Over the past month, headlines about the heart-and-stroke risks of Vioxx—and the best-selling arthritis drug’s withdrawal from the market—have been hard to miss.
Merck & Co, Inc. pulled its product from the market on September 30 after participants in a clinical trial testing Vioxx’s potential anti-cancer benefits started to show increased risk of heart attack.
In the four years since its introduction, Vioxx had been taken by 80 million people suffering from arthritis and other pain, with sales reaching a whopping $2.5 billion. By the time Vioxx (rofecoxib) was withdrawn, an estimated 80 million people worldwide had taken the drug. And, the US Food and Drug Administration (FDA) estimates that Vioxx may have contributed to almost 28,000 heart attacks in the US between 1999 and 2003.
But oddly, a key point was overlooked in all the news stories about this failed anti-inflammatory drug. As Nicholas Perricone, M.D. emphasizes in his bestselling anti-aging books, a preponderance of evidence suggests that inflammation may be the most important engine driving premature aging. And, as Dr. Perricone and other researchers say, diet-driven inflammation also underlies the epidemic of degenerative diseases—from heart disease and diabetes to Alzheimer’s and arthritis—that plagues the populations of rich industrialized societies.
Diet-driven inflammation promotes aging and disease
Inflammation is best known as a temporary immune response to infections and wounds, in which case it makes its presence felt in the form of pain, swelling, and redness.
In contrast, chronic, systemic inflammation is a “silent” phenomenon that increases as we age.
A growing body of evidence indicates that sub-clinical inflammation—that is, chronic, systemic inflammation inflammation that produces no noticeable symptoms—may be a key promoter of cardiovascular disease, diabetes, metabolic syndrome (syndrome X), Alzheimer’s, and certain common cancers (e.g., prostate, colon).
Chronic, systemic inflammation can be stimulated at any age by diet- and cooking-related processes. Cooking foods at high temperatures results in a "browning" effect, where sugars and certain oxidized fats react with proteins to damage the proteins and form tissue-damaging protein-sugar compounds called “glycotoxins.” Chief among the pro-inflammatory glycotoxins are Advanced Glycation End products or AGEs, which stimulate production of the damaging, unstable oxygen compounds known as free radicals.
Aging seen as "cooking"
In fact, normal aging resembles a slow cooking process, since these same glycotoxins form in many tissues—including skin, arteries, eye lenses, cartilage, and more—as we age. Foods high in glycotoxins induce a low-grade, chronic state of inflammation. In addition, the glycotoxins in food cooked at high temperatures also promote the formation of glycotoxins in our living tissues. The implications of these findings are profound.
Many age-related diseases—such as hardened arteries, cataracts and senility are at least partially attributable to glycation. These destructive glycation reactions render proteins in the body “cross-linked” and barely functional. As these degraded proteins accumulate, they also emit damaging free radicals—at about 50 times the rate found in normal proteins—as well as signals that induce the production of pro-inflammatory messenger chemicals called cytokines.
What one eats plays a major role in chronic inflammatory processes. Consuming low glycemic foods prevents the insulin surge that contributes to chronic inflammatory processes.
Eating too much over-cooked food causes an increase in inflammatory cytokines. Since most "junk" and “fast” foods are cooked at very 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, they also create other metabolic disorders that can induce degenerative disease.
Please don’t “SuperSize Me”
If you’ve not seen the award-winning documentary film “SuperSize Me,” I urge you to view this amusing yet alarming eye-opener. The film follows the healthy, fit young filmmaker as he subsists on nothing but MacDonald’s meals for 30 days. Within a short time, his doctors become alarmed by a steep decline in his liver function—an effect they never expected, and one that is likely caused by his consumption of huge amounts of pro-inflammatory sugars, starches, saturated fats, and glycotoxins.
Two common dietary habits are chiefly responsible for creation of pro-inflammatory AGEs:
1) Excessive consumption of sugars and refined starches—which itself stimulates silent inflammation at the cellular level—but also promotes creation of AGEs.
2) Excessive consumption of foods cooked at high temperature—a method that produces the “browning” effect, which indicates that proteins and sugars have combined chemically. Eating such foods also leads to internal formation of AGEs.
Anti- inflammatory, anti-aging foods
If asked to name some anti-inflammatory agents, most of us would respond by naming non-steroidal drugs like aspirin, ibuprofen (Advil), naproxen, Celebrex, or (no longer) Vioxx. All of these work in rather mysterious ways, but are believed to block one or both of two key pro-inflammatory enzymes, known as COX-1 and COX-2.
