conditions [8].

Oral corticosteroidsModerate

Severe COVID-19 and pneumonia in hospital

Shown to lower 28-day deaths in hospitalized COVID-19 patients, 22.9% against 25.7%, with the benefit limited to those on oxygen or a ventilator.

In severe community-acquired pneumonia, added corticosteroids lowered deaths (RR 0.47, 95% CI 0.3 to 0.74) and C-reactive protein on day 8 (SMD -0.8, 95% CI -1.11 to -0.5), with no difference in gastrointestinal bleeding or high blood sugar.

The numbers and sources

Effect: Dexamethasone 6 mg a day for up to 10 days, by mouth or vein, lowered 28-day deaths from 25.7% on usual care to 22.9% (rate ratio 0.83, 95% CI 0.75 to 0.93). Deaths were 29.3% against 41.4% in those on a ventilator and 23.3% against 26.2% in those on oxygen. In those on no respiratory support they were 17.8% against 14.0% (rate ratio 1.19, 95% CI 0.92 to 1.55) [13]. In severe community-acquired pneumonia, added corticosteroids lowered deaths (RR 0.47, 95% CI 0.3 to 0.74) and C-reactive protein on day 8 (SMD -0.8, 95% CI -1.11 to -0.5), with no difference in gastrointestinal bleeding or high blood sugar [14].
Population: 6,425 people hospitalized with COVID-19, 2,104 on dexamethasone and 4,321 on usual care [13]; 665 people with severe community-acquired pneumonia in 10 trials [14].
Sources: [13], [14]
Caveats: The COVID-19 trial was open label [13]. The pneumonia trials were small and used several corticosteroids and dosing schedules, so they do not test oral treatment alone [14].

Paleo dietModerate

Inflammation markers

Shown in two reviews to lower CRP about 0.4 to 0.8 mg/L more than comparison diets in adults, with one result sensitive to single trials.

Compared with control diets the source does not describe [1]; a control group the source does not describe [5]

The numbers and sources

Effect: CRP fell 0.41 mg/L more than on control diets (95% CI 0.008 to 0.81) [1] and 0.84 mg/L more in people with metabolic disorders (95% CI 0.06 to 1.62) [5].
Population: Adults in 8 RCTs [1]; adults with metabolic disorders in 10 RCTs [5].
Sources: [1], [5]
Caveats: Confidence intervals reach close to zero. In [1], the CRP result changed when single studies were removed. CRP is a blood marker, not a disease outcome.

ProbioticsModerate

Rheumatoid arthritis

Mixed results: reviews agree probiotics lower CRP or IL-6 in rheumatoid arthritis, but disagree on disease activity.

Across 4 RCTs (153 participants), DAS fell (SMD -0.58, 95% CI -0.97 to -0.19), CRP fell borderline (SMD -0.32, 95% CI -0.65 to 0.00), and ESR and cytokines did not change.

The numbers and sources

Effect: Across 9 studies (361 patients), probiotics lowered IL-6 (SMD -0.708) and did not change disease activity scores (MD 0.023, 95% CI -0.584 to 0.631) [8]. Across 4 RCTs (153 participants), DAS fell (SMD -0.58, 95% CI -0.97 to -0.19), CRP fell borderline (SMD -0.32, 95% CI -0.65 to 0.00), and ESR and cytokines did not change [9]. A review of 8 RA trials (344 patients) found CRP 3.04 mg/L lower (95% CI -4.47 to -1.62). With high risk-of-bias trials excluded, DAS28 did not differ from placebo (SMD -0.54, 95% CI -1.94 to 0.85) [10].
Population: Adults with rheumatoid arthritis, mostly women, over 8 weeks to 1 year [8][9][10].
Sources: [8], [9], [10]
Caveats: The reviews agree on lower CRP or IL-6 and disagree on disease activity. Strains, doses and durations varied [10].

Red light therapyModerate

Weight and waist size in obesity

Shown to reduce waist size, weight and BMI in people with obesity in one meta-analysis of 11 trials. Body fat percentage did not change.

The numbers and sources

Effect: Across 11 RCTs (569 patients), photobiomodulation improved waistline (mean difference -7.28, 95% CI -9.97 to -5.67), weight (-3.54, 95% CI -5.97 to -1.11) and BMI (-1.18, 95% CI -1.93 to -0.43), and lowered C-reactive protein, total cholesterol and HOMA-IR. Fat mass percentage (-0.28, 95% CI -1.25 to 0.69), waist-to-hip ratio and insulin did not differ [14].
Population: 569 people with obesity in 11 RCTs with varied comparators, including exercise, diet and sham light [14].
Sources: [14]
Caveats: The abstract does not give units for the mean differences. Comparators varied, and the measure of body fat itself did not change. The authors call for larger multi-center trials with longer follow-up [14].

Tart cherryModerate

Recovery after strenuous exercise

Shown to speed recovery of strength after strenuous exercise in exercising adults and athletes. Reviews disagree on whether muscle soreness falls.

A 2026 meta-analysis of 19 trials in trained athletes found faster recovery of maximal strength at every time point (ES 0.63 right after exercise to 4.82 at 96 hours) and lower CRP up to 48 hours (ES -0.46 to -0.73).

The numbers and sources

Effect: Across 14 studies, tart cherry reduced muscle soreness (ES -0.44, 95% CI -0.87 to -0.02) and sped recovery of strength (ES -0.78, 95% CI -1.11 to -0.46) and power (ES -0.53, 95% CI -0.77 to -0.29). Creatine kinase and TNF-alpha did not change [1]. A 2026 meta-analysis of 19 trials in trained athletes found faster recovery of maximal strength at every time point (ES 0.63 right after exercise to 4.82 at 96 hours) and lower CRP up to 48 hours (ES -0.46 to -0.73). Muscle soreness, creatine kinase, IL-6 and TNF-alpha did not change [2].
Population: Exercising adults in 14 studies to July 2020 [1]. Trained athletes in 19 trials to December 2025 [2].
Sources: [1], [2]
Caveats: The two meta-analyses disagree on soreness, and the later one reports strength effects several times larger, with I² of 69% to 93% [1][2]. Certainty in [2] ranged from very low to moderate, and several results depended on single studies. Products, doses and exercise protocols varied.

Vitamin DModerate

Inflammatory bowel disease

Mixed results: one review found about 36% fewer relapses in inflammatory bowel disease, mostly Crohn's in remission, while another found no change in relapse or activity.

In adults, the Harvey Bradshaw Index for Crohn's disease fell by 1.47 points (95% CI -2.47 to -0.47) and hs-CRP fell by 1.58 mg/L.

The numbers and sources

Effect: Across 7 RCTs (458 patients), vitamin D lowered clinical relapse against placebo (RR 0.64, 95% CI 0.46 to 0.89). In Crohn's disease in remission the RR was 0.47 (95% CI 0.27 to 0.82), and ulcerative colitis had only 2 studies (67 patients) [37]. In adults, the Harvey Bradshaw Index for Crohn's disease fell by 1.47 points (95% CI -2.47 to -0.47) and hs-CRP fell by 1.58 mg/L [38]. A meta-analysis of 17 trials (1,127 patients) found lower CRP (SMD -0.33) and no change in disease activity (SMD -0.13, 95% CI -0.66 to 0.39) or relapse (RR 0.59, 95% CI 0.19 to 1.86) [39].
Population: Adults with Crohn's disease or ulcerative colitis [37][38][39].
Sources: [37], [38], [39]
Caveats: The reviews disagree on relapse. Evidence for ulcerative colitis is thin [37].

