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Artificial Sweeteners May Cause Dangerous Changes in Gut Bacteria

  Researchers Found That Ingesting Artificial Sweeteners Lead To Obesity. A team of Israeli researchers has found evidence that suggests that ingesting artificial sweeteners might lead to obesity and related ailments such as diabetes. Artificial sweeteners appear to change the intestinal bacteria that direct metabolism. The Israeli group’s animal study results suggest that this connection […]

Artificial Sweeteners

 

Researchers Found That Ingesting Artificial Sweeteners Lead To Obesity. A team of Israeli researchers has found evidence that suggests that ingesting artificial sweeteners might lead to obesity and related ailments such as diabetes.

Artificial sweeteners appear to change the intestinal bacteria that direct metabolism. The Israeli group’s animal study results suggest that this connection might also exist in humans, Scientific American reports.

Digesting food and extracting energy from it is determined by genes and by the activity of the microbes that live in the digestive tract. The Israeli study results suggest that artificial sweeteners enhance the populations of gut bacteria that are more efficient at pulling energy from food and turning that energy into fat. In the Israeli experiment, one group of 10-week-old mice was fed a daily dose of aspartame, sucralose, or saccharin, while another group of mice was fed natural sugars, either glucose or sucrose. After 11 weeks, the mice in the group receiving the natural sugars were fine, but the mice consuming artificial sweeteners had abnormally high blood sugar (glucose) levels, an indication that they were having difficulty absorbing glucose from the blood, Scientific American reports.

Glucose Intolerance Can Lead To Health Problems

Glucose intolerance can lead to a range of health problems, including diabetes and a heightened risk of liver and heart disease. The researchers were able to reverse the condition: the mice received antibiotic treatment to kill all gut bacteria, and eventually their gut bacteria returned to its original makeup and balance, as did blood glucose control, Scientific American reports. Computational biologist Eran Segal of the Weizmann Institute of Science in Rehovot, Israel, was one of the scientists leading the study, which was published in Nature.

The investigators also found that the microbial populations that thrived on artificial sweeteners were the same ones found to be abundant in the guts of genetically obese mice. Jeffrey Gordon, a physician and biologist at Washington University in St. Louis, has shown that this relation between bacteria and obesity not a coincidence. More than 90 percent of the bacterial species in the gut come from just two subgroups—Bacteroidetes and Firmicutes. Gordon’s research team found that genetically obese mice had 50 percent fewer Bacteroidetes bacteria and 50 percent more Firmicutes bacteria than did normal-weight mice. When they transferred Firmicutes bacteria from the obese mice into normal-weight ones, the leaner mice became fatter. Gordon explains that the transplanted Firmicutes bacteria helped the mice extract more energy from their food and the bacteria manipulated the genes, triggering the storage of fat rather than its breakdown for energy, according to Scientific American.

In addition to the animal study, Segal’s team analyzed 381 men and women and found that those who used artificial sweeteners were more likely to be overweight and more likely to have impaired glucose tolerance. The team also tested the association in a small group of lean volunteers who do not normally consume artificial sweeteners. After the volunteers consumed the maximum dose of saccharin over a period of five days, four of seven subjects showed a reduced glucose response in addition to an abrupt change in their gut microbes. The findings warrant more research, the scientists say. The Israeli group concluded that artificial sweeteners “may have directly contributed to enhancing the exact epidemic that they themselves were intended to fight,” according to Scientific American.”

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