Upon their introduction in the late 1990’s, Celebrex and Vioxx were hailed as improvements over the older, COX-1-blocking anti-inflammatory drugs such as aspirin and ibuprofen. This was because they seem to target only the COX-2 enzyme, and it was hoped that they would not cause the adverse gastric side effects seen with the older drugs that block the COX-1 enzyme.
However, the new COX-2 drugs are not free of gastric side effects, and, as we have seen, they may have unanticipated adverse effects on heart health. They are also much more costly than aspirin and ibuprofen.
Fortunately, there are many foods with potent anti-inflammatory properties, including fish high in omega-3s, and many herbs and spices.
These are some of the best anti-inflammatory foods, whose anti-inflammatory powers derive from their high omega-3 (fish) or antioxidant (plant foods and salmon) content:
- FISH: Wild Salmon*, Sablefish, Mackerel, Herring, Sardines
- VEGETABLES: Onions, Garlic, Chives, Leeks, Greens (spinach, chard, collards, broccoli, kale), Tomatoes, Bell Peppers, Green Beans, Broccoli, Brussels sprouts, Cabbage, Lettuces
- BEANS, NUTS, SEEDS (all types)
- FRUITS: Berries (especially Blueberries and Raspberries), Capers
- SPICES: Ginger**, Turmeric**, Cinnamon, Clove
- HERBS: Rosemary, Thyme, Oregano, Parsley, Cilantro, Fennel, Mint, Dill, Tarragon
- BEVERAGES: Green tea, White tea, Black tea, Red wine, Cocoa (with minimal sugar), Pomegranate juice
- DARK CHOCOLATE (containing at least 70 percent cocoa solids; enjoy sparingly)
*Salmon offers a double anti-inflammatory punch, as it is high in both omega-3s and the uniquely potent antioxidant/ anti-inflammatory red pigment called astaxanthin (which it gets from eating zooplankton). Sockeye are highest in astaxanthin.
**Ginger and turmeric are extraordinarily potent anti-inflammatories. They rival the anti-inflammatory potency of drugs like aspirin and ibuprofen in clinical trials, but produce none of those drugs’ adverse side effects. They also hold promise as anti-cancer agents.
· Yaffe K, Kanaya A, Lindquist K, et al. The Metabolic Syndrome, Inflammation, and Risk of Cognitive Decline. JAMA. 2004 Nov 18;10:292:2237-2242.
· Yim MB, Yim HS, Lee C, Kang SO, Chock PB. Protein glycation: creation of catalytic sites for free radical generation. Ann N Y Acad Sci. 2001 Apr;928:48-53.
· Brod SA. Unregulated inflammation shortens human functional longevity. Inflamm Res. 2000 Nov;49(11):561-70. Review.
· Baynes JW, Thorpe SR. Glycoxidation and lipoxidation in atherogenesis. Free Radic Biol Med. 2000 Jun 15;28(12):1708-16. Review.
· James MJ, Gibson RA, Cleland LG. Dietary polyunsaturated fatty acids and inflammatory mediator production. Am J Clin Nutr. 2000 Jan;71(1 Suppl):343S-8S. Review.
· Zurier RB. Fatty acids, inflammation and immune responses. Prostaglandins Leukot Essent Fatty Acids. 1993 Jan;48(1):57-62. Review.
· Anderson I, Adinolfi C, Doctrow S, Huffman K, Joy KA, Malfroy B, Soden P, Rupniak HT, Barnes JC. Oxidative signalling and inflammatory pathways in Alzheimer's disease. Biochem Soc Symp. 2001;(67):141-9.
· Siskova A, Wilhelm J. [Role of nonenzymatic glycation and oxidative stress on the development of complicated diabetic cataracts] Cesk Fysiol. 2000 Feb;49(1):16-21. Review. Czech.
· Rosen P, Nawroth PP, King G, Moller W, Tritschler HJ, Packer L. The role of oxidative stress in the onset and progression of diabetes and its complications: a summary of a Congress Series sponsored by UNESCO-MCBN, the American Diabetes Association and the German Diabetes Society. Diabetes Metab Res Rev. 2001 May-Jun;17(3):189-212. Review.
· Pickup JC, Crook MA. Is type II diabetes mellitus a disease of the innate immune system? Diabetologia. 1998 Oct;41(10):1241-8. Review.
· Mene P, Festuccia F, Pugliese F. Clinical potential of advanced glycation end-product inhibitors in diabetes mellitus. Am J Cardiovasc Drugs. 2003;3(5):315-20. Review.