Article

Serotonin function following remission from bulimia nervosa

Harvard University, Cambridge, Massachusetts, United States
Neuropsychopharmacology (Impact Factor: 7.05). 04/2000; 22(3):257-63. DOI: 10.1016/S0893-133X(99)00117-7
Source: PubMed

ABSTRACT

Abnormal serotonergic regulation in bulimia nervosa is thought to contribute to recurrent binge eating, depressed mood, and impulsivity. To follow-up on previous studies showing decreased neuroendocrine responses in symptomatic patients, this study assessed serotonin-mediated prolactin responses in individuals who had remitted from bulimia nervosa. Subjects included 21 women with a history of bulimia nervosa and 21 healthy female controls, as well as an additional comparison group of 19 women with current bulimia nervosa. Placebo-controlled neuroendocrine response studies utilized a single oral dose (60 mg) of the indirect serotonin agonist d,l-fenfluramine. For the bulimia nervosa remitted group, the fenfluramine-stimulated elevation in serum prolactin concentration was not significantly different from the response in healthy controls, but was significantly larger than the response in patients with current bulimia nervosa (p < .01). These findings suggest that diminished serotonergic neuroendocrine responsiveness in bulimia nervosa reflects a state-related abnormality. The results are discussed in relationship to recent reports indicating that some alterations in central nervous system serotonin regulation may persist in symptomatically recovered individuals.

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    • "These changes to 5-HT function may only exist for the duration of the illness. For instance, researchers have shown that in REC-BN patients do not differ from controls or may be significantly higher in response to a 5-HT agonist (Wolfe et al., 2000). These data suggest the possibility that alterations to the 5-HT system may be related to pre-existing personality, change or increase as function of the bulimic symptoms, and resolve with recovery from BN. "
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    ABSTRACT: Serotonergic dysregulation is thought to underlie much of the pathology in bulimia nervosa (BN). The purpose of this review is to expand the serotonergic model by incorporating specific and nonspecific contributions of estrogens to the development and maintenance of bulimic pathology in order to guide research from molecular genetics to novel therapeutics for BN. Special emphasis is given to the organizing theory of general brain arousal which allows for integration of specific and nonspecific effects of these systems on behavioral endpoints such as binge eating or purging as well as arousal states such as fear, novelty seeking, or sex. Regulation of the serotonergic system by estrogens is explored, and genetic, epigenetic, and environmental estrogen effects on bulimic pathology and risk factors are discussed. Genetic and neuroscientific research support this two-system conceptualization of BN with both contributions to the developmental and maintenance of the disorder. Implications of an estrogenic-serotonergic model of BN are discussed as well as guidelines and suggestions for future research and novel therapeutic targets.
    Full-text · Article · Aug 2010 · Clinical psychology review
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    • "For example, we were unable to fully control for nutritionallyrelated and ''illness state'' effects in our bulimic participants. Nutritional status has been shown to be important in neuroendocrine response to 5-HT agonists in BN [e.g, Kaye et al., 1998; Wolfe et al., 2000], and we are unable to determine whether the effects of the À1438G/A polymorphism on 5-HT function would remain significant when symptoms of BN remit following treatment. Further, moderate dieting can alter prolactin response to m-CPP in otherwise healthy women [Cowen et al., 1996], and there is a tendency for prolactin response to m-CPP to normalize with short-term weight gain in anorexia nervosa [Brewerton and Jimerson, 1996]. "
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    ABSTRACT: Separate lines of research suggest that the functional alterations in the serotonin (5-HT) 2A receptor are associated with 5-HT tone, behavioral impulsiveness, and bulimia nervosa (BN). We explored the effect of allelic variations within the 5-HT2A receptor gene promoter polymorphism -1438G/A on trait impulsiveness and serotonin function in women with BN. Participants included women with BN having the A allele (i.e., AA homozygotes and AG heterozygotes, BNA+, N = 21); women with BN but without the A allele (i.e., GG homozygotes, BNGG, N = 12), and normal eater control women having the A allele (NEA+, N = 19) or without the A allele (NEGG; N = 9). The women were assessed for psychopathological tendencies and eating disorder symptoms, and provided blood samples for measurement of serial prolactin responses following oral administration of the post-synaptic partial 5-HT agonist meta-chlorophenylpiperazine (m-CPP). The BNGG group had higher scores than the other groups on self-report measures of non-planning and overall impulsiveness and had blunted prolactin response following m-CPP. The bulimic groups did not differ from each other on current eating symptoms or on frequencies of other Axis I mental disorders. Findings indicate that women with BN who are GG homozygotes on the -1438G/A promoter polymorphism are characterized by increased impulsiveness and lower sensitivity to post-synaptic serotonin activation. These findings implicate the GG genotype in the co-aggregation of impulsive behaviors and alterations of post-synaptic 5-HT functioning in women with BN.
    Full-text · Article · Aug 2005 · American Journal of Medical Genetics Part B Neuropsychiatric Genetics
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    • "Nutritional status has been shown to be important in neuroendocrine response to 5-HT agonists in BN (e.g. Kaye et al. 1998 ; Wolfe et al. 2000), and we are unable to deterimine whether the effects of avoidant PD on 5-HT function would remain significant when symptoms of BN remit following treatment . Furthermore, moderate dieting can alter prolactin response to m-CPP in otherwise healthy women (Cowen et al. 1996), and there is a tendency for prolactin response to m-CPP to normalize with short-term weight gain in anorexia nervosa (Brewerton & Jimerson, 1996). "
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    ABSTRACT: Separate lines of research link lowered serotonin tone to interpersonal submissiveness and bulimia nervosa (BN). We explored the impact of co-morbid avoidant personality disorder (APD), as a proxy for submissiveness, on behavioural inhibition and serotonin function in women with BN. Participants included women with BN with co-morbid APD (BNA +, N = 13); women with BN but without APD (BNA-, N = 23), and control women with neither BN nor APD (N = 23). The women were assessed for psychopathological tendencies and eating disorder symptoms, and participated in a computerized laboratory task that measured behavioural inhibition and disinhibition. Participants also provided blood samples for measurement of serial prolactin responses following oral administration of the partial 5-HT agonist meta-chlorophenylpiperazine (m-CPP). The BNA+ group had higher scores than the other groups on self-report measures of submissiveness, social avoidance, restricted emotional expression, affective instability and self-harming behaviours. Compared with the other groups, the BNA+ group tended to be more inhibited under cues for punishment on the computerized task and to have blunted prolactin response following m-CPP. The bulimic groups did not differ from each other on current eating symptoms or on frequencies of other mental disorders. Findings indicate that women with BN and co-morbid APD may be characterized by interpersonal submissiveness and avoidance, affective instability, self-harm, behavioural inhibition in response to threat and lower sensitivity to serotonergic activation. These findings may indicate common, serotonergic factors, associated with social submissiveness, behavioural inhibition to threat and BN.
    Full-text · Article · Feb 2004 · Psychological Medicine
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