Evidence continues to accumulate that sugar is a sweet road to obesity, diabetes, Alzheimer’s, and other maladies. As the dangers of sugar have unfolded there has been an increase in the production and consumption of sugar substitutes, five of which are currently FDA-approved. A recent study published in Nature adds to a growing set of concerns about these artificial sweeteners by presenting evidence that they, like sugar, can cause diabetes as well. The Israel-based research team presented evidence that artificial sweeteners cause this outcome by disrupting the balance of microbes that live in the body’s gut.
This isn’t the first study implicating sugar substitutes with metabolic issues. Research at Purdue University found that saccharin consumption can lead to weight gain in mice by interfering with their ability to control their appetites. Multiple studies have shown that some artificial sweeteners can mess with the body’s endocrine system, and lead to insulin resistance. Many links between the consumption of artificial sweeteners and type 2 diabetes have been uncovered as well, and studies have also shown that consumption of artificial sweeteners can change the way the body deals with food that contains actual calories.
The link between artificial sweeteners, gut bacteria and obesity has been charted as well, in a Duke University study that found that Splenda (sucralose) reduces the amount of ”good bacteria” in the intestines, increases the intestinal pH level, and leads to increased body weight.
The new Nature study moves this ball of research forward by demonstrating that several artificial sweeteners, not just sucralose, can mess with our gut bacteria, and that this disruption is directly responsible for glucose intolerance—at least in mice. The researchers added three different artificial sweeteners (AS)—saccharin, sucralose and aspartame—to the drinking water of mice. After 10 weeks, all three groups of artificial sweetener-consuming mice showed glucose intolerance. Saccharin showed the most pronounced effect.
As the Duke study had shown that sucralose causes changes in the gut microbiota in mice, the Israeli researchers used antibiotics to wipe out the microbes in the mice that had been made glucose intolerant from consuming artificial sweeteners. Eliminating the microbial community in the mice with antibiotics eliminated their glucose intolerance as well.
The researchers then preformed fecal transplants to make doubly sure that the changing character of the mice gut microbes was behind their changing tolerance of glucose. Poop from mice with AS-caused glucose intolerance was inserted into the colons of mice whose AS-induced glucose intolerance had been removed by treatment with antibiotics. After receiving fecal transplants, the mice’s glucose intolerance returned.
The team then turned its attention to humans, examining dietary data and health metrics from non-diabetic people that had been gathered in in an unrelated, ongoing nutritional study. They found correlations between AS consumption and increased ratio of waist to hip, higher blood glucose, and other metabolic markers associated with pre-diabetics.
What’s tricky about looking at this kind of human data in these cases is that those who are drinking diet sodas might very well be doing so because they are already at risk for obesity or diabetes. In other words, instead of demonstrating that artificial sweeteners make you fat, you might instead be observing that fat people are more likely to use sugar substitutes. So while interesting, this correlation in and of itself could be misleading.
To address this issue the researchers assembled a group of seven healthy volunteers who don’t normally consume artificial sweeteners. For one week, the subjects consumed the maximum FDA allotment of Saccharin. After only one week, four out of the seven volunteers began showing glucose intolerance. Those that did also showed a marked shift in their gut microbial profiles, while the microbial profiles of the subjects that did not show glucose intolerance did not show this change.