Is there an alternative way of dealing with osteoarthritis, specifically spondylitis? As you are no doubt aware, orthodox medicine has no answer. In fact, following an X-ray, which established that three of my vertebrae of the neck were without the cushioning discs, my doctor flatly stated that there is no treatment. P W B, Ipswich………
Osteoarthritis (OA) has always been considered an inevitable feature of ageing, only because it affects so many people as they grow older. Some surveys reckon that 80 per cent of those over 50 usually women have the disease. OA involves the degeneration or destruction of cartilage, after which the joint hardens and the cartilage is replaced by large bone spurs, called calcified osteophytes, in the spaces between the joints. However, unlike rheumatoid arthritis, there is only slight inflammation, if any.
Although osteoarthritis principally affects the joints of the hand, knees and hips, it can also involve the spine. Spondylitis is an inflammation of one or more vertebrae of the spine.
It is true that general wear and tear on the joints is one cause of osteoarthritis, causing a breakdown in the network of the cartilage and often the release of enzymes which further destroy collagen. The reason OA mostly affects people over 50 usually has to do with a lessening of their body’s ability to synthesise collagen.
Other causes of osteoarthritis include hormonal changes, trauma, rheumatoid arthritis or even surgery.
The usual medical solution is to offer pain killers (nonsteroidal anti inflammatory drugs NSAIDs) or to wait until the joint is completely destroyed and then to offer major joint replacement surgery.
What is little known, according to US naturopaths Joseph Pizzorno and Michael Murray, is that modern medicine’s treatment of OA usually makes the problem worse. NSAID use simply speeds the progress of the disease (Lancet, 1985; ii: 11-3; Am J Mrf, 2987; 83: Suppl 5A: 29-34), largely because NSAIDs inhibit cartilage repair and speed up cartilage destruction (J Rheumatol, 1982; 9: 3-5).
Although modern medicine argues that osteoarthritis is a natural consequence of growing older, it is not true that cartilage loss is inevitable. Poor nutritional status or food intolerance may create the deficiencies that lead to collagen destruction.
Your first port of call should be to determine whether your problem is caused by allergy or intolerance to certain foods. Although OA is often associated with the presence of certain antigens in the body, few doctors associate OA with allergies. But there is a connection with the drugs usually dispensed for this condition. NSAIDs make the gut more permeable, increasing a person’s chances of becoming food sensitive (Melvyn Werbach, Healing Through Nutrition, Thorsons, 1995).
There are also many anecdotal reports of patients whose osteoarthritis improves once they remove foods usually known to spark off arthritis such as the nightshade family (potatoes, tomato, bell peppers, aubergine). The best way of determining which foods may be exacerbating your problem is to undergo a controlled exclusion diet, noting when certain foods make your condition worse, or to use neutralising/desensitising methods to isolate the foods which may be causing the problem (see the WDDTY Allergy Handbook).
Another possible culprit is low levels of certain antioxidants. Vitamin C, which is necessary for collagen synthesis, is often deficient in the elderly. In one study, comparing OA patients given vitamin C, beta carotene and vitamin E against controls, those taking high doses of vitamin C reduced the rate in which cartilage was lost by 70 per cent (Arthritis Rheum, 1996; 39: 648-56).
Vitamin E is also essential to collagen repair. Studies have shown that vitamin E inhibits the enzymes which break down collagen; in one clinical trial, OA patients given 600 iu of vitamin E significantly improved (J Am Geriatrics Society, 1978; 26: 328-30). Both vitamins have certain synergistic effects in slowing the destruction of cartilage and so should be taken together.
Large doses of niacinamide, or vitamin B3 (900 mg 4 g taken in divided doses), have been long advocated as a treatment for OA. In one study, 663 patients receiving niacinamide had a greater range of movement , compared with controls (J Am Geriatric Society, 1955; 3: 927). One patient of WDDTY panellist Melvyn Werbach’s was so crippled she could barely get up out of her chair; three months after taking 250 mg of niacinamide every 11/2 hours (for a maxmum of 10 doses per day) she had regained her strength, could walk on her own and get in and out of chairs and bed. Setbacks only occurred if she used her hands too much in knitting, which would temporarily reduce mobility.
