Is Hypovitaminosis D one of the Environmental Risk Factors for Multiple Sclerosis?

Charles Pierrot-Deseilligny; Jean-Claude Souberbielle


Brain. 2010;133(7):1869-1888. 

In This Article


We have successively reviewed the physiological, experimental, epidemiological, immunological and biological arguments supporting a role of hypovitaminosis D in the risk of multiple sclerosis. The specific contributions of these different fields may be differentiated. The first and last groups of studies—i.e. the general physiological data and the serum level of vitamin D in multiple sclerosis—are both necessary but not sufficient in the discussion on the involvement of hypovitaminosis D in the risk of multiple sclerosis. For the physiological basis, it is for example essential to know that the basic circulating immunity cells contain receptors specific to vitamin D, but this is not sufficient to involve multiple sclerosis itself. Likewise, for the biological basis, the observation that hypovitaminosis D is widespread in patients with multiple sclerosis, in particular even at the earliest stages of the disease, is crucial for its possible involvement as a risk factor, but we have seen that such an insufficiency is not absolutely constant and, in addition, is far from specific to this disease. So, the truly significant results for implicating hypovitaminosis D in the risk of multiple sclerosis i.e. which could be both necessary and sufficient, are those of the other types of studies reviewed above. The experimental results are both necessary and sufficient for mice, but they cannot be extrapolated to humans. The epidemiological results already form a solid whole, but the relative fragility of the last link (vitamin D status and risk of multiple sclerosis), even after reinforcement with indirect arguments, may still appear to be insufficiently convincing. Lastly, the immunological results are consistent but may still be considered too recent and not yet sufficiently detailed. Therefore, although the importance of each of these different steps may still be questioned (Ascherio et al., 2010), the fact remains that they all contribute to implicating hypovitaminosis D in the risk of multiple sclerosis and that these different approaches, precisely by the consistency of their implications or conclusions, have already allowed us to reach a global level of evidence that should be considered important. However, further research is needed to confirm the involvement of hypovitaminosis D as a risk factor for multiple sclerosis and to determine whether vitamin D treatment may influence the course of the disease.


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