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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ongoing epidemics of obesity is one main health concern of the present time. Overeating in some obese individuals shares similarities with the loss of control and compulsive behavior observed in drug-addicted subjects, suggesting that obesity may involve food addiction. Here, we review the contributions provided by the use of positron emission tomography to the current understanding of the cerebral control of obesity and food intake in humans. The available studies have shown that multiple areas in the brain are involved with the reward properties of food, such as prefrontal, orbitofrontal, somatosensory cortices, insula, thalamus, hypothalamus, amygdala, and others. This review summarizes the current evidence, supporting the concepts that i) regions involved in the somatosensory response to food sight, taste, and smell are activated by palatable foods and may be hyperresponsive in obese individuals, ii) areas controlling executive drive seem to overreact to the anticipation of pleasure during cue exposure, and iii) those involved in cognitive control and inhibitory behavior may be resistant to the perception of reward after food exposure in obese subjects. All of these features may stimulate, for different reasons, ingestion of highly palatable and energy-rich foods. Though these same regions are similarly involved in drug abusers and game-addicted individuals, any direct resemblance may be an oversimplification, especially as the heterogeneities between studies and the prevalent exclusion of sensitive groups still limit a coherent interpretation of the findings. Further work is required to comprehensively tackle the multifaceted phenotype of obesity and identify the role of food dependency in its pathophysiology.
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PMID:Brain PET imaging in obesity and food addiction: current evidence and hypothesis. 2264 99

Compulsive behavior is a debilitating clinical feature of many forms of neuropsychiatric disease, including Tourette syndrome, obsessive-compulsive spectrum disorders, eating disorders, and autism. Although several studies link striatal dysfunction to compulsivity, the pathophysiology remains poorly understood. Here, we show that both constitutive and induced genetic deletion of the gene encoding the melanocortin 4 receptor (MC4R), as well as pharmacologic inhibition of MC4R signaling, normalize compulsive grooming and striatal electrophysiologic impairments in synapse-associated protein 90/postsynaptic density protein 95-associated protein 3 (SAPAP3)-null mice, a model of human obsessive-compulsive disorder. Unexpectedly, genetic deletion of SAPAP3 restores normal weight and metabolic features of MC4R-null mice, a model of human obesity. Our findings offer insights into the pathophysiology and treatment of both compulsive behavior and eating disorders.
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PMID:Double deletion of melanocortin 4 receptors and SAPAP3 corrects compulsive behavior and obesity in mice. 2375

Obesity is a heterogeneous construct that, despite multiple and diverse attempts, has been difficult to treat. One conceptualization gaining media and research attention in recent years is that foods, particularly hyperpalatable (e.g., high-fat, high sugar) ones, may possess addictive qualities. Stress is an important factor in the development of addiction and in addiction relapse, and may contribute to an increased risk for obesity and other metabolic diseases. Uncontrollable stress changes eating patterns and the salience and consumption of hyperpalatable foods; over time, this could lead to changes in allostatic load and trigger neurobiological adaptations that promote increasingly compulsive behavior. This association may be mediated by alterations in the hypothalamic-pituitary-adrenal (HPA) axis, glucose metabolism, insulin sensitivity, and other appetite-related hormones and hypothalamic neuropeptides. At a neurocircuitry level, chronic stress may affect the mesolimbic dopaminergic system and other brain regions involved in stress/motivation circuits. Together, these may synergistically potentiate reward sensitivity, food preference, and the wanting and seeking of hyperpalatable foods, as well as induce metabolic changes that promote weight and body fat mass. Individual differences in susceptibility to obesity and types of stressors may further moderate this process. Understanding the associations and interactions between stress, neurobiological adaptations, and obesity is important in the development of effective prevention and treatment strategies for obesity and related metabolic diseases.
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PMID:Stress and eating behaviors. 2412 46