One caveat: you should never embark on this kind of regime without careful medical supervision as high levels of niacinamide can cause liver damage and glucose intolerance, among other side effects.
Another good natural remedy is boron. Naturopath Rex Newnham reports positive results with boron supplementation. In one double blind (admittedly small) trial, half the boron patients improved, compared to only one tenth on placebo (J Nutri Med, 1990; 1: 127-32). Dr Werbach suggests that since the minimum daily allowance for boron hasn’t been established, patients increase consumption of boron rich foods: vegetables, such as soy, cabbage, lettuce and peas; fruits, such as apples, dates, raisins and prunes; and nuts, especially almonds, hazelnuts and peanuts.
B12 and folic acid may also play a role in controlling joint pain. In one study of 26 OA sufferers, these two B vitamins were more effective than drugs in controlling hand joint pain (J Am College Nutrition, 1994; 13; 351-6).
Some researchers have theorised that arthritis is the result of abnormal glucosamine metabolism. Glucosamine is one of the chief components of the proteoglycans, a major building block of cartilage. It seems to work by stopping the proteoglycans from breaking down and rebuilds damaged cartilage (Orthop Praxis, 1970; 9: 225). Sulphate, another naturally occurring substance, appears to strengthen glucosamine’s effect (Pharmatherpeutica, 1981; 2: 504-8).
The research on glucosamine sulphate demonstrates that it relieves pain better than NSAIDs and, unlike the drugs, apparently helps to reverse the disease process, stimulating the synthesis of cartilage.
In a large scale study of more than 1000 Portuguese arthritis patients given glucosamine sulphate for two months, pain symptoms and movement improved significantly in 59 per cent and “sufficiently” in another 36 per cent (Int J Tissue Ract, 1992; 14: 243-51).
In another study, of 80 OA patients given either 500 mg of glucosamine sulphate three times a day (a standard dose) or a placebo, those taking glucosamine had a significantly larger reduction in overall symptoms, compared with the placebo group (73 per cent vs 41 per cent), after a month on the regime. An electron microscopy sample of cartilage from the treated patients showed evidence of new growth (Clin Ther, 1980; 3: 260-72).
In another double blind study, where glucosamine sulphate was compared with ibuprofen, a popular NSAID, the ibuprofen group recorded a better response initially. However, the glucosamine group experienced a steady improvement with pain to the point where by the second month, their improvement outstripped that of the drug takers (Curr Med Res Opin, 1982; 8: 145-9).
Glucosamine is often sold with chondroitin sulphate, one of the main glycosaminoglycans found in cartilage, and so another of its building blocks. CS is generally made from bovine, whale and shark cartilage. Glucosamine sulphate and chondroitin sulphates supposedly have synergistic effects.
Patients having a proprietary form of chondroitin injections have been shown to have joint changes visible on X-ray (Semin Arth Rheum, 1987; 17: 2: Supple 1: 35-53) and a reduced narrowing of joint spaces (Rheumatol Med Int, 1986; 20: 24-8).
Although glucosamine seems to have no side effects in standard doses, intramuscular doses of chondroitin have been linked with severe kidney liver toxicity (Lancet, 1989; 1:1275).
Other potentially useful alternative solutions include New Zealand green lipped mussel extract (Lancet, 1981; i: 439); the antioxidant superoxide dismutase; omega-3 fatty acids, largely found in flaxseed and fish oils; zinc; and sulphur, taken as colloidal sulphur or sulphur baths. Capsaicin cream (made from chili peppers) has been found to reduce pain and tenderness by 40 per cent (J Rheumatology, 1992; 19: 604-7). As for herbs, extract of yucca and devil’s claw (Harpagophytum procumbens) have both been found to reduce pain and increase mobility (J Applied Nutrition, 1987; 27: 45-50).