Artificial Sweeteners Aiding the Obesity Epidemic?

Artificial Sweeteners Aiding the Obesity Epidemic?
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A new study published in the journal Nature has found that zero-calorie artificial sweeteners promote glucose intolerance in mice and humans.

Glucose intolerance is marked by higher-than-normal levels of blood sugar. It's a known precursor to diabetes and a risk factor for cardiovascular disease.

Scientists at the Weizmann Institute of Science in Israel spearheaded the research using a step-by-step approach. First, the researchers added three artificial sweeteners -- either sucralose, aspartame, or saccharin -- to the water of three groups of mice. Three other control groups of mice were given normal water or water with added sucrose or glucose. 11 weeks later, the mice consuming artificial sweeteners exhibited marked glucose intolerance compared to control groups.

Since most artificial sweeteners aren't broken down by the digestive system, the research team hypothesized that the glucose intolerance was mediated by changes to gut bacteria. To test this, they induced glucose intolerance in both lean and obese mice with the artificial sweetener saccharin, then gave both groups antibiotics to kill off gut bacteria. After the antibiotic regimen, both groups of mice saw their glucose response and blood sugar levels return to normal.

For further confirmation that the gut flora was regulating glucose intolerance, the team transplanted gut bacteria from mice fed saccharin to control mice. The control mice exhibited signs of glucose intolerance six days later.

To see whether their results in mice would carry over to humans, the researchers conducted two experiments. First, they examined a group of 381 individuals without diabetes and queried them about their intake of artificial sweeteners. They found that artificial sweetener intake was linked to various metabolic parameters, including increased weight, a larger waist-to-hip ratio, and higher blood sugar levels. Second, the researchers fed seven subjects the FDA’s maximal acceptable daily intake of saccharin per day -- equal to roughly 40 cans of diet soda -- for seven days and observed what happened. Four of the individuals developed significantly poorer glycemic responses. The other three subjects also showed worse responses, however the differences did not reach statistical significance.

The authors of the study feel their results merit a serious "reassessment" of massive artificial sweetener use. But others aren't so sure.

Professor Naveed Sattar, a Professor of Metabolic Medicine at the University of Glasgow, says that the study's findings in regards to mice are interesting, but noted that we should be skeptical of extending them to humans.

“The findings of this study do not prove that sweeteners pose any real risk to humans.  If there are any risks, we need well controlled studies in humans to find them.”

Sir Stephen O'Rahilly, a Professor of Clinical Biochemistry and Medicine at the University of Cambridge, agreed with Sattar.

"The authors report an association between artificially sweetened beverages and markers of diabetes in 381 people; however, a recent study involving more than a third of a million people showed no association between consumption of artificially sweetened drinks and the development of diabetes.  Suez et al also report adverse effects on glucose levels after 7 days of saccharin ingestion. However these experiments were undertaken in only seven people, so must be deemed preliminary."

According to the Harvard School of Public Health, "The health benefits of artificial sweeteners are inconclusive." Some studies show that they are healthy replacements for sugar, while others have showed no net benefits.

While the current study presents intriguing findings in mice, its human components lack rigor. So don't feel compelled to ditch diet soda just yet.

In general, it's probably best to avoid habitually consuming copious amounts of sugar or artificial sweeteners.

Source: Jotham Suez et. al.  "Artificial sweeteners induce glucose intolerance by altering the gut microbiota." Nature. 18 Sept. 2014. doi:10.1038/nature13793

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