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      The Neuroendocrine and Metabolic Outcomes of Bariatric Surgery Depend on Presurgical Control over Eating

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          Abstract

          Background: The outcomes of bariatric surgery are very irregular and mostly unpredictable. The search for variables of predictive value is encouraged to help preventing therapeutic failures. Objective: We aimed to confirm the hypothesis that preexisting eating behaviors could predict neuroendocrine and metabolic outcomes of gastric bypass surgery in morbidly obese subjects. Methods: Twenty-one morbidly obese patients from the Bariatric Surgery Program of our hospital were selected according to the specific inclusion and exclusion criteria for this study. The subjects filled out a validated questionnaire to quantify the “loss-of-control” (LC) dimension of food craving and provided serum samples at the onset of the study and 1 year after gastric bypass surgery. Hematological, metabolic, and hormonal variables were studied by conventional clinical tests and enzyme immunoassays and checked for correlations with LC both before and after surgery. Results: Those patients that had exhibited worse eating control at the beginning of the study experienced a better metabolic response 1 year after surgery in terms of reduction of serum insulin, HOMA1-IR, HOMA2-IR, and vitamin D<sub>1</sub>; all these variables were inversely correlated with presurgical LC. Serum brain-derived neurotrophic factor (BDNF) levels showed the same tendency; in fact, BDNF significantly decreased only in those patients with worse eating control. Conclusions: Problematic eating behaviors may predict a better response of insulin resistance and a specific reduction of serum BDNF in morbidly obese patients after gastric bypass surgery.

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          Most cited references23

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          Evidence that 'food addiction' is a valid phenotype of obesity.

          There is growing evidence of 'food addiction' (FA) in sugar- and fat-bingeing animals. The purpose of this study was to investigate the legitimacy of this disorder in the human condition. It was also our intention to extend the validation of the Yale Food Addiction Scale (YFAS) - the first tool developed to identify individuals with addictive tendencies towards food. Using a sample of obese adults (aged 25-45 years), and a case-control methodology, we focused our assessments on three domains relevant to the characterization of conventional substance-dependence disorders: clinical co-morbidities, psychological risk factors, and abnormal motivation for the addictive substance. Results were strongly supportive of the FA construct and validation of the YFAS. Those who met the diagnostic criteria for FA had a significantly greater co-morbidity with Binge Eating Disorder, depression, and attention-deficit/hyperactivity disorder compared to their age- and weight-equivalent counterparts. Those with FA were also more impulsive and displayed greater emotional reactivity than obese controls. They also displayed greater food cravings and the tendency to 'self-soothe' with food. These findings advance the quest to identify clinically relevant subtypes of obesity that may possess different vulnerabilities to environmental risk factors, and thereby could inform more personalized treatment approaches for those who struggle with overeating and weight gain. Copyright © 2011 Elsevier Ltd. All rights reserved.
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            Similarity between obesity and drug addiction as assessed by neurofunctional imaging: a concept review.

            Overeating in obese individuals shares similarities with the loss of control and compulsive drug taking behavior observed in drug-addicted subjects. The mechanism of these behaviors is not well understood. Our prior studies with positron emission tomography (PET) in drug-addicted subjects documented reductions in striatal dopamine (DA) D2 receptors. In pathologically obese subjects, we found reductions in striatal DA D2 receptors similar to that in drug-addicted subjects. Moreover, DA D2 receptor levels were found to have an inverse relationship to the body mass index of the obese subjects. We postulated that decreased levels of DA D2 receptors predisposed subjects to search for reinforcers; in the case of drug-addicted subjects for the drug and in the case of the obese subjects for food as a means to temporarily compensate for a decreased sensitivity of DA D2 regulated reward circuits. Understanding the mechanism in food intake will help to suggest strategies for the treatment of obesity.
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              Food reward, hyperphagia, and obesity.

              Given the unabated obesity problem, there is increasing appreciation of expressions like "my eyes are bigger than my stomach," and recent studies in rodents and humans suggest that dysregulated brain reward pathways may be contributing not only to drug addiction but also to increased intake of palatable foods and ultimately obesity. After describing recent progress in revealing the neural pathways and mechanisms underlying food reward and the attribution of incentive salience by internal state signals, we analyze the potentially circular relationship between palatable food intake, hyperphagia, and obesity. Are there preexisting individual differences in reward functions at an early age, and could they be responsible for development of obesity later in life? Does repeated exposure to palatable foods set off a cascade of sensitization as in drug and alcohol addiction? Are reward functions altered by secondary effects of the obese state, such as increased signaling through inflammatory, oxidative, and mitochondrial stress pathways? Answering these questions will significantly impact prevention and treatment of obesity and its ensuing comorbidities as well as eating disorders and drug and alcohol addiction.
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                Author and article information

                Journal
                NEN
                Neuroendocrinology
                10.1159/issn.0028-3835
                Neuroendocrinology
                S. Karger AG
                0028-3835
                1423-0194
                2020
                January 2020
                11 July 2019
                : 110
                : 1-2
                : 63-69
                Affiliations
                [_a] aHospital General Universitario de Ciudad Real, Ciudad Real, Spain
                [_b] bUniversidad CEU San Pablo, Alcorcón, Madrid, Spain
                Author notes
                *Luis F. Alguacil, Facultad de Farmacia, Universidad CEU San Pablo, Urb. Montepríncipe, ES–28925 Alcorcón, Madrid (Spain), E-Mail lfalguacil@ceu.es
                Author information
                https://orcid.org/0000-0002-2542-5983
                Article
                500687 Neuroendocrinology 2020;110:63–69
                10.1159/000500687
                31280270
                dcf05298-c0de-423b-a29c-b7bdc6adcdc3
                © 2019 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                : 15 January 2019
                : 01 May 2019
                Page count
                Figures: 1, Tables: 3, Pages: 7
                Categories
                Research Article

                Endocrinology & Diabetes,Neurology,Nutrition & Dietetics,Sexual medicine,Internal medicine,Pharmacology & Pharmaceutical medicine
                Insulin resistance,Brain-derived neurotrophic factor,Food craving,Gastric bypass,Eating control

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