Witkowski · European heart journal 2024 · prospective cohort and interventional study · n=3316

Xylitol is prothrombotic and associated with cardiovascular risk.

Cited 61 times in the scientific literature.

Level 3 - non-randomized controlled study

Prospective observational cohort studies with mechanistic assays and small human interventional validation

PubMed 38842092 · doi:10.1093/eurheartj/ehae244 · record verified 2026-08-26

What was done

Untargeted metabolomics on overnight fasting plasma was conducted in a discovery cohort of stable patients undergoing elective diagnostic cardiac evaluations (n = 1157). Findings were evaluated in an independent validation cohort using stable isotope dilution LC-MS/MS (n = 2149) to assess incident 3-year major adverse cardiovascular events (MACE). Complementary mechanistic assays were performed in isolated human platelets, platelet-rich plasma, whole blood, and animal models. An intervention study evaluated the acute effects of xylitol consumption on platelet responsiveness in healthy volunteers (n = 10).

What was found

In the validation cohort, circulating xylitol was significantly associated with incident 3-year MACE risk (third vs. first tertile adjusted hazard ratio: 1.57, 95% CI: 1.12–2.21, P < .01). Mechanistic studies demonstrated that xylitol enhanced platelet reactivity and in vivo thrombosis at concentrations detected in fasting plasma. In the interventional study (n = 10), ingestion of a xylitol-sweetened drink increased plasma xylitol concentrations and enhanced functional measures of platelet responsiveness in all subjects.

Why it matters

This study links the common sugar substitute xylitol to increased incident cardiovascular risk and prothrombotic platelet activation. These findings challenge the assumed cardiovascular safety of sugar alcohols widely used in processed foods.

Limits

The clinical cohorts consisted of individuals undergoing elective cardiac evaluations, potentially limiting generalizability to the general healthy population. The observational analyses could not differentiate endogenous xylitol production from dietary intake. The human feeding intervention was very small (n = 10) and only evaluated acute surrogate platelet markers rather than long-term clinical events.

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