Brain and gut microbiota disorders in the psychopathology of anorexia nervosa

Abstract

Studies of pathophysiological mechanisms involved in eating disorders (EDs) have intensified over the past several years, revealing their unprecedented and unanticipated complexity. Results from many articles highlight critical aspects in each member of ED family. Notably, anorexia nervosa (AN) is a disorder due to undefined etiology, frequently associated with symptoms of depression, anxiety, obsessive-compulsiveness, accompanied by endocrine alterations, altered immune response, increased inflammation, and dysbiosis of the gut microbiota. Hence, an advanced knowledge of how and why a multisystem involvement exists is of paramount importance to understand the pathogenetic mechanisms of AN. In this review, we describe the change in the brain structure/function focusing on hypothalamic endocrine disorders and the disequilibrium of gut microbiota in AN that might be responsible for the psychopathological complication.

Keywords: anorexia nervosa; eating disorders; gut microbiota; hypothalamic disorders.

Figure 1

HPA in AN. In AN, a stressful condition is established that can generate intestinal dysbiosis. In reverse, stress can stimulate the onset of AN and/or dysbiosis. In any case, a stressful condition acts on HPA by stimulating CRH release. The high level of CRH is responsible for a series of specific symptoms of AN. In particular, the increase in CRH induces decreased food consumption, slowed gastric emptying, and inhibition of hypothalamic secretion of GnRH resulting in ovarian cycle disorder, osteoporosis, muscle wasting, brain atrophy, and kidney damage. Furthermore, the increase in the CRH content is also responsible for a reduction in serotonin (5HT), resulting in depression and altered eating behavior.