-
Endocrinology Aug 2020Obesity is a chronic recurring disease whose prevalence has almost tripled over the past 40 years. In individuals with obesity, there is significant increased risk of... (Review)
Review
Obesity is a chronic recurring disease whose prevalence has almost tripled over the past 40 years. In individuals with obesity, there is significant increased risk of morbidity and mortality, along with decreased quality of life. Increased obesity prevalence results, at least partly, from the increased global food supply that provides ubiquitous access to tasty, energy-dense foods. These hedonic foods and the nonfood cues that through association become reward predictive cues activate brain appetitive control circuits that drive hyperphagia and weight gain by enhancing food-seeking, motivation, and reward. Behavioral therapy (diet and lifestyle modifications) is the recommended initial treatment for obesity, yet it often fails to achieve meaningful weight loss. Furthermore, those who lose weight regain it over time through biological regulation. The need to effectively treat the pathophysiology of obesity thus centers on biologically based approaches such as bariatric surgery and more recently developed drug therapies. This review highlights neurobiological aspects relevant to obesity causation and treatment by emphasizing the common aspects of the feeding-inhibitory effects of multiple signals. We focus on glucagon like peptide-1 receptor (GLP-1R) signaling as a promising obesity treatment target by discussing the activation of intestinal- and brain-derived GLP-1 and GLP-1R expressing central nervous system circuits resulting from normal eating, bariatric surgery, and GLP-1R agonist drug therapy. Given the increased availability of energy-dense foods and frequent encounters with cues that drive hyperphagia, this review also describes how bariatric surgery and GLP-1R agonist therapies influence food reward and the motivational drive to overeat.
Topics: Animals; Bariatric Surgery; Behavior Therapy; Eating; Glucagon-Like Peptide 1; Glucagon-Like Peptide-1 Receptor; Humans; Hyperphagia; Obesity; Receptors, Glucagon; Weight Loss
PubMed: 32516384
DOI: 10.1210/endocr/bqaa093 -
American Journal of Physiology.... Jun 2011Given 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... (Review)
Review
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.
Topics: Animals; Behavior, Addictive; Humans; Hyperphagia; Models, Animal; Neural Pathways; Obesity; Reward; Signal Transduction
PubMed: 21411768
DOI: 10.1152/ajpregu.00028.2011 -
Nutrients Sep 2019With the obesity epidemic being largely attributed to overeating, much research has been aimed at understanding the psychological causes of overeating and using this... (Review)
Review
With the obesity epidemic being largely attributed to overeating, much research has been aimed at understanding the psychological causes of overeating and using this knowledge to develop targeted interventions. Here, we review this literature under a model of food addiction and present evidence according to the fifth edition of the Diagnostic and Statistical Manual (DSM-5) criteria for substance use disorders. We review several innovative treatments related to a food addiction model ranging from cognitive intervention tasks to neuromodulation techniques. We conclude that there is evidence to suggest that, for some individuals, food can induce addictive-type behaviours similar to those seen with other addictive substances. However, with several DSM-5 criteria having limited application to overeating, the term 'food addiction' is likely to apply only in a minority of cases. Nevertheless, research investigating the underlying psychological causes of overeating within the context of food addiction has led to some novel and potentially effective interventions. Understanding the similarities and differences between the addictive characteristics of food and illicit substances should prove fruitful in further developing these interventions.
Topics: Food Addiction; Humans; Hyperphagia
PubMed: 31487791
DOI: 10.3390/nu11092086 -
Nature Reviews. Endocrinology Aug 2017The concept of addiction is loaded with connotations and is often used for its political as much as its medical utility. The scientific case for 'food addiction' as a... (Review)
Review
The concept of addiction is loaded with connotations and is often used for its political as much as its medical utility. The scientific case for 'food addiction' as a clinical phenotype currently rests on its association with generic diagnostic criteria for substance-related disorders being applied to everyday foods and eating-related problems. This has fused the concept of obesity with addiction regardless of whether it fits the definition. The hedonic, or reward, system can account for the ingestion of foods and drugs, confirming that they share neural substrates that differentiate liking and wanting. These are normal processes that are recruited for natural homeostatic behaviours and can explain the phenomenon of hedonic overeating as a consequence of human motivation pushed to extremes by an obesogenic environment. Food addiction constitutes a medicalization of common eating behaviours, taking on the properties of a disease. The use of this medical language has implications for the way in which society views overeating and obesity.
