Pathogenesis Of Bulimia Nervosa Research Articles

The role of blocking serotonin 2C receptor by fluoxetine in the treatment of bulimia

Fluoxetine serves as a primary drug for the pharmacological treatment of binge eating. Its activity usually consists in blocking 2C serotonin receptors. This may be considered to be controversial since agonists of this receptor are effective in pharmacological treatment of bulimia. Bulimia episodes occur as a result of a decrease in serotonergic activity in the central nervous system. The mechanism is clinically confirmed. Drugs which increase the activity of the serotonin system in suppressing binge eating proved effective. The anorexigenic effect of drugs which increase the activity of the serotonin system results from the stimulation of serotonin receptors and not from their blocking. Appetite regulation and binge eating are associated with the activity of the dopaminergic and serotonergic systems. Experimental studies conducted so far prove that the increase in dopaminergic activity in the structures of the reward system is caused by stimulation, and not blocking, of serotonin 2C receptors. The anorexigenic effect of proserotonin drugs may also result from the stimulation of type 3 serotonin receptors and possibly 2C on neurons located in the nucleus of solitary tract. The psychopharmacological investigation conducted in this paper revealed the role of 5-HT2C receptors in the pathogenesis of bulimia nervosa and the mechanism of action of fluoxetine in the treatment of binge eating. Based on existing knowledge, the fact that fluoxetine blocks these receptors does not appear to play a significant role in appetite suppression. Due to few experimental works, the problem requires further research.

Abnormal structural brain network and hemisphere-specific changes\u2002in bulimia nervosa

Bulimia nervosa (BN) is characterized by episodic binge eating and purging behaviors. Disrupted neural processes of self-regulation, taste-rewarding, and body image has been associated with the pathogenesis of BN. However, the structural basis for these behavioral and functional deficits remains largely unknown. We employed diffusion tensor imaging and graph theory approaches (including the nodal properties and network-based statistics (NBS)) to characterize the whole-brain structural network of 48 BN and 44 healthy women. For nodal measures of strength, local efficiency, and betweenness centrality, BN patients displayed abnormal increases in multiple left-lateralized nodes within the mesocorticolimbic reward circuitry (including the orbitofrontal cortex, anterior cingulate, insular, medial temporal, and subcortical areas), lateral temporal-occipital cortex, and precuneus, while reduced global efficiency was observed in the right-lateralized nodes within the dorsolateral prefrontal cortex, mesocorticolimbic circuitry, somatosensory and visuospatial system. Several mesocorticolimbic nodes significantly correlated with BN symptoms. At a network level, we found increased left-lateralized connections primarily within the orbitofrontal cortex and its connections to mesocorticolimbic and lateral temporal-occipital areas, but reduced right-lateralized connections across the inferior frontal gyrus and insula, as well as their connections to the lateral temporal cortex. This study revealed BN-related changes in white-matter connections across the prefrontal control, mesocorticolimbic reward, somatosensory and visuospatial systems. The hemispheric-specific change could be an important aspect of the pathophysiology of BN. By characterizing whole-brain structural network changes of BN, our study provides novel evidence for understanding the behavioral and functional deficits of the disorder.

Behavioral Responses to Catecholamine Depletion in Unmedicated, Remitted Subjects with Bulimia Nervosa and Healthy Subjects

BackgroundBulimia nervosa (BN) has been associated with dysregulation of the central catecholaminergic system. An instructive way to investigate the relationship between catecholaminergic function and psychiatric disorder has involved behavioral responses to experimental catecholamine depletion (CD). The purpose of this study was to examine a possible catecholaminergic dysfunction in the pathogenesis of bulimia nervosa. MethodsCD was achieved by oral administration of alpha-methyl-para-tyrosine (AMPT) in 18 remitted female subjects with BN (rBN) and 31 healthy female control subjects. The study design consisted of a randomized, double blind, placebo-controlled crossover, single-site experimental trial. The main outcome measures were bulimic symptoms assessed by the Eating Disorder Examination—Questionnaire. Measures were assessed before and 26, 30, 54, 78, 102 hours after the first AMPT or placebo administration. ResultsIn the experimental environment (controlled environment with a low level of food cues) rBN subjects had a greater increase in eating disorder symptoms during CD compared with healthy control subjects (condition × diagnosis interaction, p < .05). In the experimental environment, rBN subjects experienced fewer bulimic symptoms than in the natural environment (uncontrolled environment concerning food cues) 36 hours after the first AMPT intake (environment × diagnosis interaction, p < .05). Serum prolactin levels increased significantly, and to a comparable degree across groups, after AMPT administration. ConclusionsThis study suggests that rBN is associated with vulnerability for developing eating disorder symptoms in response to reduced catecholamine neurotransmission after CD. The findings support the notion of catecholaminergic dysfunction as a possible trait abnormality in BN.

