Syndrome X and C-reactive Protein

Syndrome X is most easily viewed as a Pre-Diabetic State,as it is characterized by hyperinsulinemia and hyperglycemia. Syndrome X can initially exist without symptoms and, as it progresses, symptoms such as fatigue can develop, which are considered a “normal” part of aging, rather than the outcome of a pathological state.

Metabolic features of syndrome X:1  

1. Increased production of pro-infl ammatory mediators: C-reactive protein (CRP), nuclear factor kappa-B (NF-kB), tumor necrosis factor (TNF), and free radicals

2. Increased platelet aggregation—platelet hyperaggregability

3. Reduced degradation of fi brin

4. Tonic vasoconstriction; reduced vasomotor regulation

5. Promotes a pro-thombotic state

6. Promotes greater infarct size

7. Leads to heart disease and stroke

As outlined above, there are numerous pro-infl ammatory factors involved in syndrome X. Perhaps the most well studied is C-reactive protein. CRP was discovered seventy years ago when scientists were studying the human infl ammatory response. It was initially characterized as an acute-phase mediator that was released during infection and trauma. However, we now know that CRP can be released chronically as part of an ongoing subclinical pro-infl ammatory state. Consider the diverse functions of CRP in the pathogenesis of heart disease.



Patients need to understand that dietary changes are the most important component for reducing the expression of syndrome X. In addition, supplements to help reduce the pro-inflammatory state include a multivitamin, magnessium, fish oil, vitamin D, and botanicals such as ginger, tumeric, and garlic.

Pro-inflammatory aspects of CRP:2

1. Localizes in atherosclerotic intima, but not normal intima

2. Induces the production of adhesion molecules

3. Reduces endothelial derived relaxing factor, which is also known as endothelial-nitic oxide

4. Induces the production of plasmin inhibitors which lead to increased fi brin deposition

5. Triggers the oxidation of LDL-cholesterol

6. Mediates the uptake of LDL by macrophages

7. Blunts normal endothelial vasoreactivity

8. Recruits circulating monocytes into the arterial wall, and their subsequent activition

9. Stimulates complement activiation


When I was in chiropractic college, as part of our training, we did blood tests on our patients, and CRP and ESR were part of the panel. Back in those days (1986) the CRP we tested for was never elevated unless there was overt trauma or infection or, perhaps, rheumatoid arthritis. Otherwise CRP was never elevated.

In recent years, a new high sensitivity CRP (hsCRP) has been developed, which can be used as a screening test for patients.3 Ridker indicates that many physicians screen for hsCRP, because it is associated with a markedly increased risk of myocardial infarction, stroke, peripheral arterial disease, and sudden cardiac death, even among apparently healthy individuals with low levels of LDL-cholesterol.2

What about musculoskeletal conditions? Most medical and chiropractic physicians have been taught that osteoarthritis (OA) is a non-infl ammatory condition caused by mechanical wear and tear. Recent research would suggest otherwise, and is consistent with most clinical presentations of osteoarthritis; that is, several joints hurt, but one may be most pronounced and perhaps associated with previous injury. We tend to forget that other joints also hurt, which takes our mind away from viewing OA, more correctly, as a systemic condition.4



In this regard, research suggests that increasing levels of CRP can predict the emergence and severity of osteoarthritis.5,6

If you decide to measure hsCRP in your offi ce, the typical interpretation is as follows: less then 1mg/L is low risk for heart disease prediction/expression; between 1-3 mg/L refl ects moderate risk; and between 3-10 mg/L suggests high risk. Greater than 10 suggests an acute phase response and, thus, a re-test in 3 weeks.3 In terms of diet, it appears that the following are associated with elevated CRP: syndrome X, low fi ber diet, low magnesium intake, low omega-3 intake, trans-fat intake, low micronutrient intake, and reduced sleep.7-15

The key to understanding elevated CRP is that it is a marker for dietary imbalances that create a pro-infl ammatory state. Syndrome X is a signifi cant metabolic driver of elevated CRP and numerous other pro-infl ammatory mediators. The dietary approach to syndrome X focuses on foods with a low glycemic index and low glycemic load, which means vegetables, lean animal products, fruits, and nuts.

