Artificial Sweetener Splenda Found to Worsen Symptoms of Crohn’s Disease in New Mouse Study

Artificial Sweetener Splenda Found to Worsen Symptoms of Crohn’s Disease in New Mouse Study
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The artificial sweetener Splenda (sucralose maltodextrin) was recently found to worsen gut inflammation in mice with Crohn’s disease, while no effects were seen in mice without the condition.

The investigation, led by researchers from Case Western Reserve University School of Medicine, found that, during a six-week period, Splenda promoted “bad” bacteria and intestinal inflammation.

These findings could have implications for humans with inflammatory bowel diseases (IBDs). In recent self-assessment dietary surveys, about 10 percent of patients living with IBDs reported that “sugary foods” worsen the severity of their symptoms and trigger flare-ups. Other epidemiological studies have also shown a strong association between the use of artificial sweeteners and an increased risk for IBD.

Findings from the study, titled “The Artificial Sweetener Splenda Promotes Gut Proteobacteria, Dysbiosis, and Myeloperoxidase Reactivity in Crohn’s Disease–Like Ileitis.”were published in the journal Inflammatory Bowel Diseases.

The findings revealed increases in the numbers of proteobacteria, a large group of microbes, in the intestines of mice that drank water supplemented with Splenda. Half of the mice studied belong to a genetic line that suffers from a Crohn’s disease variation. These mice were found to be more affected than the remaining half of the mice, which were healthy.

Proteobacteria include a variety of pathogens like E. coli, salmonella and legionellae. A certain amount of these bacteria are normal, but their overgrowth may cause health problems.

Our bodies are normally capable of eradicating these pathogens. However, if they can’t fully eliminate them, chronic inflammation may develop.

Experiments show inflammation link

In these Crohn’s disease-like mice, Splenda was found to lead to an intestinal overgrowth of E. coli and to an increase of bacterial penetration into the gut wall. To determine the effects of Splenda on these mice, researchers conducted three separate experiments with incremental adjustments:

  • In experiment 1, they added a “low dose” of Splenda (1.08 mg/mL) to the drinking water for six weeks, and then compared it to “plain water” using only the Crohn’s disease mice.
  • In experiment 2, the same protocol was repeated, but the dose was increased to the maximum recommended by the U.S. Food and Drug Administration (FDA), of 3.5 mg/mL.
  • In experiment 3, protocol from experiment 2 was repeated, but Splenda was administered at a dose 10 times higher than the maximum recommended dose (35 mg/mL).

Looking at the combined results from the three experiments, Splenda digestion resulted in an increased myeloperoxidase activity in the intestines of mice with the bowel disease. Myeloperoxidase is an enzyme in white blood cells (or leukocytes) that kills various microorganisms.

The increased presence of E. coli intensified the myeloperoxidase activity in the bowel as the body fought off the invaders. These findings suggest that the addition of Splenda could increase myeloperoxidase production in individuals with a pro-inflammatory predisposition, such as Crohn’s or other IBD. As a consequence, Splenda could exacerbate the symptoms of Crohn’s disease.

“Our findings suggest that patients with Crohn’s disease should think carefully about consuming Splenda or similar products containing sucralose and maltodextrin,” Alex Rodriguez-Palacios, PhD, the study’s lead author, said in a press release. “This study demonstrates that the sweetener induces changes in gut bacteria and gut wall immune cell reactivity, which could result in inflammation or disease flare ups in susceptible people. On the other hand, the study suggests that individuals free of intestinal diseases may not need to be overly concerned.”

The study’s senior author, Fabio Cominelli, PhD, added that these findings are based on the sole administration of a minor component of the diet, which suggests that other dietary habits or additives may also lead to similar microbiota alterations.

“For instance, diet emulsifiers used as food additives have also been shown recently to alter the gut microbiota and promote colitis in mice,” Cominelli said. “Other scenarios could put Crohn’s disease patients at risk of having exaggerated inflammation as well. This could include unexpected foodborne bacterial infections, which would further recruit myeloperoxidase-containing leukocytes to the intestinal tract and the resultant inflammation.”

Splenda was introduced in 1998 and includes an artificial sweetener suspected of being indigestible, called sucralose, in addition to maltodextrin, a digestible sweetener. It’s about 600 times as sweet as sugar and is one of the most popular artificial sweeteners on the market. Even though the FDA have confirmed the artificial sweeteners are “safe,” studies have shown that the effects of these particular artificial sweeteners across various diseases are controversial, as they vary with the diseases and human populations studied.

“This is perhaps the closest we can get to provide experimental evidence that these ingredients together induce biological changes known to cause inflammation which could be harmful over time to susceptible animal subjects,” added Rodriguez-Palacios. “Our next step would be to run experiments directly in patients, but that is more difficult to conduct given the large variability that is inherent to human genetics, microbiome and diet.”

Margarida graduated with a BS in Health Sciences from the University of Lisbon and a MSc in Biotechnology from Instituto Superior Técnico (IST-UL). She worked as a molecular biologist research associate at a Cambridge UK-based biotech company that discovers and develops therapeutic, fully human monoclonal antibodies.
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Margarida graduated with a BS in Health Sciences from the University of Lisbon and a MSc in Biotechnology from Instituto Superior Técnico (IST-UL). She worked as a molecular biologist research associate at a Cambridge UK-based biotech company that discovers and develops therapeutic, fully human monoclonal antibodies.
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