Abstract
According to the vitamin D hypothesis, demyelination in multiple sclerosis results from a breakdown of myelin due to abnormal lipid composition and structure, produced during the period of brain development. The observed abnormalities (altered lipid concentrations and fatty acid profiles) are viewed as a consequence of deficiencies in enzymes that govern myelin lipid synthesis and membrane assembly. The enzyme deficiencies, genetic in origin, are proposed to occur because of inadequate supplies of vitamin D and calcium at times of rapid myelination and growth, mainly in adolescence. If the theory proves to be correct, it may be possible to suppress the disease by dietary supplementation with vitamin D and calcium during puberty.
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