Psychopharmacological Treatment of Anorexia Nervosa and Bulimia

Johnson, Celeste; Stuckey, Marilyn; Mitchell, Janie

doi:10.1097/00005053-198309000-00002

Cited by 35 publications

(12 citation statements)

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“…Levodopa was not found to lead to significant weight gain in patients with AN (Johnson et al, 1983). Levodopa was not found to lead to significant weight gain in patients with AN (Johnson et al, 1983).…”

Section: Adultsmentioning

confidence: 70%

Dopamine in anorexia nervosa

Kontis¹,

Theochari²

2012

Behavioural Pharmacology

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Anorexia nervosa (AN) is a chronic relapsing psychiatric disorder with a largely unknown pathophysiology. Dopamine has been implicated in the pathophysiology of the disorder by preclinical and clinical evidence. Preclinical studies have examined two main characteristics of AN: reduction in food intake (diet restriction) and hyperactivity. Diet restriction has been associated with reduced dopamine levels in the hypothalamus, hippocampus, and the dorsal striatum. Animal hyperactivity following diet restriction has been linked to increased dopamine in the hypothalamus. Increased dopamine in the nucleus accumbens was associated with food administration, but not food expectation. Tyrosine and dopaminergic antagonists normalized anorexia-like behaviors in animal models of AN, but did not restore body weight. Clinical studies on the etiology of AN have produced contradictory findings. Cerebrospinal fluid concentrations of dopamine and its metabolites have been reported to be decreased or normal under conditions of low weight, whereas they tended to normalize when the weight was restored. Plasma and urinary levels of dopamine and its metabolites have been found to be normal, increased, and decreased. Neuroendocrine studies suggest that dopaminergic neurotransmission is increased in AN. However, recent neuroimaging studies lend support to the increase in binding of dopaminergic receptors in the striatum, which favors the opposite theory that intrasynaptic dopamine is indeed decreased. Genetic studies implicate dopamine D2 receptors, the dopamine transporter, and the enzyme COMT. There are promising results with respect to the use of atypical antipsychotics against symptoms of AN beyond weight gain, but further trials are required.

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Section: Adultsmentioning

confidence: 70%

Dopamine in anorexia nervosa

Kontis¹,

Theochari²

2012

Behavioural Pharmacology

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“…As described earlier, there is considerable evidence that patients with AN and BN have disturbances in dopamine, 5‐HT and noradrenaline neurotransmission. Dopamine receptor agonists, including levodopa, have not been found to produce positive effects on weight gain in AN (Johnson et al ., ). As antipsychotics affect dopamine, 5‐HT and noradrenaline systems and affect feeding and body weight, it seems possible that they might also facilitate recovery from AN and BN.…”

Section: Treatment Of An With Monoaminergic Agentsmentioning

confidence: 97%

Pharmacological manipulations in animal models of anorexia and binge eating in relation to humans

Gestel

Kostrzewa

Adan

et al. 2014

British J Pharmacology

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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‐HT2C/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. Linked Articles This article is part of a themed section on Animal Models in Psychiatry Research. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2014.171.issue-20

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“…On top of that, chlorpromazine [2] and other new psychopharmacological drugs like the antidepressant imipramine [4,5] allowed the mentally ill to live in their own homes and to obtain employment [3]. As those medications represented a massive achievement and helped with delusions, anxiety and low mood, they were also tried in patients with EDs, where these symptoms are highly prevalent [6,7].…”

Section: Historical Preliminary Remarksmentioning

confidence: 99%

Psychopharmacological advances in eating disorders

Himmerich

Treasure

2017

Expert Review of Clinical Pharmacology

100

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Anorexia nervosa (AN), bulimia nervosa (BN) and binge eating disorder (BED) are the primary eating disorders (EDs). The only psychopharmacological treatment options for EDs with approval in some countries include fluoxetine for BN and lisdexamfetamine for BED. Given the high comorbidity and genetic correlations with other psychiatric disorders, it seems possible that novel medications for these conditions might also be effective in EDs. Areas covered: The current scientific literature has increased our understanding of how medication could be beneficial for patients with EDs on a molecular, functional and behavioral level. On the basis of theoretical considerations about neurotransmitters, hormones and neural circuits, possible drug targets for the treatment of EDs may include signal molecules and receptors of the self-regulatory system such as serotonin, norepinephrine and glutamate, the hedonic system including opioids, cannabinoids and dopamine and the hypothalamic homeostatic system including histamine, ghrelin, leptin, insulin, and glucagon-like peptide-1. Expert commentary: The latest research points to an involvement of both the immune and the metabolic systems in the pathophysiology of EDs and highlights the importance of the microbiome. Therefore, the next few years may unveil drug targets for EDs not just inside and outside of the brain, but possibly even outside of the human body.

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Psychopharmacological Treatment of Anorexia Nervosa and Bulimia

Cited by 35 publications

References 0 publications

Dopamine in anorexia nervosa

Dopamine in anorexia nervosa

Pharmacological manipulations in animal models of anorexia and binge eating in relation to humans

Psychopharmacological advances in eating disorders

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