David Baxter PhD
Late Founder
Artificial Sweeteners Associated With Glucose Intolerance
by Justine Alford
September 18, 2014
Artificial sweeteners, such as aspartame, could induce the development of glucose intolerance in mice and maybe even some humans, a new study has found. As described in Nature, the researchers found that the sweeteners drove changes in the composition and function of gut microbes, which they propose is responsible for the apparent promotion of glucose intolerance. The team is therefore calling for more research and perhaps a reassessment of the use of these food additives.
Non-caloric artificial sweeteners (NAS) are synthetic substitutes for sugar that can be up to 20,000 times sweeter. They don?t contribute any calories to our diet because we can?t digest them, so they have been widely used across the globe as an aid to weight loss and diabetes prevention. However, there is a lot of controversy surrounding these additives because of conflicting research; a large body of evidence suggests they are effective at assisting weight control when part of a healthy diet, but some studies have found their use may be associated with weight gain and diabetes.
These contrasting studies spurred researchers from the Weizmann Institute to conduct a series of experiments on NAS involving both mice and humans. They started off by lacing the drinking water of young mice with three common NAS: aspartame, saccharin and sucralose. The amount used was the equivalent to the maximum acceptable daily intake in humans as decided by the FDA. After 11 weeks, mice consuming NAS showed significant glucose intolerance as compared to control mice consuming only water or water with added glucose. They also repeated the experiments with different breeds of mice and found the same thing.
Since these sweeteners are not absorbed or digested by the body, the researchers hypothesized that gut microbes may be responsible for the observed effects. To test this, they depleted the rodents? gut bacteria with antibiotics while continuing to feed them saccharin. They found that the antibiotics completely eliminated the differences in glucose tolerance between the mice fed saccharin and the control mice.
Next, they transferred the microbiota of either mice that had consumed NAS or control mice consuming glucose enriched water into sterile, ?germ-free? recipients via fecal transplant. They found that previously healthy mice developed glucose intolerance when transplanted with feces from NAS mice, but not the control mice. Transferring microbes that had been incubated in NAS outside of mice was also found to be sufficient to drive glucose intolerance in sterile mice.
Using sequencing to identify the gut microbes present in the different mice, the team found that mice fed saccharin or those that received a fecal transplant from saccharin-fed mice had markedly different bacterial populations compared to controls. Furthermore, there was an increase in certain species that had been previously linked with obesity in humans.
To find out if NAS affect humans in a similar manner, the researchers looked at data collected from 381 people. They found an association between self-reported NAS consumption and glucose intolerance and also differences in gut microbiome profiles between those consuming lots of NAS and those that did not consume them.
To take this further, they asked seven healthy volunteers that did not usually consume NAS to consume the maximum acceptable daily intake of saccharin for one week. Four showed a significant decrease in glucose tolerance, whereas three showed no change. Interestingly, the four responders had different gut microbiomes to those that didn?t respond before the experiment started. Furthermore, their microbial compositions significantly changed after consuming the sweeteners, whereas those that did not respond showed few changes.
While this research may suggest that artificial sweeteners can have metabolic consequences, at this stage it is unclear how the sweeteners are exerting this effect. Further studies are therefore needed before reassessments are made.
by Justine Alford
September 18, 2014
Artificial sweeteners, such as aspartame, could induce the development of glucose intolerance in mice and maybe even some humans, a new study has found. As described in Nature, the researchers found that the sweeteners drove changes in the composition and function of gut microbes, which they propose is responsible for the apparent promotion of glucose intolerance. The team is therefore calling for more research and perhaps a reassessment of the use of these food additives.
Non-caloric artificial sweeteners (NAS) are synthetic substitutes for sugar that can be up to 20,000 times sweeter. They don?t contribute any calories to our diet because we can?t digest them, so they have been widely used across the globe as an aid to weight loss and diabetes prevention. However, there is a lot of controversy surrounding these additives because of conflicting research; a large body of evidence suggests they are effective at assisting weight control when part of a healthy diet, but some studies have found their use may be associated with weight gain and diabetes.
These contrasting studies spurred researchers from the Weizmann Institute to conduct a series of experiments on NAS involving both mice and humans. They started off by lacing the drinking water of young mice with three common NAS: aspartame, saccharin and sucralose. The amount used was the equivalent to the maximum acceptable daily intake in humans as decided by the FDA. After 11 weeks, mice consuming NAS showed significant glucose intolerance as compared to control mice consuming only water or water with added glucose. They also repeated the experiments with different breeds of mice and found the same thing.
Since these sweeteners are not absorbed or digested by the body, the researchers hypothesized that gut microbes may be responsible for the observed effects. To test this, they depleted the rodents? gut bacteria with antibiotics while continuing to feed them saccharin. They found that the antibiotics completely eliminated the differences in glucose tolerance between the mice fed saccharin and the control mice.
Next, they transferred the microbiota of either mice that had consumed NAS or control mice consuming glucose enriched water into sterile, ?germ-free? recipients via fecal transplant. They found that previously healthy mice developed glucose intolerance when transplanted with feces from NAS mice, but not the control mice. Transferring microbes that had been incubated in NAS outside of mice was also found to be sufficient to drive glucose intolerance in sterile mice.
Using sequencing to identify the gut microbes present in the different mice, the team found that mice fed saccharin or those that received a fecal transplant from saccharin-fed mice had markedly different bacterial populations compared to controls. Furthermore, there was an increase in certain species that had been previously linked with obesity in humans.
To find out if NAS affect humans in a similar manner, the researchers looked at data collected from 381 people. They found an association between self-reported NAS consumption and glucose intolerance and also differences in gut microbiome profiles between those consuming lots of NAS and those that did not consume them.
To take this further, they asked seven healthy volunteers that did not usually consume NAS to consume the maximum acceptable daily intake of saccharin for one week. Four showed a significant decrease in glucose tolerance, whereas three showed no change. Interestingly, the four responders had different gut microbiomes to those that didn?t respond before the experiment started. Furthermore, their microbial compositions significantly changed after consuming the sweeteners, whereas those that did not respond showed few changes.
While this research may suggest that artificial sweeteners can have metabolic consequences, at this stage it is unclear how the sweeteners are exerting this effect. Further studies are therefore needed before reassessments are made.
