Testing For C-reactive Protein May Save Your Life

 

Have you had your CRP levels tested? You should—because this simple blood test might just save your life.

C-reactive protein, or CRP, has long been used as a marker of inflammation in the body.¹ High CRP levels are found in practically every known inflammatory state. Even if you have no symptoms of disease, elevated CRP levels may signal an increased risk for practically all degenerative disorders, including cardiovascular disease, cancer, diabetes, and more.^2-6

Now, it turns out that CRP is more than just a marker of inflammation—it is also a cause of inflammation.⁷

Knowing your CRP status puts you in an enviable position. If it is elevated, you can take proactive steps to lower it, thereby slashing your risk of a long list of disorders related to chronic inflammation.

What Is CRP?

C-reactive protein (CRP) is manufactured throughout the body, especially by immune cells, the liver, and by adipocytes (fat cells).⁸ During the early phase of an inflammatory stimulus (such as infection or tissue injury) CRP levels rise dramatically.

CRP is an incredibly sensitive and robust “marker” of general inflammation.¹⁰ It’s used to track the progress of chronic inflammatory conditions such as rheumatoid arthritis, vasculitis, or inflammatory bowel diseases like Crohn’s disease.^11-13 In those cases, increased symptoms accompanied by a rise in CRP signals a “flare” of the disease, and indicates the need to provide anti-inflammatory therapy.

More recently, however, CRP has been recognized as an active cause of inflammation in addition to simply being a marker of inflammation. ⁷ This important discovery opened the door for additional ways to fight chronic inflammation.

When CRP binds to specific molecules in the body, it participates in rapidly raising the production of inflammatory signaling molecules called cytokines and other inflammatory mediators.¹⁴ This is a healthy function of acute inflammation because it helps speed up the race to the scene of any damage, and quickly destroys invading organisms.¹⁵

However, when CRP rises unchecked, it can contribute to destructive chronic inflammation.

It is easy to see why Big Pharma is now hotly pursuing CRP-inhibiting drugs.¹⁶ Fortunately, there are a number of methods that lower CRP by changing the underlying conditions that cause it to rise.

What You Need To Know

CRP Predicts Heart Disease and Cancer Risk

• C-reactive protein, or CRP, is a sensitive marker of inflammation. It rises quickly after an inflammatory attack, but should return to normal levels. When CRP remains high, it is an indication of chronic inflammation.
• Elevated CRP signals increased risk for many chronic inflammation-related disorders, including cardiovascular disease, cancer, diabetes, obesity, and more.
• But CRP is much more than simply a marker of inflammation; it actively participates in the inflammatory process.
• Lowering CRP levels, then, is a vital part of a healthy lifestyle and a host of safe, affordable nutritional supplements may offer immediate help.
• Get your CRP tested, and get started today on supplements that can work for you.

What CRP Can Reveal About Your Health

The use of CRP has been a standard diagnostic practice for many years in determining the status of known inflammatory disorders,¹⁷ such as rheumatoid arthritis and Crohn’s disease, and in discriminating between inflammatory and functional bowel disorders.^12,13,18

But as we keep learning more about diseases that have been linked with inflammation, CRP is turning out to be a useful research tool for both diagnosis and risk assessment. This is especially the case with two major killers of Americans: cardiovascular disease and cancer.

What Are Optimal CRP Levels?

Heavier people usually have higher CRP levels, as abdominal fat provides fertile ground for over-production of deadly pro-inflammatory cytokines that cause CRP to increase. Obese individuals are often in a chronic pro-inflammatory state that sharply increases their risk of all degenerative diseases.

A simple way of suppressing CRP for many people is to shed abdominal fat pounds.

Optimal CRP levels for everyone to strive for are under 0.55 mg/L in men and under 1.0 mg/L in women.

