Alterations in Serotonin Activity and Psychiatric Symptoms After Recovery From Bulimia Nervosa

Department of Psychiatry, University of Pittsburgh School of Medicine, Western Psychiatric Institute and Clinic, PA 15213, USA.
Archives of General Psychiatry (Impact Factor: 14.48). 10/1998; 55(10):927-35. DOI: 10.1001/archpsyc.55.10.927
Source: PubMed


Women with bulimia nervosa (BN) have disturbances of mood and behavior and alterations of monoamine activity when they are bingeing and purging. It is not known whether these alterations are secondary to pathological eating behavior or traits that could contribute to the pathogenesis of BN.
To avoid the confounding effects of pathological eating behavior, we studied 30 women after long-term recovery (>1 year with no bingeing or purging, normal weight, and regular menstrual cycles) from BN. Subjects were compared with 31 healthy volunteer women. We assessed psychiatric diagnoses and symptoms to determine whether there was any persistent disturbance of behavior after recovery. We measured cerebrospinal fluid (CSF) levels of the major metabolites of serotonin (5-hydroxyindoleacetic acid [5-HIAA]), dopamine (homovanillic acid [HVA]), and norepinephrine (3-methoxy-4-hydroxyphenylglycol [MHPG]) as well as hormonal and behavioral response to m-chlorophenylpiperazine (m-CPP), a serotonin-specific agent.
Women who were recovered from BN had mild to moderate negative moods and obsessions with perfectionism and exactness and exaggerated core eating disorder symptoms compared with healthy volunteer women. Recovered BN women had increased levels of CSF 5-HIAA compared with control women (117 +/- 33 vs 73 +/- 15 pmol/mL; P< or =.001) but normal CSF HVA and MHPG concentrations. Recovered BN women had an anxious and disorganized behavioral response to m-CPP but a normal hormonal response.
Persistent serotonergic and behavioral abnormalities after recovery raise the possibility that these psychobiological alterations might be trait-related and contribute to the pathogenesis of BN.

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    • "Associations between serotonin genes and eating disorders, via main and G 9 E effects, align with neurobiological studies demonstrating alterations in the serotonin system in women with eating disorders . Although no longitudinal studies of serotonergic function predicting eating pathology onset exist, studies of recovered patients with AN and BN show increased cerebrospinal fluid (CSF) levels of 5-HIAA (a serotonin metabolite) compared to controls, which may reflect increased serotonin neuronal activity (Kaye, Gwirtsman, George, & Ebert, 1991; Kaye et al., 1998). Neuroimaging data also point to altered serotonin receptor activity (i.e., increased 5-HT1a and 5-HTT binding potential; reduced 5-HT2A binding potential) in several cortical and limbic regions in women recovered from AN and BN, and these serotonin receptor alterations have been associated with co-occurring features of eating disorders (i.e., increased drive for thinness and harm avoidance) (see Table 4). "
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    • "Although exact cause of 5-HT dysfunction in eating disorders is unknown, but several studies presumed that alteration of 5-HT1A and 5-HT2A receptor activities, the 5-HTT (5-HT transporter), and CSF 5-HIAA levels can be involved in patients with eating disorders.15 Several studies confirmed persistence of alterations in serotonin activity,16,17 and also persistence of anxiety, perfectionism, and obsessive behavior18 after recovery from anorexia nervosa and bulimia nervosa. "
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    • "For example, one study found that women in long-term recovery (10 years) from adolescentonset AN had higher rates of anxious and obsessive–compulsive features compared to controls (Holtkamp et al., 2005). A similar pattern emerges for those with a history of BN such that anxiety symptoms are still present after recovery (Kaye et al., 1998; Stein et al., 2002; von Ranson, Kaye, Weltzin, Rao, & Matsunaga, 1999). Finally, in line with the finding that depressive symptoms and disordered eating may share common genetic factors, Silberg and Bulik (2005) found that anxiety also shares a genetic liability with eating disorders. "
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