If a pack of sugar-free gum has ever given you a nasty stomach ache, you might have your gut bacteria to blame. New research in mice found a link between the gut microbiome and a food intolerance to sorbitol, a commonly used sugar substitute. The findings could even point to an effective treatment for the condition, though more studies will be needed to confirm the connection.
Sorbitol and similar ingredients are sugar alcohols, also called polyols. They’re derived from sugars like sucrose but carry fewer calories (about half to a third the amount), which has made them popular thickening and sweetening agents. Sugar alcohols are less sweet-tasting, however, so sugar-free products containing them often include artificial sweeteners as well. Unlike the latter type of substitute, many sugar alcohols can be found naturally in certain fruits and vegetables.
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As valuable as sugar alcohols are, it’s long been known that they can cause gastrointestinal distress. People usually don’t get sick from the small amounts of sorbitol and other polyols found in the typical diet, but some of us seem to be especially sensitive to its presence in foods—a condition known as polyol intolerance. Researchers at the University of California Davis and elsewhere say they may have figured out the reason why this happens.
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Past research in mice has suggested that disturbing the gut microbiome can temporarily induce polyol intolerance. But these scientists wanted to get a better sense of how the condition can become chronic in some people. Their previous work found that antibiotic treatment combined with a high-fat diet can extend how long it takes for the microbiome to bounce back to normal. So they wanted to see if this combination would also cause prolonged sorbitol intolerance in mice, which it did seem to. The researchers then found lower levels of an enzyme that breaks down sorbitol than usual in the feces of these affected mice—a pattern they also found in the feces of people more sensitive to sugar-free foods.
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Theorizing that the loss of this enzyme contributes to sorbitol intolerance, the team next focused on finding the gut bacteria that produce it. By scanning the genetics of the entire gut microbiome, they eventually identified bacteria belonging to the group Clostridium as likely candidates. These bacteria are known to be anaerobic, meaning they only grow well in the absence of oxygen. The combination of antibiotics plus a high-fat diet in the mice appears to produce a higher oxygen environment in the gut, reducing levels of Clostridium and then levels of the enzyme that breaks down sorbitol.
To confirm their suspicions, the team introduced another bacteria intended to restore the low-oxygen content of the mouse guts. Once they did, levels of Clostridium increased, as did levels of the enzyme that breaks down sorbitol; just as importantly, the mice also stopped having symptoms of sorbitol intolerance.
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“Our research suggests that microbial sorbitol degradation normally protects the host against sorbitol intolerance. However, an impairment in the microbial ability to break down sorbitol causes sorbitol intolerance,” said lead author Jee-Yon Lee, a microbiologist at UC Davis, in a statement from the university.
The team’s findings, published Thursday in the journal Cell, don’t yet prove that this same chain of events leads to chronic sorbitol intolerance in people. But the authors note that there are existing medications that should be able to create the same low-oxygen levels in the guts of people with this condition. These drugs include mesalazine, which is already used to help treat Crohn’s disease and other inflammatory bowel diseases. So at the very least, it’s possible to test out this hypothesis in future clinical trials and hopefully find a treatment, they argue.
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“Our study provides a completely new starting point for approaches to diagnose, prevent and treat sorbitol intolerance,” said co-author and fellow UC Davis researcher Andreas Bäumler in a statement.
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