The whole food and nothing but the food

by Judith A. DeCava, CNC, LNC, CCWFN.

Old remedies for arthritis like bee venom or wearing a copper bracelet are considered passé in the scientific world. Yet in recent years there have been even more amazing changes of viewpoint. It used to be thought that osteoarthritis was an inevitable part of aging. It isn’t. It used to be thought that osteoarthritis was caused by wear and tear on the joints. It’s not the real story. It used to be thought that osteoarthritis was just deterioration of the cartilage “shock absorber” in the joint. There’s much more involved. It used to be thought that exercise would make arthritis worse. It doesn’t. We’re all learning.

Being overweight increases your risk of osteoarthritis (OA) as does aging, having a genetic predisposition, previous injuries, being female, and (for knees) wearing high-heeled shoes. The most popular places for OA are the knees, hands, feet, hips, and spine. Currently, there are no drugs that “treat” OA directly—just pain relievers. Severely damaged joints may result in a recommendation for surgery such as arthroscopic surgery or joint replacement.

NSAIDS (non-steroidal anti-inflammatory drugs) are usually used for pain. They include COX-2 (cyclo-oxygenase-2) inhibitors (some taken off the market due to increased risk of heart attack and stroke), ibuprofen (Advil, Motrin), naproxen (Aleve), and aspirin. They can cause gastrointestinal bleeding, leaky gut, heart and lung complications, among other things, and—remember this for later—they interfere with the inflammation process. According to Dr Joseph Pizzorno and Dr Michael Murray, NSAID use can “deteriorate the very joints that they are taken for,” because they “turn off the chemistry to repair…” Sherry A Rogers, MD, says the drugs “all steal from cartilage chemistry, fostering breakdown of protective cartilage…” This ups your risk for surgery and eventual joint replacement.

Injections of cortisone are sometimes used. Cortisone blocks and suppresses the normal inflammation response of the immune system. The shots may—or may not—provide short-term pain relief and enable better joint mobility. But they don’t improve joint health. After a few series of injections there’s a buildup of adhesions, scar tissue, and damage that often leaves surgery and/or joint replacement as the only options. Potential side effects include “flares” (pain, redness, and swelling), joint infection, cartilage damage, and tendon rupture. A study reported in the New England Journal of Medicine showed that, for most people, arthroscopic surgery (insertion of a scope and scraping off any spurs [projections] from the cartilage) didn’t help any better than “fake” surgery (scope but no scraping of the cartilage) performed on other people. Spurs caused pain for only a minority of people.

There is currently no standard definition of OA, aka degenerative joint disease. It’s “often” due to deterioration of the cushiony cartilage between the two joint bones, but it’s now known to affect the whole joint. Bone, ligaments, muscles, other tissues, joint capsules (membranes that enclose bone ends), synovium (membrane containing lubricating fluid), nerves, cells that maintain all these tissues, and hormone-producing glands can all be involved. There may be stiffness, pain, tenderness, swelling, decreased joint motion, and formation of bone spurs (tiny bone growths). But, people diagnosed by x-rays don’t always have symptoms. Though joint damage may cause symptoms, the severity of damage is only “weakly related” to symptoms. Some doctors guess “that OA is a group of overlapping disorders.”
Many experts no longer believe OA is a problem of tissue wear and tear. Yet the focus of most research continues to be on cartilage or other specific tissues. What’s needed, says Paul Dieppe, MD, University of Bristol, England, “is a more holistic approach.” OA is more complex than previously thought and “has definite environmental risk factors” that include toxins (lead, other heavy metals, sodium fluoride, and smoking have been implicated) and malnutrition—a lack of needed real food components and/or disruptions causing food intolerances. (NSAIDs make the gut more permeable, decreasing digestion and increasing the risk of developing food intolerances.) Data, offers Timothy McAlinson, MD, Boston University, “suggest that optimizing the nutritional status of the population may well play some role in the secondary and possibly primary prevention of this disease.”