ZincModerate

Blood sugar

Shown to lower fasting glucose about 14 mg/dL and HbA1c about 0.55% in people with and without diabetes.

The numbers and sources

Effect: Across 32 placebo-controlled interventions (1,700 participants, 14 countries), zinc lowered fasting glucose by 14.15 mg/dL (95% CI -17.36 to -10.93), 2-hour glucose by 36.85 mg/dL, HbA1c by 0.55% (95% CI -0.84 to -0.27) and hs-CRP by 1.31 mg/L [3]. Across 18 RCTs (1,023 participants) with diabetes, gestational diabetes or prediabetes, zinc lowered serum insulin (MD -2.50, 95% CI -4.69 to -0.31) and HOMA-IR (MD -1.10, 95% CI -2.05 to -0.15), and LDL cholesterol rose slightly (MD 3.46, 95% CI 1.48 to 5.43) [4].
Population: People with and without diabetes [3]; people with diabetes or prediabetes [4].
Sources: [3], [4]
Caveats: The fasting glucose effect depended on diabetes status and on the zinc formulation [3].

BoronLimited

Joint pain and arthritis

Small trials found boron supplements eased knee discomfort over 2 weeks and lowered inflammation markers in arthritis. Several were short, and one was run by the maker.

In 60 adults with knee osteoarthritis, 15 days of calcium fructoborate improved C-reactive protein, fibrinogen and sedimentation rate against placebo, with no serious adverse events.

The numbers and sources

Effect: In 60 adults with self-reported knee discomfort, calcium fructoborate 110 mg twice a day lowered McGill Pain Questionnaire scores by 8.9 points and WOMAC scores by 13.73 points more than placebo at day 14 (both p < 0.0001), with no change on placebo [10]. In 60 adults with knee osteoarthritis, 15 days of calcium fructoborate improved C-reactive protein, fibrinogen and sedimentation rate against placebo, with no serious adverse events [11]. In 72 people with rheumatoid arthritis on etanercept, calcium fructoborate or borax (6 mg of boron a day) for 60 days improved disease activity scores and lowered ESR, hsCRP, IL-1α, IL-6 and TNF-α against placebo [12]. A 1994 review reported a 20-person trial in osteoarthritis in which 50% improved on 6 mg of boron a day against 10% on placebo [13].
Population: 60 adults aged 35 to 65 with knee discomfort in Mexico [10]. 60 middle-aged adults with knee osteoarthritis [11]. 72 adults with rheumatoid arthritis in Iraq [12]. 20 adults with osteoarthritis [13].
Sources: [10], [11], [12], [13]
Caveats: Trials ran 2 weeks to 2 months. The knee discomfort trial was designed by FutureCeuticals, which supplied the calcium fructoborate and employed most authors [10]. The 20-person trial is known only from its author's review [13]. No meta-analysis was located.

Grape seed extractLimited

Inflammation

Limited evidence: a 50-trial review found lower CRP, while an earlier review found no effect.

The numbers and sources

Effect: Across 50 trials, C-reactive protein fell (WMD -0.81, 95% CI -1.25 to -0.38) [5]. An earlier meta-analysis found no significant effect on C-reactive protein [2].
Population: Adults in RCTs [5][2].
Sources: [5], [2]
Caveats: C-reactive protein is a blood marker, not a symptom. The two reviews disagree.

Juice cleanseLimitedStudied in women

Inflammation

One trial found the inflammation marker hs-CRP fell on a 7-day lemon detox but not on a calorie-matched placebo juice, in overweight Korean women.

Compared with before the diet, in the same people (overweight Korean women), with a calorie-matched placebo juice group measured the same way [1]

The numbers and sources

Effect: Serum hs-CRP fell only in the lemon detox group. Hemoglobin and hematocrit stayed stable on the lemon detox and fell in the other two groups [1].
Population: 84 premenopausal overweight Korean women [1].
Sources: [1]
Caveats: One short trial, with a blood marker rather than a disease outcome. Each group was measured against its own starting level, and no test between the groups is reported for hs-CRP [1].

Lymphatic drainage massageLimited

Muscle recovery after hard exercise

One trial of 36 combat athletes found drainage after jumping exercise raised pain thresholds and lowered creatine kinase and C-reactive protein more than passive rest.

Compared with passive rest [10]; intense sports massage [10]

Creatine kinase and C-reactive protein were lower than with rest (p < 0.001 to 0.017).

The numbers and sources

Effect: Six 30-minute drainage sessions over 72 hours raised pressure pain thresholds more than passive rest at 24, 48 and 72 hours (p = 0.004 to < 0.001), with larger gains than sports massage at 24 hours. Creatine kinase and C-reactive protein were lower than with rest (p < 0.001 to 0.017). Sports massage increased muscle blood flow more [10].
Population: 36 combat sports athletes, 24 men and 12 women, mean age 27.4 [10].
Sources: [10]
Caveats: One small trial with no sham. Perceived recovery was measured, and the abstract does not report its result [10].

Tart cherryLimited

Knee osteoarthritis pain

One trial found knee pain scores did not differ significantly from placebo in adults with knee osteoarthritis, though CRP fell.

The numbers and sources

Effect: In 58 patients drinking two 8 oz bottles a day for 6 weeks, WOMAC scores fell during cherry juice but the difference from placebo was not significant (P = 0.16). hsCRP fell compared with placebo [14].
Population: Non-diabetic adults with Kellgren grade 2 to 3 knee osteoarthritis, crossover [14].
Sources: [14]
Caveats: One trial.

Urolithin ALimited

Mitochondrial and cellular markers

Small trials found changes in mitochondrial and inflammation blood markers in middle-aged and older adults. All were run or funded by the maker.

Acylcarnitines, ceramides and CRP fell more than on placebo in older adults over 4 months, and acylcarnitines and CRP fell in middle-aged adults.

The numbers and sources

Effect: Four weeks at 500 or 1,000 mg a day changed plasma acylcarnitines and muscle mitochondrial gene expression in older adults [4]. Acylcarnitines, ceramides and CRP fell more than on placebo in older adults over 4 months [3], and acylcarnitines and CRP fell in middle-aged adults [2].
Population: Healthy, sedentary older adults [4]; 66 older adults [3]; middle-aged adults [2].
Sources: [4], [3], [2]
Caveats: These are markers, not health outcomes. All three trials were run or funded by the maker.

Shown to raise it1

CLAModerateHow often is not known

Inflammation and oxidative stress markers

Shown to raise CRP in adults across 14 studies. Sources disagree on oxidative stress, with one marker rising and another falling.

The numbers and sources

How common: How often is not known: the sources give no rate.
Effect: Across 14 studies, CLA raised serum CRP by 0.63 mg/dL, the unit as the review's abstract prints it (95% CI 0.13 to 1.13, I² 52.3%), independent of dose or duration [7]. In the 12-week trial in obese men, trans-10 cis-12 CLA raised the lipid peroxidation marker 8-iso-PGF2α by 578% and CRP by 110% compared with placebo [8]. A separate pooled analysis of 22 RCTs found malondialdehyde, another oxidative stress marker, lower with CLA [9].
Population: Adults in prospective studies [7]; 60 men with metabolic syndrome randomized to trans-10 cis-12 CLA, a CLA mixture or placebo, the same design as [6] [8]; adults in RCTs [9].
Sources: [7], [8], [9]
Caveats: The size of the CRP rise is uncertain. The abstract of [7] gives it in mg/dL, and 0.63 mg/dL is 6.3 mg/L, a large change for a pooled result. The full text could not be read to confirm the unit, so the direction is reported here and the size is not relied on. Sources disagree on oxidative stress. The isoprostane rise [8] and the malondialdehyde fall [9] used different markers and mostly different products.