Obesity is a globally widespread disease. Approximately 35% of world population has the problem of inappropriate body weight due to sedentary lifestyle, excessive food consumption and the lack of physical activity. In the course of many years, several pharmacological anti-obesity drugs have been discovered. Most of them, however, possess severe side effects. Recent findings suggest that disturbed functioning of the reward system can be involved in the development of obesity. The data coming from clinical and animal studies provide new evidence that links excessive food consumption with compulsive behavior that can lead to binge eating disease occurrence. In this review we discuss most commonly used animal models of binge eating such as restriction/refeeding, limited access and stress schedule model, and related to them neurobiological findings as well. We also present new, anti-obesity drugs, which are characterized by central mechanism of action.
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PMID:Binge eating in pre-clinical models. 2593 62

Obesity has proven difficult to treat. Many approaches neglect to address the deep-rooted underlying psychological issues. This paper describes a psychodynamically oriented approach to treating compulsive overeating as an addiction. Common to all addictions is a compulsion to consume a substance or engage in a behavior, a preoccupation with using behavior and rituals, and a lifestyle marked by an inability to manage the behavior and its harmful consequences. The approach represents a shift away from primarily medical models of intervention to integrated models focusing on the psychological underpinnings of obesity. Long-term psychodynamic group psychotherapy is recommended as a primary treatment.
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PMID:A Substance Called Food: Long-Term Psychodynamic Group Treatment for Compulsive Overeating. 2607 5

The changes in eating patterns that have occurred in recent decades are an important cause of obesity. Food intake and energy expenditure are controlled by a complex neural system involving the hypothalamic centers and peripheral satiety system (gastrointestinal and pancreatic hormones). Highly palatable and caloric food disrupts appetite regulation; however, palatable foods induce pleasure and reward. The cafeteria diet is such a palatable diet and has been shown consistently to increase body weight and induce hyperplasia in animal obesity models. Moreover, palatable high-fat foods (such as those of the cafeteria diet) can induce addiction-like deficits in brain reward function and are considered to be an important source of motivation that might drive overeating and contribute to the development of obesity. The mechanism of neural adaptation triggered by palatable foods is similar to those that have been reported for nondrug addictions and long-term drug use. Thus, this review attempts to describe the potential mechanisms that might lead to highly palatable diets, such as the cafeteria diet, triggering addiction, or compulsion through the reward system.
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PMID:The Influence of Palatable Diets in Reward System Activation: A Mini Review. 2708 6

Compulsive eating behavior is a transdiagnostic construct that is characteristic of medical and psychiatric conditions such as forms of obesity and eating disorders. Although feeding research is moving toward a better understanding of the proposed addictive properties of food, the components and the mechanisms contributing to compulsive eating are not yet clearly defined or understood. Current understanding highlights three elements of compulsive behavior as it applies to pathological overeating: (1) habitual overeating; (2) overeating to relieve a negative emotional state; and (3) overeating despite aversive consequences. These elements emerge through mechanisms involving pathological habit formation through an aberrant learning process, the emergence of a negative emotional state, and dysfunctions in behavioral control. Dysfunctions in systems within neurocircuitries that comprise the basal ganglia, the extended amygdala, and the prefrontal cortex result in compulsive eating behaviors. Here, we present evidence to relate compulsive eating behavior and addiction and to characterize their underlying neurobiological mechanisms. A major need to improve understanding of compulsive eating through the integration of complex motivational, emotional, and cognitive constructs is warranted.
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PMID:Pathological Overeating: Emerging Evidence for a Compulsivity Construct. 2792 96

