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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Is starvation in anorexia nervosa (AN) or overeating in bulimia nervosa (BN) a form of addiction? Alternatively, why are individuals with BN more vulnerable and individuals with AN protected from substance abuse? Such questions have been generated by recent studies suggesting that there are overlapping neural circuits for foods and drugs of abuse. To determine whether a shared neurobiology contributes to eating disorders and substance abuse, this review focused on imaging studies that investigated response to tastes of food and tasks designed to characterize reward and behavioral inhibition in AN and BN. BN and those with substance abuse disorders may share dopamine D2 receptor-related vulnerabilities, and opposite findings may contribute to "protection" from substance abuse in AN. Moreover, imaging studies provide insights into executive corticostriatal processes related to extraordinary inhibition and self-control in AN and diminished inhibitory self-control in BN that may influence the rewarding aspect of palatable foods and likely other consummatory behaviors. AN and BN tend to have premorbid traits, such as perfectionism and anxiety that make them vulnerable to using extremes of food ingestion, which serve to reduce negative mood states. Dysregulation within and/or between limbic and executive corticostriatal circuits contributes to such symptoms. Limited data support the hypothesis that reward and inhibitory processes may contribute to symptoms in eating disorders and addictive disorders, but little is known about the molecular biology of such mechanisms in terms of shared or independent processes.
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PMID:Does a shared neurobiology for foods and drugs of abuse contribute to extremes of food ingestion in anorexia and bulimia nervosa? 2338 Jul 16

The worldwide obesity epidemic poses an enormous and growing threat to public health. However, the neurobehavioral mechanisms of overeating and obesity are incompletely understood. It has been proposed that addiction-like processes may underlie certain forms of obesity, in particular those associated with binge eating disorder. To investigate the role of addiction-like processes in obesity, we adapted a model of cocaine addiction-like behavior in rats responding for highly palatable food. Here, we tested whether rats responding for highly palatable chocolate Ensure would come to show three criteria of addiction-like behavior, i.e., high motivation, continued seeking despite signaled non-availability and persistence of seeking despite aversive consequences. We also investigated whether exposure to a binge model (a diet consisting of alternating periods of limited food access and access to highly palatable food), promotes the appearance of food addiction-like behavior. Our data show substantial individual differences in control over palatable food seeking and taking, but no distinct subgroup of animals showing addiction-like behavior could be identified. Instead, we observed a wide range extending from low to very high control over palatable food intake. Exposure to the binge model did not affect control over palatable food seeking and taking, however. Animals that showed low control over palatable food intake (i.e., scored high on the three criteria for addiction-like behavior) were less sensitive to devaluation of the food reward and more prone to food-induced reinstatement of extinguished responding, indicating that control over palatable food intake is associated with habitual food intake and vulnerability to relapse. In conclusion, we present an animal model to assess control over food seeking and taking. Since diminished control over food intake is a major factor in the development of obesity, understanding its behavioral and neural underpinnings may facilitate improved management of the obesity epidemic.
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PMID:Low control over palatable food intake in rats is associated with habitual behavior and relapse vulnerability: individual differences. 2405 16

The purpose of this study was to extend existing work that examines the role of cravings in Binge Eating Disorder (BED). The current study uses a case-control design to establish a relationship between cravings and food exposure, and between cravings and food consumption in individuals diagnosed with BED. Twenty-nine females with BED, 40 obese controls, and 50 normal-weight controls were first presented with a neutral cue and completed a food-craving measure. They were then presented with their favourite snack food and completed the craving measure again, after which they were allowed to consume the food. The BED group had significantly higher scores for pre- and post-craving measures, and consumed more food compared to the controls. There was, however, no significant interaction between group and craving scores. Results also showed a positive correlation between food consumption and cravings scores both before and after food exposure for individuals with BED. The findings suggest that the level of cravings prior to food exposure may be sufficient to predict overeating in BED and that treatment may want to target this as a defining feature that differentiates individuals with BED from those who do not binge eat.
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PMID:Cravings and food consumption in Binge Eating Disorder. 2418 39

The diagnostic criteria for the Night Eating Syndrome (NES) published in 2010 require the presence of two core criteria: evening hyperphagia and/or nocturnal awakenings for ingestion of food and three of five diagnostic descriptors. One of the descriptors is as follows: "The belief that one must eat in order to fall asleep". In this study we evaluated whether this conviction is significantly more prominent in obese individuals suffering from insomnia and nocturnal eating, than among obese patients with insomnia who do not eat at night. Ninety-eight obese subjects afflicted by insomnia were included in this study. Eight were affected by NES, 33 by Binge Eating Disorder (BED), and 13 by both BED and NES. Subjects' insomnia and sleep disturbances were assessed using the Insomnia Severity Index and the Sleep Disturbance Questionnaire. The presence of the belief that one must eat at night in order to sleep was evaluated with the question: "Do you need to eat in order to get back to sleep when you wake up at night?" Patients affected by NES and by both BED and NES were convinced that nocturnal food intake was necessary in order to fall back asleep after a night time awakening. The presence of this belief seemed to be a critical factor in identifying the presence of the Night Eating Syndrome among obese subjects suffering from insomnia.
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PMID:Clinical validity of the descriptor. "presence of a belief that one must eat in order to get to sleep" in diagnosing the Night Eating Syndrome. 2436 11