“We’ve learned,” says Dr Dieppe, “that OA, rather than a passive ‘falling to bits’ of the joints, is an active form of joint disease that seems to stem from an out-of-kilter degradation and repair response of the matrix.” A clue! It’s “thought to be a mechanically driven, but chemically mediated, process that seems to be dominated by an attempt by joints to repair damage or abnormal biomechanics.” Aha! To translate: There is injury or damage to the joint and the body attempts to repair it. The problem arises when the body isn’t able to properly repair the joint. That’s why an under-recognized aspect of OA is that the body’s attempt at repair of the damaged joint is often successful. “Most of my patients get better, not because I do anything to them—I’m a therapeutic minimalist—I just watch it and it gets better. Some of this is due to social and behavioral adaptation, but a lot results from the repair process.” (Emphasis added) What’s the repair process? It’s mostly the natural process of inflammation—the body’s way of getting rid of damaged or dead cells and laying down a matrix of cells for replacement. Ironic, isn’t it, that the drugs given to people with OA are designed to interfere with or stop inflammation! When the immune system is healthy and allowed to do its job, there’s a healthy inflammation response and repair. The degree of healing depends on the degree of the person’s resources, including nutritional reserves.

Some doctors use prolotherapy—injections of substances like a sugar, salt or corn extract into tissues surrounding the affected joints. Why? To stimulate the immune system “by tricking the body into thinking a new injury has occurred.” In other words, the injections cause irritation to which the body responds with inflammation. It’s the inflammation process (removal of debris or irritants and rebuilding of tissues) that does the trick. Wouldn’t it be better to support the inflammation process from the start, allowing the body to do what it wants to do, giving it what it requires to do so, rather than interfering with that process by drugs and then later trying to stimulate an inflammation response? [i]


A high quality diet comprised mainly of fresh, whole real foods is imperative. Eating more fruits and vegetables lowers the risk of developing OA. Dr Royal Lee referred to OA as “cooked food disease,” so include plenty of raw foods. Avoid refined carbohydrates (white flour products, white rice, refined sugars, and the like) as well as processed deviant or fake fats. If you’re overweight, take steps to lose that ballast! Both diet and exercise are essential. Studies show that diet plus exercise results in less inflammation, improved function, less pain, improved mobility—plus weight and fat loss and muscle gain. Diet or exercise alone may result in weight loss, but less improvement in the joints. Knees are especially vulnerable to excess weight—each pound you lose means 4 less pounds of pressure on your knee joint.

Food allergies or intolerances may worsen symptoms. Not all people with OA have food sensitivities, but identifying them in those who do can make a huge difference. Eliminate suspected foods from your diet for 3 weeks; then reintroduce one at a time to identify specific triggers. The most common are wheat, red meats, dairy products, eggs, peanuts, caffeine, and corn. Nightshades (tomato, potato, chili peppers, eggplant) have also been implicated. One study found that eliminating common allergic foods decreased joint stiffness, swelling, and tenderness. A year later, the benefits were still there. A few studies accused a high intake of red meat of upping risk, but meat itself may not be the culprit. The toxic, unnatural environment in which meat animals are now raised skews the fatty acid content and leaves residues of hormones, drugs, and pesticides. And people eating a lot of meat may simply not be consuming enough vegetables and fruits for other needed nutrients. A Mediterranean-type diet seems to help reduce pain, joint swelling, and tenderness as well as improve movement and vitality. It consists mostly of vegetables, fruit, fish, cereals, beans, and unrefined olive oil with little or no ‘junk’ food—a diet high in compounds supportive to inflammation and repair.

Numerous studies found links between nutrients and improvement in OA. In one large study, those with OA who consumed the most vitamin C were 3 times less likely to have suffered worsening of symptoms over a 10-year period than people who got the least. A 2003 study also found a strong link between vitamin C consumption—via fruits and vegetables—and lowered risk of developing OA. Carotenoids—like beta-carotene, beta-cryptoxanthin and zeaxanthin—have been linked to a lower risk of developing inflammatory arthritis. The carotenes in just one glass of freshly squeezed orange juice each day could play a role in preventing arthritis. B vitamins—particularly niacinamide, B12, and folate—may be involved in joint repair and may help impaired joint mobility. One reason there are so many B vitamin deficiencies is the increased use of medications. To properly absorb B vitamins, you need high levels of active bacterial flora in your intestines. Antibiotics, oral contraceptives, anti-cholesterol drugs, diuretics, stomach acid blockers, and most pain killers either destroy beneficial bacteria in the intestines and/or interfere with absorption of B vitamins. Most people over age 50—those most likely to have OA—presently take one or more drugs like these.