Cholecystokinin in the Pathogenesis of Bulimia Nervosa

Objective: This review aims to describe the role of the hormone cholecystokinin (CCK) in the pathogenesis of bulimia nervosa (BN), the perpetuation of this illness and the possibility of its use as a target for future therapeutic advances. Methods: Search for cholecystokinin AND bulimia nervosa in Pubmed Central, with no limits, identified 38 articles published up to the present date. Results: It is well established that CCK is altered in the pathogenesis of BN, and that its main role is in the perpetuation of the disorder rather than the cause of it. Discussion: Additional studies will be needed to further understand the mechanisms by which CCK regulates orexigenic pathways. If an orally active, longer acting analogue of CCK could be developed, it would be of significant interest as an appetite suppressant and a key adjuvant in the treatment of patients suffering from BN, particularly in refractory cases.

Altered ghrelin and peptide YY responses to meals in bulimia nervosa

In recent years great advances have been made in our understanding of the peripheral signals produced within the gastrointestinal tract that regulate appetite, such as ghrelin and peptide YY (PYY). While ghrelin elicites hunger signals, PYY elicites satiety. Therefore, alterations in hormone physiology may play a role in the pathogenesis of bulimia nervosa (BN). In this study, we investigated the postprandial profile of ghrelin and PYY levels in patients with BN. Postprandial plasma ghrelin and PYY levels and insulin and glucose responses were measured in 10 patients with BN and 12 control patients in response to a standard 400 kcal meal. Basal ghrelin levels present in BN subjects (265.0 +/- 25.5 pmol/l) were significantly higher than those in healthy controls (199.3 +/- 18.4 pmol/l, P < 0.05), while basal PYY levels were equivalent in BN (14.6 +/- 1.3 pmol/l) and control (12.8 +/- 1.1 pmol/l, P = 0.30) subjects. Postprandial ghrelin suppression (decremental ghrelin area under the curve) was significantly attenuated in BN patients, compared to controls (-96.3 +/- 26.8 pmol/l x 3 h vs. -178.2 +/- 25.7 pmol/l x 3 h, P < 0.05). After a meal, the incremental PYY area under the curve in BN patients was significantly blunted from that observed in controls (9.2 +/- 2.6 pmol/l x 3 h vs. 26.8 +/- 3.2 pmol/l x 3 h, P < 0.01). Glucose and insulin responses to meals were similar between the two groups. BN patients exhibit elevated ghrelin levels before meals with reduced ghrelin suppression after eating. In bulimia nervosa subjects, the rise in PYY levels after meals is also blunted. A gut-hypothalamic pathway involving peripheral signals, such as ghrelin and PYY, may be involved in the pathophysiology of BN.

Which comes first in the pathogenesis of bulimia nervosa: dieting or bingeing?

Clinical experience has indicated that dieting usually precedes the onset of binge eating in the development of bulimia nervosa (BN). However, data confirming this in nonclinical, representative samples are lacking. Using results obtained from the National Women's Study (NWS), we were able to determine the chronological relationship between age of onset of significant dieting (attempting to lose 15 lbs) and onset of bingeing in 85 respondents who met DSM-III-R criteria for BN. These respondents were a subset of over 3,000 female adult U.S. women who completed a random telephone interview (averaging 40 min and including screenings for rape, sexual molestation, aggravated assault, posttraumatic stress disorder [PTSD], and BN). We found that the age of first serious attempt to diet preceded the age of first binge in 46% of cases. There were no significant differences in histories of victimization experiences among the groups. First binge preceded first serious diet in 37% of cases, and these behaviors occurred during the same age in 17% of cases. These data confirm that dieting is more likely to precede binge eating, although binge eating precedes significant dieting in a substantial proportion of bulimic respondents.