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Sugar and artificial sweeteners and risk of cardiovascular disease.

Created on 31 Jul 2026

Authors

Antonis A Manolis, Theodora A Manolis, Apostolos Vouliotis, Antonis S Manolis

Published in

European journal of internal medicine. Pages 107090. Jul 30, 2026. Epub Jul 30, 2026.

Abstract

Humans have an innate preference for sweetness; in this regard, dietary sugar consumption patterns are established early in life. Although moderate consumption of naturally occurring sugars from whole foods contributes to metabolic and physiological functions, excessive consumption of free sugars, particularly those added during processing, such as in sugar-sweetened beverages (SSB), may largely lead to obesity and metabolic syndrome (MetS). SSB consumption has increased since 1990 and is projected to rise further by 2050, contributing considerably to the global burden of noncommunicable diseases, including cardiovascular (CV) disease (CVD). As non-sugar sweeteners (NSS) have been widely adopted as sugar substitutes to reduce caloric intake, the metabolic disturbances that they produce have also increased. Sucrose, a disaccharide composed of glucose and fructose, is one of the most widely consumed dietary sugars. Over the years, concerns have been raised regarding CV health and relevant SSB-related problems like hypertension, diabetes mellitus (DM), obesity, MetS, atherosclerotic heart disease, valvular heart disease, kidney disease, and cerebrovascular disease and attendant mortality. However, the biological effects of natural sweeteners such as steviol, monk fruit extract, tagatose, allulose, and sweet proteins (eg, brazzien, miraculin, thaumatin) are not well studied. Eating less sugar is a prudent thing to do; for people with DM and those at risk of DM, diversifying the type of the sweetener and limiting the quantity may also be a prudent strategy. All these issues are herein reviewed; results of meta-analyses of studies reporting on the CV risk of artificial sweeteners are tabulated and pictorially illustrated.

PMID:
42532778
Bibliographic data and abstract were imported from PubMed on 31 Jul 2026.

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