10 June 2024

The sweetener xylitol increased the risk of serious heart abnormalities

A comprehensive study with experiments on mice and observations on humans has shown an association between the sweetener xylitol and the risk of serious cardiovascular events. Xylitol increases the risk of thrombosis, and in humans, ingestion of xylitol increases platelet reactivity. The results of the study are published in the European Heart Journal.

Due to the growing problem of obesity worldwide, measures to reduce sugar intake have become a public health priority. One such measure has been the proliferation of artificial sweeteners in processed foods that are advertised as healthy alternatives to sugar. While artificial sweeteners are generally recognised as safe and approved by public health authorities, some have raised concerns among doctors due to negative health effects. To learn more about how much to worry about the recognition of the sweetener aspartame as "potentially carcinogenic," check out our editorial podcast.

Over the past decade, the use of artificial sweeteners has increased markedly almost universally, and they have been recommended to patients with cardiometabolic disease. In several epidemiological studies, their use has been associated with the development of insulin resistance, increased risk of type 2 diabetes and cardiovascular disease. However, little is known about xylitol, a popular sweetener among manufacturers, a five-carbon sugar alcohol that is added to candy, chewing gum and oral care products. Xylitol is also produced endogenously as a by-product of glucose metabolism in the human body in small amounts and has little effect on blood sugar levels and insulin secretion.

A team of researchers led by Stanley Hazen of the Cleveland Clinic conducted a multifaceted study involving experiments in mice and human observation to examine the association between xylitol exposure and the risk of cardiovascular disease as well as increased platelet reactivity.

A preliminary plasma metabolomics study showed that levels of polyols, including a metabolite tentatively classified as xylitol, differed significantly between those who had cardiovascular events and those who did not. Further examination showed patients with higher plasma xylitol levels had a significantly increased risk of a serious adverse cardiovascular event within three years (adjusted relative risk 1.57, p < 0.01). The increased risk was observed in both sexes, and statistical significance was maintained in several statistical models at once.

The researchers also found an association between high xylitol levels and the risk of thrombotic complications, suggesting a potential effect of xylitol on platelet function. In vitro experiments with human platelets showed that xylitol increased intracellular calcium concentration, which led to their activation and aggregation. In addition, xylitol significantly accelerated the rate of collagen-dependent platelet adhesion.

Intraperitoneal injections of xylitol into mice resulted in similar changes in the alcohol concentration in mouse plasma. After such exposure, changes similar to those in the in vitro experiments occurred in mouse platelets. The scientists observed the same platelet activation and increased adhesion in platelets of people who drank a solution with 30 grams of xylitol (its level in the plasma of volunteers increased a thousand times).

Overall, this comprehensive study shows the negative effects of xylitol exposure on cardiovascular health. First and foremost, xylitol increases the risk of thrombosis through platelet activation, which can lead to myocardial infarction or stroke. According to the authors of the paper, regulators should pay attention to the increasing use of xylitol in the manufacture of products.

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