There’s a connection between low vitamin D and OA. Sunlight on your skin stimulates your body to make vitamin D and is the best way to get what you need. Low blood levels of vitamin D and low intake of vitamin D may up the risk of progressive OA three-fold. Fish like salmon, mackerel, and tuna give you vitamin D complex and supportive nutrients. Vitamins A, C, D and E complexes in foods all help prevent arthritis. One reason may be their roles in the inflammation and repair processes. But d-alpha tocopherol (so-called “vitamin E,” a separated fraction) doesn’t seem to relieve arthritis pain or stiffness.

Minerals including calcium, magnesium, manganese, potassium, silica, boron, copper, zinc, selenium, and sulfur have all been shown to play a protective and healing role. A mineral-rich seaweed supplement was found to improve pain and reduce stiffness. Most popular supplements for treating OA contain chemically unrelated forms of sulfur—condroitin sulfate, SAMe, MSM, acetyl-cysteine, etc. Many people don’t get enough sulfur and sulfur-containing amino acids. Studies show that 70 to 90% of people with arthritis obtain relief with boron, essential in the metabolism of vitamin D, calcium, phosphorus, and steroidal hormones like estrogen and cortisol. A deficit of boron may cause a deficit of these other nutrients or hormones. Zinc and manganese are both needed to manufacture joint structures and for producing SOD (superoxide dismustase)—important for protection against cellular damage.

Omega-3 fatty acids (in fatty fish, fish oils, flaxseed, green leafy veggies, walnuts, meat or milk from pasture-fed animals) play a big part in the successful resolution of inflammation. Research in Great Britain demonstrated that cod liver oil helps relieve pain and stiffness of OA as well as help reverse destruction of joint cartilage. Borage oil, evening primrose oil, hemp oil, or black currant oil are rich in the fatty acid gamma-linolenic acid (GLA). GLA can be made in the body, but many people don’t make enough. Low GLA levels are linked with immune system dysfunction and arthritis. Another fatty acid—cetyl myristoleate (CM)—may help decrease arthritic symptoms and help protect against getting arthritis in the first place. CM is found in fish oils, coconut oil, and other fatty, unrefined, natural foods. Consuming olive oil has been shown to decrease pain and improve activities of daily living. Avoiding “bad” fats like trans fats, refined overheated oils, fake fats, fried foods, and the like is vital too.

Years ago, Dr Weston Price identified “activator X” and Dr Rosalind Wulzen found the “Wulzen anti-stiffness factor” in foods like liver and raw milk products from grass-fed animals as well as some fish eggs. These food components work synergistically with other food factors to help protect against arthritis, help the repair and rebuilding of bone or other tissues, improve mineral absorption, assist hormone production, and much more. Both activator X and the anti-stiffness factor can be destroyed by excessive heat or pasteurization.

Hyaluronic acid (HA) in drug form is approved by the FDA for treating knee OA. In the body, HA is a natural lubricant and shock absorber found in synovial fluid of joints. It enhances the ability of cartilage to resist frictional force (as would occur walking down stairs, for example) and maintain resiliency. Levels of HA in the blood have been linked with severity of OA. The HA drug is administered as a series of injections directly into the knees. The small relief of pain “may be overestimated.” Plus it’s “not clear whether these injections alter or slow the progression of OA.” So you may feel better for a while but the underlying problem may not improve. Oral HA supplements (usually made from rooster combs) aren’t well absorbed and aren’t as “effective” as the injections. The best way to get HA is to make it in your body or get it from whole foods containing the entire package of co-factors. Good toxin-free bone-meal supplements are a great way to get HA. Another terrific source is bone broth. Broths made from beef, chicken, or fish bones benefit bones, joints, cartilage, other musculoskeletal tissues, skin, and overall health. One reason is HA—in cooperation with all the minerals, proteins, and other components supportive to joint health, including sulfur compounds. Vegetables or meat can be added or the broth can be used as stock. When you make broth, throw in egg shells leftover from breakfast and strain them out after cooking. The membrane that separates the egg white from its shell is mostly made of protein, plus HA, glucosamine, and chondroitin. (HA breaks down into glucosamine.) A small study showed that people who took supplements containing 500 milligrams of eggshell membrane enjoyed reduced joint and muscle pain after just 7 days—relief continued through the end of the study at 30 days.

