A human study was conducted by examining the relationship between long-term NAS consumption, based on a validated food frequency questionnaire, and various clinical parameters in an ongoing clinical nutritional study.

There were significant positive correlations between NAS consumption and several symptoms of metabolic syndrome, including:

    • Increased weight
    • Increased waist-to-hip ratio
    • Higher fasting blood glucose
    • Increased glucose intolerance
    • Glycosylated haemoglobin

The levels of glycosylated haemoglobin was significantly increased in a subgroup of individuals of NAS consumers to non-NAS consumers. Of this cohort, the 16S rRNA were characterised and a statistically positive correlation between multiple taxonomic entities and NAS consumption.

In an initial assessment of whether the relationship was causal, seven healthy volunteers who did not normally consume NAS were followed for a week, during which they consumed the maximal acceptable daily intake of commercial saccharin as recommended by the FDA. Four of the seven individuals developed a significantly poorer glycaemic response after NAS consumption after around five days of NAS consumption. The other three did not feature improved glucose tolerance.

The microbiome configurations of the NAS responders were assessed by 16S rRNA analysis, and clustering of the microbiota appeared different to that of the non-responders, both before and after NAS consumption. The microbiomes from the non-responders also showed little change in composition during the week of study, while there were pronounced compositional changes observed in the NAS responders.

NAS exposure was then transferred from two NAS responders and two NAS non-responders into groups of normal-chow-fed mice. The transfer of post-NAS exposure stool from NAS responders induced a significant glucose intolerance in the recipients compared to the response from pre-NAS exposure stool from the same responders. The post-NAS exposure stool of the non-responders, however, did not induce abnormal glucose tolerance in the mice. The response was indistinguishable from that of pre-NSA exposure stools from the same individuals.

Reference: Suez, Jotham et al. ‘Artificial Sweeteners Induce Glucose Intolerance By Altering The Gut Microbiota’. Nature (2014)

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