[123I] β-CIT and single photon emission computed tomography reveal reduced brain serotonin transporter availability in bulimia nervosa

Background: Impaired serotonin transmission has been implicated in the pathophysiology of eating disorders. We investigated the in vivo availability of brain serotonin transporters and dopamine transporters in bulimia nervosa patients. Methods: Approximately 24 hours after injection of [123I]-2β-carbomethoxy-3β-(4-iodophenyl)tropane ([123I] β-CIT), single photon emission computed tomography scans were performed in 10 medication-free, female bulimic patients and 10 age-matched, healthy females. For quantification of brain serotonin transporter and dopamine transporter availability, a ratio of specific to nonspecific [123I] β-CIT brain binding was used (V3″ = target region − cerebellum/cerebellum). Results: Drug-free bulimia nervosa patients showed a 17% reduced brain serotonin transporter availability in the hypothalamus and thalamus, as compared with healthy control subjects (2.4 ± 0.4 vs. 2.9 ± 0.4, p = .026), and a similar reduction in striatal dopamine transporter availability. There was a negative correlation of illness duration and serotonin transporter availability (r = −.65; p = .042) and a strong positive correlation between hypothalamic/thalamic and striatal V3″ (r = .80, p< .001). Conclusions: This first report of reduced [123I] β-CIT binding in a relatively small group of patients with bulimia nervosa suggests a reduced hypothalamic and thalamic serotonin transporter availability in bulimia, which is more pronounced with longer duration of illness.