Studies disagree11

Dietary nitrateStrong

Recovery from muscle damage

Shown to speed strength and jump recovery after damaging exercise with beetroot juice, in small trials. The reviews disagree on creatine kinase.

Creatine kinase and oxidative stress did not change; C-reactive protein was higher than placebo at 48 hours (SMD 0.55).

The numbers and sources

Effect: In 6 pooled studies, beetroot juice sped isometric strength recovery at 72 hours (SMD 0.54) and countermovement jump recovery at 24 to 72 hours (SMD 0.75 to 1.32), and raised pressure pain threshold at 48 and 72 hours. Creatine kinase and oxidative stress did not change; C-reactive protein was higher than placebo at 48 hours (SMD 0.55) [12]. In 7 trials, beetroot juice lowered creatine kinase by 98.67 IU/L (95% CI -122.14 to -75.21, I² 74.2%) and improved recovery of isometric strength (8.93%, I² 81.2%), jump height (4.72%) and pressure pain threshold (7.22%) against placebo. CRP, IL-6 and TNF-α did not change [13].
Population: Adults after damaging exercise [12][13].
Sources: [12], [13]
Caveats: Both reviews pooled 6 or 7 small, overlapping trials, and heterogeneity was high for creatine kinase and strength [13]. The two disagree on creatine kinase. All pooled trials in [12] had some concerns for risk of bias and used beetroot juice rather than isolated nitrate, so other juice compounds cannot be ruled out [12].

Tart cherryStrong

Blood pressure and cardiometabolic markers

Not shown to change blood pressure, cholesterol or body fat in adults. Fasting glucose and CRP fell very slightly.

Across 21 trials, blood pressure, heart rate, hs-CRP and IL-6 did not change, while CRP fell by 0.39 mg/L (95% CI -0.74 to -0.05, moderate certainty).

The numbers and sources

Effect: Across 10 RCTs, tart cherry juice did not change blood pressure, cholesterol, triglycerides or body fat. Fasting glucose fell by 0.51 mg/dL [4]. Across 21 trials, blood pressure, heart rate, hs-CRP and IL-6 did not change, while CRP fell by 0.39 mg/L (95% CI -0.74 to -0.05, moderate certainty) [5]. A 3-month trial in 50 middle-aged adults found no change in vascular or metabolic measures [6].
Population: Adults across 10 to 21 RCTs [4][5]; middle-aged adults, 30 mL concentrate twice a day [6].
Sources: [4], [5], [6]
Caveats: A 0.51 mg/dL glucose change is very small. The 3-month trial was funded by the Cherry Research Committee [6].

Vitamin DStrong

Rheumatoid arthritis disease activity

Shown to lower disease activity modestly in adults with rheumatoid arthritis. Reviews disagree on CRP, ESR and pain.

Across 11 RCTs, it lowered pain scores (WMD -1.30) and DAS28-CRP (WMD -0.58, 95% CI -0.86 to -0.31), while CRP, ESR and HAQ did not change.

The numbers and sources

Effect: Across 6 studies (438 patients), vitamin D lowered DAS28 (WMD -0.41, 95% CI -0.59 to -0.23), ESR (WMD -3.40) and tender joint count (WMD -1.44) against control [6]. Across 11 RCTs, it lowered pain scores (WMD -1.30) and DAS28-CRP (WMD -0.58, 95% CI -0.86 to -0.31), while CRP, ESR and HAQ did not change [7]. A third meta-analysis of 11 studies found lower DAS28 (WMD -0.83, 95% CI -1.38 to -0.28), CRP and ESR, with no change in HAQ or pain scores [8].
Population: Adults with rheumatoid arthritis in RCTs [6][7][8].
Sources: [6], [7], [8]
Caveats: The reviews disagree on CRP, ESR and pain, and heterogeneity was high [7].

Fermented foodsModerate

Inflammation and C-reactive protein

Mixed results: one meta-analysis found fermented dairy lowered C-reactive protein slightly, while two meta-analyses of kefir trials found no change.

Compared with control groups the abstract does not describe [5]; people who did not drink kefir [6]; control groups [7]; a high-fiber diet, with changes measured over time in each group [8]

The numbers and sources

Effect: Across 14 trials of yogurt, fermented milk and kefir, C-reactive protein fell (SMD -0.21, 95% CI -0.40 to -0.02), mainly in people with metabolic disease, and TNF-alpha and interleukin-6 did not change [5]. Kefir did not change C-reactive protein (WMD -0.17 mg/L, 95% CI -0.84 to 0.49), though it fell in trials of 8 weeks or longer [6]. A second kefir review found no significant effect on inflammatory markers [7]. In a 17-week trial, a high fermented food diet steadily raised gut microbiome diversity and lowered inflammatory markers [8].
Population: 14 trials [5]. 385 adults in 7 trials [6]. 24 studies [7]. 36 healthy adults, 18 in each diet group [8].
Sources: [5], [6], [7], [8]
Caveats: Few small trials with different foods. The abstract of [8] does not name C-reactive protein among the markers that fell.

Keto dietModerate

Inflammation markers

Mixed results: CRP fell 0.62 mg/dL in one review of short and long trials, and a review of trials lasting a year or more found no CRP difference.

Compared with diets that did not restrict carbohydrates to the level of ketosis

The numbers and sources

Effect: In 5 RCTs pooled, CRP fell 0.62 mg/dL (95% CI 0.40 to 0.84) and IL-6 did not change significantly (-1.31 pg/mL, 95% CI -2.86 to 0.25) [11]. In 13 trials of 12 months or more, CRP was measured and was not among the outcomes that differed from low-fat diets [1].
Population: 218 adults with overweight or obesity in 7 RCTs of 8 weeks to 2 years [11]; adults in trials against low-fat diets [1].
Sources: [1], [11]
Caveats: Few small trials. The abstract of [11] does not say whether the CRP change was measured against the control diet or from baseline. CRP is a blood marker, not a disease outcome.

Olive oilModerate

Inflammation

Mixed results: one pooled analysis found C-reactive protein fell 0.64 mg/L with olive oil, while a later one found no change in C-reactive protein or interleukin-6.

Compared with control groups, with control diets that varied [12]; trials comparing olive oil or flaxseed oil with controls [13]

The numbers and sources

Effect: Olive oil lowered C-reactive protein (mean difference -0.64 mg/L, 95% CI -0.96 to -0.31, 15 trials) and interleukin-6 (-0.29) and raised flow-mediated dilation by 0.76% against controls [12]. A pooling of trials in adults with normal or mildly raised blood pressure found no effect on C-reactive protein (8 trials) or interleukin-6 (3 trials) [13].
Population: 3,106 participants in 30 randomized trials [12]. 17 randomized trials, 14 of olive oil [13].
Sources: [12], [13]
Caveats: The first review calls for conservative reading because olive oil was given as a supplement or within a diet and control diets varied [12].

