TOPLINE:
METHODOLOGY:
- Food addiction, characterized by a loss of control over food intake, may promote obesity and alter gut microbiota composition.
- Researchers used the Yale Food Addiction Scale 2.0 criteria to classify extreme food addiction and nonaddiction in mouse models and humans.
- The gut microbiota between addicted and nonaddicted mice were compared to identify factors related to food addiction in the murine model. Researchers subsequently gave mice drinking water with the prebiotics lactulose or rhamnose and the bacterium Blautia wexlerae, which has been associated with a reduced risk for obesity and diabetes.
- Gut microbiota signatures were also analyzed in 15 individuals with food addiction and 13 matched controls.
TAKEAWAY:
- In both humans and mice, gut microbiome signatures suggested possible nonbeneficial effects of bacteria in the Proteobacteria phylum and potential protective effects of Actinobacteria against the development of food addiction.
- In correlational analyses, decreased relative abundance of the species B wexlerae was observed in addicted humans and of the Blautia genus in addicted mice.
- Administration of the nondigestible carbohydrates lactulose and rhamnose, known to favor Blautia growth, led to increased relative abundance of Blautia in mouse feces, as well as “dramatic improvements” in food addiction.
- In functional validation experiments, oral administration of B wexlerae in mice led to similar improvement.
IN PRACTICE:
“This novel understanding of the role of gut microbiota in the development of food addiction may open new approaches for developing biomarkers and innovative therapies for food addiction and related eating disorders,” the authors wrote.
SOURCE:
The study, led by Solveiga Samulėnaitė, a doctoral student at Vilnius University, Vilnius, Lithuania, was published online in Gut.
LIMITATIONS:
Further research is needed to elucidate the exact mechanisms underlying the potential use of gut microbiota for treating food addiction and to test the safety and efficacy in humans.
DISCLOSURES:
This work was supported by La Caixa Health and numerous grants from Spanish ministries and institutions and the European Union. No competing interests were declared.
A version of this article first appeared on Medscape.com.