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Best Years in Life)
published in the prestigious
journal Nature has revealed
how non-caloric artificial
sweeteners (NAS) drive
diabetes-related changes in
both mice and humans.
The study titled,
induce glucose intolerance
by altering the gut
Finally, in order to test whether the role of microbiota in upsetting blood sugar balance was 'cause and effect' they performed a fecal transplant from mice receiving saccharin or glucose into germ-free mice receiving the same normal-chow diet. Their results confirmed the crucial role of the microbiota in inducing blood sugar disturbing effects:
Artificial Sweeteners Induce Negative Changes In Gut Bacteria
Notably, the researchers found that many of the strains that were increased in relative abundance belonged to the Bacteroides genus and Clostridiales order, both of which contain members linked to obesity and opportunistic infections. They also observed that these microbiota changes lead to 1) increased lipopolysaccharide biosynthesis often found in harmful bacteria overgrowth and linked to metabolic endotoxemia 2) increased bacterial chemotaxis (an indication of increased bacterial activity;movement) previously observed in obese mice. 3) increased microbial energy harvest (e.g. increased carbohydrate metabolism and fatty acid biosynthesis) linked to obesity and glucose intolerance.
Part 2: Artificial Sweeteners Drive Similar Adverse Changes in Humans
In order to confirm that artificial sweeteners also drive adverse changes in humans, the researchers enrolled 381 non-diabetic individuals (44% males and 56% females) in a clinical nutritional study. Their results were reported as follows:
They also observed significant changes in the bacterial composition in those subjects consuming artificial sweeteners, with a shift towards the Enterobacteriaceae family, the Deltaproteobacteria class and the Actinobacteria phylum.
Finally, the researchers took fecal samples from subjects with artificial sweetener induced adverse bacterial changes (dysbios) and transplanted them into germ-free mice, resulting in impaired glucose tolerance and some replication of the adversely altered microbiome within the mice – confirming that micobiota mediate the adverse effects of artificial sweeteners on metabolism.
This latest study provides a physiological basis for the observed blood sugar impairing and weight-promoting properties of artificial sweeteners, and may help to explain why we have a burgeoning epidemic of pre- and type 2 diabetes, overweight and obesity, and related metabolic syndrome associated conditions in countries where artificial sweeteners are found everywhere.
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