Topics: Animals; Behavior, Addictive; Feeding Behavior; Humans; Hyperphagia; Medicalization; Obesity; Philosophy
PubMed: 28549063
DOI: 10.1038/nrendo.2017.61 -
The Journal of Neuroscience : the... Sep 2010
Review
Topics: Animals; Humans; Hyperphagia; Neurosciences; Translational Research, Biomedical
PubMed: 20810875
DOI: 10.1523/JNEUROSCI.2578-10.2010 -
The Journal of Clinical Endocrinology... Aug 2023
Topics: Humans; Prader-Willi Syndrome; Hyperphagia; Oxytocin; Anxiety
PubMed: 36896885
DOI: 10.1210/clinem/dgad131 -
Psychogeriatrics : the Official Journal... Nov 2019
Topics: Aged, 80 and over; Alzheimer Disease; Antineoplastic Agents, Hormonal; Humans; Hyperphagia; Male; Megestrol; Off-Label Use
PubMed: 30809875
DOI: 10.1111/psyg.12432 -
Eating Behaviors Jan 2008The purpose of this study was to evaluate the Night Eating Questionnaire (NEQ) as a measure of severity of the Night Eating Syndrome (NES). The 14-item NEQ assesses the...
The purpose of this study was to evaluate the Night Eating Questionnaire (NEQ) as a measure of severity of the Night Eating Syndrome (NES). The 14-item NEQ assesses the behavioral and psychological symptoms of NES. The NEQ was evaluated in three samples: 1980 persons who completed the NEQ on the Internet; 81 persons diagnosed with NES; and 194 bariatric surgery candidates. Study 1, using principal components analysis, generated four factors (nocturnal ingestions, evening hyperphagia, morning anorexia, and mood/sleep) and an acceptable alpha (.70). Confirmatory factor analysis suggested that 99% of covariation among factors is accounted for by a higher-order construct. Study 2 found convergent validity of the NEQ with additional measures of night eating, disordered eating, sleep, mood, and stress. Study 3 compared scores from obese bariatric surgery candidates with and without NES and found appropriate discriminant validity of the NEQ. The NEQ appears to be an efficient, valid measure of severity for NES.
Topics: Adult; Affect; Bariatric Surgery; Body Mass Index; Circadian Rhythm; Factor Analysis, Statistical; Feeding Behavior; Female; Humans; Hyperphagia; Internet; Patient Selection; Psychometrics; Reproducibility of Results; Severity of Illness Index; Stress, Psychological; Surveys and Questionnaires; Syndrome
PubMed: 18167324
DOI: 10.1016/j.eatbeh.2007.03.007 -
European Journal of Medical Genetics Jan 2022Prader-Willi Syndrome (PWS) is a multi-system genetically determined neurodevelopmental disorder and the commonest cause of syndromal obesity. The development of... (Meta-Analysis)
Meta-Analysis
Prader-Willi Syndrome (PWS) is a multi-system genetically determined neurodevelopmental disorder and the commonest cause of syndromal obesity. The development of hyperphagia in early childhood is part of the phenotype arising as a result of an impaired neural response to food intake and the inability to regulate food intake in line with energy needs. Severe obesity develops if access to food is not controlled. In this review we evaluate the evidence for increased morbidity and mortality in PWS in order to establish the extent to which it is directly related to the obesity; a consequence of the eating behaviour itself independent of obesity; or associated with other characteristics of the syndrome. Medline, Cochrane, PsychINFO, CINAHL, Web of Science and Scopus databases were used to systematically identify published material on PWS and hyperphagia and syndrome-related morbidity and mortality. One hundred and ten key papers were selected. Data on 500 people with PWS indicated that the average age of death was 21 years and obesity was, as expected, a significant factor. However, the behaviour of hyperphagia itself, independent of obesity, was also important, associated with choking, gastric rupture, and/or respiratory illness. Other syndrome-related factors increased the risk for, and seriousness of, co-morbid illness or accidents. We conclude that improving life-expectancy largely depends on managing the immediate non-obesity and obesity-related consequences of the hyperphagia, through improved support. The development of new treatments that significantly reduce the drive to eat are likely to decrease morbidity and mortality improving quality of life and life expectancy.
Topics: Humans; Hyperphagia; Morbidity; Prader-Willi Syndrome
PubMed: 34748997
DOI: 10.1016/j.ejmg.2021.104379 -
Revue Medicale Suisse Mar 2015Food addiction is a common term used in everyday language by obese patients. Although the neurobiological evidence points to some similarities between addictive... (Review)
Review
Food addiction is a common term used in everyday language by obese patients. Although the neurobiological evidence points to some similarities between addictive mechanisms and the consumption of certain foods, this diagnosis is not yet officially recognized. After a brief history of food addiction compared to other eating disorders, we review the neurobiological processes underlying this concept. A food addiction assessment tool is presented and discussed with the current literature and new classifications of the DSM-5. The concept of food addiction needs to be rethought and requires further research.
Topics: Behavior, Addictive; Feeding Behavior; Humans; Hyperphagia; Nutrition Disorders; Substance-Related Disorders
PubMed: 26027200
DOI: No ID Found