What about popular glucosamine (GS) and chondroitin sulfate (CS) supplements? In the body these naturally-produced substances are involved in cartilage repair, elasticity, and maintenance. Many people don’t make enough. And they don’t chew on bones or eat gristle (cartilage) to get more. Historically, people worldwide chewed on or cooked with animal bones and cartilage. But taking GS or CS supplements has yielded mixed results. Some studies showed they reduce pain and disability, increase mobility, strengthen and support existing cartilage, and slow deterioration of tissues like cartilage in the joints. Yet questions remain as to whether they actually help rebuild cartilage or other tissues. On the other hand, a review of 53 studies found that GS and CS “appear to be no more effective than placebo.” A large trial funded by the National Institutes of Health showed that after 24 weeks of treatment, neither GS or CS, nor a combination of the two, was more effective than a placebo for pain. Other studies indicated the supplements were not very effective, didn’t reduce pain or improve function, or relieved pain only for a while. Many say benefits are “exaggerated.” One foible may be study funding—funding by supplement companies often produce far more positive findings than studies without such funding. Another problem may be the supplements themselves—what’s on the label isn’t always in the supplement. You need quality supplements from a company you can trust! GS and CS may be manufactured from lobster, crab, or shrimp shells; shark cartilage; cow trachea; or outer skeletons of beetles and certain micro-organisms. The question is: do supplements of separated GS and CS perform as well as whole food sources that contain other components that all work together to help the body repair damaged tissues? A couple of studies added the mineral manganese to GS and CS and got even better relief. Harvard researchers showed that collagen from chicken cartilage (rich in GS and CS) contains other substances that aids inflammation and accelerate healing. So, separated GS and CS may relieve symptoms somewhat. But it’s best to get real foods containing the whole package of natural factors that will support repair of joint tissues.

SAMe (a derivative of the amino acid methionine) is said to decrease joint discomfort. But many studies on SAM-e were poorly designed and included only small numbers of people. Studies that showed good results found modest pain relief—“not dramatic.” One study indicated SAMe relieved pain as well as NSAID drugs. Some studies found “no consistent effect” on pain. SAMe supplies sulfur—supportive to the inflammation process and good for building collagen (protein fiber) bonds that strengthen joints. But you’d have to take huge amounts to imitate most of the studies. Taking mega-doses of an amino acid derivative can cause gastrointestinal distress and a number of biochemical imbalances. People with bipolar disorder, Parkinson’s disease, and those using anti-depressants should not take SAM-e. Does that sound like a food? Real foods like Brazil nuts and sunflower seeds are good sources of SAMe containing all other synergistic components.

MSM (methyl sulfonylmethane) is often added to glucosamine or chondroitin products. MSM is naturally present in tiny amounts in many foods. But the supplement is not real food—it’s an oxidized form of DMSO (dimethl-sulfoxide), a drug. A 2004 study concluded that a combination of MSM and glucosamine worked better than either alone. The small trial of 10 volunteers used 2250-milligram MSM doses (a lot more than the 250 to 1000 mg usually in supplements) for 6 weeks. There was improvement in pain. A study involving 50 people also showed decreases in pain and function impairment. There’s still no evidence that MSM protects or repairs cartilage or other tissues or that it alters the progression of tissue damage. Stanley Jacobs, MD, the developer of MSM supplements, acknowledges that MSM is overhyped as an arthritis cure but claims it does relieve pain. Taking large amounts of one chemical is a drug approach, not nutritional support.

