Motivation: The last few months have been a haze - the typical residency experience. Apologies for the sparse posts. We will begin again with a relatively shocking news topic. The reputation of artificial sweeteners is under attack with allegations that glucose tolerance levels may worsen with these artificial sweeteners. Is this true or craze?
Paper: Suez, J, Korem, T, Zeevi, D, et. al. "Artificial sweeteners induce glucose intolerance by altering the gut microbiota." Nature (2014) epub.
Methods: This study consisted of two parts. The first part was in mice divided into cohorts fed water mixed with saccharin, sucralose, aspartame, or glucose/sucrose. The metabolic profile was then determined of these mice. The second part consisted of observational human data and a small trial of saccharin in control human adults.
Results:
Non-Caloric Sweeteners in Mice: After 11 weeks of mice being fed saccharin, sucralose, aspartame, or glucose/sucrose, all three artifical sweetener cohorts had significantly worse glucose tolerance with saccharin being the worst offender. Note that these doses of sweeteners where under the FDA approved dose limit by weight. The authors replicated this finding for saccharin in two other mice cohorts randomized to either glucose or saccharin.
The author's next postulated that this effect is mediated by the gut bacteria. Treatment with ciprofloxacin and metronidazole or vancomycin abolished the glucose intolerance effect of artificial sweeteners. Furthermore, fecal transplant from mice consuming saccharin also induced glucose intolerance in the transplanted mice. The authors further postulate that short chain fatty acid production is increased in the gut with artificial sweeteners and may be part of the causal chain to increased glucose resistance.
Non-Caloric Sweeteners in Human Beings: 381 non-diabetic adults (mean age 43.3) were studied next in a cross-sectional manner. Increased consumption of non-caloric sweeteners was associated with increased weight, higher fasting blood glucose, elevated glycosylated hemoglobin, and impaired glucose tolerance test. These associations held true independent of adjustment for body mass index.
A small trial was conducted next in seven adults who do not consume artificial sweeteners. For six days, they were fed daily saccharin up to 5 mg/kg (FDA maximum limit). After this six-day experiment, 4 out of 7 subjects developed impaired glucose tolerance. Transplant of the feces from the subjects with impaired glucose tolerance into mice elicited impaired glucose tolerance in the mice suggesting that a change in the gut microbiome may be causal.
Discussion: This paper strongly shows that use of artificial sweeteners (particularly saccharin) is associated with impairment in glucose tolerance. Although this relationship is shown most conclusively in mice, the small trial also suggests a similar process occurring in adult human beings. Furthermore the elegant fecal transplant experiments suggest that alterations in gut flora are probably to blame. This study raises serious concerns about the artificial sweeteners. However, prior to discarding the artifical sweeteners, we need larger scale observational human studies verifying that the imbalance in glucose tolerance seen within the short duration of the trial does in fact translate to increased risk of long-term glucose intolerance and development of diabetes. Moreover, these studies again highlight the fact that when these sweeteners were approved by the FDA, no clinical endpoints were used!
Paper: Suez, J, Korem, T, Zeevi, D, et. al. "Artificial sweeteners induce glucose intolerance by altering the gut microbiota." Nature (2014) epub.
Methods: This study consisted of two parts. The first part was in mice divided into cohorts fed water mixed with saccharin, sucralose, aspartame, or glucose/sucrose. The metabolic profile was then determined of these mice. The second part consisted of observational human data and a small trial of saccharin in control human adults.
Results:
Non-Caloric Sweeteners in Mice: After 11 weeks of mice being fed saccharin, sucralose, aspartame, or glucose/sucrose, all three artifical sweetener cohorts had significantly worse glucose tolerance with saccharin being the worst offender. Note that these doses of sweeteners where under the FDA approved dose limit by weight. The authors replicated this finding for saccharin in two other mice cohorts randomized to either glucose or saccharin.
The author's next postulated that this effect is mediated by the gut bacteria. Treatment with ciprofloxacin and metronidazole or vancomycin abolished the glucose intolerance effect of artificial sweeteners. Furthermore, fecal transplant from mice consuming saccharin also induced glucose intolerance in the transplanted mice. The authors further postulate that short chain fatty acid production is increased in the gut with artificial sweeteners and may be part of the causal chain to increased glucose resistance.
Non-Caloric Sweeteners in Human Beings: 381 non-diabetic adults (mean age 43.3) were studied next in a cross-sectional manner. Increased consumption of non-caloric sweeteners was associated with increased weight, higher fasting blood glucose, elevated glycosylated hemoglobin, and impaired glucose tolerance test. These associations held true independent of adjustment for body mass index.
A small trial was conducted next in seven adults who do not consume artificial sweeteners. For six days, they were fed daily saccharin up to 5 mg/kg (FDA maximum limit). After this six-day experiment, 4 out of 7 subjects developed impaired glucose tolerance. Transplant of the feces from the subjects with impaired glucose tolerance into mice elicited impaired glucose tolerance in the mice suggesting that a change in the gut microbiome may be causal.
Discussion: This paper strongly shows that use of artificial sweeteners (particularly saccharin) is associated with impairment in glucose tolerance. Although this relationship is shown most conclusively in mice, the small trial also suggests a similar process occurring in adult human beings. Furthermore the elegant fecal transplant experiments suggest that alterations in gut flora are probably to blame. This study raises serious concerns about the artificial sweeteners. However, prior to discarding the artifical sweeteners, we need larger scale observational human studies verifying that the imbalance in glucose tolerance seen within the short duration of the trial does in fact translate to increased risk of long-term glucose intolerance and development of diabetes. Moreover, these studies again highlight the fact that when these sweeteners were approved by the FDA, no clinical endpoints were used!
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