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Here, Hedstrom and colleagues show that lifestyle/environmental/genetic relationships seen for relapsing-onset multiple sclerosis (MS) are also seen for progressive-onset MS
The aetiology of multiple sclerosis (MS) reflects a complicated interrelationship of environmental, lifestyle and genetic risk factors, each comprising a unique causal pie to realise disease in each patient. Of these factors, there is variable evidence in support of each, though some of the strongest and most consistent have been tobacco smoke,1 Epstein-Barr virus (EBV) exposure2 and the major histocompatibility locus, particularly the HLA-DRB1*15:01 allele,3 while less consistent evidence exists for factors including sun exposure/vitamin D,4 5 alcohol intake6 and BMI.7 In addition to exploring direct effects of these risk factors, the interaction between them, particularly gene–environment interaction, is of great interest as well as highly biologically plausible. A seminal publication by van der Mei et al explored the interaction between early childhood infant sibling exposure, a measure of early pathogen exposure and HLA-DRB1 genotype, finding those with less infant sibling exposure had a greater …
Correction notice This article has been corrected since ti appeared Online First. Title has been abbreviated.
Contributors SS-Y authored the editorial.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.