(P13-043-24) Association of Habitual Glucosamine Use With All-Cause and Cause-Specific Mortality Among Individuals With Type 2 Diabetes: A Prospective Study in UK Biobank

Objectives: Evidence is limited regarding the impact of glucosamine on the risk of subsequent premature death among individuals with diabetes. We prospectively analyzed the association of habitual glucosamine use with mortality risk among individuals with type 2 diabetes (T2D); and explored the potential mediation effects of metabolic biomarkers.

Methods: This analysis included 19 125 participants with T2D from the UK Biobank who completed the questionnaire on supplement use. Survival models were used to calculate adjusted hazard ratios of all-cause and cause-specific mortality with habitual glucosamine use. We evaluated potential effect modification by examining the interaction of glucosamine use with stratified factors, including diabetes severity, demographic characteristics, lifestyle behaviors, and history of medication use.

Results: During a median of 12.3-13.5 years of follow-up, 2552 death cases were documented, with 1095 from cancer, and 741 from cardiovascular disease. After multivariable adjustment for sociodemographic characteristics, history of diseases, glycemic control, medication histories, and other supplement use, the hazard ratios (95% confidence interval) associated with glucosamine use were 0.75 (95% confidence interval, 0.66 to 0.86) for all-cause mortality, 0.82 (0.68 to 0.99) for cancer mortality, 0.73 (0.57 to 0.94) for CVD mortality. Stratified factors including diabetes severity factors did not modify the associations between glucosamine use and mortality. Moreover, a range of biochemistry markers including cystatin C, alanine aminotransferase, LDL-cholesterol, and C-reactive protein collectively explained 40.0% (14.0% to 73.2%) of the association between glucosamine use and CVD mortality.

Conclusions: Habitual glucosamine use is associated with lower risks of all-cause and cause-specific mortality among individuals with T2D. These associations were partly explained by some clinical markers but the exact mechanisms remain to be explored.

Funding Sources: This study was funded by the National Natural Science Foundation of China, the National Key Research and Development Program of China, the Hubei Province Science Fund for Distinguished Young Scholars, and the Fundamental Research Funds for Central Universities.