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

Overeating in industrial societies is a significant problem, linked to an increasing incidence of overweight and obesity, and the resultant adverse health consequences. We advance the hypothesis that a possible explanation for overeating is that processed foods with high concentrations of sugar and other refined sweeteners, refined carbohydrates, fat, salt, and caffeine are addictive substances. Therefore, many people lose control over their ability to regulate their consumption of such foods. The loss of control over these foods could account for the global epidemic of obesity and other metabolic disorders. We assert that overeating can be described as an addiction to refined foods that conforms to the DSM-IV criteria for substance use disorders. To examine the hypothesis, we relied on experience with self-identified refined foods addicts, as well as critical reading of the literature on obesity, eating behavior, and drug addiction. Reports by self-identified food addicts illustrate behaviors that conform to the 7 DSM-IV criteria for substance use disorders. The literature also supports use of the DSM-IV criteria to describe overeating as a substance use disorder. The observational and empirical data strengthen the hypothesis that certain refined food consumption behaviors meet the criteria for substance use disorders, not unlike tobacco and alcohol. This hypothesis could lead to a new diagnostic category, as well as therapeutic approaches to changing overeating behaviors.
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PMID:Refined food addiction: a classic substance use disorder. 1922 27

In this paper we argue that compulsive overeating has compelling similarities to conventional drug addiction. Our case is based on their comparable clinical features, the biological mechanisms they have in common, and on evidence that the two disorders have a shared diathesis. In making the argument for overeating as an addictive behaviour, it is clearly not appropriate to include all cases of excessive food consumption in this taxon. Nor are we claiming that obesity and addiction are one and the same. However, it is proposed that Binge Eating Disorder (BED) is a phenotype particularly well-suited to such a conceptualization, and that sound clinical and scientific evidence exists to support this viewpoint. We have provided some recommendations for treatment modifications that recognize the similarities between treating drug dependence and compulsive overeating.
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PMID:Compulsive overeating as an addiction disorder. A review of theory and evidence. 1950 Jun 25

Our dramatically changed food environment--since periods in our history when food sources were highly constrained--has presented new challenges for obesity research. For example, these alterations have strongly emphasized the physiological differences between the homeostatic and the hedonic regulation of food intake--the latter being largely responsible for the pronounced increase in obesity in the past few decades. There is also increasing agreement that compulsive overeating shares many parallels with addiction disorders such as drug abuse. These factors have also fostered a renewed interest in identifying individual differences in personality and motivational systems that increase the risk for overeating and weight gain in our population. Reward sensitivity has been the focus of a recent body of compelling research, with evidence favoring two seemingly opposite points of view. On the one hand, studies have found support for a link between low reward sensitivity and obesity, whereas other evidence suggests that a strong appetitive motivation leads to overeating and weight gain. Arguments are provided to reconcile these apparently disparate theories. Finally, the role of impulsivity and its links with symptoms of attention deficit/hyperactivity disorder are discussed, as well as their respective roles in the risk profile for obesity.
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PMID:Psychobiological traits in the risk profile for overeating and weight gain. 1952 80

In North American society, it is all too common for the intake of calories to outweigh an individual's energy demands. Such over-consumption where high-energy foods are readily available undoubtedly contributes to the growing problem of obesity. Palatable food stimulates brain circuits similar to those that mediate behavioral responses to drugs of abuse, which may underlie the continuation of food intake long after energy requirements are met. Among the brain areas implicated in reward and food intake, the lateral hypothalamus (LH) has long been recognized as a common region involved in both. It has been suggested that orexin neurons that are expressed exclusively within and adjacent to the LH comprise a major cellular substrate for the functioning of the LH. Here, we review the idea that the orexin neuropeptides play a key role in the rewarding aspects of food intake through interactions with both peripheral and central signals reflecting current energy stores as well as the classic reward pathway--the mesolimbic dopamine system. Furthermore, a possible heterogeneity of orexin neurons is discussed. Uncovering orexin's role in food reinforcement may provide insight into hyperphagia and obesity. In addition, the idea that food intake and substance abuse involve similar brain circuitry suggests potential for a single treatment aiding both obesity and addiction.
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PMID:Interaction between orexins and the mesolimbic system for overriding satiety. 1954 24

Obesity is a major public health problem and notoriously difficult to treat. There are many parallels between obesity/overeating and addictions to alcohol and drugs. This paper discusses similarities between obesity and addictive disorders, including common personality characteristics, disruptive behavior syndromes, and brain mechanisms. Although there are important differences between overeating and other addictive behaviors, an addiction model of overeating may effectively inform prevention and treatment of obesity.
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PMID:Obesity and its relationship to addictions: is overeating a form of addictive behavior? 1987 65

Dysregulation of the dopamine system is linked to various aberrant behaviors, including addiction, compulsive exercise, and hyperphagia leading to obesity. The goal of the present experiments was to determine how dopamine contributes to the expression of opposing phenotypes, excessive exercise and obesity. We hypothesized that similar alterations in dopamine and dopamine-related gene expression may underly obesity and excessive exercise, as competing traits for central reward pathways. Moreover, we hypothesized that selective breeding for high levels of exercise or obesity may have influenced genetic variation controlling these pathways, manifesting as opposing complex traits. Dopamine, dopamine-related peptide concentrations, and gene expression were evaluated in dorsal striatum (DS) and nucleus accumbens (NA) of mice from lines selectively bred for high rates of wheel running (HR) or obesity (M16), and the non-selected ICR strain from which these lines were derived. HPLC analysis showed significantly greater neurotransmitter concentrations in DS and NA of HR mice compared to M16 and ICR. Microarray analysis showed significant gene expression differences between HR and M16 compared to ICR in both brain areas, with changes revealed throughout the dopamine pathway including D1 and D2 receptors, associated G-proteins (e.g., Golf), and adenylate cyclase (e.g., Adcy5). The results suggest that similar modifications within the dopamine system may contribute to the expression of opposite phenotypes in mice, demonstrating that alterations within central reward pathways can contribute to both obesity and excessive exercise.
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PMID:Dopaminergic dysregulation in mice selectively bred for excessive exercise or obesity. 2015 88

