The Scoop on Inflammation



Conventional Treatments for Inflammation

Cox-2 inhibitor drugs such as Celebrex and Vioxx are often prescribed by medical doctors to treat arthritis, inflammation, pain, premenstrual syndrome, and potentially even cancer. Cox-2 is short for cyclooxygenase-2, one of the key enzymes that help the body produce inflammatory hormone-like compounds called prostaglandins and cytokines. Cox-2 is essential; without it we wouldn't be able to fight infections or heal injuries. When the body overproduces Cox-2, the end result is chronic inflammation and pain. The intensive marketing and advertising of Cox-2 inhibitors fails to address why many individuals overproduce the enzyme. Too high of levels of Cox-2 often results from imbalances and deficiencies of certain nutrients. Rather than correct these underlying dietary problems, pharmaceutical Cox-2 inhibitors only mask the most visible symptoms. Relatively minor dietary changes, with the addition of some vitamin and herbal supplements, can help correct the underlying problems.

Problems with Cox-2 Inhibitor Drugs

For years, people have used nonsteroidal anti-inflammatory drugs (NSAIDS), such as ibuprofen, to treat the inflammation and pain associated with rheumatoid arthritis and osteoarthritis. NSAIDS ease inflammation by inhibiting the activity of both Cox-2 and Cox-1, the latter an enzyme that helps maintain homeostasis (biological equilibrium) and protect the stomach lining. Because stomach ulcers occur in about 25 percent of NSAID users, pharmaceutical companies worked to develop NSAIDS that blocked only the activity of Cox-2. The idea was that a selective Cox-2 inhibitor would reduce inflammation but not irritate the stomach. Though touted for their relative safety, Cox-2 inhibitors may be far more hazardous than originally believed. While gastrointestinal problems with Cox-2 inhibitors occur less frequently, they can be severe. Just four months after the FDA approved Celebrex, 10 deaths from the drug were reported. One study has even suggested that Cox-2 is important to the gut and healing ulcers, suggesting that pharmaceutical tampering with the enzyme may not be wise.

Inflammation and Nutrition

Nutrients supply the most basic building blocks of the body's powerful inflammatory compounds. The "parent" nutrient is linoleic acid, found in many foods but especially concentrated in vegetable oils (e.g., corn, soy, and safflower oils). The body converts linoleic acid to the omega-6 family of fatty acids, including arachidonic acid. Cox-2 plays a critical role in converting arachidonic acid to the hormone-like prostaglandin E2 (PGE2) and to the cytokines interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNFa), all of which promote inflammation. Once an infection or injury stimulates production of IL-1 and TNFa, these two pro-inflammatory compounds can further stimulate each other. In addition, These compounds trigger the production of free radicals, which encourage the production of more pro-inflammatory cytokines. The pro-inflammatory reaction essentially feeds on itself, setting the stage for chronic inflammation. Ideally, the body balances these compounds with a group of anti-inflammatory compounds that originate with alpha-linolenic acid, found in cold-water fish, leafy green vegetables, and flaxseed. The body converts alpha-linolenic acid to the omega-3 family of fatty acids, which include eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Much of the problem with inflammatory disorders actually stems from an imbalance in dietary intake of the omega-6 and omega-3 fatty acids and the consequential cascade in pro-inflammatory activity. A study at the Center for Genetics, Nutrition and Health in Washington, D.C., has shown that people historically consumed roughly equal amounts of the pro-inflammatory omega-6 fatty acids and the anti-inflammatory omega-3 fatty acids. However, over the past 30 years or so, Americans have replaced much of their dietary saturated fat with omega-6 fatty acids. It’s estimated that Americans are now eating 20 times more omega-6s than omega-3s. From a biochemical standpoint, this sets the stage for powerful and chronic pro-inflammatory reactions. In addition to a diet containing too many omega-6 fatty acids, a shortage of nutritional antioxidants, such as vitamin E, also contributes to chronic inflammation. The pro-inflammatory cytokines, trigger the release of free radicals. A diet rich in antioxidants-found chiefly in vegetables and fruit-can help neutralize these free radicals. But relatively few people-9 to 34 percent, eat the recommended five daily servings of vegetables and fruit. Excess omega-6 fatty acids, lack of omega-3 fatty acids, and inadequate intake of antioxidants allows the body's pro-inflammatory reaction to get out of control, leading to chronic inflammation and pain. Inflammation plays a role in a host of diseases, including arthritis, bursitis, tendonitis and most of "-itis" diseases. Recent research has pointed to the role of inflammation in heart disease, stroke, and even Alzheimer's disease. It’s even estimated that chronic inflammation and infection cause about one-third of all cancers.