Another ‘hot’ treatment consists of compounds derived from oils of avocados and soybeans (avocado-soybean unsaponifiables—ASU or FASU). A Belgian study involving people with arthritis of the knee gave subjects either 300 mg or 600 mg of ASU/FASU or a placebo daily. After 3 months, those taking either of the ASU/FASU supplements had reduced pain and increased function. Further, 71% of them reduced their pain pill intake by more than half. A few other studies also suggested efficacy. But the only real long-term trial found no benefit. [ii]


There are now oodles of studies that show exercise doesn’t cause or worsen OA and that exercise actually helps to prevent OA or to benefit the joints when you do have OA. People who exercise have better cartilage in their knees and other joints. Physical activity helps relieve the pain of OA, even in older people. It staves off functional decline. Strength training can reduce the rate of space narrowing in joints (indicating less deterioration of cartilage). Range-of-motion exercises (like dance or yoga), strengthening exercises (like weight training), and aerobic exercises (like walking, bike riding, swimming) are all best for people with OA. Tai Chi improves OA symptoms, functional mobility, levels of tension, and general health. Exercising in water particularly decreases pain and improves function. Options should be discussed with a health professional. Regular, moderate exercise is needed to maintain joint function no matter who you are. Exercise stimulates cartilage and supporting tissues to take up more nutrients and repair themselves. Another case of use ‘em or lose ‘em. [iii]

To supplement a whole-food, preferably organic, diet, the following may be considered:

Just Before Two Meals:
2 Calcifood wafers – chew
1 Cataplex C or Echinacea-C – chew
1 Thymex – chew
1 SP Green Food
1 Nutrimere (6 months only)
After Two Meals:
1 Chlorophyll Complex
1 Tuna Omega-3 Oil

After One Meal:
1 Glucosamine Synergy (90 caps only)

