Vitamin E and Rheumatoid Arthritis

During the course of inflammation in the joints of patients with rheumatoid arthritis, a number of mediators or agents that can bring about inflammation and joint destruction are released. There is now no doubt that in rheumatoid arthritis joint inflammation swelling, heat, pain, tenderness of the joint can be separated from joint destruction. Usually, of course these two processes go hand in hand. Nevertheless, it is possible for a therapy to affect the one and not the other.

One group of inflammatory mediators are called "reactive oxygen species"("ROS"). One example of ROS it that of hydrogen peroxide. I do not need to remind you that it is used to bleach hair to give it a "peroxide blonde" colour! ROS can be neutralised by anti-oxidants present in the food. There are epidemiological surveys that show that low levels of circulating anti-oxidants may be linked to the development of rheumatoid arthritis. Such circulating anti-oxidants are beta-keratin, selenium, vitamin E and vitamin D. The results of therapeutic trials with these anti-oxidants have been controversial largely on the basis that the clinical studies have not been particularly well planned. However, they have shown little or no effect on inflammation. This particularly applies to at least two studies with Vitamin E.

It would be ideal to try and establish, by appropriate experiments, whether supplementation of the diet with anti-oxidants, such as Vitamin E, could lead to benefit, as this would then give an impetus to carrying out studies on patients.

The experimental model of rheumatoid arthritis

The development of any new therapy for any drug for any disease demands a sequence of steps. First, there are experiments in test tubes to see if the idea is correct. Second there are experiments, conducted under properly supervised and humane condition, that establish whether the potential therapy is safe and efficacious. Thirdly, clinical trials in patients to establish efficacy and lack of side effects.

Recently a mouse model of rheumatoid arthritis has been described in the KRN/NOD mice. These mice spontaneously develop arthritis very similar to rheumatoid arthritis by day 30 of life. The investigators, in the work to be described, therefore used this model in order to study the effect of vitamin E on this model.

The experiment

The mice were given vitamin E by mouth starting on day 21 of life (1 week before the onset of arthritis) and continuing for 6 weeks. Vitamin E had no effect whatsoever on the clinical features of disease such as joint swelling so that the date of onset or disease intensity was not affected. However, joint destruction was markedly prevented. This again is an extremely interesting and intriguing finding supporting other joints in which the effects of a therapy on inflammation and joint damage can be separated.

Of further interest, was the fact that there was only a very slight difference in the ROS between the treated and non-treated mice. However, in the treated mice there was a very marked reduction in the levels of the inflammatory mediator interleukin-1 but not tumor necrosis factor . Thus vitamin E may not be acting by inhibiting the release of ROS.

Conclusions

There are several conclusions to be drawn from this study. Any future studies of anti-oxidants, including Vitamin E, may have to focus more on joint damage than on symptoms and signs of inflammation. Properly planned and conducted studies of such anti-oxidants are clearly warranted.

DO NOT GO OUT AND BUY VITAMIN E FOR YOUR RHEUMATOID ARTHRITIS, AS THESE EXPERIMENTS WILL HAVE TO BE CONFIRMED BY CLINICAL TRIALS IN HUMANS. These experiments are reported to you for information and to emphasise that research into new therapies for rheumatoid arthritis are constantly going on.

This study was reported in the journal "Arthritis & Rheumatism" 2002 Volume 46, pages 522 532 by De Bandt and his colleagues, Faculte Xavier Bichat, Paris, France. (http://www3.interscience.wiley.com/journal/76509746/home)