Cardiovascular Disease

 

CRP levels are closely correlated with the risk of cardiovascular disease; the higher the CRP, the greater the risk.^19,20 Even otherwise healthy people with modestly raised CRP levels have a significantly higher risk of future cardiovascular events.²⁰

In one important study, patients with the highest CRP levels were at a 45% increased risk for coronary heart disease compared with those having the lowest levels.²¹ Another study found that people with elevated CRP levels were 60% more likely to develop ischemic heart disease and 30% more likely to have a cerebrovascular event, compared to those with normal levels.²² In addition, CRP levels have now been shown to be capable of predicting serious complications in hospitalized patients with coronary artery disease.²³

Preliminary evidence suggests that CRP levels may even help distinguish between your risk for a fatal vs. a non-fatal heart attack, but that is far from established.²⁴

Such risk increases seem to hold true for other conditions, such as diabetes, that also contribute to cardiovascular disease.^25,26 Indeed, in one study, women with the highest CRP levels had a 16-fold risk for developing diabetes compared with those at the lowest levels.²⁵ In another study, the risk was about 2.8-fold for both sexes.^25,26

CRP is also associated with other cardiovascular-related conditions such as high blood pressure.

In people with high blood pressure, CRP levels are correlated with stiffness of arteries and atherosclerosis, as well as damage to organs such as the heart and kidney.²⁷

In people with normal baseline blood pressure, CRP levels have repeatedly been shown to predict the later development of hypertension.²⁷

And people with heart rhythm disturbances, such as atrial fibrillation, have significantly higher CRP levels than do normal controls.²⁸

CRP levels are such strong indicators of cardiovascular risk that circulating levels of CRP are now being used to predict the likelihood of cardiovascular events and to assist in choosing therapy.²⁷

In addition to being a marker of risk, there is growing evidence that CRP contributes directly to cardiovascular and diabetes risk. ^26,27 Studies have shown the presence of CRP directly inside of most arterial plaques—and all heart lesions—after a heart attack.²⁰ Indeed, in a damaged brain or heart after a stroke or heart attack, there is a correlation between CRP and the size of the affected area; this is strong support for a contributing role of CRP in these diseases.¹⁶

Cancer

With the discovery that cancer is strongly related to overall inflammation status, there’s been growing interest in CRP as a predictor of prognosis in a variety of cancer types.^29,30 And, with strong evidence that CRP is an active (and destructive) participant in promoting inflammation, there’s equally strong interest in discovering ways to actively lower a person’s CRP levels to reduce their cancer risk—or to promote their recovery if they already have cancer.

Optimal CRP levels for everyone to strive for are under 0.55 mg/L in men and under 1.0 mg/L in women.

Interestingly, CRP is now associated with a number of cancers as a powerful tool for determining prognosis and survival.^29-36 When CRP is measured at the time of diagnosis, high levels consistently predict poor survival, whereas normal (especially the lower-end of normal) levels predict good outcomes.^30-36

For example:

In men with penile cancer, a CRP level greater than 20 mg/L at diagnosis is significantly associated with the probability of developing lymph node metastases, a sign of poor outcome.³¹

In patients with advanced stomach cancer, those with a CRP level greater than 17 mg/L had an 11% greater chance of dying within 3 months after diagnosis, compared to those with lower levels.³² A later study found that CRP greater than 10 mg/L was associated with a 77% increase in poor overall survival, with a 196% greater chance of having a higher disease stage, and an 81% increase in the likelihood of tumor recurrence.³³

CRP is strongly associated with survival in patients with colon and/or rectum cancers. Those with elevated levels of CRP were more likely to have lymph node (local) and distant metastases, invasion of blood vessels and nerves, and a higher stage diagnosis.³⁴ For patients with CRP greater than 5 mg/L, only 13.3% survived after 5 years, while 57% of patients with lower CRP were still alive 5 years later.³⁴ Indeed, one study indicated that CRP was the only marker that was an independent predictor of disease-free survival.³⁰ CRP concentrations were higher in a group of colorectal cancer patients, at 2.4 mg/L, compared with 1.9 mg/L in healthy controls, and those with the highest CRP were 2.6 times as likely as those with the lowest levels to develop such cancers.³⁵

In pancreatic cancer, high plasma CRP levels at diagnosis indicated a 121% increased risk of dying from the disease.²⁹

In breast cancer, a CRP level of greater than 10 mg/L, compared with a level of less than 1 mg/L,predicted³⁶:

• A 96% greater risk of dying from any cause,
• A 91% greater risk of dying from breast cancer specifically, and
• A 69% greater risk of having additional breast cancer-related events.