ResveratrolModerate

Inflammation and blood lipids

Mixed results: reviews disagree on whether CRP falls, and most found no change in LDL or triglycerides.

The numbers and sources

Effect: One meta-analysis found no change in CRP (WMD -0.144 mg/L, 95% CI -0.968 to 0.680), total cholesterol, LDL, triglycerides or glucose. HDL fell slightly (WMD -4.18 mg/dL, 95% CI -6.54 to -1.82) [4]. A later meta-analysis found lower TNF-α (WMD -0.44, 95% CI -0.71 to -0.16) and hs-CRP (WMD -0.27, 95% CI -0.5 to -0.02), with no change in IL-6 [6]. In 25 RCTs in metabolic disorders, CRP fell (SMD -0.18, 95% CI -0.33 to -0.03), and IL-6 and TNF-α did not change significantly [7]. In 6 RCTs in type 2 diabetes (533 participants), CRP fell (SMD -1.40, 95% CI -2.60 to -0.21) [8]. Apolipoprotein B (WMD 2.11 mg/dL, 95% CI -1.53 to 5.75) and apolipoprotein A-I did not change in 7 RCTs [9]. An umbrella review rated as high certainty a 0.19 mmol/L drop in total cholesterol in adults with overweight (95% CI 0.06 to 0.32) [5].
Population: 10 RCTs [4]; 17 RCTs with 736 adults [6]; adults with metabolic disorders [7]; adults with type 2 diabetes [8]; 7 RCTs [9]; meta-analyses of RCTs [5].
Sources: [4], [6], [7], [8], [9], [5]
Caveats: The reviews disagree on CRP, and the CRP effect in [8] is several times the size of that in [7]. Heterogeneity in [6] was about 50%. Evidence in [8] was low certainty. CRP is a marker, not a clinical outcome [7].

Whole grainsModerate

C-reactive protein and inflammation

Mixed results: two pooled analyses of trials found whole grains lowered C-reactive protein slightly, while a third found no significant change.

Compared with refined grains [11]; refined grains or placebo [9]; control diets low in or without whole grains [10]

The numbers and sources

Effect: Whole grains lowered high-sensitivity C-reactive protein (Hedges' g -0.22, 95% CI -0.45 to 0.00) and interleukin-6, with no change in TNF-alpha, and high heterogeneity (I² 69%) [11]. Another review found lower C-reactive protein (SMD -0.22, 95% CI -0.44 to 0.00) [9]. A third found no significant change in C-reactive protein (-0.29 mg/L, 95% CI -1.10 to 0.52), interleukin-6 or TNF-alpha, with effects in people with raised C-reactive protein and in trials with matched calories [10].
Population: 466 participants in 13 trials [11]. 25 trials [9]. 1,238 adults in 14 trials [10].
Sources: [11], [9], [10]
Caveats: Heterogeneity was high across reviews [10][11]. The intervals of the two reviews that found a fall reach zero.

Fish oilLimited

Inflammation markers (CRP)

Limited evidence: CRP fell in hemodialysis patients but not with high-dose EPA, in knee osteoarthritis, or in most trials of trained people.

The numbers and sources

Effect: In 13 hemodialysis trials (678 patients), omega-3 in triglyceride form lowered CRP (SMD -0.62, 95% CI -1.22 to -0.03, I² 74%), and so did doses under 2,000 mg a day (SMD -0.32) [32]. In 3 trials of trained people, only 1 found a significant drop in CRP after exercise [33]. High-dose EPA did not change hs-CRP across 6 outcome trials [9], and krill oil did not change CRP in knee osteoarthritis [29].
Population: Hemodialysis patients [32]; trained individuals [33]; cardiovascular and osteoarthritis trials [9][29].
Sources: [32], [33], [9], [29]
Caveats: The reviews disagree by population. In rheumatoid arthritis, only leukotriene B4 of five inflammatory markers fell [11].

MeditationLimited

Inflammation and C-reactive protein

Mixed results: one meta-analysis found C-reactive protein fell against active controls, while a review of trials found a fall in three of six that measured it.

Compared with active control groups [17]; waiting list, usual care and active control groups [18]

The numbers and sources

Effect: Across 45 trials against active controls, meditation reduced cortisol, C-reactive protein, blood pressure, heart rate, triglycerides and tumor necrosis factor alpha [17]. In a systematic review of 20 randomized trials, six measured C-reactive protein. One found a reduction and two found a trend toward reduction. The reviewers called the immune findings tentative and heterogeneous [18].
Population: Participants in 45 randomized trials [17]. Participants in 20 randomized trials, including people with cancer, HIV and ulcerative colitis [18].
Sources: [17], [18]
Caveats: The meta-analysis abstract gives no effect sizes [17]. Assay methods and populations varied widely [18].

PalmitoylethanolamideLimited

Inflammation markers (CRP, IL-6)

Small trials found lower IL-6 and CRP in diabetic nerve pain, while a COVID-19 trial lowered other markers but not those two.

IL-6 and CRP were primary outcomes and are not among the markers reported as reduced.

The numbers and sources

Effect: In 70 people with diabetic nerve pain, IL-6 and raised CRP fell more on 600 mg a day than on placebo (p 0.05), and fibrinogen did not differ [5]. In 60 unvaccinated adults recently diagnosed with COVID-19, 600 mg twice a day for 4 weeks lowered soluble P-selectin, IL-1 beta and IL-2 against placebo. IL-6 and CRP were primary outcomes and are not among the markers reported as reduced [9].
Population: 70 adults with type 1 or type 2 diabetes [5], and 60 adults aged 19 to 53 with COVID-19 not in hospital [9].
Sources: [5], [9]
Caveats: Two small trials. A systematic review of 47 RCTs lists 10 that measured blood or tissue markers but gives no pooled estimate [10].

Tested, and not shown to change it16

NutsStrong

Inflammation and blood vessel function

Not shown to lower C-reactive protein in two meta-analyses of nut trials. Blood vessel widening, a measure of vessel function, improved in one.

Compared with control conditions the abstract does not describe [13]; control arms without nuts [4]

The numbers and sources

Effect: Across 25 trials, nuts made no significant difference to C-reactive protein (WMD -0.01 mg/L, 95% CI -0.06 to 0.03) or other inflammation markers. Flow-mediated dilation rose 0.79% (95% CI 0.35 to 1.23) across 8 trials [13]. Tree nuts had no significant effect on C-reactive protein in 61 trials [4].
Population: 32 randomized trials in adults, 652 participants for vessel function [13]. 2,582 adults in 61 trials [4].
Sources: [13], [4]
Caveats: The authors note the C-reactive protein result may have been influenced by two studies [13].

TMGStrongHow often is not known

Higher cholesterol

Shown to raise total cholesterol, about 14 mg/dL in one review, at 4 g a day or more. Reviews differ on whether LDL rises.

Triglycerides, HDL, glucose, CRP, liver enzymes and blood pressure did not change.

