Life Extension Magazine May 2003
As We See It
Eating Food Cooked At High
What you should do
Most Life Extension members follow a healthy lifestyle that helps prevent glycation and chronic inflammation.
Inflammatory cytokine production can be suppressed with the proper supplementation of fish oil, DHEA, vitamin K and nettle leaf extract. If blood tests reveal persistently high levels of inflammatory cytokines, then 400 mg twice a day of a low-cost drug called pentoxiphylline may bring inflammatory cytokine levels down to safe ranges.
What one eats plays a major role in chronic inflammatory processes. Consuming low glycemic foods reduces the insulin surge that contributes to chronic inflammatory processes. It is also important to avoid over consumption of foods high in arachidonic acid (beef, egg yolk, dairy, etc.).
We now know that eating too much over cooked food causes an increase in inflammatory cytokines. Since most "junk" foods are cooked at extremely high temperatures, it makes sense to avoid french fries, hamburgers, potato chips, fried food and other snacks. These foods not only contain lots of glycotoxins, but they also create other metabolic disorders that can induce degenerative disease.
Consuming at least 1000 mg a day of carnosine, and/or 300 mg of the European drug aminoguanidine can inhibit pathological glycation reactions in the body. Avoiding foods cooked at high temperature not only reduces pathological glycation processes, but also prevents the formation of numerous gene-mutating toxins that are known carcinogens.
When food is cooked at high temperatures, deadly gene-mutating toxins are created that increase human cancer risk. This warning has been communicated to readers of this publication for many years. Now that overheated food is associated with accelerated aging, health conscious individuals have an even greater incentive to pay attention to their diet. As a member of the Life Extension Foundation, you learn about documented methods of reducing disease risk years before the general public.
Those concerned that they are already suffering from the effects of a chronic inflammatory disorder should turn to the next page to learn how they can measure and suppress lethal pro-inflammatory cytokines.
For longer life,
Further Reading: Protecting against the lethal effects of chronic inflammation
Caution: Food is cooked to destroy bacteria and other pathogens that could cause a serious illness. It is important not to eat undercooked food, but avoiding food unnecessarily cooked at higher temperatures is desirable. Certain foods (like fried foods) have to cook at high temperatures. Health conscious people are increasingly avoiding fried foods because they are associated with many health risks.
Note: For more information about eating healthier, log on to www.lef.org and access the Obesity and Inflammation (Chronic) protocols listed under Health Concerns. Also refer to the January 2001 issue of Life Extension on this website and click the article Drugs That Inhibit Cox-2 May Cause Tissue Damage.
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).