Vitamin D plays an important role in bone metabolism and may also have immunomodulatory effects. Specifically, it has been shown in animals that vitamin D can suppress the effects of autoimmunity. Although we do not know whether a similar effect would be found in humans, no studies have assessed the association between Vitamin D and rheumatoid arthritis (RA), a devastating autoimmune disease. To address this issue, Merlino and associates (Arthritis and Rheumatism, 50:72-77, 2004) analyzed data from a large prospective cohort of women aged 55-69 in 1986 who were followed for 11 years.
To assess the association between vitamin D and RA, data on 29,368 women from the Iowa Womens Health Study (IWHS) were used. The IWHS is a population-based prospective cohort study initiated in 1986. Using a self-administered questionnaire the IWHS collects demographic data, medical and reproductive history, lifestyle factors, and a 127-item food frequency questionnaire that included supplement use. Vitamin D intake was estimated by calculating the vitamin D content of foods, as well as from the intake of vitamins and mineral supplements. Cox proportional hazards regression was used to estimate the association between vitamin D intake and RA incidence, adjusting for several factors including age, smoking, and hormone replacement therapy.
Through the 11 years of follow-up, 152 cases of RA were validated medically. Greater intake of vitamin D was associated with reduced risk of RA. That is, those with greater intake of vitamin D were 67% as likely to as those with lesser intake of vitamin D to have RA. This association was present for both dietary and supplemental vitamin D; however, vitamin D derived from supplements reduced the risk of RA to a greater extent than did vitamin D derived from the diet (66% vs. 72%).
Greater vitamin D intake may associate with lower risk of RA in older women.
Although there is a biological explanation for the observed association between vitamin D and RA (i.e., animal models suggest that vitamin D may be an immunosuppressant), this study was not hypothesis driven. Thus, it is possible, though unlikely, that chance alone may account for the observed association. Apart from this, there are several other considerations that may attenuate the studys findings. First, vitamin D intake was assessed only once in 1986. Although this assessment was prior to the development of RA, it is possible that in the intervening 11 years participants increased their vitamin D intake. Second, sun exposure, an important source of vitamin D, was not assessed and may represent an important unmeasured confounding variable. Finally, because the IWHS population was made up of predominantly white women, the results may not generalize to other groups of adults with RA. Although the immunomodulatory effects of vitamin D are unknown in humans, this study suggests that vitamin D may play a role in reducing the risk of immunologic disorders such as RA.
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