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Arthritis Benefits of Diet Revision
Several diet revision studies have shown benefit for patients with rheumatoid arthritis. These studies support the more common and persistent claims in the community that diet revision has benefits. The occurrence of transient inflammatory arthritis after eating reactive foods with improvement between attacks is one pattern of food allergy. The food connection to more chronic and progressive inflammatory disease is difficult to recognize because the reactions are delayed and there may be little or no improvement between attacks.
Carinini and Brostoff reviewed the concepts of and evidence for food-induced arthritis. They stated: "Despite an increasing interest in food allergy and the conviction of innumerable patients with joint disease that certain foods exacerbate their symptoms, relatively little scientific attention has been paid to this relationship. Abnormalities of the gastrointestinal tract are commonly found in rheumatic disease...Support for an intestinal origin of antigens comes from studies of patients whose joint symptoms have improved on the avoidance of certain foods antigens, and become worse on consuming them. These have included patients with both intermittent symptoms, palindromic rheumatism and more chronic disease."
In one study of diet revision, 33 of 45 patients with rheumatoid arthritis improved significantly on a hypoallergenic diet. The authors concluded: "Increasing numbers of scientific studies suggest that dietary manipulation may help at least some rheumatoid patients and perhaps the greatest need now is for more careful and well-designed research so that preconceptions may be put aside and role of diet, as a specific or even a non-specific adjunctive therapy, may be determined."
In a review article, Darlington and Ramsey suggest that there are now enough good studies that show that diet therapy in some cases may improve symptoms and possibly halt the progression of arthritis. They review both supplementation and food elimination approaches. They suggested that diet therapy should begin with elimination of all foods which might be causing symptoms, followed by single food re-introductions to discover which foods reproduce symptoms. They list corn, wheat, cow's milk, pork, oranges, oats, rye, eggs, beef, coffee, malt, cheese, grapefruit, lemon, tomato, peanuts, and soya as the foods most likely to cause arthritis.
Appelboom et al reported benefit from the exclusion of dairy products in patients with ankylosing spondylitis and related spondyloarthropathies; 18 of 25 patients complied with 6 weeks of dairy exclusion - 13 had major improvement and 8 of these discontinued NSAID use; another 4 had moderate improvement.
Food Proteins Cause Arthritis
Sr. Wm. Osler had first suggested that dietary proteins were important in the pathogenesis of Henoch-Schonlein purpura and arthritis. The term "palindromic arthritis" was used to describe transient synovitis in food-sensitive patients. The occurrence of transient episodes of inflammatory arthritis with the complete absence of signs and symptoms between attacks is typical of one pattern of food allergy, but the connection to more chronic and progressive disease has been more difficult to recognize.
The frequent occurrence of arthritis in patients with digestive tract disease is a major clue. About 20% of patients with regional enteritis and 10% with ulcerative colitis develop inflammatory arthritis. Intestinal bypass for obesity leads to polyarthritis in 20 % of patients and is associated with other features of "autoimmune" disease. Another clue is that people with celiac disease who continue to eat gluten-containing foods such as bread, pasta, cakes and cookies develop rheumatoid arthritis. Another clue is an animal model of rheumatoid arthritis in rabbits who develop typical joint lesions when they are fed cow's milk.
A wheat gluten mechanism has been studied in rheumatoid arthritis patients. Careful observation revealed that wheat ingestion is followed within hours by increased joint swelling and pain. Little and his colleagues studied the mechanism, as it developed sequentially following gluten ingestion. Parke et al concurred with this explanation of the gut-arthritis link in their report of three patients with celiac disease and rheumatoid arthritis. The mechanism they postulated involves several stages:
The digestive tract must be permeable to antigenic proteins or peptide fragments, derived from digested food. The food antigens appear in the blood stream and are bound by a specific antibody (probably of IgA or IgG, not IgE class), forming an antigen-antibody complex, a circulating immune complex (CIC). The antigen-antibody complexes activate the rest of the immune response, beginning with the release of mediators - serotonin is released from the blood platelets. Serotonin release causes "symptoms" as it circulates in the blood stream and enhances the deposition of CICs in joint tissues.
Once in the joint, the immune complexes activate complement, which in turn damages cells and activates inflammation. Inflammation causes pain, swelling, stiffness, and loss of mobility.
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