Wednesday Sep 24, 2014 (foodconsumer.org) -- An excellent study recently published in the prestigious scientific journal Science provides evidence indicating that many cases of type 2 diabetes and obesity may be caused by artificial sweeteners.

The study finds that artificial sweeteners induce glucose intolerance, which is a prime feature in diabetes mellitus and pre-diabetes, which together affect tens of millions of Americans.

Artificial sweeteners are considered safe to use by governments worldwide and food industry and probably the majority of food consumers.  These non-caloric artificial sweeteners are commonly used in diet drinks such as diet coke and foods.  People use these products maybe because they are diabetic or suffering obesity or want to prevent diabetes mellitus or obesity.

The study led by Eran Elinav at Weizmann Institute of Science in Israel and colleagues shows that non-caloric artificial sweeteners actually change the microbial flora in the gut or gut microbiota, that is, the artificial compounds promote the growth of harmful bacteria like bacteroides vulgatus in the intestinal tract while suppressing growth of beneficial bacteria like the probiotic called akkermansia muciniphila, which is associated with weight loss.

The researchers find that when the harmful fecal bacteria from mice or human volunteers drinking water with artificial sweeteners are transferred  to germ-free mice that are not exposed to artificial sweeteners, the recipient mice developed glucose intolerance.

And researchers validate the assumption that the gut micro flora modified by artificial sweeteners is the cause for glucose intolerance.  They use antibiotics to kill the harmful bacteria in the gut of mice and the glucose intolerance is reversed.

The harmful effect of artificial sweeteners has been duplicated in healthy individuals who do not usually drink any diet drinks or eat any foods with artificial sweeteners.  Just after one week of consumption of drinks sweetened with artificial sweeteners, glucose intolerance is developed.

Tested artificial sweeteners includes saccharine and two other artificial sweeteners, sucralose and aspartame, which are approved by the US Food and Drug Administration and more commonly used in diet drinks and foods.

Early studies have found that use of probiotics can help fight obesity and type 2 diabetes mellitus. The findings suggest that harmful bacteria in the gut mcrobiota can be a risk factor for metabolic diseases like diabetes melltus type 2 and obesity.

Another study conducted in Mexico indicates that drinking diet soda does not lower fasting glucose, compared to drinking regular soda in adults with diabetes mellitus.  Australian researchers conducted a study and came to a similar conclusion - drinking diet soda does not lower glucose, compared to using a diet with added sugar.

The current study in Nature is not the first to link drinking soda sweetened with artificial sweeteners like aspartame, sucralose, and saccharin to diabetes mellitus and other cardiometabolic diseases.

In 2013, S. E. Swithers of Purdue University published a review to conclude that "frequent consumers of these sugar substitutes may also be at increased risk of excessive weight gain, metabolic syndrome, type 2 diabetes, and cardiovascular disease. " (David Liu, PHD)

References

1. H Shapiro, Z Halpern, E Segal, E Elinav Artificial sweeteners induce glucose intolerance by altering the gut microbiota,  Nature, 2014 - nature.com

2. Olalde-Mendoza L, Moreno-González YE. [Modification of fasting blood glucose in adults with diabetes mellitus type 2 after regular soda and diet soda intake in the State of Querétaro, Mexico].  [Article in Spanish] Arch Latinoam Nutr. 2013 Jun;63(2):142-7.

3. Swithers SE.  Artificial sweeteners produce the counterintuitive effect of inducing metabolic derangements.  Trends Endocrinol Metab. 2013 Sep;24(9):431-41.  

4. Colagiuri S , Miller JJ, Edwards RA.  Metabolic effects of adding sucrose and aspartame to the diet of subjects with noninsulin-dependent diabetes mellitus.  Am J Clin Nutr. 1989 Sep;50(3):474-8.