Artificial sweeteners may not prevent the current diabetes and obesity epidemic as others claimed and promoted, the Immunology Department of the Weizmann Institute discovered in its new research.

The researchers said that artificial sweeteners in food and beverages instead speed up the development of metabolic disease and glucose intolerance by altering the function and composition of the gut microbiota, which is the substantial bacteria population living in human intestines.

“Non-caloric artificial sweeteners (NAS) are among the most widely used food additives worldwide, regularly consumed by lean and obese individuals alike. NAS consumption is considered safe and beneficial owing to their low caloric content, yet supporting scientific data remain sparse and controversial,” the researchers wrote in the study.

Although the sweeteners don’t contain sugar, they were found to have a direct effect on the ability of the body to use glucose. Glucose intolerance, according to the researchers, leads to adult-onset diabetes and metabolic syndrome.

The researchers experimented with humans and mice. They gave water with three most often used sweeteners to the mice, but only in amounts permitted by the U.S. Food and Drug Administration.

As compared to mice that only drank water or sugar water, the mice with sweetener-based water developed intolerance to glucose. They achieved the same results even when the experiment involved various types of mice and sweeteners in different doses.

The researchers thereafter looked into the premise that gut microbiota may be involved in such occurrence, thinking the bacteria might have been reacting to new substances—such as the artificial sweeteners—which may not be recognized as food by the body.

True enough, the gastrointestinal tract doesn’t absorb these sweeteners. As the sweeteners pass through, they come across trillions of bacteria found in gut microbiota.

To get rid of many gut bacteria, the mice were treated with antibiotics, which led to a full reversal of the effects of artificial sweeteners on the metabolism of glucose. After which, they moved the microbiota in mice consuming sweeteners to the germ-free mice, resulting in a full transmission of glucose intolerance into the receiver-mice.

The researchers also learned that the incubation of microbiota and artificial sweeteners outside the body was enough to stimulate glucose intolerance in the germ-free mice.

When tested in humans, the researchers also found that the involved respondents developed glucose intolerance following a week of consuming artificial sweeteners. They examined information gathered from their Personalized Nutrition Project and discovered an important association among self-reported sweetener consumption, tendency on glucose intolerance and personal configurations of bacteria in the gut.

The researchers also uncovered a difference in the composition of human’s gut microbiota: one that stimulated glucose intolerance because of exposure to sweeteners, and the other that has no effect at all.

“The results of our experiments highlight the importance of personalized medicine and nutrition to our overall health,” Eran Segal, professor at the Computer Science and Applied Mathematics Department, said in a statement.

Dr. Eran Elinav, lead researcher from the Immunology Department, also said “this calls for reassessment of today’s massive, unsupervised consumption of these substances.”

The study, Artificial sweeteners induce glucose intolerance by altering the gut microbiota, was published in the Nature journal.

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