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Artificial sweeteners induce glucose intolerance by altering the gut microbiota

By SugarScience Editor

This groundbreaking study suggests that artificial sweeteners may be a major cause of our epidemic of obesity and diabetes in North America.  A team of scientists found that artificial sweeteners change the huge colony of bacteria in your intestines to favor the harmful bacteria that increase risk for diabetes. Scientists fed 10-week-old mice drinks containing either: saccharin (the sweetener in the pink packets of Sweet’N Low), sucralose (the yellow packets of Splenda), aspartame (the blue packets of Equal), sugar, plain water.

The amount given to the mice was equivalent to four diet sodas per day for a human. After one week, the mice fed diet drinks had higher than normal blood sugar levels in response to eating sugar, while those that drank sugared water or plain water did not. Saccharin, aspartame and sucralose are chemically very different from each other, but they all caused the same abnormal rise in blood sugar. A high rise in blood sugar after eating sugar is called “glucose intolerance”, which is a marker for diabetes and increased risk for heart attacks.

ABSTRACT: 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. Here we demonstrate that consumption of commonly used NAS formulations drives the development of glucose intolerance through induction of compositional and functional alterations to the intestinal microbiota. These NAS-mediated deleterious metabolic effects are abrogated by antibiotic treatment, and are fully transferrable to germ-free mice upon faecal transplantation of microbiota configurations from NAS-consuming mice, or of microbiota anaerobically incubated in the presence of NAS. We identify NAS-altered microbial metabolic pathways that are linked to host susceptibility to metabolic disease, and demonstrate similar NAS-induced dysbiosis and glucose intolerance in healthy human subjects. Collectively, our results link NAS consumption, dysbiosis and metabolic abnormalities, thereby calling for a reassessment of massive NAS usage.

READ THE  FULL PUBLICATION:  NATURE JOURNAL ARTICLE