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Revisiting the Compensatory Theory as an explanatory model for relapse in obesity management
Weight regain remains the main challenge in obesity management, and its etiology remains elusive. The aim of the present review was to revise the available evidence regarding the “Compensatory Theory,” which is an explanatory model of relapse in obesity treatment, and to propose alternative mechanis...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7657332/ https://www.ncbi.nlm.nih.gov/pubmed/32936896 http://dx.doi.org/10.1093/ajcn/nqaa243 |
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author | Martins, Catia Dutton, Gareth R Hunter, Gary R Gower, Barbara A |
author_facet | Martins, Catia Dutton, Gareth R Hunter, Gary R Gower, Barbara A |
author_sort | Martins, Catia |
collection | PubMed |
description | Weight regain remains the main challenge in obesity management, and its etiology remains elusive. The aim of the present review was to revise the available evidence regarding the “Compensatory Theory,” which is an explanatory model of relapse in obesity treatment, and to propose alternative mechanisms that can contribute to weight regain. It has been proposed, and generally accepted as true, that when a person loses weight the body fights back, with physiological adaptations on both sides of the energy balance equation that try to bring body weight back to its original state: this is the Compensatory Theory. This theory proposes that the increased orexigenic drive to eat and the reduced energy expenditure that follow weight loss are the main drivers of relapse. However, evidence showing a link between these physiological adaptations to weight loss and weight regain is lacking. Here, we propose that the physiological adaptations to weight loss, both at the level of the homeostatic appetite control system and energy expenditure, are in fact a normalization to a lower body weight and not drivers of weight regain. In light of this we explore other potential mechanisms, both physiological and behavioral, that can contribute to the high incidence of relapse in obesity management. More research is needed to clearly ascertain whether the changes in energy expenditure and homeostatic appetite markers seen in reduced-obese individuals are a compensatory mechanism that drives relapse or a normalization towards a lower body weight, and to explore alternative hypotheses that explain relapse in obesity management. |
format | Online Article Text |
id | pubmed-7657332 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-76573322020-11-18 Revisiting the Compensatory Theory as an explanatory model for relapse in obesity management Martins, Catia Dutton, Gareth R Hunter, Gary R Gower, Barbara A Am J Clin Nutr Narrative Review Weight regain remains the main challenge in obesity management, and its etiology remains elusive. The aim of the present review was to revise the available evidence regarding the “Compensatory Theory,” which is an explanatory model of relapse in obesity treatment, and to propose alternative mechanisms that can contribute to weight regain. It has been proposed, and generally accepted as true, that when a person loses weight the body fights back, with physiological adaptations on both sides of the energy balance equation that try to bring body weight back to its original state: this is the Compensatory Theory. This theory proposes that the increased orexigenic drive to eat and the reduced energy expenditure that follow weight loss are the main drivers of relapse. However, evidence showing a link between these physiological adaptations to weight loss and weight regain is lacking. Here, we propose that the physiological adaptations to weight loss, both at the level of the homeostatic appetite control system and energy expenditure, are in fact a normalization to a lower body weight and not drivers of weight regain. In light of this we explore other potential mechanisms, both physiological and behavioral, that can contribute to the high incidence of relapse in obesity management. More research is needed to clearly ascertain whether the changes in energy expenditure and homeostatic appetite markers seen in reduced-obese individuals are a compensatory mechanism that drives relapse or a normalization towards a lower body weight, and to explore alternative hypotheses that explain relapse in obesity management. Oxford University Press 2020-09-16 /pmc/articles/PMC7657332/ /pubmed/32936896 http://dx.doi.org/10.1093/ajcn/nqaa243 Text en © The Author(s) 2020. Published by Oxford University Press on behalf of the American Society for Nutrition. http://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com |
spellingShingle | Narrative Review Martins, Catia Dutton, Gareth R Hunter, Gary R Gower, Barbara A Revisiting the Compensatory Theory as an explanatory model for relapse in obesity management |
title | Revisiting the Compensatory Theory as an explanatory model for relapse in obesity management |
title_full | Revisiting the Compensatory Theory as an explanatory model for relapse in obesity management |
title_fullStr | Revisiting the Compensatory Theory as an explanatory model for relapse in obesity management |
title_full_unstemmed | Revisiting the Compensatory Theory as an explanatory model for relapse in obesity management |
title_short | Revisiting the Compensatory Theory as an explanatory model for relapse in obesity management |
title_sort | revisiting the compensatory theory as an explanatory model for relapse in obesity management |
topic | Narrative Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7657332/ https://www.ncbi.nlm.nih.gov/pubmed/32936896 http://dx.doi.org/10.1093/ajcn/nqaa243 |
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