Patients need to understand that dietary changes are the most important component for reducing the expression of syndrome X. In addition, supplements to help reduce the pro-infl ammatory state include a multivitamin, magnesium, fi sh oil, vitamin D, and botanicals such as ginger, turmeric, and garlic.


Dr. Seaman is the Clinical Chiropractic Consultant for Anabolic Laboratories, one of the fi rst supplement manufacturers to service the chiropractic profession. He is on the postgraduate faculties of several chiropractic colleges, providing nutrition seminars that focus on the needs of the chiropractic patient. He is also a faculty member at Palmer College of Chiropractic Florida, where he teaches nutrition and subluxation theories. He can be reached by e-mail at [email protected].



  1. Dandona P, Aljada A, Chaudhuri A, Mohanty P, Garg R. Metabolic Syndrome – A Comprehensive Perspective Based on Interactions Between Obesity, Diabetes, and Inflammation. Circulation 2005; 111:1448-54
  2. Ridker PM. Rosuvastatin in the primary prevention of cardiovascular disease among patients with low levels of low-density lipoprotein cholesterol and elevated high-sensitivity C-reactive protein: rationale and design of the JUPITER trial. Circulation. 2003; 108: 2292–2297
  3. Ridker PM. C-reactive protein. A simple test to help predict risk of heart attack and stroke. Circulation. 2003:108:381-e85
  4. Aspden RM, Scheven BA, Hutchison JD. Osteoarthritis as a systemic disorder including stromal cell differentation and lipid metabolism. Lancet. 2001:357:1118-20.

5.      Pearle AD, Warren RF, Rodeo SA. Basic science of articular cartilage and osteoarthritis. Clin Sports Med.  2005; 24:1-12

  1. Sharif M et al. Elevated serum C-reactive protein levels in osteoarthritis. Brit J Rheumatol  1997; 36:140-49
  2. Ajani UA, Ford ES, Mokdad AH. Dietary fiber and C-reactive protein: findings from national health and nutrition examination survey data. J Nutr. 2004; 134:1181-5.
  3. Lopez-Garcia E, Schulze MB, Manson JE et al. Consumption of (n-3) fatty acids is related to plasma biomarkers of inflammation and endothelial activation in women. J Nutr. 2004; 134:1806-11
  4. Ma Y, Griffith JA, Chasan-Taber L et al. Association between dietary fiber and serum C-reactive protein. Am J Clin Nutr 2006;83:760–66.
  5. King DE Mainous AG, Geesey ME, Woolson RF. Dietary magnesium and C-reactive protein levels. J AM Coll Nutr. 2005; 24L3):166-71.
  6. Church TS, Earnest CP,  Wood KA, Kampert JB. Reduction of C-reactive protein levels through use of a multivitamin. Am J Med. 2003;115:702–707.
  7. Lopez-Garcia E, Schulze MB, Meigs JB et al. Consumption of trans fatty acids is related to biomarkers of inflammation and endothelial dysfunction. J Nutr. 2005; 135(3):562-66.
  8. Pfutzner A, Forst T. High-sensitivity C-reactive protein as cardiovascular risk marker in patients with diabetes mellitus.  Diabetes Technol Ther. 2006; 8(1):28-36.
  9. Dandona P, Aljada A, Chaudhuri A, Mohanty P, Garg R. Metabolic Syndrome – A Comprehensive Perspective Based on Interactions Between Obesity, Diabetes, and Inflammation. Circulation. 2005; 111:1448-54.
  10. Meier-Ewert HK, Ridker PM, Rifai N et al. Effect of sleep loss on C-reactive protein, an inflammatory marker of cardiovascular risk. J Am Coll Cardiol. 2004; 43(4):678-83.

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