A Correlation Between Increase In Popularity Of Nas And The Large Spike In The Obesity And Diabetes Epidemics
Non-caloric artificial sweeteners (NAS) are a popular food additive used among people of different body types. Initially, NAS were marketed to be “healthy” and a lower calorie option than for example sucrose, common table sugar. NAS are commonly found in an array of food items ingested by the population. NAS are also the center of many studies that conflict on whether or not these popular food additives have adverse health effects. There has been a greater amount of studies that indicate correlations between eating NAS and increase in body weight or a heightened risk of type 2 diabetes, than there has been studies that show negligent glycemic response. NAS, when ingested by humans, interact with the commensal microbiota in the gastrointestinal tract. Problems with blood-glucose level, weight gain and actions and type of microbiota present are causal factors in both directions.
The increase in popularity of NAS being an addition to food products is linear with the large spike in the obesity and diabetes epidemics, so it is important for people to be able to understand this correlation and why it occurred. Also its important to shed light on the increasingly growing area of research of ties between gut microbiome and health. The experimenters wanted to prove that NAS directly effects the makeup and roles of the microbiota in the host and in addition causes a dysbiosis, which leads to a host phenotype for glucose intolerance.
The beginning experiment of adding different NAS to the drinking water of lean 10-week old C57Bl/6 mice produced results that showed all but the control groups had developed significant glucose intolerance. Saccharin, out of the three NAS tested, showed the greatest outcome. The next experiment showed that both mice fed a high fat diet (HFD) and a normal chow diet developed glucose intolerance when fed commercial saccharin. A later experiment showed that a group of HFD mice fed a dosage of pure saccharin corresponding with that of the FDA limit for humans also developed great glucose intolerance. After this set of experiments, all mouse groups treated with pure saccharin and with commercial saccharin were treated with both gram-negative and gram-positive targeting antibiotics. Both treatments caused the glucose intolerance to subside in the saccharin consuming mice. These results together show that there is a vast range of types of microbiota present, and that glucose intolerance is affected by changing these commensal bacteria. Later on, fecal matter transplants from normal chow eating mice drinking commercial saccharin were put into normal chow consuming germ-free specimens. The transplanted mice later on exhibited higher glucose intolerance to that of the controls. This showed that the problems with metabolism that come from NAS are internally controlled by the gut microbiota. Much later the fecal microbiota present in the mouse groups was gene sequenced for the 16S ribosomal RNA gene. The saccharin drinking mice had increased numbers of Bacteroides and Clostridiales present, indicating saccharin consumption leads to dysbiosis. Further on, metagenomic sequencing of fecal samples before and after saccharin consumption was performed. The saccharin treatments showed the largest change in pathways, including higher amounts of glycan degrading pathways, in which short-chain fatty acids are made by fermentation. These pathways have been linked before with obesity in both human and mice hosts.
Other pathways were also noted to have been enriched. These results showed that the microbiota were performing at a higher energy expenditure due to increase in saccharin consumption. Towards the end of the experiments, fecal matter from young mice was cultured under anaerobic conditions with saccharin presence. After incubation and administration, the culture in vitro showed changes in gut microbiota ratios of phyla, this treated microbiome was transferred to a group of germ free mice whom then exhibited a rise in glucose intolerance. These results were consistent with showing saccharin changes the role and types of bacteria in the microbiome which further leads to glucose intolerance.
Lastly, humans were observed and the results showed consistent linkages between NAS consumption and criterion that were necessary for metabolic issues. Some of these included weight gain and glycosylated hemoglobin. To end out the experiments normal human volunteers who do not consume NAS normally were observed while taking extreme amounts of saccharin. Most showed poor glycemic responses. Later in this experiment the microbiota’s were analyzed by 16S rRNA analysis, which results agreed with saccharin causing a dysbiosis.
Overall the experiments all contributed to the main result that NAS is linked to increase in role and type of gut microbiota and increases glucose intolerance by proliferation of pathways prevalent in metabolic disorders.
This article gave valuable insight into the inner workings of how the fad of NAS is actually a negative trend for human health. The amount of different experiments that were collected in this article helped to bolster the credibility of the overall study. Also, the statistics showed that the data was accurate and there seemed to be no statistically significant regions of error. One critique of the paper was that the figures at times were hard to read and the captions didn’t seem to explain them quite well enough.
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