Anorexia nervosa, zinc deficiency and the glutamate system: The ketamine option

Daniel F Hermens; Gabrielle Simcock; Megan Dutton; A P Bouças; Adem T Can; Chris Lilley; Jim Lagopoulos

doi:10.1016/j.pnpbp.2020.109921

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Anorexia nervosa, zinc deficiency and the glutamate system: The ketamine option

Journal article

Open access

Peer reviewed

Anorexia nervosa, zinc deficiency and the glutamate system: The ketamine option

Daniel F Hermens, Gabrielle Simcock, Megan Dutton, A P Bouças, Adem T Can, Chris Lilley and Jim Lagopoulos

Progress in Neuro-Psychopharmacology and Biological Psychiatry, Vol.101, pp.1-7

2020

DOI: https://doi.org/10.1016/j.pnpbp.2020.109921

PMID: 32169564

Appears in Thompson Institute Research Collection

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Abstract

Anorexia nervosa

zinc

glutamate

NMDA receptors

ketamine

Eating disorders

Ketamine

Thompson Institute Special Collection

UniSC Diversity Area - Disability and Inclusion

Anorexia nervosa (AN) is a severe, biological brain disorder with significant medical risks and a tenacious development over time. Unfortunately, few treatments show efficacy in people with AN although numerous therapies including pharmacological have been explored. Zinc deficiency has been implicated in AN and zinc is important in a large range of processes in the brain. In particular, it is an allosteric modulator of NMDA receptors - the maintenance of zinc levels within a normal, narrow range is essential for glutamatergic functioning. Chronic zinc deficiency increases neuronal stores of calcium and reduces direct modulation of NMDA receptors which collectively lead to overactivation and upregulation of NMDA receptors. This may facilitate pathologically high levels of glutamate, calcium influx and subsequent excitotoxicity, which can disrupt synaptogenesis and synaptic plasticity. While studies of zinc supplementation in AN have shown some promise, the efficacy of this treatment is limited. This may be due to AN illness chronicity and the significant changes already made, as well as a reduced potency of zinc to inhibit NMDA receptors in a pathological state. Thus, we propose that the safe (at low doses) yet more potent NMDA receptor antagonist, ketamine, may act to normalise a perturbed glutamatergic system and increase synaptogenesis in the short term. This 'kickstart' via ketamine could then allow zinc supplementation and other forms of treatment to enhance recovery in AN.

Details

Title: Anorexia nervosa, zinc deficiency and the glutamate system: The ketamine option
Authors: Daniel F Hermens (Author) - University of the Sunshine Coast
Gabrielle Simcock (Author) - University of the Sunshine Coast
Megan Dutton (Author) - University of the Sunshine Coast
A P Bouças (Author) - University of the Sunshine Coast
Adem T Can (Author) - University of the Sunshine Coast
Chris Lilley (Author) - University of the Sunshine Coast
Jim Lagopoulos (Author) - University of the Sunshine Coast
Publication details: Progress in Neuro-Psychopharmacology and Biological Psychiatry, Vol.101, pp.1-7
Publisher: Elsevier Inc.
Date published: 2020
DOI: 10.1016/j.pnpbp.2020.109921
ISSN: 0278-5846
PMID: 32169564
Organisation Unit: School of Social Sciences - Legacy; Thompson Institute
Language: English
Record Identifier: 99450947102621
Output Type: Journal article

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