Bulimia nervosa

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april 10, 2026

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april 10, 2026

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"Bulimia nervosa is a serious eating disorder. People with bulimia nervosa are overly concerned with their body’s shape and weight and engage in detrimental behaviors in an attempt to control their body image. Bulimia nervosa is often characterized by a destructive pattern of binging (eating too much unhealthy food) and inappropriate, reactionary behaviors to control one’s weight following these episodes. Binge eating is the rapid consumption of an unusually-large amount of food in a short period of time. Unlike simple overeating, people who binge feel “out of control” during these episodes. This means that one “cannot stop the urge to eat” once it has begun, even after their stomach is full. Binging may “feel good” initially, but it quickly becomes distressing for the person who is absorbed in this behavior. Food is often eaten secretly and quickly. A binge is usually ended only with abdominal discomfort, social interruption or running out of food. When the binge is over, the person with bulimia often feels guilty and will engage in inappropriate behaviors to rid their body of the excess calories that were eaten. Inappropriate behaviors to control one’s weight can include purging. Purging behaviors are potentially dangerous and can consist of a wide variety of actions “to get rid of everything I ate.” This can include self-induced vomiting, the abuse of laxatives, enemas or diuretics (e.g., caffeine). Other behaviors such as “fasting” or restrictive dieting following binge-eating episodes are also common, as well as excessive exercising."

- Bulimia nervosa

• 0 likes• eating-disorders•
"Previously, we identified that a majority of patients with anorexia nervosa (AN) and bulimia nervosa (BN) as well as some control subjects display autoantibodies (autoAbs) reacting with alpha-melanocyte-stimulating hormone (alpha-MSH) or adrenocorticotropic hormone, melanocortin peptides involved in appetite control and the stress response. In this work, we studied the relevance of such autoAbs to AN and BN. In addition to previously identified neuropeptide autoAbs, the current study revealed the presence of autoAbs reacting with oxytocin (OT) or vasopressin (VP) in both patients and controls. Analysis of serum levels of identified autoAbs showed an increase of IgM autoAbs against alpha-MSH, OT, and VP as well as of IgG autoAbs against VP in AN patients when compared with BN patients and controls. Further, we investigated whether levels of these autoAbs correlated with psychological traits characteristic for eating disorders. We found significantly altered correlations between alpha-MSH autoAb levels and the total Eating Disorder Inventory-2 score, as well as most of its subscale dimensions in AN and BN patients vs. controls. Remarkably, these correlations were opposite in AN vs. BN patients. In contrast, levels of autoAbs reacting with adrenocorticotropic hormone, OT, or VP had only few altered correlations with the Eating Disorder Inventory-2 subscale dimensions in AN and BN patients. Thus, our data reveal that core psychobehavioral abnormalities characteristic for eating disorders correlate with the levels of autoAbs against alpha-MSH, suggesting that AN and BN may be associated with autoAb-mediated dysfunctions of primarily the melanocortin system."

- Bulimia nervosa

• 0 likes• eating-disorders•
"With the apparent increase in prevalence of anorexic and bulimic eating disorders, the search for effective treatments for these disorders has been intensified in recent years. In this review the results of psychopharmacological studies of patients with anorexia or bulimia nervosa are presented and analysed. The focus of this review is on controlled studies. Although a variety of psychopharmacological substances has been tested in patients with anorexia nervosa, the outcome of controlled studies has been generally disappointing. A possible differential therapy effect of cyproheptadine needs replication: in one study it enhanced body weight gain in non-bulimic anorexics, while it appeared to hinder weight gain in bulimic anorexics. The issue of prophylaxis of osteoporosis in chronic low-weight anorexics has received increasing attention in recent years, and pharmacological prophylaxis appears indicated in this patient group. The results of psychopharmacological treatment studies of patients with bulimia nervosa have overall been more favourable than those of anorexic patients. Statistically significant effects concerning the reduction of bulimic or depressive symptoms in bulimia nervosa has been demonstrated for tricyclic antidepressants (imipramine, desipramine), serotonergic agents (fluoxetine, d-fenfluramine), non-selective monoamine-oxydase-inhibitors (isocarboxazide, phenelzine) and trazodone. The antibulimic effect appears not to be associated with the antidepressant effect. Theoretical, methodological and practical issues concerning pharmacological treatment of anorexic and bulimic eating disorders are presented and discussed."

- Bulimia nervosa

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"Studies of the role of leptin in patients with anorexia nervosa and bulimia nervosa have conflicted in their data and interpretation. Such differences may be a result of the assay methods used or the way results are compared with those from normal controls. To investigate these possibilities, we analyzed serum leptin levels in anorexic, bulimic, obese, and control individuals, thereby spanning the full range of human body weights, using three frequently employed commercial kits. Kits from Linco (St Louis, MO) and DSL (Webster, TX) employ a radioimmunoassay method, and the R&D Systems kit (Minneapolis, MN) uses an enzyme-linked immunosorbent assay. We found that the three kits provide results that are highly linearly correlated with each other and remarkably linearly related to percent ideal body weight (%IBW) over more than three orders of magnitude (Linco, r = 0.90; R&D, r = 0.87; DSL, r = 0.86). For very low leptin levels, the more sensitive kits from R&D and Linco appeared to give more reliable results. Measurement method does not appear to explain the literature conflicts. We found that patients with anorexia nervosa have serum leptin values that lie above the line extrapolated from the %IBW/leptin curve generated from analysis of all non-anorexic patients. Therefore, in anorexia nervosa, inappropriately high leptin levels for %IBW may contribute to a blunted physiologic response to underweight and consequent resistance to dietary treatment. By contrast, most bulimic patients have leptin levels significantly below those predicted from the same %IBW/leptin curve. The relative leptin deficiency in bulimic subjects may contribute to food-craving behavior. We propose that using the %IBW/ leptin curve can facilitate identification of true pathophysiologic abnormalities in eating-disordered individuals and provide a basis for the design of therapeutic interventions or monitoring of response to treatment."

- Bulimia nervosa

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"Eating disorders, such as anorexia nervosa (AN), bulimia nervosa (BN) and binge eating disorders (BED), are described as abnormal eating habits that usually involve insufficient or excessive food intake. Animal models have been developed that provide insight into certain aspects of eating disorders. Several drugs have been found efficacious in these animal models and some of them have eventually proven useful in the treatment of eating disorders. This review will cover the role of monoaminergic neurotransmitters in eating disorders and their pharmacological manipulations in animal models and humans. Dopamine, 5-HT (serotonin) and noradrenaline in hypothalamic and striatal regions regulate food intake by affecting hunger and satiety and by affecting rewarding and motivational aspects of feeding. Reduced neurotransmission by dopamine, 5-HT and noradrenaline and compensatory changes, at least in dopamine D2 and 5-HT(2C/2A) receptors, have been related to the pathophysiology of AN in humans and animal models. Also, in disorders and animal models of BN and BED, monoaminergic neurotransmission is down-regulated but receptor level changes are different from those seen in AN. A hypofunctional dopamine system or overactive α2-adrenoceptors may contribute to an attenuated response to (palatable) food and result in hedonic binge eating. Evidence for the efficacy of monoaminergic treatments for AN is limited, while more support exists for the treatment of BN or BED with monoaminergic drugs."

- Bulimia nervosa

• 0 likes• eating-disorders•