Measuring CRP In The Laboratory

A laboratory test measurement called “high sensitivity CRP (or “hs-CRP”) is now often used to measure inflammation, especially in cardiovascular disease. This newer test uses the same scale as previous standard CRP measurements, but because of its higher sensitivity, it is better at discriminating even very small increases in CRP measurements at the lowest levels. While Life Extension currently recommends an optimal hs-CRP of less than 1.0 mg/L for women and less than .55 mg/L for men, standard laboratory testing uses the following risk stratification for hs-CRP:

• The “lowest risk” range is less than 1.0 mg/L.
• “Average risk” is 1.0 to 3.0 mg/L.
• The “highest risk” category is greater than 3.0 mg/L.⁶⁹

How To Lower Your CRP

With high levels of CRP being so closely tied to cardiovascular disease and cancer, the question you’re probably wondering right now is, “How do I lower my CRP levels?”

For starters, your lifestyle has a direct impact on CRP levels. Certain dietary habits, such as a high intake of trans-fatty acids, can increase CRP levels, leading to a reason why trans fats increase cardiovascular risk to a greater degree than one would expect based on its adverse effects on blood fat levels.³⁷ 

A 2013 study found that ideal health behaviors (such as diet, exercise, etc.) could lower CRP.³⁸ In that study, people having four to six “ideal behaviors” had up to a 32% reduction in their CRP levels. Exercise alone has been shown to be a means of lowering high CRP. In fact, the higher the baseline CRP, the greater the impact of a reasonable exercise regimen on CRP.³⁹

Eating foods cooked at high temperature can increase inflammation.^40-42

Avoiding high temperature-cooked food can reduce production of pro-inflammatory cytokines and CRP, thus helping to extinguish the inflammatory fire raging in the bodies of most aging people today.^40-43

Wouldn’t it be incredible if Americans could throw away side effect-laden pain killing drugs just by changing the way their food is prepared?

Some drugs, such as statins, have been shown to lower CRP levels in patients with elevated blood lipids.^19,44 In fact, one study using rosuvastatin (Crestor^®) showed that healthy people without raised blood cholesterol but with CRP levels greater than 2.0 mg/L reduced hs-CRP levels by 37% and reduced the frequency of major cardiovascular events (though the study didn’t address the long-term consequences of statin therapy).⁴⁵ There are, however, other ways to lower CRP without a prescription.

Over a dozen dietary supplements have been shown to bring down CRP levels in laboratory or human models. Red yeast rice, for example, lowered CRP by nearly 24% in people with moderately high cholesterol;⁴⁶ ginger reduced CRP in diabetic adults;⁴⁷ and vitamin C reduced plasma CRP 24% in smokers.⁴⁸

The table above describes 17 nutrients that have been shown to favorably influence CRP levels.

In order to determine your CRP level, all it requires is a low-cost blood test.

By lowering your CRP, you’ll be protecting yourself against chronic inflammation before it progresses to a life-threatening disease.

Clinical Uses Of CRP In Diagnosis

C-reactive protein has been in use as a screening measure for inflammation almost since its original discovery.⁷⁰

Levels of CRP begin to rise in the body usually 6 to 12 hours after an inflammatory stimulus and peak around 48 to 96 hours after the event.^71,72 Changes in repeated measurements of CRP are often used as a way to track a patient’s inflammatory course, helping to identify improvement (falling CRP) or relapse (rising CRP).⁷³

While CRP is never diagnostic of a specific condition, if interpreted in terms of clinical context, it does help to determine if inflammation is the source of worrisome signs and symptoms, and whether symptoms are being caused by infections or by other causes.^70,74 In infants and toddlers with high fevers, for example, a CRP below 5 mg/dL was shown to rule out a serious bacterial infection.⁷⁵

In a similar fashion, CRP is frequently used diagnostically to rule out a potentially dangerous diagnosis in adults. For example, adult patients with chest pain were found to be safe to go home from the hospital if they had CRP levels within the normal range.⁷⁶

