Anorexia nervosa

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April 10, 2026

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April 10, 2026

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"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."

- Anorexia 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."

- Anorexia 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."

- Anorexia nervosa

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"The aim of this study is to obtain CRF (Corticotropin Releasing Factor) stimulation at a suprahypothalamic level with a psychological stressor and to evaluate its response in anorexia nervosa. CRF plays a major role in the mechanisms underlying the hypothalamo-pituitary-adrenal (HPA) system's response to stress. Animal studies clearly showed that CRF is involved both in the adaptation to a novel environment and the regulation of eating behaviour. CRF's staietogenic effect is mediated via the paraventricular nucleus. Three groups of age matched young women were studied: 8 patients meeting the DSM III-R criteria for anorexia nervosa, 8 underweight healthy volunteers and 10 normal weight volunteers. All subjects were submitted to an auditory stimulation test ("psychosocial stress test") consisting of an intellectual task in which maximal performance is impossible to achieve, the subjects being permanently disturbed by various meaningful noises. Subjects were asked to answer self-rating scales for anxiety and tension prior to and after the test. CRF reactivity was measured by salivary cortisol (RIA). After the test, anorexia nervosa patients exhibit a significantly higher salivary cortisol response compared to the normal weight volunteers. In most of cases, salivary cortisol response was not correlated with the psychological variables. The range of the response is very explosive in two anorectic patients. Our data are consistent with the hyperactivity of the corticotropic axis stress response in anorexia nervosa, but request further investigations to prove that."

- Anorexia nervosa

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"Although many women diet, relatively few develop the extreme weight loss and the clinical symptoms of anorexia nervosa. An underlying biological diathesis and temperament may place someone at risk for developing anorexia nervosa. Certain traits, such as negative affect, behavioral inhibition, compliance, high harm avoidance, and an obsessive concern with symmetry, exactness, and perfectionism, persist after recovery from anorexia nervosa. These persistent symptoms raise the possibility that such traits exist premorbidly and contribute to the pathogenesis of this disorder. Such traits could be associated with increased brain serotonin activity. After recovery, anorexics have increased levels of 5-HIAA, the major metabolite of serotonin, in the cerebrospinal fluid (CSF). Low CSF 5-HIAA levels have been associated with impulsive and aggressive behaviors, which are opposite to those typically found in anorexia nervosa. Increased serotonin activity could contribute to many behavioral symptoms, such as increased satiety. Moreover, recent data suggest that selective serotonin reuptake inhibitor (SSRI)-type medication improves outcome and prevents relapse in people with anorexia nervosa. These theoretical issues have important clinical implications in this era of diminished support for treatment of eating disorders. Anorexia nervosa, like other major psychiatric disorders, has contributory pathophysiology and can benefit from and deserves appropriate treatment resources."

- Anorexia nervosa

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"Premorbid, childhood personality and temperament traits, which are thought to be genetically-determined, are thought to contribute to a vulnerability to develop AN. These include negative emotionality, harm avoidance, perfectionism, inhibition, a drive for thinness, altered interoceptive awareness and obsessive-compulsive personality traits. Individuals with AN seem to have a paradoxical response to eating; they engage in dietary restraint in order to reduce anxiety, because eating stimulates dysphoric mood. Several lines of evidence raise the possibility that altered serotonin (5-HT) function contributes to anxiety in subjects with AN, and starvation is a means of diminishing 5-HT functional activity. Individuals with AN might have a trait towards an imbalance between serotonin and dopamine pathways, which may have a role in an altered interaction between ventral (limbic) neurocircuits, which are important for identifying the emotional significance of stimuli and for generating an affective response to these stimuli, and dorsal (cognitive) neurocircuits that modulate selective attention, planning and effortful regulation of affective states. Recent functional MRI studies support the possibility that individuals with AN might be less able to precisely modulate affective responses to immediately salient stimuli but have increased activity in neurocircuits concerned with planning and consequences. Coding the awareness of pleasant sensation from the taste experience through the anterior insula might be altered in individuals with AN, tipping the balance of striatal processes away from normal, automatic reward responses mediated by the ventral striatum and towards a more 'strategic' approach mediated by the dorsal striatum. Perfectionism and obsessional personality traits could be related to exaggerated cognitive control by the dorsal lateral prefrontal cortex (which may have excessive inhibitory activity and thus dampen information processing through reward pathways) or to compensation for primary deficits in limbic function. When there are deficits in emotional regulation, overdependence upon cognitive rules is a reasonable strategy of self-management. <br. The temperament and personality traits that create a vulnerability to develop AN also persist after recovery. After recovery, these traits tend to have positive aspects, including attention to detail, concern about consequences and a drive to accomplish and succeed."

