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Over 2 million persons worldwide have multiple sclerosis (MS),1 and the burden of the disease for affected individuals and society is substantial. A recent study estimated that by 2031, 133,635 Canadians would be living with MS, and that the direct costs of their care would reach a staggering $2 billion annually.2 Therefore, identifying modifiable risk factors for MS remains vitally important. Researchers still seek to firmly demonstrate a causal role for vitamin D, a biologically plausible etiologic factor which is modifiable. Vitamin D receptors are ubiquitous, being expressed on immune cells and in the CNS; immune responses are affected by variations in 25-hydroxyvitamin D (25[OH]D) levels; and 1,25-dihydroxycholecaliferol can prevent the emergence of experimental autoimmune encephalomyelitis,3,4 an animal model of demyelinating disease. However, epidemiologic studies have often been hindered by the inability to demonstrate temporality; that is, that the exposure to inadequate 25(OH)D occurred before the onset of MS.
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See page 1578
- © 2017 American Academy of Neurology
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