Artificial Sweeteners, Microbes and Blood Sugar Control
A paper in Nature back in 2014 noted that artificial non-caloric sweeteners (NAS) when consumed by mice had a detrimental effect of their metabolic health and microbiota, and the authors suggested that this connection may be an indication of risk in humans who consume these additives. The study used three artificial sweeteners: saccharin, sucralose (which is Splenda®), and aspartame.
It Seems These Are Also Seen In Humans
Next, they tested these findings in humans, using a database with nutritional profiling in a large number of patients, with ongoing data collection. They identified 381 non-diabetics in their database, with about 44% males. They looked at associations with glycaemic control and ingestion of NAS. They had a very dynamic way to look at dietary recall with a validated dietary history questionnaire.
When they looked at this and corrected for exposure to NAS, there were increases in things that you would expect from the mouse model. There were increases in haemoglobin A1c, more prediabetes, reduced glucose tolerance, impaired fasting glucose, and increased body weight and waist-to-hip ratios. In effect a central obesity pattern seen in metabolic syndrome began to develop. These changes were all related to this exposure to NAS, and there seemed to be a dose-related effect. In other words, those people who used more of these NAS had even more pronounced effects.
Following this they conducted a small but interesting experiment where they looked at seven healthy, lean participants and fed them the US FDA acceptable daily intake of saccharin. They looked at glycaemic effect as a response only to the saccharin ingestion, with standardised meals. Of these 4 out of the 7 participants actually developed impaired glucose tolerance, and their glycaemic response relative to what they were at baseline was strikingly aberrant.
They also looked at the response in their microbiome, and they found that there were profound changes in these 4 participants. The 3 participants who didn’t have glucose intolerance also had a microbiome analysis, but it didn’t seem to differ from their baseline analysis. So something in these 4 participants really seemed to change. When these patients resumed their normal diet and stopped their saccharin intake, they returned to having normal glucose tolerance but it does not appear a microbiome reanalysis was undertaken, which is a shame.
They then took the stool from these 7 participants, and they transposed this into germ free mice. Those that received the stool from the 4 participants with glucose intolerance, developed glucose intolerance as well. This suggests that glucose intolerance is a transmissible event using faecal matter as the vector.
What Can We Take Away
Artificial sweeteners are frequently used around the world to try to decrease glucose exposure, increase glycaemic control, and decrease the tendency for obesity.
Ironically this series of early studies suggest that NAS are not always as benign as some may like, and they have an effect on bacterial compositional balance, which in turn precipitates a change in the metabolic management of sugars, preceding the events that determine the diagnosis of metabolic syndrome. Those already diabetic may well see an increasing difficulty to manage their sugars. This also seems to support the notion that the dysbiotic event results in change in body composition leading to obesity developing.
Ironically people may be doing their utmost to reduce weight or improve glycaemic management by using NAS and experience the opposite as their microbiota are reactive to the NAS.
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