Artificial Sweeteners? Not so Sweet for Your Health.
Sugar in our blood can be a blessing or a curse. As a means of fueling our bodies when brought into our cells by insulin, it is fine. But when our cells stop responding to insulin because we’ve overloaded the system with too frequent sugary foods, it’s a curse. And that curse is called “type 2 diabetes.”
We may have been tempted to think that artificial sweeteners can help overcome this problem. Unfortunately, they don’t.
Sucralose is an artificial sweetener that is engineered to not add calories, but only a sweeter flavor to foods. Frequently used as an ingredient in soft drinks and packaged snacks, it can actually decrease insulin sensitivity when consumed along with (or included in) a carbohydrate in just 10 days.
There’s no shortcut to good health. While sucralose is a popular sweetener, it is no substitute for limiting sugars of all kinds and being wise about food choices whenever possible.
Dalenberg JR, Patel BP, Denis R, et al. Short-Term Consumption of Sucralose with, but Not without, Carbohydrate Impairs Neural and Metabolic Sensitivity to Sugar in Humans. Cell Metab. 2020;31(3):493‐502.e7.
There is a general consensus that overconsumption of sugar-sweetened beverages contributes to the prevalence of obesity and related comorbidities such as type 2 diabetes (T2D). Whether a similar relationship exists for no- or low-calorie "diet" drinks is a subject of intensive debate and controversy. Here, we demonstrate that consuming seven sucralose-sweetened beverages with, but not without, a carbohydrate over 10 days decreases insulin sensitivity in healthy human participants, an effect that correlates with reductions in midbrain, insular, and cingulate responses to sweet, but not sour, salty, or savory, taste as assessed with fMRI. Taste perception was unaltered and consuming the carbohydrate alone had no effect. These findings indicate that consumption of sucralose in the presence of a carbohydrate rapidly impairs glucose metabolism and results in longer-term decreases in brain, but not perceptual sensitivity to sweet taste, suggesting dysregulation of gut-brain control of glucose metabolism.