Reducing Inflammation Naturally

The simplest physiological way of turning down the body's pro-inflammatory prostaglandins and cytokines is by restoring a balance between pro- and anti-inflammatory foods. From a dietary standpoint, this means switching from vegetable oils to extra-virgin olive oil (high in anti-inflammatory omega-9 fatty acids). It also means avoiding most processed (boxed, canned, or frozen) foods, because their makers frequently add omega-6 fatty acids. By eating simple unprocessed foods-such as baked chicken, a salad, and steamed vegetables-it becomes easier to consume a more balanced ratio of omega-6 and omega-3 fatty acids. Other foods which are pro-inflammatory and should be avoided include peanuts, wheat, red meats, alcohol, the nightshade family (white potatoes, tomatoes, eggplant, tobacco, red and green peppers, paprika), carbonated drinks and fried foods. However, most people have been eating a diet high in omega-6 fatty acids and low in antioxidants for years. Simply restoring a balance is not enough to quickly offset accumulated damage, because the fatty acid composition of the body's cells reflects their dietary ratios. It's imperative to increase consumption of anti-inflammatory fatty acids and antioxidants. The take home message in all this is relatively simple: pharmaceutical drugs, while providing rapid relief of symptoms, do not correct the underlying cause of chronic inflammation. The cause is often a diet that's either unbalanced or lacking in key nutrients. No drug can correct a nutritional deficiency or imbalance. Only nutrients can do that

Supplements with Anti-Inflammatory Properties

  • Omega-3 essential fatty acids EPA and DHA are essential building blocks for the body's anti-inflammatory prostaglandins (e.g., prostaglandin E1) and for turning off Cox-2 and the body's pro-inflammatory cytokines (IL-1, IL-6, and TNFa). In addition, omega-3 fatty acids block the activity of an enzyme that breaks down joint cartilage.
  • Gamma-linolenic acid Although GLA is an omega-6 fatty acid, it has anti-inflammatory properties. Relatively little GLA is converted to arachidonic acid and prostaglandin E2. Instead, GLA increases production of the anti-inflammatory prostaglandin E1.
  • Vitamin E Although Cox-2 and prostaglandin E2 levels rise with age, animal studies have shown that vitamin E supplements reverse the increase in Cox-2 and prostaglandin E2. Vitamin E also turns off nuclear factor-kB (NF-kB) and activator protein-1 (AP-1), compounds that turn on inflammatory genes. One recent study found that arthritics taking supplements of natural vitamin E (600 mg twice daily) for 12 weeks had their pain reduced by about half.
  • Vitamin C Long recognized for its anti-inflammatory properties, the effects of vitamin C are enhanced by other nutrients. In a study of people exposed to simulated sunlight, researchers found that vitamin C and E worked synergistically to reduce skin inflammation. In a cell study, Italian researchers noted that quercetin and vitamin C worked together to protect cells from inflammation-induced damage.
  • Polyphenols and Flavonoids The antioxidant polyphenols in green tea have anti-inflammatory properties by inhibiting Cox-2 and TNFa. Genistein inhibits prostaglandin E2 and Cox-2, and quercetin inhibits the activity of inflammation-promoting "adhesion" molecules. It's likely that Pycnogenol, grape seed extract, and other flavonoids work through similar mechanisms.
  • St. John's wort Better known for its antidepressant effect, this herb also has anti-inflammatory properties. In a laboratory experiment, researchers from the University of Frieburg, Germany found that hypericin, one of the constituents of St. John's wort, inhibited NF-kB, which activates pro-inflammatory genes.
  • Ginger With a long history as a folk medicine, ginger inhibits Cox-2 and another proinflammatory compound, 5-lipoxygenase. This simple herb and condiment contains almost 500 different compounds, many of which are anti-inflammatory.
  • Rosemary This common kitchen herb is rich in ursolic acid and many of its derivatives. In laboratory experiments, Swedish researchers found that the ursolic acid extract of rosemary was a potent inhibitor of Cox-2 activity.
  • Curcumin A natural pigment that accounts for the yellow color of the spice turmeric, curcumin is also a powerful antioxidant. A recent cell study by researchers at Cornell University, New York, found that curcumin blocked the activity of Cox-2. The researchers suggested that this property might explain some of the herb's anticancer effects.
  • Cat's Claw Known as una de gato and Uncaria tomentosa, this Peruvian herb has a long history as a remedy for inflammatory arthritis. Recent cell-culture and animal experiments at the Albany Medical College, New York, found that cat's claw inhibited inflammation by blocking the activity of NF-kB.

The information provided by Dr. Stewart is strictly educational and not intended as medical advice. For diagnosis and treatment, consult your healthcare practitioner. References available by request.