To assist discomfort, 1 Saligesic (MediHerb) can be taken 2 to

[i] UC Berkeley Wellness Lttr, Dec 2003, 20(3):2-3 & Apr 2007, 23(7):1 & Jul 2007, 23(10):7; Altern Med Alert, Feb 2003, 6(2):13-6; Hlth, Apr 2006, 20(3):26; S Lark, Women’s Wellness Today, Oct 2007, 14(10):1-5; Worst Pills, Best Pills News, May 2006, 12(5):35-6; S Rogers, Total Wellness, Sept 2003:7 & Feb 2008:6-7; Duke Med HlthNews, May 2007, 13(5):12; HealthFacts, Aug 2007, 32(8): 1-2; DC Kerrigan, JL Lelas, et al, Lancet, 7 Apr 2001, 357(9262):1097-8; P Creamer, M Hochberg, Lancet, 16 Aug 1997, 350(9076):503-9; S Parmet, JAMA, 26 Feb 2003, 289(8):1068; A Gelber, et al, Ann Internal Med, 2000, 133:321-8; Hlth News, Dec 2005, 11(12):2 & Jul 2006, 12(7):9; MC Nevitt, et al, Arthritis & Rheumatism, 2002, 46:1773-9; PA Dieppe, SS Lohmander, Lancet, 12 Mar 2005, 365(9463):965-73; ES Kurland, et al, J Bone Miner Res, 2007, 22:163-70; Hlth & Healing, Feb 2007, 17(2):5; K Senior, Lancet, 15 Jan 2000, 355(9199):208; RM Aspden, BA Scheven, et al, Lancet, 7 Apr 2001, 357(9262):1118-20; MJ Friedrich, JAMA, 15 Sept 1999, 282(11):1023-6; JB Moseley, K O’Malley, et al, N Engl J Med, 11 Jul 2002, 347(2):81-8; EW McDonagh, Acres USA, Dec 2002, 32(12):32-3; RJ Rowan, Sec Opin, Apr 2005, 15(4):4-7.
[ii] HealthNews, Oct 2005, 11(10):10-11; Altern Med Alert, Feb 2003, 6(2):S1-S2; S Boshert, Fam Prac News, 15 Mar 2003:22; SP Messier, RF Loeser, et al, Arth Rheum, May 2004, 50(5):1501-10; Tufts Univ Hlth & Nutr Lttr, Oct 2007, 25(8):Suppl 3-4 & Feb 2006, 23(12):1-2 & Nov 2005, 23(9):1-2; Duke Med HealthNews, Dec 2006, 12(12):12 & Sept 2007, 13(9):10; G Nick, Townsend Lttr D&P, Apr 2004, 249:131-2; NK Fuchs, Women’s Hlth Lttr, Apr 2003, 9(4):3-6 & Oct 2003, 9(10):1-5; R Farid, Z Mirfeizi, et al, Nutr Res, 2007, 27:692-7; D Williams, Alternatives, Oct 2006, 11(16):121-28; KL Soeken, WL Lee, et al, J Fam Pract, Aug 2002, 51(5):425-30; D Schardt, Nutr Action Healthlttr, Jun 2003, 30(5):8-11 & Oct 2000, 27(8):10; S Kolasinski, Alternative Med Alter, Oct 2000, 3(10):1115-9 & July 2001, 4(7):73-7 & Nov 2003, 6(11):121-5 & Jul 2006, 9(7):73-8; PR Usha, MUR Naidu, Clin Drug Invest, 2004, 24:353-63; GH Lo, M LaValley, et al, JAMA, 17 Dec 2003, 290(23):3115-21; R Greenfield, Altern Med Alert, Oct 2005, 8(10):118-9; LS Kim, LJ Axelrod, et al, Osteoarthritis Cartilage, 2006, 14(3):286-94; Environ Nutr, Aug 2007, 30(8);1, 4; S Lark, Women’s Wellness Today, Oct 2007, 14(10):1-5; WC Douglass, Douglass Report, Sept 2007:3-5; B Kuehn, JAMA, 28 Nov 2007, 298(20):2361; LS Lohmander, EM Roos, Lancet, 22/29 Dec 2007, 370(9605):2082-4; JL Frestedt, M Walsh, et al Nutr J, 2008, 7(1):9; UC Berkeley Wellness Lttr, Jan 2001, 17(4):4 & May 2001, 17(8):1-2; M Larkin, Lancet, 18 Mar 2000, 355(9208):993; T McAlindon, M LaValley, et al, JAMA, 15 Mar 2000, 283(11):1469-75; T Klepser, N NIsly, Alternative Med Altert, Aug 2000, 3(8):85-9; G Mautone, JAMA, 13 Sept 2000, 284(10):1241; A Hume, Complemen Med Phys, Sept 2000, 5(7):52; J Reginster, R Deroisy, et al, Lancet, 27 Jan 2001, 357(9252):251-6; M McClure, Altern Med Alert, Feb 2001, 4(2):22; BF Leeb, H Schweitzer, et al, J Rheumatol, 2000, 27:205-11; A Gaby, Townsend Lttr D&P, Jul 2001, 216:12; R Braham, B Dawson, et al, Br J Sports Med, 2003, 37:45-9; S Wolfe, Worst Pills, Best Pills News, Mar 2001, 7(3):20-1; Health Facts, Jan 2002, 27(1):3; C Tsourounis, Altern Med Alert, Feb 2002, 5(2):22; J Bland, Intern J