The numbers and sources

How common: How often is not known: the sources give no rate.
Effect: At 4 g a day or more, betaine raised total cholesterol by 0.34 mmol/L (95% CI 0.02 to 0.65). LDL, HDL and triglycerides did not change significantly [7]. A second meta-analysis found total cholesterol 14.12 mg/dL higher (95% CI 9.23 to 19.02) and LDL 10.26 mg/dL higher (95% CI 6.14 to 14.38). Triglycerides, HDL, glucose, CRP, liver enzymes and blood pressure did not change [2].
Population: Adults in 6 RCTs from 2002 to 2018 [7]; RCTs pooled up to February 2021 [2].
Sources: [7], [2]
Caveats: The reviews differ on LDL. Subgroup analysis suggested the rise appears at 4 g a day or more [2]. In uncontrolled liver pilot trials at 2 to 8 g a day, LDL did not change and HDL rose at 2 and 4 g [6].

Vitamin DStrong

Psoriasis severity

Not shown to lower psoriasis severity with oral vitamin D in adults. One small pooled effect lost significance after adjustment.

Across 4 studies (333 patients), PASI, DLQI and CRP changes did not differ from control.

The numbers and sources

Effect: Across 3 trials, oral vitamin D lowered PASI at 6 months (MD -0.92, 95% CI -1.72 to -0.11), and the result lost significance after Hartung-Knapp adjustment (95% CI -2.21 to 0.38) [9]. Across 4 studies (333 patients), PASI, DLQI and CRP changes did not differ from control [10]. In 122 adults in Norway with low vitamin D, 100,000 IU then 20,000 IU a week for 4 months did not change PASI against placebo (adjusted difference 0.11, 95% CI -0.23 to 0.45) [11].
Population: Adults with plaque psoriasis [9][10][11].
Sources: [9], [10], [11]
Caveats: Baseline severity was low in the Norwegian trial (mean PASI 3.1) [11]. This concerns oral vitamin D, not topical vitamin D analogue creams.

AstaxanthinModerate

Oxidative stress and inflammation

Shown to lower blood malondialdehyde, an oxidative stress marker, and IL-6 in type 2 diabetes. CRP and TNF-alpha did not change.

CRP and TNF-α did not change.

The numbers and sources

Effect: Astaxanthin lowered blood malondialdehyde (SMD -0.95, 95% CI -1.67 to -0.23). IL-6 fell in type 2 diabetes (WMD -0.70 pg/mL, 95% CI -1.29 to -0.11). CRP and TNF-α did not change [7].
Population: 380 participants in 12 RCTs [7].
Sources: [7]
Caveats: Few trials measured each marker. These are biomarkers, not disease outcomes.

Cold water immersionModerate

Inflammation

Not shown to lower inflammation. Inflammatory markers rose in the hour after immersion, and post-exercise reviews found no change in C-reactive protein or interleukin-6.

Across meta-analyses of post-exercise immersion, there were no significant effects on C-reactive protein or interleukin-6 up to 72 hours.

The numbers and sources

Effect: In healthy adults, inflammation markers were higher immediately after immersion (SMD 1.03, 95% CI 0.37 to 1.68) and 1 hour after (SMD 1.26, 95% CI 0.59 to 1.94) [14]. Across meta-analyses of post-exercise immersion, there were no significant effects on C-reactive protein or interleukin-6 up to 72 hours [6]. Five weeks of immersion after interval training did not change inflammatory markers in muscle [12].
Population: Healthy adults in 11 randomized trials [14]. Healthy people in 15 meta-analyses of post-exercise immersion [6]. 16 men [12].
Sources: [14], [6], [12]
Caveats: The acute rise was measured within an hour and the reviewers call it an acute inflammatory response. Long-term markers in everyday users were not pooled [14].

Fish oilModerate

Cardiovascular outcomes with purified EPA (prescription)

Mixed results: one review found fewer cardiovascular deaths with prescription purified EPA, and another found no change in cardiovascular death at high doses.

Across 6 trials (42,738 adults) of 1.8 g a day or more of EPA-dominant omega-3, hospitalization for unstable angina fell (RR 0.75, 95% CI 0.66 to 0.87), while cardiovascular death, ischemic stroke and hs-CRP did not change significantly.

The numbers and sources

Effect: Across 16 RCTs (127,771 patients, median 3.7 years), cardiovascular death fell with purified EPA (HR 0.79, 95% CI 0.67 to 0.94) and less with mixed EPA and DHA (HR 0.92, 95% CI 0.84 to 1.00) [8]. Across 6 trials (42,738 adults) of 1.8 g a day or more of EPA-dominant omega-3, hospitalization for unstable angina fell (RR 0.75, 95% CI 0.66 to 0.87), while cardiovascular death, ischemic stroke and hs-CRP did not change significantly. Recurrent heart attack and revascularization fell only after excluding STRENGTH, the one mixed EPA and DHA outcome trial [9]. Across 10 imaging trials (860 patients) on statins, total coronary plaque volume changed by -10.0% with added EPA, -3.3% with added EPA and DHA and +1.9% on statin alone [10]. In 23 RCTs of omega-3 in general, plaque volume did not change [2].
Population: Adults in primary or secondary prevention trials [8]; adults with established cardiovascular disease or high risk [9]; patients with coronary artery disease [10][2].
Sources: [8], [9], [10], [2]
Caveats: Purified EPA (icosapent ethyl) is a prescription drug, not an over-the-counter fish oil. The two outcome reviews disagree on cardiovascular death [8][9]. Authors of [8] and [10] include a REDUCE-IT investigator with Amarin research funding and an Amarin speakers bureau member [8].

Fish oilModerate

Rheumatoid arthritis

Mixed results: one review found better disease activity markers in rheumatoid arthritis, while others found small or no effects on pain and swollen joints.

Across 18 RCTs (1,018 patients), tender joint count fell (SMD -0.59, 95% CI -0.79 to -0.39), while ESR, CRP and DAS28 did not change significantly.

The numbers and sources

Effect: Across 20 RCTs (1,252 patients), omega-3 improved eight disease activity markers. Of five inflammatory markers, only leukotriene B4 fell (SMD -0.440, 95% CI -0.676 to -0.205) [11]. Across 23 placebo-controlled trials, pooled effects on pain (SMD -0.16, 95% CI -0.40 to 0.09), tender joints (SMD -0.20, 95% CI -0.46 to 0.05) and swollen joints (SMD -0.10, 95% CI -0.28 to 0.07) were small, with intervals that include no effect [12]. Across 18 RCTs (1,018 patients), tender joint count fell (SMD -0.59, 95% CI -0.79 to -0.39), while ESR, CRP and DAS28 did not change significantly [13].
Population: Adults with rheumatoid arthritis in RCTs [11][12][13].
Sources: [11], [12], [13]
Caveats: The certainty of the evidence was mostly very low or low [12]. The authors of [12] note that earlier findings of lower NSAID use may reflect inadequate blinding.

High-protein dietModerate

Blood pressure and triglycerides

Mixed results: triglycerides fell more on higher-protein diets in two meta-analyses, while blood pressure fell slightly in one and did not differ in another.

Compared with diets with less protein

Total and LDL cholesterol, C-reactive protein and HbA1c did not change.

The numbers and sources

Effect: Across 74 trials, higher-protein diets lowered systolic (SMD -0.21, 95% CI -0.32 to -0.09) and diastolic blood pressure (SMD -0.18, 95% CI -0.29 to -0.06) and triglycerides (SMD -0.51, 95% CI -0.78 to -0.24). Total and LDL cholesterol, C-reactive protein and HbA1c did not change [6]. In energy-restricted trials, triglycerides fell 0.23 mmol/L more (95% CI 0.12 to 0.33), and blood pressure and total, LDL and HDL cholesterol did not differ [1].
Population: Adults in 74 trials [6] and in 24 weight-loss trials [1].
Sources: [1], [6]
Caveats: Restricting to studies at lower risk of bias reduced the triglyceride effect [6]. In type 2 diabetes, blood pressure changes were not significant [8].