Obesity has become a major health problem and epidemic. However, much of the current debate has been fractious and etiologies of obesity have been attributed to eating behavior or fast food, personality issues, depression, addiction, or genetics. One of the interesting new hypotheses for epidemic obesity is food addiction, which is associated with both substance-related disorder and eating disorder. Accumulating evidences have shown that there are many shared neural and hormonal pathways as well as distinct differences that may help researchers find why certain individuals overeat and become obese. Functional neuroimaging studies have further revealed that good or great smelling, looking, tasting, and reinforcing food has characteristics similar to that of drugs of abuse. Many of the brain changes reported for hedonic eating and obesity are also seen in various forms of addictions. Most importantly, overeating and obesity may have an acquired drive like drug addiction with respect to motivation and incentive; craving, wanting, and liking occur after early and repeated exposures to stimuli. The acquired drive for great food and relative weakness of the satiety signal would cause an imbalance between the drive and hunger/reward centers in the brain and their regulation.
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PMID:Food addiction and obesity: evidence from bench to bedside. 2064 9

Alterations of both central and peripheral feeding regulatory substances occur in the acute phases of anorexia nervosa (AN) and bulimia nervosa (BN) and, generally, reverse after recovery. Some of these alterations are believed not only to sustain the altered eating behavior but also to contribute to certain psychopathological aspects and/or etiopathogenetic processes of eating disorders (EDs). It has been suggested that EDs are clinical conditions linked to reward-related mechanisms leading to a kind of addiction to self-starvation and/or overeating. Most of the feeding regulatory substances, which are dysregulated in EDs, are also implicated in the modulation of reward, emotional, and cognitive functions, thus representing possible links between altered nutritional regulation, motivated behaviors and reward processes. In this chapter, the ED literature dealing with ghrelin, brain-derived neurotrophic factor, opioid peptides, and endocannabinoids, which have prominent effects on eating behavior, body weight, reward, emotional, and cognitive functions, is reviewed in view of the above suggested links. Moreover, the potential therapeutics of new medications developed on the basis of neuroendocrine aberrations found in EDs is also presented.
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PMID:New frontiers in endocrinology of eating disorders. 2124 77

The alarming increase in the incidence of obesity and obesity-associated disorders makes the etiology of obesity a widely studied topic today. As opposed to 'homeostatic feeding', where food intake is restricted to satisfy one's biological needs, the term 'non-homeostatic' feeding refers to eating for pleasure or the trend to over-consume (palatable) food. Overconsumption is considered a crucial factor in the development of obesity. Exaggerated consumption of (palatable) food, coupled to a loss of control over food intake despite awareness of its negative consequences, suggests that overeating may be a form of addiction. At a molecular level, insulin and leptin resistance are hallmarks of obesity. In this review, we specifically address the question how leptin resistance contributes to enhanced craving for (palatable) food. Since dopamine is a key player in the motivation for food, the interconnection between dopamine, leptin and neuropeptides related to feeding will be discussed. Understanding the mechanisms by which these neuropeptidergic systems hijack the homeostatic feeding mechanisms, thus leading to overeating and obesity is the primary aim of this review. The melanocortin system, one of the crucial neuropeptidergic systems modulating feeding behavior will be extensively discussed. The inter-relationship between neuronal populations in the arcuate nucleus and other areas regulating energy homeostasis (lateral hypothalamus, paraventricular nucleus, ventromedial hypothalamus etc.) and reward circuitry (the ventral tegmental area and nucleus accumbens) will be evaluated and scrutinized.
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PMID:Neurobiology of overeating and obesity: the role of melanocortins and beyond. 2129 24

Obesity has become a serious epidemic and one of the leading global health problems. However, much of the current debate has been fractious, and etiologies of obesity have been attributed to eating behavior (i.e. fast food consumption), personality, depression, addiction or genetics. One of the interesting new hypotheses for explaining the development of obesity involves a food addiction model, which suggests that food is not eaten as much for survival as pleasure and that hedonic overeating is relevant to both substance-related disorders and eating disorders. Accumulating evidence has shown that there are a number of shared neural and hormonal pathways as well as distinct differences in these pathways that may help researchers discover why certain individuals continue to overeat despite health and other consequences, and becomes more and more obese. Functional neuroimaging studies have further revealed that pleasant smelling, looking, and tasting food has reinforcing characteristics similar to drugs of abuse. Many of the brain changes reported for hedonic eating and obesity are also seen in various types of addictions. Most importantly, overeating and obesity may have an acquired drive similar to drug addiction with respect to motivation and incentive craving. In both cases, the desire and continued satisfaction occur after early and repeated exposure to stimuli. The acquired drive for eating food and relative weakness of the satiety signal would cause an imbalance between the drive and hunger/reward centers in the brain and their regulation. In the current paper, we first provide a summary of literature on food addition from eight different perspectives, and then we proposed a research paradigm that may allow screening of new pharmacological treatment on the basis of functional magnetic resonance imaging (fMRI).
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PMID:Food addiction and neuroimaging. 2149 80


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