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Phobic memory and somatic vulnerabilities in anorexia nervosa: a necessary unity?

Anorexia nervosa is a clinically significant illness that may be associated with permanent medical complications involving almost every organ system. The paper raises a question whether some of them are associated with premorbid vulnerability such as subcellular ion channel abnormalities ('chan...

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Autor principal: Myslobodsky, Michael
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2005
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1260012/
https://www.ncbi.nlm.nih.gov/pubmed/16144551
http://dx.doi.org/10.1186/1744-859X-4-15
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author Myslobodsky, Michael
author_facet Myslobodsky, Michael
author_sort Myslobodsky, Michael
collection PubMed
description Anorexia nervosa is a clinically significant illness that may be associated with permanent medical complications involving almost every organ system. The paper raises a question whether some of them are associated with premorbid vulnerability such as subcellular ion channel abnormalities ('channelopathy') that determines the clinical expression of the bodily response to self-imposed malnutrition. Aberrant channels emerge as a tempting, if rather speculative alternative to the notion of cognitively-driven neurotransmitter modulation deficit in anorexia nervosa. The concept of channelopathies is in keeping with some characteristics of anorexia nervosa, such as a genetically-based predisposition to hypophagia, early onset, cardiac abnormalities, an appetite-enhancing efficacy of some antiepileptic drugs, and others. The purpose of this article is to stimulate further basic research of ion channel biophysics in relation to restrictive anorexia.
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spelling pubmed-12600122005-10-21 Phobic memory and somatic vulnerabilities in anorexia nervosa: a necessary unity? Myslobodsky, Michael Ann Gen Psychiatry Review Anorexia nervosa is a clinically significant illness that may be associated with permanent medical complications involving almost every organ system. The paper raises a question whether some of them are associated with premorbid vulnerability such as subcellular ion channel abnormalities ('channelopathy') that determines the clinical expression of the bodily response to self-imposed malnutrition. Aberrant channels emerge as a tempting, if rather speculative alternative to the notion of cognitively-driven neurotransmitter modulation deficit in anorexia nervosa. The concept of channelopathies is in keeping with some characteristics of anorexia nervosa, such as a genetically-based predisposition to hypophagia, early onset, cardiac abnormalities, an appetite-enhancing efficacy of some antiepileptic drugs, and others. The purpose of this article is to stimulate further basic research of ion channel biophysics in relation to restrictive anorexia. BioMed Central 2005-09-06 /pmc/articles/PMC1260012/ /pubmed/16144551 http://dx.doi.org/10.1186/1744-859X-4-15 Text en Copyright © 2005 Myslobodsky; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Myslobodsky, Michael
Phobic memory and somatic vulnerabilities in anorexia nervosa: a necessary unity?
title Phobic memory and somatic vulnerabilities in anorexia nervosa: a necessary unity?
title_full Phobic memory and somatic vulnerabilities in anorexia nervosa: a necessary unity?
title_fullStr Phobic memory and somatic vulnerabilities in anorexia nervosa: a necessary unity?
title_full_unstemmed Phobic memory and somatic vulnerabilities in anorexia nervosa: a necessary unity?
title_short Phobic memory and somatic vulnerabilities in anorexia nervosa: a necessary unity?
title_sort phobic memory and somatic vulnerabilities in anorexia nervosa: a necessary unity?
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1260012/
https://www.ncbi.nlm.nih.gov/pubmed/16144551
http://dx.doi.org/10.1186/1744-859X-4-15
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