LactoferrinModerate

Respiratory infections

Mixed results: one review found fewer respiratory infections in children but not adults, and another found no difference in children.

In adults, IL-6 fell by 24.9 pg/mL, while CRP and NK cell activity did not change.

The numbers and sources

Effect: Across 25 studies, respiratory infection incidence fell in infants and children (OR 0.78, 95% CI 0.61 to 0.98) but not in adults (OR 1.00, 95% CI 0.76 to 1.32). In adults, IL-6 fell by 24.9 pg/mL, while CRP and NK cell activity did not change [4]. A 2025 meta-analysis of 8 trials in people under 18 found no significant difference in upper respiratory infections (OR 0.61, 95% CI 0.27 to 1.40) [2].
Population: 20 studies in adults and 5 in children [4]. 8 trials in children [2].
Sources: [4], [2]
Caveats: The two reviews differ on children [4][2]. The authors of the first describe the clinical studies as limited. The review was supported by an Australian government grant in partnership with Freedom Foods Group Nutritionals [4].

Nordic dietModerate

Inflammation markers

Not shown to change CRP, IL-6 or TNF-alpha in adults in Nordic countries.

Compared with control groups the source does not describe [8], [9]

The numbers and sources

Effect: In 6 trials (613 adults), CRP did not change (-0.17 mg/L, 95% CI -0.69 to 0.35), and TNF-alpha and IL-6 did not change in 3 trials [8]. A 2025 meta-analysis also found no effect on CRP [9].
Population: Adults in Nordic countries [8]; adults in 15 RCTs [9].
Sources: [8], [9]
Caveats: Short trials. In SYSDIET, IL-1 receptor antagonist rose on the control diet and not on the Nordic diet [4], a finding not tested in the pooled analyses.

RhodiolaModerate

Endurance performance

Mixed results: a review of 26 trials found better VO2 max and endurance in healthy young adults, and a later review of 9 trials found no VO2 max effect.

Creatine kinase (ES -0.84) and lactate fell, and IL-6 and CRP did not change.

The numbers and sources

Effect: Across 26 RCTs (668 healthy participants, mean age 22), rhodiola improved VO2 max (11 studies, ES 0.32), time to exhaustion (7 studies, ES 0.38) and time trial performance (5 studies, ES -0.40). Creatine kinase (ES -0.84) and lactate fell, and IL-6 and CRP did not change. VO2 max gains were larger above 600 mg a day [4]. A systematic review of 10 papers reported less pain and muscle damage after training and improved explosive power [5]. A 2026 meta-analysis of 9 RCTs (424 healthy adults) found no significant effect on VO2 max (95% CI -0.91 to 2.99) [6].
Population: Healthy young adults, mean intervention 33 days [4]; exercise studies [5]; healthy adults [6].
Sources: [4], [5], [6]
Caveats: The two meta-analyses disagree on VO2 max [4][6]. The 2025 abstract reports no confidence intervals and notes heterogeneity [4]. Reference [5] is narrative.

Whole-body cryotherapyModerate

Ankylosing spondylitis

Shown to improve pain, function and disease activity scores in people with ankylosing spondylitis in a meta-analysis of 5 studies. C-reactive protein did not change.

C-reactive protein did not change (p = 0.684).

The numbers and sources

Effect: Across 5 studies (310 patients), cryotherapy improved the BASDAI disease activity index (p < 0.001), ASDAS (p = 0.015), BASFI function index (p = 0.006) and pain scores (p = 0.005). C-reactive protein did not change (p = 0.684) [11].
Population: 310 people with ankylosing spondylitis in 5 studies with varied temperatures and session lengths of 80 seconds to 3 minutes [11].
Sources: [11]
Caveats: Five studies, with protocols that varied. The abstract gives p values without effect sizes, and the authors call for studies of tolerance and long-term results.

CuppingLimited

Inflammation, wet cupping

One trial of 126 people with metabolic syndrome found wet cupping did not change high-sensitivity C-reactive protein over 12 weeks.

Compared with dietary advice alone [13]

The numbers and sources

Effect: Serum hs-CRP did not change between groups (p > 0.05) or over time when wet cupping was added to dietary advice, measured at 6 and 12 weeks [13].
Population: 126 patients aged 18 to 65 with metabolic syndrome [13].
Sources: [13]
Caveats: One trial without a sham.

Deer antler velvetLimited

Arthritis

One trial found elk velvet antler did not differ from placebo over 6 months in 168 adults with rheumatoid arthritis.

The numbers and sources

Effect: In 168 people with rheumatoid arthritis on standard treatment, 6 months of elk velvet antler did not differ from placebo on joint pain and swelling, disease activity, function, quality of life or CRP [4]. A systematic review identified 2 rheumatoid arthritis trials and 1 osteoarthritis trial, and its authors wrote that the osteoarthritis findings may have some promise [5].
Population: Adults with stage 2 to 3 rheumatoid arthritis [4]; RCTs [5].
Sources: [4], [5]
Caveats: One osteoarthritis trial.

Green-lipped musselLimited

Inflammation markers (CRP)

Small trials found no change in CRP in knee osteoarthritis, and lower airway inflammation markers in asthma.

The numbers and sources

Effect: In 100 adults with knee osteoarthritis, CRP and ESR did not differ between powder and placebo after 12 weeks [3]. In the asthma crossover trial, airway markers including cysteinyl leukotrienes and 8-isoprostane in exhaled breath fell on PCSO-524 against placebo [6].
Population: 100 adults with knee osteoarthritis [3] and 20 adults with asthma [6].
Sources: [3], [6]
Caveats: Two small trials measuring different markers. No meta-analysis of inflammation markers was located.

L-carnitineLimitedHow often is not known

TMAO and cardiovascular markers

Limited evidence: L-carnitine raised blood TMAO tenfold in older women without changing inflammation or lipids. The heart disease link is from mice and observational data.

In healthy older women, 24 weeks of L-carnitine raised plasma TMAO tenfold but did not change CRP, IL-6, adhesion molecules or lipids.

The numbers and sources

How common: How often is not known: the sources give no rate.
Effect: In mice, carnitine supplements raised TMAO and increased atherosclerosis, which did not occur when gut bacteria were suppressed. In 2,595 people having cardiac evaluation, plasma carnitine predicted cardiovascular disease and major adverse cardiac events only when TMAO was also high. Omnivores produced more TMAO than vegans after carnitine [10]. In healthy older women, 24 weeks of L-carnitine raised plasma TMAO tenfold but did not change CRP, IL-6, adhesion molecules or lipids [11]. In healthy volunteers given 0.5 or 1.5 g of carnitine or acetylcarnitine, about 90% of both was metabolized to TMAO, with plasma levels reaching 50 µM [12].
Population: Mice and observational cohorts [10]; healthy older women [11]; healthy volunteers given single doses [12].
Sources: [10], [11], [12]
Caveats: The heart disease link is from animals and observational data. The one supplement trial measured markers, not events, for 24 weeks.