Elevated CRP levels are also useful as early markers of the seriousness of inflammation in a very wide range of disorders, from urinary tract infections and appendicitis to heart attacks.^15,70,76 And CRP has been shown to help in discriminating Crohn’s disease from non-inflammatory bowel disorders, including intestinal lymphoma.⁷⁷

Another widespread use of CRP is as a means of following a patient’s progress after a major diagnosis has already been made. In such patients, the CRP level correlates with the severity of the ongoing disease, and therefore rising levels can be used as an early warning that the disease is rapidly worsening, and that aggressive treatment is necessary.⁷⁸

Summary

We’ve known for years that C-reactive protein (CRP) is an important marker of dangerous inflammation in the body, but we’ve recently discovered that it also actively participates in the inflammatory process.^1,7

High CRP levels are found in practically every known inflammatory state. Even if you have no symptoms of disease, elevated CRP signals increased risk for cardiovascular disease, cancer, diabetes, obesity, and more.²

Additionally, there’s strong evidence that people with lower CRP levels have fewer inflammation-related diseases.^{21,22,30,34,63}

This knowledge has opened the door to a new way of treating chronic inflammation: by lowering your CRP level back to a safe, normal range. There are drugs such as statins that lower CRP levels, but high-dose statin drugs have proven side effects.⁴⁵ Fortunately, over a dozen nutrients have been found to have a safe, immediate impact on this dangerous cause of chronic inflammation.

Don’t delay—get your CRP checked, and get started on a lifestyle, supplement, hormone or drug regimen that works for you. 

If you have any questions on the scientific content of this article, please call a Life Extension^® Health Advisor at 1-866-864-3027.

Obesity And CRP

Two conditions that contribute to a rise in CRP levels are obesity and diabetes—an effect that may be the reason behind the rise in inflammation seen in those conditions.^79,80

Obese individuals experience a double threat from CRP. First, while much of the circulating CRP is made in the liver, human fat tissue also produces substantial amounts of CRP.^8,79 Second, obese individuals experience a rapid rise in cytokines, particularly the one known as interleukin-6 (IL-6),⁸¹ which may induce CRP production in the liver—potentially causing CRP levels to climb even higher and promoting additional inflammation.⁸²

In this way, CRP may be at least part of the missing link between obesity, diabetes, and cardiovascular disease, in which inflammation plays such a major part.^79,80,82

