The Truth About Diet Soda: Do Artificial Sweeteners Increase Rates of Obesity?

In modern America, much emphasis has been placed on the issue of rising rates of obesity and type two diabetes. In 2015, more than 2/3 of Americans are overweight (body mass index of 25-29 kg/m2,) and 1/3 are obese (body mass index great than 30 kg/m2.) Because of this obesity epidemic, many Americans are becoming more health-conscious and beginning to shift their dietary tendencies. A decision that generally goes hand in hand with increased focus on obesity prevention is switching to “diet” drinks, usually soda. The popular belief around the non-caloric artificial sweeteners (NAS) used to replace sugar in these drinks is that they lower caloric intake and reduce weight. “Diet” drinks are seen as the perfect beverage by many health-conscious people; they seem to aid in diet and normalize blood sugar while retaining the taste of the original drink containing sugar. Recently however, NAS has come under fire for, in fact, causing weight gain rather than loss. Critics of NAS struggled to find definitive proof of its negative effects, though, because many, if not most, people who drink diet sodas are already overweight, or suffer from metabolic syndrome manifestations. Since using humans for observation of artificial sweeteners' effect usually led to inconclusive conclusions, a group of Israeli researchers at the Weizmann Institute of Science conducted a study on mice. The results were, in the words of Cathryn Nagler, a pathology professor at the University of Chicago, “very compelling.”

          The researchers set up three different mouse groups (every mouse was lean and healthy.) One group was given water with saccharin (a commonly used NAS in diet drinks), one group was given water supplemented with glucose or sucrose (sugar), and the control group was given only water. As the experiment carried on, it became increasingly clear to the researchers that NAS had detrimental effects on the body. The control mouse group and the sugar water group demonstrated similar, “normal,” glucose tolerance, while the NAS group developed glucose intolerance. To add on to this telling finding, the researchers started a new group of obese and lean mice. Both groups were given a daily dose of saccharin that corresponds to the FDA labeled “acceptable intake” in humans. Despite differences in weight, both mouse groups developed glucose intolerance after only 5 weeks. The researchers also found the NAS fed rats to have insulin intolerance. Both of these rat groups' diets were constructed to parallel a typical human diet, making these findings critically important. The intolerances identified in the NAS rat groups reduces the bodies' ability to metabolize glucose, leading to increased chance of type two diabetes and obesity.

Source: http://www.weightlosstips.co.uk/western-obesity-epidemic-is-spreading-world-wide/

    

         Although these initial observations are intriguing, and certainly of utmost importance, the researchers were not fully satisfied at this stage. They wanted to delve deeper, and uncover the underlying cause of the NAS-sparked glucose and insulin intolerance. The researchers treated a control group and a NAS fed group of mice with antibiotics. After 4 weeks of this treatment the glucose intolerance in the NAS group leveled out to match the healthy tolerance that the control group had. This result informed the researchers that the cause of the glucose intolerance was gut microbiota that was altered by the artificial sweeteners. Microbiota is a bacteria in the digestive system that plays a crucial role in metabolism and blood sugar regulation. To test this hypothesis, the researchers transferred microbiota from the control rats and microbiota from the NAS rats to two new groups of rats. On par with the researchers's prediction, the rats who received microbiota from the NAS rats demonstrated glucose intolerance, while the control rats did not

          While this finding showed a correlation between NAS rat microbiota and glucose intolerance, it did not definitively prove that artificial sweeteners were the reason behind the altered microbiota. The researchers constructed yet another experiment to confirm NAS's altering role. The research team cultured stool in conditions with saccharine and a control condition. After 9 days of culturing these microbiota configurations in the form of stool, the researchers transferred the saccharin-cultured microbiota to a group of mice, which resulted in a high glucose intolerance. Conversely, the control mice did not develop this intolerance. This finding proves NAS's negative impact on microbiota.

Since rats have similar anatomy, and the same microbiota digestive usage as humans, these results should be taken quite seriously. People who drink diet drinks with the intention of weight loss and diabetes prevention are blind to the fact that this artificial sweetener intake is, in fact, kindling a lower ability to metabolize glucose and hurting their body's ability to regulate blood sugar. The findings of this experiment have exploded in the media, with articles in the New York Times, the LA Times, and Science World, among many others. Americans need to realize that, while dieting is a great thing to do, it should be done without the diet drinks. In the war against obesity and diabetes type two, people are currently funding the wrong side through their endorsement of artificial sweeteners. While water and some juices are preferential beverages for a diet, regular soda should take preference to diet.

References

Breindl, A. (2014). Artificial sweeteners backfire via gut microbiome. Retrieved from http://www.bioworld.com/content/artificial-sweeteners-backfire-gut-microbiome-0

Chang, K. (2014). Artificial sweeteners may disrupt body's blood sugar controls. Retrieved from http://well.blogs.nytimes.com/2014/09/17/artificial-sweeteners-may-disrupt-bodys-blood-sugar-controls/?_r=1

Elinav, E., Segal, E., Suez, J., & Korem, T. (2014). "Artificial sweeteners induce glucose intolerance by altering the gut microbiota". Nature.Com, 514