The data in this study do not support the general statement that ?artificial sweeteners? induce glucose intolerance and thus cause obesity by altering the gut microbiome?.
The extensive research conducted on aspartame and sucralose has clearly demonstrated that these compounds do not affect the gut microbiota (1,2). Aspartame is completely digested into amino acids and methanol, which are absorbed in the small intestine. Neither aspartame nor its digestion products ever reach the colon; thus aspartame itself cannot affect gut microbiota. Sucralose is not digested, and passes unchanged to the large intestine; however numerous studies show pure sucralose cannot be metabolized by microflora.
So how is it possible that these 2 sweeteners reportedly altered the gut microbiota in this study? The answer ? inappropriate statistics and huge changes in overall diet composition.
Firstly, to achieve statistical significance, the authors combined all 3 different sweetener groups (n=20/group) together into one group (n=60) and compared against the combined control groups to obtain 1 statistically significant p value! So 6 groups of 20 became 2 groups of 60, making it impossible to determine which, if any, individual sweetener had a significant effect.
Secondly, the notable impact on intake of mouse chow, by adding extremely high doses of sweetener to drinking water, was ignored. Doses and food intake can only be estimated as data were reported for just 4 of the 20 mice per group and for only 3 days of the 11-week study. Doses of the sweeteners were up to 1000 times the acceptable daily intake (ADI), and consumption of mouse chow dropped by 50% in some groups in just 72 hr. Mouse chow contains fiber, protein, fat, fermentable carbohydrates and a host of other components that have repeatedly been shown to affect both gut microbiota and glycemic indices. Clearly, these dramatic changes in diet would result in changes in microbiota, and glycemic responses. Other dietary factors were similarly not considered in the human studies.
Lastly, these conclusions do not agree with the results of the extensive testing of these sweeteners required for approval, including human clinical studies conducted in healthy and diabetic participants for periods of several weeks to months, on parameters including glycemic indices and insulin (1,2). These studies must include control groups, baseline measurements, blinding, crossover designs, and appropriate statistics to ensure no effects on these parameters with continual exposure of sweeteners, at maximum expected uses.
Thus this study provides no evidence that aspartame or sucralose alters gut microbiota or glycemic response. In contrast, the observation that saccharin at high doses alters gut microbiota was known in the 80s, and contributed to the establishment of the ADI for saccharin (3). Therefore, extrapolation of findings of effects of saccharin on the gut microbiome to all artificial sweeteners has no scientific basis and overlooks well-established differences in chemistry and metabolism.
Also not mentioned are the numerous studies demonstrating that use of low calorie sweeteners, including aspartame and sucralose, are beneficial in weight loss and weight loss maintenance programs (4,5).
The allegations that ?artificial sweeteners? contribute to glucose intolerance and obesity based on studies in this report, are unfounded and should be withdrawn.