Type in your own result

How it compares with the reference method

Mixed results2

Moderate

Repeat testing in one person

Mixed results: one study found 63% of repeat hs-CRP results stayed in the same quartile, and another found 69% of results above 3 mg/L later fell to a lower band.

The numbers and sources

Compared with: A repeat measurement in the same person
Effect: In adults measured five times at quarterly intervals, 63% of first and second hs-CRP results fell in the same quartile and 90% were within one quartile, similar to total cholesterol at 60%. The authors concluded hs-CRP is about as stable as total cholesterol [17]. In a US cohort, the intraclass correlation of CRP was 0.62 (95% CI 0.55 to 0.68), lower than 0.75 for total cholesterol. Half of participants in the highest third at baseline were in a different third at follow-up, and among those above 3 mg/L at baseline, 69% had a later result in a lower risk category [18]. FDA guidance, citing the AHA/CDC statement, calls for the average of two results about two weeks apart [2].
Population: 113 healthy adults over 1 year [17]. 760 participants in the Multi-Ethnic Study of Atherosclerosis, 255 with serial values, after excluding those with conditions or drugs known to affect CRP or CRP of 10 mg/L or above [18].
Sources: [17], [18], [2]
Caveats: The two studies reach different conclusions about stability. The intervals between measurements were months to years, not the two weeks used in practice [17][18].

Limited

Agreement between assays

Limited evidence: in a 2001 comparison of nine hs-CRP methods, four placed 92 to 95% of people in the comparison method's quartile and four placed 68 to 77%.

The numbers and sources

Compared with: A comparison hs-CRP method, in samples from apparently healthy people
Effect: Among nine automated hs-CRP methods tested on samples from 388 apparently healthy people, the concentrations marking each quartile depended on the method. Four methods classified 92 to 95% of subjects into the same quartile as the comparison method and four classified 68 to 77%, with no subject differing by more than one quartile. All methods were linear from 0.3 to 10 mg/L, and four had imprecision above 10% at 0.15 mg/L [19]. A standardization study of 28 assays from 21 manufacturers stated that variability among hs-CRP assays can lead to misclassification of patients, and selected a certified reference material for the next phase of standardization [20]. FDA guidance asks that cardiac CRP assays be standardized to that reference material and show a coefficient of variation of 10% or less at 1.0 mg/L [2].
Population: 388 apparently healthy individuals [19]. 28 assays from 21 manufacturers [20].
Sources: [19], [20], [2]
Caveats: Both comparisons date from 2001 to 2003, before standardization, so they may not describe assays in use now. No recent head-to-head comparison was sourced.

Did not match the reference method1

LimitedStudied in women

Detecting endometriosis

Limited evidence: in a Cochrane review, three studies of hs-CRP gave sensitivities of 41% to 83% and specificities of 47% to 87% against surgery.

The numbers and sources

Compared with: Endometriosis seen at surgery (laparoscopy)
Effect: Three studies with six data sets tested hs-CRP against surgical findings at cut-offs that varied, with sensitivities of 0.41 to 0.83 and specificities of 0.47 to 0.87. The highest figures, 0.83 and 0.87, came from one study of 95 women sampled in the follicular phase. Five of the data sets drew on overlapping groups of women, so the results were not pooled. The review set a sensitivity of 0.94 and a specificity of 0.79 as the accuracy a blood test would need to replace diagnostic surgery. Across 122 blood markers in 141 studies, none consistently met its criteria for replacing surgery or for triage, and the reviewers concluded that none was accurate enough for clinical use outside research [23].
Population: 506 participants in three studies of hs-CRP, within 141 studies of 15,141 women [23].
Sources: [23]
Caveats: The review rated every included study as of poor methodological quality, and the women were already having surgery, with endometriosis in 10% to 85% of them, so the figures may not hold for women tested for symptoms alone. Its searches ran to 2015 [23].

What studies tie it to

Linked in research6

Strong

Coronary heart disease and stroke

Linked to more coronary heart disease and stroke at higher levels, about 37% more coronary disease per threefold rise after adjusting for standard risk factors.

The numbers and sources

Effect: In pooled individual records from 54 prospective studies, the risk ratio for coronary heart disease per one standard deviation higher log CRP (a threefold higher level) was 1.63 (95% CI 1.51 to 1.76) adjusted for age and sex, 1.37 (1.27 to 1.48) after conventional risk factors and 1.23 (1.07 to 1.42) after fibrinogen as well. For ischemic stroke the figures were 1.44, 1.27 and 1.32 [6]. In initially healthy US women followed for 30 years, the top fifth of hs-CRP had a hazard ratio for a first major cardiovascular event of 1.70 against the bottom fifth (95% CI 1.52 to 1.90), compared with 1.36 for LDL cholesterol [7]. In statin-treated patients from three trials, the top quarter of hs-CRP had hazard ratios of 1.31 for major cardiovascular events (95% CI 1.20 to 1.43) and 2.68 for cardiovascular death (2.22 to 3.23) against the bottom quarter [8].
Population: 160,309 people without vascular disease in 54 studies, 27,769 outcomes [6]. 27,939 women, mean age 54.7, with 3,662 events [7]. 31,245 patients with or at high risk of atherosclerotic disease on statins [8].
Sources: [6], [7], [8]
Caveats: Observational. The pooled analysis found the association depends considerably on conventional risk factors and other markers of inflammation, and that CRP was tied about as strongly to deaths from several cancers and lung disease, which its authors say leaves its relevance unclear [6].

Strong

Death from any cause

Linked to more deaths at higher levels, about 75% more in the highest than the lowest category across pooled general population studies.

The numbers and sources

Effect: In a meta-analysis of prospective studies in the general population, the highest category of hs-CRP had a pooled risk ratio of 1.75 for death from any cause against the lowest (95% CI 1.55 to 1.98), 2.03 for cardiovascular death (1.65 to 2.50) and 1.25 for cancer death (1.13 to 1.38) [10]. In pooled individual records, the risk ratio per threefold higher CRP after adjustment for conventional risk factors was 1.55 for vascular death (95% CI 1.37 to 1.76) and 1.54 for non-vascular death (1.40 to 1.68) [6].
Population: 83,995 participants in 14 studies [10]. 160,309 people in 54 studies [6].
Sources: [10], [6]
Caveats: Observational. CRP rises with many illnesses, so a higher level may mark disease already present. The link with cancer death was seen in men and not in women [10].

Moderate

Type 2 diabetes

Linked to more type 2 diabetes at higher levels, with a 26% higher risk in a meta-analysis of 22 cohorts.

The numbers and sources

Effect: A meta-analysis of prospective studies found elevated CRP was associated with a higher risk of type 2 diabetes (relative risk 1.26, 95% CI 1.16 to 1.37), with no sign of publication bias [11].
Population: 40,735 participants with 5,753 cases in 22 cohorts [11].
Sources: [11]
Caveats: Observational, and the abstract does not give the size of the CRP difference the estimate refers to [11].

Strong

Cardiovascular events in trials that selected people by hs-CRP or lowered inflammation

Shown in trials: a drug that lowered hs-CRP without changing cholesterol cut cardiovascular events 15%, while one that did not lower it made no difference.

