RESUMEN
Central serotonin pathways modulate eating patterns, and may also participate in the regulation of behavioral impulsivity and mood. Recent studies lend support to the hypothesis that impaired postingestive satiety in bulimia nervosa is associated with reduced hypothalamic serotonergic responsiveness. Serotonin dysregulation has been implicated in major depression, and may play a role in the increased prevalence of depressive episodes in patients with eating disorders. This review compares evidence for alterations in central serotonin regulation in patients with anorexia nervosa, bulimia nervosa, and depression. It is proposed that impaired synaptic transmission in functionally distinct serotonin pathways may result in concurrent or sequential periods of binge eating, behavioral impulsivity, and depression in patients with eating disorders.
Asunto(s)
Anorexia Nerviosa/fisiopatología , Encéfalo/fisiopatología , Bulimia/fisiopatología , Trastorno Depresivo/fisiopatología , Serotonina/fisiología , Humanos , Receptores de Serotonina/fisiologíaRESUMEN
The onset and progression of symptomatology in patients with anorexia nervosa and bulimia nervosa is complex. It is unlikely that dysregulation of a single neurotransmitter system would be sufficient to explain the pathophysiology of these disorders. The studies reviewed above provide preliminary evidence that decreased central serotonin function may contribute to the onset or persistence of binge eating episodes in patients with bulimia nervosa, including low weight anorexic patients with bulimic symptoms. Future clinical studies will benefit from the availability of selective serotonin receptor agonists and antagonists. Longitudinal studies through progressive phases of treatment and clinical remission will be important to clarify the contribution of dietary and body weight changes to results of neurotransmitter studies with eating disorder patients.