References

1. Tillett WS, Francis T. Serological reactions in pneumonia with a non-protein somatic fraction of pneumococcus. J Exp Med. 1930 Sep 30;52(4):561-71.
2. Trichopoulos D, Psaltopoulou T, Orfanos P, Trichopoulou A, Boffetta P. Plasma C-reactive protein and risk of cancer: a prospective study from Greece. Cancer Epidemiol Biomarkers Prev. 2006 Feb;15(2):381-4.
3. Poole EM, Lee IM, Ridker PM, Buring JE, Hankinson SE, Tworoger SS. A prospective study of circulating C-reactive protein, interleukin-6, and tumor necrosis factor α receptor 2 levels and risk of ovarian cancer. Am J Epidemiol. 2013 Oct 15;178(8):1256-64.
4. Pradhan AD, Manson JE, Rifai N, Buring JE, Ridker PM. C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus. JAMA. 2001 Jul 18;286(3):327-34.
5. Oei L, Campos-Obando N, Dehghan A, et al. Dissecting the relationship between high-sensitivity serum C-reactive protein and increased fracture risk: the Rotterdam Study. Osteoporos Int. 2013 Dec 13.
6. Wium-Andersen M, Ørsted D, Nordestgaard B. Elevated C-reactive protein associated with schizophrenia in the general population: a prospective study. APA 2013; Poster NR10-23.
7. Li JJ, Fang CH. C-reactive protein is not only an inflammatory marker but also a direct cause of cardiovascular diseases. Med Hypotheses. 2004;62(4):499-506.
8. Available at: http://circres.ahajournals.org/content/97/7/609.full. Accessed February 18, 2014.
9. Thompson D, Pepys MB, Wood SP. The physiological structure of human C-reactive protein and its complex with phosphocholine. Structure. 1999 Feb 15;7(2):169-77.
10. Available at: http://circ.ahajournals.org/content/99/2/237.full. Accessed February 18, 2014.
11. Deodhar SD. C-reactive protein: the best laboratory indicator available for monitoring disease activity. Cleve Clin J Med. 1989 Mar-Apr;56(2):126-30.
12. Du Clos TW. C-reactive protein as a regulator of autoimmunity and inflammation. Arthritis Rheum. 2003 Jun;48(6):1475-7.
13. Vermeire S, Van Assche G, Rutgeerts P. C-reactive protein as a marker for inflammatory bowel disease. Inflamm Bowel Dis. 2004 Sep;10(5):661-5.
14. Available at: http://www.jimmunol.org/content/176/12/7598.full. Accessed February 6, 2014.
15. Zimmerman MA, Selzman CH, Cothren C, Sorensen AC, Raeburn CD, Harken AH. Diagnostic implications of C-reactive protein. Arch Surg. 2003 Feb;138(2):220-4.
16. Pepys MB, Hirschfield GM, Tennent GA, et al. Targeting C-reactive protein for the treatment of cardiovascular disease. Nature. 2006 Apr 27;440(7088):1217-21.
17. Clyne B, Olshaker JS. The C-reactive protein. J Emerg Med. 1999 Nov-Dec;17(6):1019-25.
18. Available at: https://blogs.commons.georgetown.edu/journal-of-health-sciences/issues-2/previous-volumes/vol-4-no-1-march-2007/the-role-of-c-reactive-protein-in-inflammatory-bowel-disease. Accessed February 6, 2014.
19. Jialal I, Stein D, Balis D, Grundy SM, Adams-Huet B, Devaraj S. Effect of hydroxymethyl glutaryl coenzyme a reductase inhibitor therapy on high sensitive C-reactive protein levels. Circulation. 2001 Apr 17;103(15):1933-5.
20. Hirschfield GM, Pepys MB. C-reactive protein and cardiovascular disease: new insights from an old molecule. Qjm. 2003 Nov;96(11):793-807.
21. Danesh J, Wheeler JG, Hirschfield GM, et al. C-reactive protein and other circulating markers of inflammation in the prediction of coronary heart disease. N Engl J Med. 2004 Apr 1;350(14):1387-97.
22. Zacho J, Tybjaerg-Hansen A, Jensen JS, Grande P, Sillesen H, Nordestgaard BG. Genetically elevated C-reactive protein and ischemic vascular disease. N Engl J Med. 2008 Oct 30;359(18):1897-908.
23. Elgharib N, Chi DS, Younis W, Wehbe S, Krishnaswamy G. C-reactive protein as a novel biomarker. Reactant can flag atherosclerosis and help predict cardiac events. Postgrad Med. 2003 Dec;114(6):39-44; quiz 16.
24. van Wijk DF, Boekholdt SM, Wareham NJ, et al. C-reactive protein, fatal and nonfatal coronary artery disease, stroke, and peripheral artery disease in the prospective EPIC-Norfolk cohort study. Arterioscler Thromb Vasc Biol. 2013 Dec;33(12):2888-94.
25. Pradhan AD, Manson JE, Rifai N, Buring JE, Ridker PM. C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus. JAMA. 2001 Jul 18;286(3):327-34.
26. Dehghan A, Kardys I, de Maat MP, et al. Genetic variation, C-reactive protein levels, and incidence of diabetes. Diabetes. 2007 Mar;56(3):872-8.
