Food additives that are commonly used to thicken and stabilize processed foods may disrupt the bacterial makeup of the gut, causing health problems, a new study in animals suggests.
In the study, mice that were fed two chemicals that are commonly added to foods gained weight, had altered blood sugar and developed intestinal problems. The chemicals were "emulsifying agents," chemicals that hold together mixtures that include both fat and water, which would otherwise separate.
The chemicals were "able to trigger low-grade inflammation and metabolic syndrome," in the mice, said study co-author Benoit Chassaing, a microbiologist at Georgia State University in Atlanta.
The food additives may also have harmed the mice by promoting the growth of bacteria that eat through the protective mucus lining of the gut, the study found. [ 5 Ways Gut Bacteria Affect Your Health ]
Widely used products
Generally, emulsifying agents are chemicals that thicken foods. For instance, emulsifiers help make ice cream stay creamy even after several cycles of freezing and thawing, whereas otherwise it would turn into a hard, icelike block, Chassaing said.
"If you want to make a product that gels together and liquefies together, you need to add these compounds," said Christian Jobin, a microbial immunologist at the University of Florida in Gainesville, who was not involved in the study.
Past studies in mice had shown that a food additive called carboxymethylcellulose changed the composition of the bacterial communities that line the gut. So Chassaing and his colleagues wondered how this affected the animals' health.
The team fed healthy mice a diet with either 1 percent carboxymethylcellulose, or 1 percent polysorbate 80, another popular emulsifier found in many foods. (Processed foods typically contain about 1 percent emulsifiers.)
The healthy mice soon began eating more, gaining weight and had blood sugar control problems, compared with control mice. These symptoms are important to look at because in humans, they are involved in "metabolic syndrome," which is a generally unhealthy state (defined as having high blood pressure, low levels of HDL, or "good" cholesterol, high blood sugar and increased levels of triglycerides).
When the researchers looked at the mice's gut tissue under a microscope, they saw more signs of low-grade inflammation.
The team also fed the food additives to mice genetically predisposed to develop diseases such as inflammatory bowel disease and colitis. In these mice, the emulsifiers seemed to worsen the disease.
To understand why the food additives caused low-grade inflammation in the mice, the researchers looked at the layer of protective mucus that lines the gut. They found that emulsifiers contributed to the growth of bacteria that live deeper in the mucous layer, closer to the intestinal tissue itself. The food additives also promoted the growth of bacteria that can digest the mucous.
The findings are part of a growing body of literature that suggests that the bacteria that live in the human body play an important role in health, the researchers said.
Jobin noted that mice eat a very different diet than humans, so repeating this study in animals such as pigs, which eat a very similar diet to humans, could be more informative.
Ultimately, the ideal experiment would be to compare people who are eating foods with and without these agents in them, Jobin said. But completely eliminating these compounds from a person's diet could be tricky.
"We are just bombarded with these things," Jobin told Live Science.
People who want to avoid these food additives should eat more whole foods and fresh foods, Chassaing said.
"Packaged products are very loaded with emulsifiers and freshly cooked foods are not, so this is one of the simplest ways to avoid these agents," Chassaing told Live Science.
The research team is currently starting a test in people, and the members are also following up to see if other natural emulsifying agents, such as soy lecithin and guar gum, have similar effects, Chassaing said.
The findings were published today (Feb. 25) in the journal Nature.