Life Extension Magazine®
People suffering from chronic disease often have elevated levels of C-reactive protein in their blood. C-reactive protein indicates an inflammatory process is going on in the body, but does not identify the specific pro-inflammatory cytokine that may be the underlying cause. Testing for pro-inflammatory cytokines has been prohibitively expensive because there has been so little demand for it. The Life Extension Foundation has spent more than a year establishing a relationship with the largest blood-testing laboratory in the United States to offer an inflammatory cytokine profile at an affordable price. Here is the new cytokine panel along with the optimal anti-inflammatory ranges:
The importance of cytokine testing for those suffering from chronic illness From a practical standpoint, if you suffer from congestive heart failure, and your levels of TNF-a remain persistently high, you may ask your doctor to prescribe the drug Enbrel®, which specifically counteracts the destructive effects of TNF-a. If you suffer from cancer and your levels of IL-6 remain persistently high, you may consider high dose DHEA or asking your doctor to prescribe a bisphosphonate drug (such as Zometa® that protects against bone destruction that releases excess IL-6 into the body). Those with prostate, certain types of breast cancer, and other hormonally driven cancer should consider other IL-6 lowering therapies (such as high dose DHA fish oil extract) in lieu of DHEA. Those with systemic inflammatory disease often manifest high levels of IL-1b. If diet, the anti-inflammatory supplements (fish oil, borage oil, DHEA, etc.) and cytokine-suppressing drugs (pentoxifylline, 400 mg twice a day) fail to suppress this destructive cytokine, then ask your doctor to prescribe the drug Arava (leflunomide), starting at the low dose of 10 mg a day. Methods of lowering elevated C-reactive protein Those who are in relative good health, but have elevated C-reactive protein, can try to lower it using a variety of diet modifications, supplements and/or drugs. Supplements such as vitamin E, borage oil, fish oil, DHEA, vitamin K and nettle leaf extract can lower C-reactive protein. Diets low in arachidonic acid, omega-6 fatty acids, saturated fats, high-glycemic and overcooked food can suppress inflammatory factors in the body. If diet and supplements fail, drugs such as ibuprofen, aspirin, pentoxifylline or one of the statins (such as Pravachol®) should be taken. If the modified diet, nutrients and/or drugs lower C-reactive protein to below 1.3 (mg/L) of blood, then this is an indication that the underlying inflammatory fire has been extinguished. (Make sure to always ask for the high-sensitivity C-reactive protein blood test). Individuals with chronic disease sometimes find it difficult to suppress C-reactive protein. In these cases, it is important to identify the specific inflammatory cytokines that are responsible for the destructive inflammatory processes that is causing or contributing to the underlying disease state. This enables a custom tailored program to be implemented, and its success measured by suppressing the pro-inflammatory cytokine culprits. For instance, if TNF-a levels are elevated and natural approaches fail to lower it, the prescription drug Enbrel should be considered. Low-cost cytokine testing Few physicians have recognized the critical importance of suppressing pro-inflammatory cytokines in the treatment of degenerative disease. As a result, there has been little demand for them and commercial blood laboratories have been charging exorbitant prices (around $645.00) for the four most important inflammatory cytokine tests. The Life Extension Buyers Club has negotiated a favorable pricing arrangement with the largest blood-testing laboratory in America to offer the complete inflammatory cytokine panel for only $435.00. The cost of individual cytokine tests to Life Extension members is then discounted as follows:
