Bulimia nervosa is an
eating disorder characterised by recurrent episodes of
binge eating and associated efforts to purge the ingested calories through self-induced
vomiting,
laxative or
diuretic abuse, fasting or intensive exercise. The aetiopathogenesis and pathophysiology of the disorder are currently unclear.
Biological bases have been proposed repeatedly, based on several lines of evidence: hunger, satiety and food choice are regulated by
neurotransmitters and
neuropeptides, and impairment of eating habits may be related to alterations in the secretion of these chemicals; genetic studies suggest that these
neurotransmitter systems are dysfunctional in individuals with
bulimia nervosa; and the frequent comorbidity of
bulimia nervosa with major depressive and
obsessive-compulsive disorders, conditions in which multiple alterations of brain biochemical functions have been demonstrated. Data in the literature suggest that levels of
noradrenaline (
norepinephrine) and
serotonin (
5-hydroxytryptamine; 5-HT) are lower in individuals with
bulimia nervosa than in healthy controls. Levels of
dopamine are similar to, or lower than, those in controls. After remission of the disorder, noradrenergic function returns to that seen in controls, whereas dopaminergic and serotonergic function rebound to levels higher than in controls. Among the
neuropeptides, alterations in the levels of
neuropeptide Y,
peptide YY,
beta-endorphin,
corticotrophin-releasing
hormone,
somatostatin,
cholecystokinin and
vasopressin have been found in the symptomatic phase of
bulimia nervosa, with a return to levels seen in controls after remission. Pharmacological treatment of
bulimia nervosa that is directed at correction of the neurochemical alterations observed is difficult because of the complexity of the impairments. However, such treatment is necessary and should be continued long after symptomatic remission to ensure reinstitution of cerebral biochemical homeostasis.