Maternal obesity is known to predispose offspring to metabolic and neurodevelopmental abnormalities. While the mechanisms underlying these phenomena are unclear, high fat diets dramatically alter intestinal microbiota, and gut microbiota can impact physiological function. To determine if maternal diet-induced gut dysbiosis can disrupt offspring neurobehavioral function, we transplanted high fat diet- (HFD) or control low fat diet-associated (CD) gut microbiota to conventionally-housed female mice. Recipient mice were then bred and the behavioral phenotype of male and female offspring was tracked. While maternal behavior was unaffected, neonatal offspring from HFD dams vocalized less upon maternal separation than pups from CD dams. Furthermore, weaned male offspring from HFD dams had significant and selective disruptions in exploratory, cognitive, and stereotypical/compulsive behavior compared to male offspring from CD dams; while female offspring from HFD dams had increases in body weight and adiposity. 16S metagenomic analyses confirmed establishment of divergent microbiota in CD and HFD dams, with alterations in diversity and taxonomic distribution throughout pregnancy and lactation. Likewise, significant alterations in gut microbial diversity and distribution were noted in offspring from HFD dams compared to CD dams, and in males compared to females. Regression analyses of behavioral performance against differentially represented taxa suggest that decreased representation of specific members of the Firmicutes phylum predict behavioral decline in male offspring. Collectively, these data establish that high fat diet-induced maternal dysbiosis is sufficient to disrupt behavioral function in murine offspring in a sex-specific manner. Thus these data reinforce the essential link between maternal diet and neurologic programming in offspring and suggest that intestinal dysbiosis could link unhealthy modern diets to the increased prevalence of neurodevelopmental and childhood disorders.
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PMID:Maternal obese-type gut microbiota differentially impact cognition, anxiety and compulsive behavior in male and female offspring in mice. 2844 94

A major problem in treating obesity is the high rate of relapse to abnormal food-taking habits after maintaining an energy balanced diet. Alterations of eating behavior such as compulsive-like behavior and lack of self-control over food intake play a critical role in relapse. In this study, we used an operant paradigm of food-seeking behavior on two different diet-induced obesity models, a free-choice chocolate-mixture diet and a high-fat diet with face validity for a rapid development of obesity or for unhealthy food regularly consumed in our societies. A reduced operant performance and motivation for the hedonic value of palatable chocolate pellets was revealed in both obesity mouse models. However, only mice exposed to high-fat diet showed an increased compulsive-like behavior in the absence of the reinforcer further characterized by impaired operant learning, enhanced impulsivity and intensified inflexibility. We used principal component analysis to globally identify the specific behaviors responsible for the differences among diet groups. Learning impairment and inflexible behaviors contributed to a first principal component, explaining the largest proportion of the variance in the high-fat diet mice phenotype. Reinforcement, impulsion and compulsion were the main contributors to the second principal component explaining the differences in the chocolate-mixture mice behavioral phenotype. These behaviors were not exclusive of chocolate group because some high-fat individuals showed similar values on this component. These data indicate that extended access to hypercaloric diets differentially modifies operant behavior learning, behavioral flexibility, impulsive-like and compulsive-like behavior, and these effects were dependent on the exposure to each specific diet.
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PMID:Extinction and reinstatement of an operant responding maintained by food in different models of obesity. 2928 13

The overarching goal of video games is to amuse the end-users by means of interactive systems that are now existent across numerous platforms such as personal computer, mobile phones, tablets and game consoles. Player Unknown's Battlegrounds (PUBG) is a multiplayer online game. The addiction of PUBG is soaring worldwide and it has thick user-base. It is suggested that inhuman attitudes such as lack of empathy and war-related sentiments are likely to emerge among children who play aggressive and violent games like PUBG. In 2018, World Health Organisation (WHO) acknowledged online gaming compulsion as a grave mental health problem. Some of the well-known repercussions of playing PUBG video game are eyes strain, exhaustion, headache, obesity, poor quality of sleep, insomnia, withdrawal symptoms (rage and irritability) and even drug abuse owing to compulsive disorder. This game craze is unfortunately triggering world's young population to invest their valuable time, money and effort in a no-return business, and therefore needs urgent measures.
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PMID:Playerunknown's Battlegrounds: Yet Another Internet Gaming Addiction. 3246 76


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