Compulsive eating and obesity may be triggered by a specific gut bacteria, a new study suggests, and the breakthrough could lead to new treatments to tackle the problem of food addiction.
The bacteria identified by an international research team is associated with the development of food addiction that can lead to obesity in humans and mice. They have also identified bacteria that play a beneficial role in preventing food addiction.
“A number of factors contribute to food addiction, characterised by a loss of control over food consumption and associated with obesity, other eating disorders and alterations in the composition of bacteria in the gut microbiome,” said Professor Elena Martín-García, from Pompeu Fabra University, Spain.
“Until now, the mechanisms underlying this behavioral disorder were largely unknown.”
Professor Rafael Maldonado, who heads the university’s neuropharmacology laboratory, said: “These results from our study could allow us to identify new biomarkers of food addiction and, above all, to evaluate whether beneficial bacteria could be used as potential new treatments for this obesity-related behaviour, which currently lacks effective therapeutic approaches.
“Potential new treatments could involve the use of beneficial bacteria and dietary supplements.”
The team used the Yale Food Addiction Scale to diagnose food addiction in mice and humans. It contains 35 questions for people to answer, and these can also be grouped into three criteria for use in mice: persistent search for food, high motivation to obtain food, and compulsive behavior.
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In the gut bacteria of food-dependent and non-food-dependent mice, the researchers found an increase in bacteria belonging to a group called the Proteobacteria phylum and a decrease in bacteria belonging to the Actinobacteria phylum in the food-dependent mice.
These mice also had a decrease in the amount of another type of bacteria called Blautia from the phylum Bacillota.
88 patients were classified as food addicted or not. Similar to the results observed in mice, a decrease in the phyla Actinobacteria and Blautia was observed in food addicted humans, as well as an increase in the phyla Proteobacteria.
Prevention on the horizon
“The results obtained in mice and humans suggest that the specific microbiota could have a protective effect in preventing food addiction,” said Professor Martín-García. “In particular, the strong similarities in the quantity of Blautia highlighted the potential beneficial effects of this particular gut bacteria. »
“Therefore, we investigated the protective effects of oral administration of lactulose and rhamnose, which are non-digestible carbohydrates called ‘prebiotics’ that can increase the amount of Blautia in the intestine.
“We did this in mice and found that it led to an increase in the abundance of Blautia in mouse feces, in parallel with dramatic improvements in food addiction.
“We saw similar improvements when we gave mice a species of Blautia called Blautia wexlerae orally as a probiotic.
“Gut microbiota signatures in mice and humans suggest possible non-beneficial effects of bacteria (belonging to the phylum Proteobacteria) and potential protective effects of increased abundance of Actinobacteria and Bacillota against the development of food addiction.”
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Professor Martín-García says the results show how bacteria in the gut influence brain function and vice versa.
“We have demonstrated for the first time a direct interaction between intestinal composition and brain gene expression, revealing the complex and multifactorial origin of this important obesity-related behavioral disorder.
“Understanding the interactions between behavioral changes and bacteria in the gut is a step forward for future treatments of food addiction and related eating disorders.”
The crucial connection between the gut and the brain
Professor Martín-García also described work to determine how microRNAs (miRNAs) – small, single-stranded molecules that regulate gene expression and contribute to almost all cellular processes – are involved in food addiction.
According to her, changes in miRNA expression may be involved in the mechanisms underlying this disorder. The researchers used a technique called Tough Decoy to inhibit specific miRNAs in the medial prefrontal cortex (mPFC) of the mouse brain to produce mice vulnerable to developing food addiction.
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They explained that part of the prefrontal cortex is the part of the brain involved in self-control and decision-making.
They found that inhibition of miRNA-29c-3p promoted response persistence and increased the mice’s vulnerability to developing food addiction. Inhibition of another miRNA called miRNA-665-3p promoted compulsive behavior and vulnerability to food addiction.
“These two microRNAs could act as protective factors against food addiction,” said Professor Maldonado. “This helps us understand the neurobiology of loss of eating control, which plays a crucial role in obesity and related disorders.”
“To better understand these mechanisms, we are now exploring how the expression of gut microbiota and miRNAs in the brain interact in mice.”
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Professor Richard Roche of Maynooth University, who was not involved in the research, welcomed the new information on food addiction.
“Many factors contribute to this phenomenon, including the environment people live in and the availability of certain types of food. However, we have known for some time that there are likely contributing factors to eating disorders. »
The research, which paves the way for the development of potential new treatments, was presented Thursday at the Federation of European Neuroscience Societies Forum in Austria and published in the journal Gut.
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