27. Hage FG. C-reactive protein and Hypertension. J Hum Hypertens. 2013 Nov 14.
28. Polovina M, Potpara T, Giga V, Stepanovic J, Ostojic M. Impaired endothelial function in lone atrial fibrillation. Vojnosanit Pregl. 2013 Oct;70(10):908-14.
29. Szkandera J, Stotz M, Absenger G, et al. Validation of C-reactive protein levels as a prognostic indicator for survival in a large cohort of pancreatic cancer patients. Br J Cancer. 2013 Nov 7.
30. Toiyama Y, Inoue Y, Saigusa S, et al. C-reactive protein as predictor of recurrence in patients with rectal cancer undergoing chemoradiotherapy followed by surgery. Anticancer Res. 2013 Nov;33(11):5065-74.
31. Al Ghazal A, Steffens S, Steinestel J, et al. Elevated C-reactive protein values predict nodal metastasis in patients with penile cancer. BMC Urol. 2013 Oct 22;13(1):53.
32. Baba H, Kuwabara K, Ishiguro T, et al. C-reactive protein as a significant prognostic factor for stage IV gastric cancer patients. Anticancer Res. 2013 Dec;33(12):5591-5.
33. Yu Q, Yu XF, Zhang SD, Wang HH, Wang HY, Teng LS. Prognostic role of C-reactive protein in gastric cancer: A meta-analysis. Asian Pac J Cancer Prev. 2013;14(10):5735-40.
34. Lin M, Huang J, Zhu J, Shen H. Elevated pre-treatment levels of high sensitivity C-reactive protein as a potential prognosticator in patients with colorectal cancer. Exp Ther Med. 2013 Dec;6(6):1369-74.
35. Erlinger TP, Platz EA, Rifai N, Helzlsouer KJ. C-reactive protein and the risk of incident colorectal cancer. JAMA. 2004 Feb 4;291(5):585-90.
36. Villasenor A, Flatt SW, Marinac C, Natarajan L, Pierce JP, Patterson RE. Postdiagnosis C-reactive protein and breast cancer survivorship: Findings from the WHEL Study. Cancer Epidemiol Biomarkers Prev. 2013 Dec 26.
37. Lopez-Garcia E, Schulze MB, Meigs JB, et al. Consumption of trans fatty acids is related to plasma biomarkers of inflammation and endothelial dysfunction. J Nutr. 2005 Mar;135(3):562-6.
38. Xue H, Wang J, Hou J, et al. Association of ideal cardiovascular metrics and serum high-sensitivity C-reactive protein in hypertensive population. PLoS One. 2013;8(12):e81597.
39. Swardfager W, Herrmann N, Cornish S, et al. Exercise intervention and inflammatory markers in coronary artery disease: a meta-analysis. Am Heart J. 2012 Apr;163(4):666-76.e1-3.
40. Birlouez-Aragon I, Saavedra G, Tessier FJ, et al. A diet based on high-heat-treated foods promotes risk factors for diabetes mellitus and cardiovascular diseases. Am J Clin Nutr. 2010 May;91(5):1220-6.
41. Vlassara H, Cai W, Crandall J, et al. Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy. Proc Natl Acad Sci U S A. 2002 Nov 26;99(24):15596-601.
42. Uribarri J, Woodruff S, Goodman S, et al. Advanced glycation end products in foods and a practical guide to their reduction in the diet. J Am Diet Assoc. 2010 Jun;110(6):911-16.e12.
43. Available at: https://www.lifeextension.com/magazine/mag2013/jan2013_Are-You-Cooking-Yourself-to-Death_01.htm. Accessed February 21, 2014.
44. Jonathan E, Derrick B, Emma L, et al. C-reactive protein concentration and the vascular benefits of statin therapy: an analysis of 20,536 patients in the Heart Protection Study. Lancet. 2011 Feb 5;377(9764):469-76.
45. Ridker PM, Danielson E, Fonseca FA, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med. 2008 Nov 20;359(21):2195-207.
46. Cicero AF, Derosa G, Parini A, et al. Red yeast rice improves lipid pattern, high-sensitivity C-reactive protein, and vascular remodeling parameters in moderately hypercholesterolemic Italian subjects. Nutr Res. 2013 Aug;33(8):622-8.
47. Mahluji S, Ostadrahimi A, Mobasseri M, Ebrahimzade Attari V, Payahoo L. Anti-inflammatory effects of zingiber officinale in type 2 diabetic patients. Adv Pharm Bull. 2013;3(2):273-6.
48. Block G, Jensen C, Dietrich M, Norkus EP, Hudes M, Packer L. Plasma C-reactive protein concentrations in active and passive smokers: influence of antioxidant supplementation. J Am Coll Nutr. 2004 Apr;23(2):141-7.
49. Deminice R, Rosa FT, Franco GS, Jordao AA, de Freitas EC. Effects of creatine supplementation on oxidative stress and inflammatory markers after repeated-sprint exercise in humans. Nutrition. 2013 Sep;29(9):1127-32.
50. Panahi Y, Sahebkar A, Parvin S, Saadat A. A randomized controlled trial on the anti-inflammatory effects of curcumin in patients with chronic sulphur mustard-induced cutaneous complications. Ann Clin Biochem. 2012 Nov;49(Pt 6):580-8.