If you add up the members price for all four of these tests, the cost comes out to $376.00. If all four of these tests are ordered at once, the member's price is reduced to $295.00 a 54% savings compared to commercial lab charges. To order a high sensitivity C-reactive protein blood test, the Inflammatory Cytokine Blood Panel, or any other blood tests by mail order, call 1-800-208-3444. Until June 1, 2003, the price of a high-sensitivity C-reactive protein test is only $42.00. References 1. Vlassara H 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. 2. Kanda T. C-reactive protein (CRP) in the cardiovascular system. Rinsho Byori 2001 Apr;49(4):395-401. 3. Smith DA et al. Serum levels of the antiinflammatory cytokine interleukin-10 are decreased in patients with unstable angina. Circulation 2001 Aug 14;104(7):746-9. 4. Speer P. New insights into the pathogenesis of pulmonary inflammation in preterm infants. Biol Neonate 2001;79(3-4):205-9. 5. Glabinski AR et al. CXC chemokine receptors expression during chronic relapsing experimental autoimmune encephalomyelitis. Ann N Y Acad Sci 2000;917:135-44. 6. Ajuebor MN, et al. The chemokine RANTES is a crucial mediator of the progression from acute to chronic colitis in the rat. J Immunol 2001 Jan 1;166(1):552-8. 7. Hogan SP, et al. A pathological function for eotaxin and eosinophils in eosinophilic gastrointestinal inflammation. Nat Immunol 2001 Apr;2(4):353-60. 8. Shiels IA, et al. Cell phenotype as a target of drug therapy in chronic inflammatory diseases. Med Hypotheses 2000 Feb;54(2):193-7. 9. Licinio J, et al. The role of inflammatory mediators in the biology of major depression: central nervous system cytokines modulate the biological substrate of depressive symptoms, regulate stress-responsive systems, and contribute to neurotoxicity and neuroprotection. Mol Psychiatry 1999 Jul;4(4):317-27. 10. Willard LB, et al. Pathological and biochemical consequences of acute and chronic neuroinflammation within the basal forebrain cholinergic system of rats. Neuroscience 1999 Jan;88(1):193-200. 11. Van der Meide PH, et al. Cytokines and the immune response. Biotherapy 1996;8(3-4):243-9. 12. Blaser MJ. Hypotheses on the pathogenesis and natural history of Helicobacter pylori-induced inflammation. Gastroenterology 1992 Feb;102(2):720-7. 13. Cominelli F, et al. Interleukin-1 in the pathogenesis of and protection from inflammatory bowel disease. Biotherapy 1989;1(4):369-75. 14. Deon D, et al. Cross-talk between il-1 and il-6 signaling pathways in rheumatoid arthritis synovial fibroblasts. J Immunol 2001 Nov 1;167(9):5395-403. 15. Baynes JW, et al. Glycoxidation and lipoxidation in atherogenesis. Free Radic Bio. Med 28, 1708-1716 (2000). 16. Sell DR, et al. Longitudinal determination of skin collagen glycation and glycoxidation rates predicts early death in C57Bl/6NNIA mice. FASEB J 14,145-156 (2000). 17. Dyer DG, et al. The Maillard Reaction in vivo. Z Ernahrungswiss 30,29-45(1991). 18. Monnier VM, et al. Acelerated age-related browning of human collagen in diabetes mellitus. Proc Natl Acad Sci, USA 81,583-587(1984). 19. Monnier VM, et al. Skin collagen glycation, glycoxidation, and crosslinking are lower in subjects with long-term intensive versus conventional therapy of type 1 diabetes: relevance of glycated collagen products versus HbA1c as markers of diabetic complications. Diabetes 48, 870-880(1999). 20. Schmidt AM, et al. The multiligand receptor RAGE as a progression factor amplifying immune and inflammatory responses. J Clin Invest 108,949-955(2001). 21. [Don't have the authors] Role of Inflammatory and Hemostatic mediators in preclinical endothelial dysfunction: Relevance to high-risk patients with hypertension. JACC (Supplement A) 2002 Mar 6; 39 (5):p.209A. 22. Pradhan AD, et al. C-reactive protein, interleukin 6 and risk of developing type 2 diabetes mellitus. JAMA 2001;286:327-334. 23. Harris TB, et al. Associations of elevated interleukin-6 and C-reactive protein levels with mortality in the elderly. Am J Med 1999 May;106(5):506-12. 24. Walston J, et al. Frailty and activation of the inflammation and coagulation systems with and without clinical comorbidities; results from the cardiovascular health study. Archives of Internal Medicine (2002;162:2333-2341). |