- Anorexia nervosa

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"Individuals with anorexia nervosa (AN) demonstrate a relentless engagement in behaviors aimed to reduce their weight, which leads to severe underweight status, and occasionally death. Neurobiological abnormalities, as a consequence of starvation are controversial: evidence, however, demonstrates abnormalities in the reward system of patients, and recovered individuals. Despite this, a unifying explanation for reward abnormalities observed in AN and their relevance to symptoms of the illness, remains incompletely understood. Theories explaining reward dysfunction have conventionally focused on anhedonia, describing that patients have an impaired ability to experience reward or pleasure. We review taste reward literature and propose that patients' reduced responses to conventional taste-reward tasks may reflect a fear of weight gain associated with the caloric nature of the tasks, rather than an impaired ability to experience reward. Consistent with this, we propose that patients are capable of 'liking' hedonic taste stimuli (e.g., identifying them), however, they do not 'want' or feel motivated for the stimuli in the same way that healthy controls report. Recent brain imaging data on more complex reward processing tasks provide insights into fronto-striatal neural circuit dysfunction related to altered reward processing in AN that challenges the relevance of anhedonia in explaining reward dysfunction in AN. In this way, altered activity of the anterior cingulate cortex and striatum could explain patients' pathological engagement in behaviors they consider rewarding (e.g., self-starvation) that are otherwise aversive or punishing, to those without the eating disorder. Such evidence for altered patterns of brain activity associated with reward processing tasks in patients and recovered individuals may provide important information about mechanisms underlying symptoms of AN, their future investigation, and the development of treatment approaches."

- Anorexia nervosa

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"Anorexia nervosa is an eating disorder defined by a symptomatic triad, anorexia, emaciation and amenorrhoea. This disease mainly affects young women. Besides these three symptoms, hyperactivity is often associated with anorexia nervosa. Hyperactivity can be considered as a strategy to lose weight, but studies on animal models have shown that it could be explained by more complicated mechanisms. Hyperactivity is defined by an excess of physical activity, which can induce social, professional and family consequences. Hyperactivity can take different forms, most striking is the restless one. Patients with anorexia nervosa are not all hyperactive. Brewerton et al. have compared patients with anorexia nervosa and hyperactivity to patients without hyperactivity. Hyperactive patients are more dissatisfied by their body image, they use less means of purging (laxatives, vomiting), and they start starving earlier than patients without hyperactivity. Many factors can promote the emergence and maintenance of hyperactivity, especially social and cultural requirements, sports environment, family influences. Various models can explain the links between excessive exercise and anorexia nervosa. Epling and Pierce have exposed a behavioural model which shows how hyperactivity can lead to starvation, creating a self-maintained cycle. Eisler and Le Grande have described four models to explain the links between hyperactivity and anorexia nervosa. First, excessive exercise can be considered as a symptom of anorexia nervosa. It can also promote the development of eating disorders. Anorexia nervosa and hyperactivity can be a manifestation of an other psychiatric disorder. At least, hyperactivity can be a variant of anorexia nervosa, which has the same effects, as weight loss. Hyperactivity can also be considered as a kind of obsessive compulsive disorder. Hyperactivity and obsessive compulsive disorders actually share some clinical and neurochemical characteristics. An other model consists in comparing excessive exercise in anorexia nervosa to an addictive behaviour. Self-starvation exacerbated by hyperactivity can be considered as an addiction to endogenous opioid."

- Anorexia nervosa

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"Few studies are carried out in order to estimate the prevalence of high level exercise in the eating disorders. Davis et al. have achieved a prevalence study. The results indicate that a large majority of patients with anorexia nervosa (80,8%) were exercising excessively during an acute phase of the disorder. Research on animals, specially on rats, brings us an interesting model explaining interactions between anorexia nervosa and hyperactivity. With animal models, we have noticed that, when rats with access to a running wheel, are restricted in their food intake, they become excessively active, and paradoxically reduce food consumption. Many searchers have tried to explain this phenomenon. Morse et al. have pointed from animal models that the level of hyperactivity was linked to the severity of food restriction. This result can be explained by a failure of a part of the brain involved in rest and activity regulation. Animal research brings us explanations about the effects of starvation on the endocrine system and the neurotransmitters. Broocks et al. have shown that corticosterone concentration in plasma was synergistically increased by semi starvation and exercise, and the reduction of triiodothyronine by semi starvation was significantly greater in the running wheel group. An other study of Broocks et al. has revealed an increased hypothalamic serotonin metabolism with the combined effect of hyperactivity and food restriction. Tryptophan, an amid acid involved in serotonin synthesis, can also play a role in the maintenance of anorexia nervosa. In starvation conditions, opioid releasing caused by physical exercise would decrease food intake. Exner's study and Adan's one have shown that leptin would be involved in semi starvation induced hyperactivity mechanisms. In spite of animal models can not be entirely generalized to human, they are useful to try to explain biological supports of hyperactivity. Hyperactivity is not only a strategy to lose weight, but also a specific symptom which completes the clinical triad. Animal studies have led to promising results; we might use medicine, such as serotonin reuptake inhibitors or opioid antagonists in the treatment of hyperactivity in anorexia nervosa."

- Anorexia nervosa

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