51. Sahebkar A. Are curcuminoids effective C-reactive protein-lowering agents in clinical practice? Evidence from a meta-analysis. Phytother Res. 2013 Aug 7.
52. Sindhu G, Ratheesh M, Shyni GL, Nambisan B, Helen A. Anti-inflammatory and antioxidative effects of mucilage of Trigonella foenum graecum (Fenugreek) on adjuvant induced arthritic rats. Int Immunopharmacol. 2012 Jan;12(1):205-11.
53. Bornhoeft J, Castaneda D, Nemoseck T, Wang P, Henning SM, Hong MY. The protective effects of green tea polyphenols: lipid profile, inflammation, and antioxidant capacity in rats fed an atherogenic diet and dextran sodium sulfate. J Med Food. 2012 Aug;15(8):726-32.
54. Lebon J, Riesco E, Tessier D, Dionne IJ. Additive effects of isoflavones and exercise training on inflammatory cytokines and body composition in overweight and obese postmenopausal women: a randomized controlled trial. Menopause. 2013 Dec 30.
55. Chen Y, Abbate M, Tang L, et al. L-Carnitine supplementation for adults with end-stage kidney disease requiring maintenance hemodialysis: a systematic review and meta-analysis. Am J Clin Nutr. 2013 Dec 24.
56. Moslehi N, Vafa M, Rahimi-Foroushani A, Golestan B. Effects of oral magnesium supplementation on inflammatory markers in middle-aged overweight women. J Res Med Sci. 2012 Jul;17(7):607-14.
57. Asemi Z, Zare Z, Shakeri H, Sabihi SS, Esmaillzadeh A. Effect of multispecies probiotic supplements on metabolic profiles, hs-CRP, and oxidative stress in patients with type 2 diabetes. Ann Nutr Metab. 2013;63(1-2):1-9.
58. Grenon SM, Conte MS, Nosova E, et al. Association between n-3 polyunsaturated fatty acid content of red blood cells and inflammatory biomarkers in patients with peripheral artery disease. J Vasc Surg. 2013 Nov;58(5):1283-90.
59. Khajehnasiri F, Mortazavi SB, Allameh A, Akhondzadeh S. Effect of omega-3 and ascorbic acid on inflammation markers in depressed shift workers in Shahid Tondgoyan Oil Refinery, Iran: a randomized double-blind placebo-controlled study. J Clin Biochem Nutr. 2013 Jul;53(1):36-40.
60. Mocellin MC, Pastore e Silva Jde A, Camargo Cde Q, et al. Fish oil decreases C-reactive protein/albumin ratio improving nutritional prognosis and plasma fatty acid profile in colorectal cancer patients. Lipids. 2013 Sep;48(9):879-88.
61. Askari G, Ghiasvand R, Feizi A, Ghanadian SM, Karimian J. The effect of quercetin supplementation on selected markers of inflammation and oxidative stress. J Res Med Sci. 2012 Jul;17(7):637-41.
62. Zhang K, Li Y, Cheng X, et al. Cross-over study of influence of oral vitamin C supplementation on inflammatory status in maintenance hemodialysis patients. BMC Nephrol. 2013 Nov 14;14(1):252.
63. Kostoglou-Athanassiou I, Athanassiou P, Lyraki A, Raftakis I, Antoniadis C. Vitamin D and rheumatoid arthritis. Ther Adv Endocrinol Metab. 2012 Dec;3(6):181-7.
64. Asemi Z, Samimi M, Tabassi Z, Shakeri H, Esmaillzadeh A. Vitamin D supplementation affects serum high-sensitivity C-reactive protein, insulin resistance, and biomarkers of oxidative stress in pregnant women. J Nutr. 2013 Sep;143(9):1432-8.
65. Singh U, Devaraj S. Vitamin E: inflammation and atherosclerosis. Vitam Horm. 2007;76:519-49.
66. Khan MI, Siddique KU, Ashfaq F, Ali W, Reddy HD, Mishra A. Effect of high-dose zinc supplementation with oral hypoglycemic agents on glycemic control and inflammation in type-2 diabetic nephropathy patients. J Nat Sci Biol Med. 2013 Jul;4(2):336-40.
67. Kim J, Ahn J. Effect of zinc supplementation on inflammatory markers and adipokines in young obese women. Biol Trace Elem Res. 2014 Jan 10.
68. Qureshi AA, Khan DA, Mahjabeen W, Papasian CJ, Qureshi N. Nutritional supplement-5 with a combination of proteasome inhibitors (resveratrol, quercetin, -tocotrienol) modulate age-associated biomarkers and cardiovascular lipid parameters in human subjects. J Clin Exp Cardiolog. 2013 Mar 2;4(3).
69. Available at: http://www.webmd.com/a-to-z-guides/c-reactive-protein-crp?page=2. Accessed January 12, 2014.
70. Clyne B, Olshaker JS. The C-reactive protein. J Emerg Med. 1999 Nov-Dec;17(6):1019-25.
71. Hansen JG, Dahler-Eriksen BS. C-reactive protein and infections in general practice. Ugeskr Laeger. 2000 Apr 24;162(17):2457-60.
    
