Scientists have discovered a possible link between eating disorders and specific types of bacteria in the intestines.
The biological mechanisms behind eating disorders such as anorexia nervosa, bulimia, and binge eating disorder are unknown. So a team led by Dr. Serguei Fetissov from the Inserm Laboratory on Nutrition, Gut and Brain in Rouen, France, looked at a protein that mimics a “satiety” protein.
The protein, ClpB, is made by bacteria such as E. coli that are often seen in the intestinal flora. The team say ClpB can mimic a hormone known as alpha-melanotropin, which controls skin pigmentation and plays a role as a satiety signal in the hypothalamus of the brain.
If this mechanism is found to be faulty in some individuals with eating disorders, correcting it and normalizing satiety signals could potentially help restore a healthy food intake.
Full details of the study are published in the journal Translational Psychiatry. To test their theory, the team altered the intestinal flora of mice to see the impact of different types of E. coli on their immune system and behavior.
When the animals were given E. coli that produced ClpB, disordered eating behavior was observed. Eating behavior was normal in mice given mutated E. coli bacteria that did not produce ClpB.
Tests on 60 eating disorder patients showed greater antibodies to ClpB and alpha-melanotropin compared with the general population, suggesting raised levels of ClpB.
Said Fetissov, “We are presently working to develop a blood test based on detection of the bacterial protein ClpB. If we are successful in this, we will be able to establish specific and individualized treatments for eating disorders.”
A molecular mechanism linked to risk for anorexia nervosa, bulimia, and binge eating disorder has never been established. This study confirms the involvement of ClpB in appetite regulation, suggesting that “specific alterations of gut microbiota may lead to behavioral and emotional abnormalities as observed in eating disorder patients.”
Fetissov and colleagues point out that the role of gut microbiota in eating disorder risk factors is in line with other data “supporting an infectious origin of neuropsychiatric disorders” such as schizophrenia.
“Our findings of increased levels of anti-ClpB antibodies in eating disorder patients, and correlations of anti-ClpB antibodies with patients’ psychopathological traits, support the involvement of ClpB-expressing microorganisms in abnormal feeding behavior,” they state.
This “opens up new perspectives for the diagnosis and specific treatment of eating disorders,” says the team. “According to our initial observations, it would indeed be possible to neutralize this bacterial protein using specific antibodies, without affecting the satiety hormone.”
In addition to pharmaceutical drugs, the human gut microbiome can also be altered via diet. This phenomenon has been explored by Peter J. Turnbaugh, Ph.D., assistant professor of microbiology & immunology at Harvard University, Cambridge, Mass.
He explains, “Dietary intake influences the structure and activity of the trillions of microorganisms residing in the human gut.” He adds that even short-term consumption of diets composed entirely of animal or plant products “alters microbial community structure.”
Animal-based diets increase microorganisms including Alistipes, Bilophila and Bacteroides, and reduce the levels of bacteria that metabolize plant components. The changes reflect “trade-offs between carbohydrate and protein fermentation,” he says. His findings also support a link between dietary fat and “the outgrowth of microorganisms capable of triggering inflammatory bowel disease.”
“These results demonstrate that the gut microbiome can rapidly respond to altered diet, potentially facilitating the diversity of human dietary lifestyles,” Turnbaugh said.
Regarding eating disorders, and specifically anorexia, Fetissov and colleagues add that a range of hormonal pathways involved in regulation of appetite and emotion may be involved.
Akio Inui, M.D., Ph.D., of Kobe University School of Medicine, Japan, outlines some of these mechanisms. Many hormonal and metabolic changes occur after prolonged starvation, to conserve energy and protein, he said.
However, anorexia differs from ordinary starvation in an excess of both feeding-stimulatory signaling, led by the neurotransmitter neuropeptide Y, and feeding-inhibitory signalling, led by the hormone corticotropin-releasing factor, “producing the ‘mixed’ signal about satiety and desire to feed.”
“Therapeutic intervention using such receptor antagonists may lead to more successful and targeted psychopharmacological treatment,” Inui said.
First, though, much more work needs to be carried out in this area. The origins of eating disorders are extremely complex and require a great deal of work to disentangle. For example, raised levels of the ClpB protein in eating disorder patients could be a consequence, rather than a cause of their disorder.
The “diagnostically relevant” psychopathological features of eating disorders, such as intense fear of gaining weight or becoming fat, and the undue influence of body weight or shape on self-evaluation, clearly distinguish eating disorder patients from other individuals who may simply have a lower appetite or weight than average.
Tennoune, N. et al. Bacterial ClpB heat-shock protein, an antigen-mimetic of the anorexigenic peptide a-MSH, at the origin of eating disorders. Translational Psychiatry, 7 October 2014 doi:10.1038/nn.3773
David, L. A. et al. Diet rapidly and reproducibly alters the human gut microbiome. Nature, 23 January 2014, doi:10.1038/nature12820
Inui, A. Eating behavior in anorexia nervosa, an excess of both orexigenic and anorexigenic signalling? Molecular Psychiatry, November 2001, Volume 6, Number 6, Pages 620-624