Glucosamine and osteoarthritis: time to quit?

Abstract

Glucosamine (2-amino-2-deoxy-D-glucose), an amino monosaccharide derivative of glucose, is a precursor of the glycosaminoglycans and proteoglycans that make up articular cartilage. The notion that augmenting the intake of the precursor molecule, glucosamine, may directly stimulate articular proteoglycan synthesis to modulate osteoarthritis has provided the rationale for its widespread use. Theoretically, exogenous glucosamine may augment glycosaminoglycan synthesis in cartilage. There is a simultaneous theoretical concern that it might also induce insulin resistance in insulin-sensitive tissues.In a previous issue of DMRR, Simon et al. conclude that typical doses of oral glucosamine have no significant effects on glucose metabolism or insulin sensitivity. On the basis of the results from clinical, animal, and cell-based studies they conclude that oral glucosamine neither augments the hexosamine biosynthetic pathway nor reduces insulin-mediated glucose uptake. In recent meta-analyses restricted to well-designed randomized controlled trials that include adequate allocation concealment or to nonindustry-funded studies, oral glucosamine fails to show any significant clinical benefit in individuals with osteoarthritis. These data should raise serious questions from patients and their health care providers about its continued use.