Integrative Med, Feb/Mar 2002, 4(1):34-7; A Das Jr, TA Hammad, Osteoarthritis Cartilage, Sept 2000, 8(5):343-50; J Reginster, L Rovati, et al, ULAR 2002 European Congress of Rheumatology, 12-15 June 2002, Stockholm, Sweden; K Pavelka, J Gatterova, et al, Arch Intern Med, 14 Oct 2002, 162:2113-23; T McAlindon, M Formica, et al, Am J Med, 1 Nov 2004, 117:643-9; S Owens, P Wagner, et al, J Knee Surg, Oct 2004, 17(4):185-93; J Cibere, A Thorne, et al, J Rheumatol, 2005, 32(5):896-902; D Priebe, T McDiarmid, L Mackler, J Fam Pract, Mar 2003, 52(3):237-8; L Lippiello, Osteoarthritis Cartilage, 2003, 11:335-42; IA Zupanets, NV Bezdetko, et al, Eksp Klin Farmakol, Nov-Dec 2002, 65(6):67-9; N Walsh, Fam Prac News, 1 Jan 2004:22; Arch Intern Med, 14 Jul 2003; C Bitler, K Matt, et al, Nutr Res, 2007, 27(8):470-7; O Bruyere, K Pavelka, et al, Osteoarth Cartilage, 2007, Epub ahead of print; TF Kirn, Fam Prac News, 1 Dec 2004:51; JW Anderson, RJ Nicolosi, et al, Food Technol, Dec 2004, 58(12):105; N Poolsup, C Suthisisang, et al, Ann Pharmacolther, 2005, 39(6):1080-7; GR Dodge, SA Jimenez, Osteoarthritis Cartilage, 2003, 11:424-32; JA Blakeley, VES Ribeiro, AJN, Feb 2004, 104(2):54-9; N Volpi, Osteoarthritis Cartilage, 2003, 11(6):433-41; DO Clegg, RJ Domenic, et al, N Engl J Med, 23 Feb 2006, 354(8):795-808; SX Wang, S Laverty, et al Arthritis Rheum, 2007, 56(5):1537-48; R Liva, Integrative Med, Dec 2006/Jan 2007, 5(6):44-5; T Hampton, JAMA, 24/31 Jan 2007, 297(4):351-2; S Messier, S Mihalko, et al, Osteoarthritis Cartilage, 2007, 15(11):1256-66; JAMA, 28 Nov 2007, 298(20):2361; Altern Med Alert, Feb 2003, 6(2):S1-S2; HealthNews, 26 Aug 1997, 3(11):7; S Rogers, Total Wellness, Oct 2002:4; T Batchelder, Townsend Lttr D&P, May 2002, 226:136-8; J Abel, Townsend Lttr D&P, May 2003, 238:99-100; DJ Pattison, DPM Symmons, et al, Arthritis Rheum, Dec 2004, 50(12):3804-12; S Worcester, Fam Prac News, 15 Oct 2002:27; N Walsh, Fam Prac News, 15 May 2003:22; DJ Pattison, DP Symmons, et al, Am J Clin Nutr, 2005, 82(2):451-5; E Ernst, Clin Rheumatol, 2003, 22:285-8; Sala Horowitz, Altern Complement Ther, Oct 2005, 11(5):235-40; What Doctors Don’t Tell You, Sept 2003, 14(6):10; Y Wang, Am Hodge, et al, Athritis Res Ther, 2007, 9(4):R66; LG Cleland, MJ James, et al, World Rev Nutr Diet, 2003, 92:152-68; Ann Rheum Dis, 2001, 60:946; O Bruyere, K Pavelka, et al, Osteoarthritis Cartilage, 2008, 16(2):254-60; RM Rozendall, BW Koes, et al, Ann Intern Med, 2008, 148(4):268-77.
[iii] K Baker, Nutr in Clin Care, Jul/Aug 2000, 3(4):216-24; S Messier, R Loeser, et al, J Am Geriatr Soc, Sept 2000, 48:1062-72; B Penninx, et al, Arch Inter Med, 2001, 161:2309-16; W Nagler, Fam Prac News, 1 May 2005:63; Tufts Univ Hlth & Nutr Lttr, Aug 2003, 21(6):S1-S4 & Jul 2005, 23(5):1-2 & Mar 2006, 24(1):3 & Dec 2007, 25(10:6; Alter Med Alert, Nov 2003, 6(11):S1-S2 & Jul 2006, 9(7):S1-S2; A Foley, J Halbert, et al, Ann Rheuma Dis, 2003, 62:1162-7; P Wendling, Fam Prac News, 15 Jan 2005:55; HealthNews, Aug 2005, 11(8):7-9 & Mar 2006, 12(3):12; UC Berkeley Wellness Lttr, Jul 2005, 21(10):8 & Apr 2007, 23(7):1 ; Duke Med Hlth News, Jan 2007, 13(1):4 & Mar 2007, 13(3):8-9 & Apr 2007, 13(4):6-7 & Jul 2007, 13(7):7-8 & Jan 2008, 14(1):10; CA Hartman, TM Manos, et al, J Am Geriatr Soc, Dec 2000, 48(12):1553-9; M Blum & S Kolasinski, Altern Med Alert, Dec 2007, 10(12):136-40; B Bates, Fam Prac News, 1 Nov 2004:49.

© 1995-2009, Judith A. DeCava