The purpose of this study was to explore how obese women with and without binge eating disorder (BED) experience overeating in relation to the DSM-5 symptoms of addiction. Findings from this study demonstrate that food addiction can occur in obese individuals with and without BED. It is important that health care professionals identify individuals who may require a specific treatment approach that incorporates techniques used in the treatment of addictions.
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PMID:A qualitative study of binge eating and obesity from an addiction perspective. 2436 25

A psychobiological dimension of eating behaviour is proposed, which is anchored at the low end by energy intake that is relatively well matched to energy output and is reflected by a stable body mass index (BMI) in the healthy range. Further along the continuum are increasing degrees of overeating (and BMI) characterized by more severe and more compulsive ingestive behaviours. In light of the many similarities between chronic binge eating and drug abuse, several authorities have adopted the perspective that an apparent dependence on highly palatable food-accompanied by emotional and social distress-can be best conceptualized as an addiction disorder. Therefore, this review also considers the overlapping symptoms and characteristics of binge eating disorder (BED) and models of food addiction, both in preclinical animal studies and in human research. It also presents this work in the context of the modern and "toxic" food environment and therein the ubiquitous triggers for over-consumption. We complete the review by providing evidence that what we have come to call "food addiction" may simply be a more acute and pathologically dense form of BED.
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PMID:From passive overeating to "food addiction": a spectrum of compulsion and severity. 2455 43

Eating pathology in Seasonal Affective Disorder (SAD) may be more severe than hyperphagia during winter. Although research has documented elevated rates of subclinical binge eating in women with SAD, the prevalence and correlates of binge eating disorder (BED) in SAD remain largely uncharacterized. We examined the prevalence and correlates of binge eating, weekly binge eating with distress, and BED as defined by the DSM-IV-TR in SAD. We also tested whether binge eating exhibits a seasonal pattern among individuals with BED. Two samples were combined to form a sample of individuals with SAD (N=112). A third sample included non-depressed adults with clinical (n=12) and subclinical (n=11) BED. All participants completed the Questionnaire of Eating and Weight Patterns-Revised (QEWP-R) and modified Seasonal Pattern Assessment Questionnaire (M-SPAQ). In the SAD sample, 26.5% reported binge eating, 11.6% met criteria for weekly binge eating with distress, and 8.9% met criteria for BED. Atypical symptom severity predicted binge eating and BED. In the BED sample, 30% endorsed seasonal worsening of mood, and 26% reported a winter pattern of binge eating. The spectrum of eating pathology in SAD includes symptoms of BED, which are associated with atypical depression symptoms, but typical depression symptoms.
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PMID:Prevalence and correlates of binge eating in seasonal affective disorder. 2468 Aug 72

Eating disorders are characterized by uncontrolled eating behaviors. The core psychopathology is expressed in a variety of ways: body image distortion, preoccupation with food and weight, fear of weight gain, and so on. Brain-imaging techniques provide many opportunities to study neural circuits related symptoms in eating disorder. The present article focuses studies about functional magnetic resonance imaging (fMRI) of eating disorders. Studies of anorexia nervosa suggest 1) relationship between amygdala activation and fear of weight gain, 2) relationship between prefrontal cortex activity and cognitive flexibility. Studies of bulimic eating disorder (bulimia nervosa, binge eating disorder, and so on) suggest 1) relationship between brain reward system and overeating, 2) relationship between prefrontal cortex activity and impulse control.
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PMID:[Cognitive function in eating disorders]. 2479 94

This study sought to examine risk and onset patterns in anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED). Women with AN (n=71), BN (n=66), BED (n=160) and non-psychiatric controls (n=323) were compared retrospectively on risk factors, symptom onset, and diagnostic migration. Eating disorder groups reported greater risk exposure than non-psychiatric controls. AN and BED differed on premorbid personality/behavioral problems, childhood obesity, and family overeating. Risk factors for BN were shared with AN and BED. Dieting was the most common onset symptom in AN, whereas binge eating was most common in BN and BED. Migration between AN and BED was rare, but more frequent between AN and BN and between BN and BED. AN and BED have distinct risk factors and onset patterns, while BN shares similar risk factors and onset patterns with both AN and BED. Results should inform future classification schemes and prevention programs.
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PMID:Risk factors across the eating disorders. 2510 74

We aimed to determine whether variability in the melanocortin-4 receptor (MC4R) gene, predisposing to hyperphagia and obesity, may also be present in nonobese patients with binge-eating behavior or be related to anthropometric or psychopathological parameters in these patients. The coding region of the MC4R gene was sequenced in nonobese patients with binge-eating behavior diagnosed with bulimia nervosa or binge-eating disorder (n=77); individuals with severe early-onset obesity (n=170); and lean women with anorexia nervosa (n=20). A psychometric evaluation (Eating Disorders Inventory-2 and Symptom Checklist 90 Revised inventories) was carried out for all the patients with eating disorders. In the obesity group, 10 different variants were identified, whereas in the binge-eating patients, only two individuals with bulimia nervosa were found to carry the I251L polymorphism, which did not correlate with weight, BMI, or psychopathological features. We found no evidence that mutations in the MC4R gene are associated with binge-eating behavior in nonobese eating disorder patients.
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PMID:Melanocortin-4 receptor gene variants are not associated with binge-eating behavior in nonobese patients with eating disorders. 2541 36


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