03/21/2026
Many people regularly take glucosamine for osteoarthritis (OA). When the 2019 UK Biobank study first reported a 15% lower risk of cardiovascular disease (CVD) among habitual glucosamine users, it was met with both surprise and considerable scepticism. Several mainstream clinicians and scientists questioned how such a widely used joint supplement could plausibly confer cardioprotection, or suggested that this observational finding was confounded, simply reflecting a healthy-user bias rather than a true biological effect.
In this prospective (following forward rather than looking back) UK Biobank analysis of 466,039 participants without CVD at baseline, habitual glucosamine use over about 7 years was linked to a 15% lower risk of total CVD events (hazard ratio, HR, 0.85, 95% confidence interval, CI, 0.80 to 0.90), a 22% lower risk of CVD death (similar effect to statin drugs) (HR 0.78, CI 0.70 to 0.87), an 18% lower risk of coronary heart disease (HR 0.82, CI 0.76–0.88), and a weaker association for stroke (HR 0.91, CI 0.83–1.00). Apparent benefit was even larger in the 2020 US NHANES study, where regular glucosamine/chondroitin users had substantially lower CVD mortality (HR 0.42, CI 0.23–0.75) and lower all-cause mortality (HR 0.73, CI 0.57–0.93), although the exposure was combined and therefore not glucosamine alone. More recently, an observational plus Mendelian randomisation (MR) study suggested a modest reduction in incident heart failure over 9 years (MR HR 0.92, CI 0.87–0.96).
However, the evidence is not uniformly protective. In a very large OA cohort in China (about 686,000 participants), glucosamine use over about 6 years was associated with a 10% higher overall CVD risk (HR 1.10, CI 1.08–1.11) and a 12% higher coronary heart disease risk (HR 1.12, CI 1.09–1.15), with an even stronger association among adherent users (HR 1.68, CI 1.59–1.78). It should be noted that the Biobank/NHANES databases are generally more transparent, more comprehensively adjusted and one is prospective (Biobank). The Chinese study may have been confounded by NSAID use, although the authors did adjust for this on the information they had (that did not cover OTC use).
Randomised trial data for glucosamine on hard cardiovascular outcomes are lacking. In a very small, randomised crossover trial, glucosamine hydrochloride (1500 mg/d) plus chondroitin sulfate (1200 mg/d) for 28 days reduced C-reactive protein by approximately 23% compared to placebo. This is compatible with an anti-inflammatory mechanism, and CRP is now a widely recognised risk factor in CVD.
Now a newer 2026 UK Biobank analysis has focused specifically on 54,096 high-risk people with prediabetes or diabetes (type 1 and type 2). Over a median 10.6 years, habitual glucosamine use was associated with a 6% lower overall CVD risk (HR 0.94, 0.91–0.96), a 11% lower heart failure risk (HR 0.89, 0.81–0.99), a 11% lower ischaemic heart disease risk (HR 0.89, 0.84–0.95), and a 14% lower stroke risk (HR 0.86, 0.77–0.97). Paradoxically, the lowest risks were observed among users with low CRP at the beginning of the study (HR 0.85, 0.82–0.89). Multiple sensitivity analyses yielded comparable results.
While this new study strengthens the consistency of the protective association with glucosamine use in a higher-risk metabolic group, it remains observational, based on self-reported supplement use without dosage data, and therefore cannot establish causality. At this point in time glucosamine should not be recommended as a proven strategy for cardiovascular prevention, but there should be no harm (despite the Chinese study) in prioritising its use (probably with chondroitin) in patients with OA who are also at risk of CVD.
For more information see:
https://pubmed.ncbi.nlm.nih.gov/31088786/
https://pubmed.ncbi.nlm.nih.gov/33219063/
https://pubmed.ncbi.nlm.nih.gov/37422736/
https://pubmed.ncbi.nlm.nih.gov/36145069/
https://pubmed.ncbi.nlm.nih.gov/25719429/
https://pubmed.ncbi.nlm.nih.gov/41712318/