Commonly, we see different eating disorders, like anorexia and bulimia, as types of psychiatric illness, but recent research suggests they may be forms of a more generalized illness. The digestive tract itself plays a key role in these disorders, researchers now believe, with one study in particular having identified a protein produced by our intestinal bacteria and functioning as a possible source of the problem. “Specific alterations of gut microbiota may lead to behavioral and emotional abnormalities as observed in [eating disorder] patients,” suggest the authors in their new study.

As different as they are, anorexia nervosa, bulimia, and binge eating disorder are all eating disorders (ED). The only common characteristic of these different EDs is dysregulation of food intake, which is either radically decreased or radically increased, depending on the disorder. If atypical forms of ED are included, these disorders affect about 15 percent to 20 percent of the population, particularly adolescents and young adults. Despite the many studies that have already been conducted, the psychiatric, genetic, and neurobiological basis remains unclear while the molecular mechanism responsible for these disorders is also mysterious.

Protein Mimics the Hormone That Makes Us Feel Full

For the current study, scientists from France’s University of Rouen and Institut National de la Santé et de la Recherche Médicale began with past findings that identified a protein, known as ClpB, which mimics the hormone that makes us feel sated (melanotropin). This protein is produced by some of our gut bacteria, including the commonplace E. coli. Where this protein is present, our bodies produce antibodies against it, and these bind to the satiety hormone because it is structurally similar to ClpB. As a result, researchers theorize the hormone’s usual satiety effects become modified. Simply put, when this happens, someone with anorexia would feel they’ve eaten enough, while someone with bulimia or an overeating disorder would feel the opposite, that they haven’t eaten enough.

To see whether this theory is correct, the researchers modified the composition of the intestinal flora of mice and watched how they responded. In one group of mice, which were given mutant E. coli bacteria that did not produce ClpB, food intake and level of antibodies against melanotropin did not change. In a second group of mice, which received E. coli producing the ClpB protein, antibody levels and food intake did change. Next, the researchers analyzed data from 60 patients with an eating disorder. In these patients, the researchers found, levels of antibodies to ClpB and melanotropin were higher than normal.

To continue this line of research, the scientists are once again using mice and have found it may be possible to neutralize ClpB. “We are presently working to develop a blood test based on detection of the bacterial protein ClpB,” noted the authors of the study. “If we are successful in this, we will be able to establish specific and individualized treatments for eating disorders.”

Source: Tennoune N, Chan P, Breton J, et al. Bacterial ClpB heat-shock protein, an antigen-mimetic of the anorexigenic peptide α-MSH, at the origin of eating disorders. Translational Psychiatry. 2014.