The genetic and neurobiological etiology of anorexia nervosa

Anorexia nervosa (AN) is a life-threatening eating disorder (ED) characterized by restrictive eating, the pursuit of thinness and an obsessive fear of being fat. The lifetime prevalence of AN is 0.3-1% with morality rates approximately 8-15%, higher than in any other mental illness. Unfortunately, treatment therapies have remained generally unsuccessful. Relapse is common, disordered eating patterns persistent in majority of the cases and as many as 20% remaining chronically ill. Despite the severity and chronicity of the disorder, the etiology of AN is largely unknown. Multiple theories have been developed outlining the biological, psychological and cultural factors contributing to AN pathogenesis. However, there is a growing consensus that understanding the predisposing genetic and neurobiological factors leading to AN is critical in order to improve treatment outcomes. The purpose of this mini-review is to summarize the current evidence pointing to alterations in serotonin (5-HT) and dopamine (DA) function in AN pathology. Disturbances in these neurotransmitter systems may explain the underlying genetic component and common psychiatric traits and comorbid disorders present in AN.