The numbers and sources

Effect: In people with a previous heart attack and hs-CRP of 2 mg/L or more, canakinumab lowered hs-CRP by 26 to 41 percentage points more than placebo without lowering lipids. At 150 mg it reduced the primary end point of heart attack, stroke or cardiovascular death (HR 0.85, 95% CI 0.74 to 0.98). Fatal infection was more frequent, and death from any cause did not differ (HR 0.94, 95% CI 0.83 to 1.06) [12]. Low-dose methotrexate did not lower C-reactive protein and did not reduce cardiovascular events (HR 0.96, 95% CI 0.79 to 1.16) [13]. In apparently healthy adults with hs-CRP of 2.0 mg/L or higher and LDL cholesterol below 130 mg/dL, rosuvastatin reduced the primary cardiovascular end point (HR 0.56, 95% CI 0.46 to 0.69) while lowering LDL cholesterol by 50% and hs-CRP by 37% [14].
Population: 10,061 patients followed a median 3.7 years [12]. 4,786 patients with stable atherosclerosis and diabetes or metabolic syndrome followed a median 2.3 years [13]. 17,802 men and women followed a median 1.9 years [14].
Sources: [12], [13], [14]
Caveats: The statin trial lowered LDL cholesterol and hs-CRP together, and had no group with low hs-CRP, so it cannot show that hs-CRP identified who benefited [14]. Canakinumab acts on interleukin-1 beta, upstream of CRP, so the trial tests lowering inflammation, not lowering CRP itself. The canakinumab trial was funded by its maker [12].

StrongStudied in women

Polycystic ovary syndrome

Linked to higher CRP in women with polycystic ovary syndrome, about twice the level of women without it, in two meta-analyses that held after accounting for obesity.

The numbers and sources

Effect: In 31 studies, mean CRP was 96% higher in women with PCOS than in controls without it (95% CI 71% to 122%), with no sign of publication bias. The difference persisted after excluding five studies in which body mass or the frequency of obesity differed between the groups. The same review found no difference in interleukin-6 or tumor necrosis factor alpha, in 10 and 9 studies [21]. In 63 studies, CRP was higher in women with PCOS than in controls (standardized mean difference 1.26, 95% CI 0.99 to 1.53), and in 35 higher quality studies that included non-obese women the difference was 1.80 (1.36 to 2.25) [22].
Population: 3,648 women, 2,359 with PCOS and 1,289 controls, in 31 studies [21]. 4,086 women with PCOS and 3,120 controls in 63 studies [22].
Sources: [21], [22]
Caveats: Observational comparisons of women with and without the condition, which cannot show which came first. Body weight raises CRP. The reviews dealt with it by setting aside studies with mismatched weight or by analyzing non-obese women, not by adjusting each result for body mass index [21][22].

LimitedStudied in women

Premenstrual symptoms and period cramps

One cohort of midlife women linked hs-CRP above 3 mg/L to more premenstrual mood symptoms, cramps or back pain, bloating and breast pain, but not headaches.

The numbers and sources

Effect: Against hs-CRP of 3 mg/L or below, a level above 3 mg/L had adjusted odds ratios of 1.27 for premenstrual mood symptoms (95% CI 1.02 to 1.58), 1.40 for abdominal cramps or back pain (1.09 to 1.80), 1.41 for appetite cravings, weight gain or bloating (1.04 to 1.89) and 1.26 for breast pain (1.02 to 1.55). It was not associated with premenstrual headaches or with reporting three or more symptoms [25].
Population: 2,939 women aged 42 to 52, before or early in the menopausal transition, at the start of the Study of Women's Health Across the Nation, from several racial and ethnic groups [25].
Sources: [25]
Caveats: Cross-sectional, so it cannot show which came first. Covariates, body mass index among those tested, stayed in each model only if they were significant [25]. The women were in midlife, so the result may not describe younger women with period pain.

Mixed results2

Strong

Risk prediction beyond standard risk factors

Mixed results: adding CRP to standard risk factors improved prediction slightly in 52 pooled cohorts, and the US Preventive Services Task Force judged the evidence insufficient.

The numbers and sources

Effect: Across 52 prospective studies, adding CRP to a model of conventional risk factors raised the C-index by 0.0039 and gave a net reclassification improvement of 1.52%. The authors estimated that measuring CRP in people at intermediate risk could prevent one additional cardiovascular event over 10 years for every 400 to 500 people screened [15]. The US Preventive Services Task Force found that adding hs-CRP to existing risk models gives small improvements in discrimination and reclassification whose clinical meaning is largely unknown, and concluded the evidence is insufficient to assess the balance of benefits and harms [16].
Population: 246,669 participants without cardiovascular disease in 52 studies [15]. Asymptomatic adults [16].
Sources: [15], [16]
Caveats: The estimate of events prevented assumes statin treatment decisions under older US guidelines [15].

LimitedStudied in women

Endometriosis

Mixed results: six studies in a Cochrane review found no CRP difference with endometriosis, while a US survey linked endometriosis to 60% higher odds of CRP above 3 mg/L.

The numbers and sources

Effect: A Cochrane review of blood tests for endometriosis found six studies that showed no difference in CRP or hs-CRP between women with endometriosis confirmed at surgery and women without it, across stages I to IV. One used an hs-CRP assay in 834 participants and the others a standard CRP assay in 499. The reviewers concluded that CRP measured either way is not a reliable marker of endometriosis [23]. In a national US survey, women who reported a diagnosis of endometriosis had greater odds of CRP above 3.0 mg/L than women without it (adjusted odds ratio 1.60, 95% CI 1.05 to 2.45) [24].
Population: 1,333 participants in six studies, within a review whose studies enrolled women having surgery for suspected endometriosis, infertility or an ovarian mass [23]. 2,342 women in the National Health and Nutrition Examination Survey, 1999 to 2002 [24].
Sources: [23], [24]
Caveats: Observational. In the survey, endometriosis was self-reported, and the abstract does not list what the model adjusted for, so body weight may not be accounted for [24]. The Cochrane review rated all its included studies as of poor methodological quality [23].

Checked, no link found2

Moderate

Coronary heart disease in genetic studies

Not shown to cause coronary heart disease: gene variants that raise CRP did not raise risk in 194,418 people.

The numbers and sources

Effect: In a Mendelian randomization meta-analysis, variants in the CRP gene each changed CRP concentration by up to 30% per allele and were unrelated to other risk factors. The risk ratio for coronary heart disease was 1.00 (95% CI 0.90 to 1.13) per standard deviation higher genetically raised log CRP, against 1.33 (1.23 to 1.43) for the same difference in measured CRP in prospective studies (P = 0.001 for the difference). The authors concluded that CRP concentration itself is unlikely to be even a modest causal factor in coronary heart disease [9].
Population: 194,418 participants in 47 studies in 15 countries, including 46,557 with coronary heart disease [9].
Sources: [9]
Caveats: The finding concerns CRP itself. It does not test whether the inflammation that CRP reflects is a cause [9].

LimitedStudied in women

Uterine fibroids

One US survey found no clear link between uterine fibroids and CRP above 3 mg/L.

The numbers and sources

Effect: In the same national survey that linked endometriosis to higher CRP, the authors report that no substantive patterns emerged between uterine fibroids and CRP above 3.0 mg/L or leukocyte telomere length [24].
Population: 2,342 women in the National Health and Nutrition Examination Survey, 1999 to 2002 [24].
Sources: [24]
Caveats: One cross-sectional analysis with self-reported diagnoses, and the abstract gives no odds ratio for fibroids [24]. No meta-analysis of inflammation markers in women with fibroids was located.

Sources

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