72. Melbye H, Hvidsten D, Holm A, Nordbø SA, Brox J. The course of C-reactive protein response in untreated upper respiratory tract infection. Br J Gen Pract. 2004 Sep;54(506):653-8.
73. Vermeire S, Van Assche G, Rutgeerts P. The role of C-reactive protein as an inflammatory marker in gastrointestinal diseases. Nat Clin Pract Gastroenterol Hepatol. 2005 Dec;2(12):580-6.
74. Mitaka C. Clinical laboratory differentiation of infectious versus non-infectious systemic inflammatory response syndrome. Clin Chim Acta. 2005 Jan;351(1-2):17-29.
75. Pulliam PN, Attia MW, Cronan KM. C-reactive protein in febrile children 1 to 36 months of age with clinically undetectable serious bacterial infection. Pediatrics. 2001 Dec;108(6):1275-9.
76. Magadle R, Weiner P, Beckerman M, Berar-Yanay N. C-reactive protein as a marker for active coronary artery disease in patients with chest pain in the emergency room. Clin Cardiol. 2002 Oct;25(10):456-60.
77. Liu S, Ren J, Xia Q, et al. Preliminary case-control study to evaluate diagnostic values of C-reactive protein and erythrocyte sedimentation rate in differentiating active Crohn’s Disease from intestinal lymphoma, intestinal tuberculosis and Behcet’s Syndrome. Am J Med Sci. 2013 Dec;346(6):467-72.
78. Muangchant C, Pope JE. The significance of interleukin-6 and C-reactive protein in systemic sclerosis: a systematic literature review. Clin Exp Rheumatol. 2013 Mar-Apr;31(2 Suppl 76):122-34.
79. Lau DC, Dhillon B, Yan H, Szmitko PE, Verma S. Adipokines: molecular links between obesity and atheroslcerosis. Am J Physiol Heart Circ Physiol. 2005 May;288(5):H2031-41.
80. Greenfield JR, Campbell LV. Relationship between inflammation, insulin resistance and type 2 diabetes: ‘cause or effect’? Curr Diabetes Rev. 2006 May;2(2):195-211.
81. Fain JN. Release of interleukins and other inflammatory cytokines by human adipose tissue is enhanced in obesity and primarily due to the nonfat cells. Vitam Horm. 2006;74:443-77.
82. Bastard JP, Maachi M, Lagathu C, et al. Recent advances in the relationship between obesity, inflammation, and insulin resistance. Eur Cytokine Netw. 2006 Mar;17(1):4-12.