Systematic Review of the Effect of Glucosamine on Joint Health while Focused on the Evaluation of Claims for Health Functional Food

Abstract

Although the functional ingredient has been evaluated based on scientific evidence by the Ministry of Food and Drug Safety (MFDS), the levels of scientific evidence and consistency of the results might vary according to the emerging data. Therefore, a periodic re-evaluation may be needed in some functional ingredients. In this study, we re-evaluated the scientific evidence for the joint health of glucosamine as a functional ingredient in health functional food. Literature searches were conducted using Pubmed, Cochrane, KISS, and IBIDS databases with the search term of glucosamine in combination with osteoarthritis. The search was limited to human studies published in English, Korean and Japanese. Using the MFDS's evidence based evaluation system for scientific evaluation of health claims, 34 human studies were identified and reviewed in order to evaluate the strength of the evidence supporting the relation between glucosamine and joint health. Among the 34 studies, significant effects for joint health were reported in 28 studies, and their daily intake amount was 1.5 to 2 g. Eleven out of 34 studies were identified, excluding severe radiographic osteoarthritis, and ten from those eleven studies reported significant effects for joint health. Based on this systematic review, we concluded that there was possible evidence to support a relation between glucosamine intake and joint health.

Herring and chicken/pork meals lead to differences in plasma levels of TCA intermediates and arginine metabolites in overweight and obese men and women

“…Glucosamine is an amino‐monosaccharide, a constituent of cartilage, not regularly consumed in high amounts . Dietary intake of glucosamine has been associated with affecting joint health , though glucosamine supplementation has not been found to have any consistent effect on joint health . The change in plasma glucosamine between the diets may be due to endogenous regulation rather than to glucosamine intake, though the glucosamine content of the diets was not measured.…”