Artificial sweeteners may contribute to obesity, diabetes, CVD

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Artificially sweetened foods and beverages may have the counterintuitive effect of increasing the risk for obesity, type 2 diabetes, metabolic syndrome and cardiovascular events, according to an opinion article recently published in Trends in Endocrinology and Metabolism.
“Public health officials are rightfully concerned about the consequences of consuming sugar-sweetened beverages, such as soft drinks, but these warnings may need to be expanded to advocate limiting the intake of all sweeteners, including no-calorie sweeteners and so-called diet soft drinks,” Susan E. Swithers, PhD, a professor of psychological sciences and a behavioral neuroscientist at Purdue University, said in a press release. “Although it seems like common sense that diet sodas would not be problematic, that doesn’t appear to be the case. Findings from a variety of studies show that routine consumption of diet sodas, even one per day, can be connected to higher likelihood of heart disease, stroke, diabetes, metabolic syndrome and high blood pressure, in addition to contributing to weight gain.”
Susan E. Swithers
Swithers reviewed data from recent studies on the effects of consuming artificial sweeteners and identifying the underlying mechanisms between these sweeteners and potential adverse health outcomes.
According to Swithers, data suggest that patients who regularly consume artificially sweetened beverages have an increased risk for negative health outcomes, including type 2 diabetes, metabolic syndrome and CVD, compared with those who do not. The magnitude of these increased risks was similar to those observed with sugar-sweetened beverages.
Swithers’ article cited the San Antonio Heart Study, among other prospective cohort and interventional studies, which linked artificially sweetened beverages to hypertension, CV risk and increased BMI. Further, Swithers wrote that in several studies, the increased risks associated with artificial sweeteners were not sufficiently explained by baseline characteristics, family history or BMI.
Recent data support evidence showing that regular ingestion of artificial sweeteners appears to stimulate food intake by reducing a patient’s ability to compensate for energy provided by caloric sweeteners in the diet, she added. Due to this physiological response, sugar-sweetened beverages could impair the ability to predict the arrival of energy in the gut, thus weakening the underlying mechanism for satiety, Swithers wrote.
Furthermore, imaging studies of the human brain have shown that metabolic and hormonal factors are caused by the intake of caloric sweeteners. According to Swithers, sucrose, but not sucralose, activates the dopaminergic midbrain areas related to reward or pleasantness. These data also show that sucralose leads to decreased activation in other taste-related pathways.
Additionally, other studies suggest that the typical release of hormones and markers of postprandial glucose homeostasis do not occur after ingestion of artificial sweeteners.
“This somewhat counterintuitive result may reflect negative consequences of interfering with learned relationships between sweet tastes and typical post-ingestive outcomes, which may result in impaired ability to compensate for energy provided when caloric sweeteners are consumed,” she wrote.
Swithers concluded that current findings suggest caution about the overall sweetening of the diet is warranted.
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