NEW YORK (Reuters Health) - French scientists have found that vitamin E can reduce joint destruction in mice with a rheumatoid arthritis-like condition--suggesting, they say, that the vitamin should be studied as a potential therapy for the human disease.

The vitamin did not help the symptoms of the disease in mice, but it did prevent some breakdown in the animals' joints, according to researchers led by Dr. Michel De Bandt, of the Centre Hospitalo-Universitaire Xavier Bichat in Paris.

Rheumatoid arthritis is an inflammatory condition in which the immune system mistakenly attacks the lining of the joints, leading to pain, swelling and loss of mobility. Joint destruction occurs over time.

According to De Bandt's team, potentially damaging forms of oxygen in the body called reactive oxygen species are thought to play a role in this process. In line with this theory, rheumatoid arthritis patients have been found to have low blood levels of antioxidants like vitamins E and C, which help neutralize reactive oxygen species.

There have been some clinical trials of using antioxidants to treat rheumatoid arthritis, but the results have been mixed, the researchers note. So they sought to weed out the effects of vitamin E alone in a mouse "model" of the disease.

The investigators found that after 6 weeks of vitamin E treatment, mice with the arthritic condition showed symptoms, but the destruction in their bone and cartilage was much less severe than that in animals not given the vitamin. The vitamin-treated mice also showed lower blood levels of an inflammatory protein produced by the immune system called interleukin-1beta--which, De Bandt and colleagues note, is involved in joint destruction.

Exactly how vitamin E might have prevented joint destruction is unclear. The researchers found no evidence that the antioxidant altered the oxidation process in the animals' circulation.

"Our results," they conclude, "emphasize the potential interest of vitamin E in arthritis and deserve further evaluation in order to fully understand its precise mechanism of action."

SOURCE: Arthritis and Rheumatism 2002;46:522-532.

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