From bacteria to binge eating When loss of F. prausnitzii leads to binge eating

Binge eating of fatty and sugary foods is classically observed in patients with eating disorders. For those with binge eating disorder (sidenote: Binge eating disorder Binge eating disorder is an eating disorder whose diagnosis is based on:

• clinical criteria : binge eating, on average at least once a week for three months; feeling of lack of control over eating.
 
• and on the presence of three or more of the following five criteria: eating much more quickly than normal; eating to the point of feeling uncomfortable; eating large quantities of food without physically feeling hungry; eating alone because of shame; feeling disgusted, depressed or guilty about having eaten too much.
 
  Binge eating behavior is a source of marked suffering. 

  Source: Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition Text Revision, DSM-5-TRTM, Feeding and eating disorders. ) , these episodes go hand in hand with unhappiness and excess weight, even obesity. It seems that the gut microbiota is involved. But what are the mechanisms involved? What are the effects of this eating disorder on the gut microbiota, and of the latter on behavior? To find out, researchers ¹ have deciphered the gut-brain axis step by step.

Binge eating and gut dysbiosis

After stress and dieting, mice, like humans, are more inclined to nibble on highly appetizing cookies, increase their calorie intake, and indulge in binge eating. This behavior seems to be linked to the rodents' gut microbiota, whose diversity and richness are altered, with a loss of Lactobacillus and Ruminococcaceae and an increase in Bacteroides, Roseburia and Alistipes.

Fecal microbiota transplantation (FMT) experiments suggest that the flora of the hyperphagic mice is depleted in protective bacteria: FMT from healthy mice causes hyperphagic mice to stop binge eating, suggesting the return of protective bacteria; conversely, FMT from hyperphagic mice to healthy mice does not induce binge eating, suggesting the absence of bacteria inducing this disorder.

Deciphering the mechanisms

Additional experiments show that binge eating in mice originates from disinhibition of the vagus nerve, leading to hyperactivation of the gut-brain axis, passing through the paraventricular nucleus of the thalamus (associated with reward, motivation and energy homeostasis) and the nucleus of the solitary tract. The trigger could be low production of a gut microbial metabolite, kynurenic acid (KYNA), in hyperphagic mice. Giving the mice KYNA supplements is enough to put them back on the road to a balanced diet.

What if all it took was a probiotic?

To confirm the results of the mouse model, the researchers analyzed fecal samples from eleven patients with binge eating disorder and nine healthy controls. The patients' microbiota showed a loss of Faecalibacterium prausnitzii (family Ruminococcaceae) and a drop in KYNA levels. There is every reason to believe that a reduction in F. prausnitzii could accompany a reduction in luminal KYNA and consequent eating disorders triggered via the gut-brain axis. This hypothesis seems to be confirmed in animals: inoculation of hyperphagic mice with F. prausnitzii raises KYNA levels and reduces their attraction to cookies and their binge eating.