This apparent paradox may be explained by the fact that, at a given level of BMD, MS patients present lower bone quality by means of various mechanisms, including hyperinsulinemia, deposition of advanced glycosylation endproducts (AGEs) in collagen, reduced serum levels of IGF-1, hypercalciuria, renal failure, microangiopathy and inflammation. This evidence concerns the gene IGF1 and hyperinsulinism.