Abstract
Recent emerging data indicate that obesity is an important risk factor for multiple sclerosis (MS) susceptibility and may be associated with MS disability progression. Marked interactions between obesity and human leukocyte antigen (HLA) genotype with regard to the risk of MS have been reported. Evidence from Mendelian randomization studies also point to a causal relationship between obesity and MS risk. In this report, we aimed to analyze the current evidence of the relationship between obesity and risk of MS and disability progression, examine data on the interaction between obesity and HLA risk genes of MS and Mendelian randomization studies and to explore the plausible biological mechanisms that may underlie this relationship.
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