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      Revisiting the Compensatory Theory as an explanatory model for relapse in obesity management

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          ABSTRACT

          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.

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          Changes in energy expenditure resulting from altered body weight.

          No current treatment for obesity reliably sustains weight loss, perhaps because compensatory metabolic processes resist the maintenance of the altered body weight. We examined the effects of experimental perturbations of body weight on energy expenditure to determine whether they lead to metabolic changes and whether obese subjects and those who have never been obese respond similarly. We repeatedly measured 24-hour total energy expenditure, resting and nonresting energy expenditure, and the thermic effect of feeding in 18 obese subjects and 23 subjects who had never been obese. The subjects were studied at their usual body weight and after losing 10 to 20 percent of their body weight by underfeeding or gaining 10 percent by overfeeding. Maintenance of a body weight at a level 10 percent or more below the initial weight was associated with a mean (+/- SD) reduction in total energy expenditure of 6 +/- 3 kcal per kilogram of fat-free mass per day in the subjects who had never been obese (P < 0.001) and 8 +/- 5 kcal per kilogram per day in the obese subjects (P < 0.001). Resting energy expenditure and nonresting energy expenditure each decreased 3 to 4 kcal per kilogram of fat-free mass per day in both groups of subjects. Maintenance of body weight at a level 10 percent above the usual weight was associated with an increase in total energy expenditure of 9 +/- 7 kcal per kilogram of fat-free mass per day in the subjects who had never been obese (P < 0.001) and 8 +/- 4 kcal per kilogram per day in the obese subjects (P < 0.001). The thermic effect of feeding and nonresting energy expenditure increased by approximately 1 to 2 and 8 to 9 kcal per kilogram of fat-free mass per day, respectively, after weight gain. These changes in energy expenditure were not related to the degree of adiposity or the sex of the subjects. Maintenance of a reduced or elevated body weight is associated with compensatory changes in energy expenditure, which oppose the maintenance of a body weight that is different from the usual weight. These compensatory changes may account for the poor long-term efficacy of treatments for obesity.
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            Trends in Obesity Among Adults in the United States, 2005 to 2014.

            Between 1980 and 2000, the prevalence of obesity increased significantly among adult men and women in the United States; further significant increases were observed through 2003-2004 for men but not women. Subsequent comparisons of data from 2003-2004 with data through 2011-2012 showed no significant increases for men or women.
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              Obesity: a chronic relapsing progressive disease process. A position statement of the World Obesity Federation

              This paper considers the argument for obesity as a chronic relapsing disease process. Obesity is viewed from an epidemiological model, with an agent affecting the host and producing disease. Food is the primary agent, particularly foods that are high in energy density such as fat, or in sugar-sweetened beverages. An abundance of food, low physical activity and several other environmental factors interact with the genetic susceptibility of the host to produce positive energy balance. The majority of this excess energy is stored as fat in enlarged, and often more numerous fat cells, but some lipid may infiltrate other organs such as the liver (ectopic fat). The enlarged fat cells and ectopic fat produce and secrete a variety of metabolic, hormonal and inflammatory products that produce damage in organs such as the arteries, heart, liver, muscle and pancreas. The magnitude of the obesity and its adverse effects in individuals may relate to the virulence or toxicity of the environment and its interaction with the host. Thus, obesity fits the epidemiological model of a disease process except that the toxic or pathological agent is food rather than a microbe. Reversing obesity will prevent most of its detrimental effects.
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                Author and article information

                Contributors
                Journal
                Am J Clin Nutr
                Am J Clin Nutr
                ajcn
                The American Journal of Clinical Nutrition
                Oxford University Press
                0002-9165
                1938-3207
                November 2020
                16 September 2020
                16 September 2020
                : 112
                : 5
                : 1170-1179
                Affiliations
                Obesity Research Group, Department of Clinical Research and Molecular Medicine, Faculty of Medicine, Norwegian University of Science and Technology , Trondheim, Norway
                Centre for Obesity and Innovation, Clinic of Surgery, St. Olav University Hospital , Trondheim, Norway
                Department of Nutrition Sciences, University of Alabama at Birmingham , Birmingham, AL
                Division of Preventive Medicine, Department of Medicine, University of Alabama at Birmingham , Birmingham, AL
                Department of Nutrition Sciences, University of Alabama at Birmingham , Birmingham, AL
                Department of Nutrition Sciences, University of Alabama at Birmingham , Birmingham, AL
                Author notes
                Address correspondence to CM (E-mail: catia.martins@ 123456ntnu.no ).
                Article
                nqaa243
                10.1093/ajcn/nqaa243
                7657332
                32936896
                3757f15c-9862-4ae8-99ca-0fa1e03d0ace
                © The Author(s) 2020. Published by Oxford University Press on behalf of the American Society for Nutrition.

                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@ 123456oup.com

                History
                : 28 January 2020
                : 04 August 2020
                Page count
                Pages: 10
                Funding
                Funded by: Norwegian University of Science and Technology, DOI 10.13039/100009123;
                Categories
                Narrative Review
                AcademicSubjects/MED00060
                AcademicSubjects/MED00160

                Nutrition & Dietetics
                relapse,metabolic adaptation,hunger,ghrelin,weight loss,weight regain,energy expenditure,resting metabolic rate

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