Eating disorders Ketamine Thompson Institute Special Collection UniSC Diversity Area - Disability and Inclusion
Anorexia nervosa is a disorder associated with serious adverse health outcomes, for which there is currently considerable treatment ineffectiveness. Characterised by restrictive eating behaviours, distorted body image perceptions and excessive physical activity, there is growing recognition anorexia nervosa is associated with underlying dysfunction in excitatory and inhibitory neurometabolite metabolism and signalling. This narrative review critically explores the role of N-methyl-D-aspartate receptor-mediated excitatory and inhibitory neurometabolite dysfunction in anorexia nervosa and its associated biomarkers. The existing magnetic resonance spectroscopy literature in anorexia nervosa is reviewed and we outline the brain region-specific neurometabolite changes that have been reported and their connection to anorexia nervosa psychopathology. Considering the proposed role of dysfunctional neurotransmission in anorexia nervosa, the potential utility of zinc supplementation and sub-anaesthetic doses of ketamine in normalising this is discussed with reference to previous research in anorexia nervosa and other neuropsychiatric conditions. The rationale for future research to investigate the combined use of low-dose ketamine and zinc supplementation to potentially extend the therapeutic benefits in anorexia nervosa is subsequently explored and promising biological markers for assessing and potentially predicting treatment response are outlined.
Details
Title
Ketamine and Zinc: Treatment of Anorexia Nervosa Via Dual NMDA Receptor Modulation
Authors
Jules S Mitchell (Corresponding Author) - University of the Sunshine Coast, Queensland, Thompson Institute
Daniel F Hermens (Author) - University of the Sunshine Coast, Queensland, Thompson Institute
Maxwell R Bennett (Author) - The University of Sydney
Adem T Can (Author) - University of the Sunshine Coast, Queensland, Thompson Institute
Jim Lagopoulos (Author) - University of the Sunshine Coast, Queensland, Thompson Institute
Publication details
CNS Drugs, Vol.37(2), pp.159-180
Publisher
Adis International Ltd.
Date published
2023
DOI
10.1007/s40263-022-00984-4
ISSN
1179-1934; 1172-7047
PMID
36681939
Copyright note
This article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, which permits any non-commercial use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc/4.0/.
Grant note
Open Access funding enabled and organized by CAUL and its Member Institutions. This work forms part of the corresponding author’s PhD supported by the Australian Government Research Training Program scholarship. Open access publication was funded by University of the Sunshine Coast.
Organisation Unit
School of Health - Biomedicine; Thompson Institute