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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    • "RBN individuals had a history of past binge eating and purging behaviors, but had never been emaciated and had maintained a weight above 85% average body weight (ABW). RAN and RBN subjects must have had: (a) no restrictive eating or other eating disorder related behaviors in the preceding 12 months; (b) a stable weight ( 73.0 kg) between 90% and 120% ABW for at least 12 months (Metropolitan Life Insurance Company, 1959); (c) regular menstrual cycles for the preceding 12 months; and (d) normal plasma b-hydroxybutyric acid (BHBA), glucose, and insulin concentrations during the evaluation phase as previously described (Kaye et al., 1991, 1998; Srinivasagam et al., 1995). CW had no history of an eating disorder or any psychiatric or serious medical or neurological illness, no first-degree relatives with an eating disorder, and had been within normal weight range since menarche. "
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    ABSTRACT: Recent studies show that higher-order appetitive neural circuitry may contribute to restricted eating in anorexia nervosa (AN) and overeating in bulimia nervosa (BN). The purpose of this study was to determine whether sensitization effects might underlie pathologic eating behavior when a taste stimulus is administered repeatedly. Recovered AN (RAN, n=14) and BN (RBN, n=15) subjects were studied in order to avoid the confounding effects of altered nutritional state. Functional magnetic resonance imaging (fMRI) measured higher-order brain response to repeated tastes of sucrose (caloric) and sucralose (non-caloric). To test sensitization, the neuronal response to the first and second administration was compared. RAN patients demonstrated a decreased sensitization to sucrose in contrast to RBN patients who displayed the opposite pattern, increased sensitization to sucrose. However, the latter was not as pronounced as in healthy control women (n=13). While both eating disorder subgroups showed increased sensitization to sucralose, the healthy controls revealed decreased sensitization. These findings could reflect on a neuronal level the high caloric intake of RBN during binges and the low energy intake for RAN. RAN seem to distinguish between high energy and low energy sweet stimuli while RBN do not.
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    • "These preliminary findings await classification, but align with emerging data from neurobiological studies suggesting dopaminergic disturbances in patients recovered from AN, and to some extent, BN (see Table 4). Lower CSF levels of dopamine metabolites, which may reflect decreased neuronal dopamine function, have been found in women recovered from AN-R (but not those recovered from BN or AN-B/P;Kaye et al., 1998Kaye et al., , 1991Kaye, Frank, &amp; McConaha, 1999). Increased binding of dopamine D2/D3 receptors (i.e., reflective of reduced intrasynaptic dopamine or elevated affinity/density of receptors) is present in women recovered from AN and, to a limited degree, in women recovered from BN (see Table 4). "
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    ABSTRACT: Eating disorders are severe psychiatric disorders with a complex etiology involving transactions among sociocultural, psychological, and biological influences. Most research and reviews, however, focus on only one level of analysis. To address this gap, we provide a qualitative review and summary using an integrative biopsychosocial approach. We selected variables for which there were available data using integrative methodologies (e.g., twin studies, gene-environment interactions) and/or data at the biological and behavioral level (e.g., neuroimaging). Factors that met these inclusion criteria were idealization of thinness, negative emotionality, perfectionism, negative urgency, inhibitory control, cognitive inflexibility, serotonin, dopamine, ovarian hormones. Literature searches were conducted using PubMed. Variables were classified as risk factors or correlates of eating disorder diagnoses and disordered eating symptoms using Kraemer et al.'s (1997) criteria. Sociocultural idealization of thinness variables (media exposure, pressures for thinness, thin-ideal internalization, thinness expectancies) and personality traits (negative emotionality, perfectionism, negative urgency) attained 'risk status' for eating disorders and/or disordered eating symptoms. Other factors were identified as correlates of eating pathology or were not classified given limited data. Effect sizes for risk factors and correlates were generally small-to-moderate in magnitude. Multiple biopsychosocial influences are implicated in eating disorders and/or disordered eating symptoms and several can now be considered established risk factors. Data suggest that psychological and environmental factors interact with and influence the expression of genetic risk to cause eating pathology. Additional studies that examine risk variables across multiple levels of analysis and that consider specific transactional processes amongst variables are needed to further elucidate the intersection of sociocultural, psychological, and biological influences on eating disorders. © 2015 Association for Child and Adolescent Mental Health.
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    • "Individuals with AN have been shown in prospective studies to display higher neuroticism than controls before the onset of their illness (Bulik et al., 2006), and individuals with AN, bulimia nervosa (BN) or an eating disorder not otherwise specified (EDNOS) have shown lower emotional stability (Ghaderi & Scott, 2000). Based on retrospective parental reports, Strober (1981) found that childhood affective instability and premorbidly high perfectionism were common in individuals with AN, and higher perfectionism has also been shown to remain after recovery from AN and BN (Kaye et al., 1998; Kaye, Bulik, Thornton, Barbarich, & Masters, 2004). Premorbid or childhood obsessive-compulsive traits, as assessed retrospectively, were frequent among those with eating disorders (Anderluh et al., 2003; Halmi, 1974), and von Ranson et al. (1999) observed that obsessive-compulsive symptoms persist after recovery from BN. "
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