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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

The increase in the incidence of obesity and eating disorders has promoted research aimed at understanding the aetiology of abnormal eating behaviours. Apart from metabolic factors, obesity is caused by overeating. Clinical reports have led to the suggestion that some individuals may develop addictive-like behaviours when consuming palatable foods, and compulsive eating plays a similar dominant role in obesity as compulsive drug taking does in drug addiction. The progress made in the development of treatment strategies for obesity is limited, in part, because the physiological and neurological causes and consequences of compulsive eating behaviour are not clearly understood and cannot readily be studied in human subjects. We have developed experimental approaches that reflect the functioning of the components of eating control, including compulsive food taking in rats. Rats that are given free choice between standard chow and a palatable, chocolate-containing 'Cafeteria Diet' (CD) develop distinct signs of compulsive food taking that appear at an early stage. These include the inability to adapt intake behaviour in periods of limited or bitter-tasting CD access, continued food intake during resting phases and changes in fine structure of feeding (duration, distribution and recurrence of feeding bouts). The model will help examine the neurobiological underpinnings of compulsive food seeking and food taking and provides a possibility to study the effects of novel anti-obesity compounds on compulsive eating and other components of food-taking behaviour in detail. For future use of genetic models, the possibility of a transfer to a mouse was discussed.
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PMID:An animal model of compulsive food-taking behaviour. 1974 Mar 65

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

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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PMID:Food reward, hyperphagia, and obesity. 2141 68

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

The food addiction model of overeating has been proposed to help explain the widespread advancement of obesity over the last 30 years. Parallels in neural substrates and neurochemistry, as well as corresponding motivational and behavioral traits, are increasingly coming to light; however, there are still key differences between the two disorders that must be acknowledged. We critically examine these common and divergent characteristics using the theoretical framework of prominent drug addiction models, investigating the neurobiological underpinnings of both behaviors in an attempt to justify whether classification of obesity and binge eating as an addictive disorder is merited.
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PMID:The neurobiological underpinnings of obesity and binge eating: a rationale for adopting the food addiction model. 2372 9

One of the defining characteristics of the research of Ann E. Kelley was her recognition that the neuroscience underlying basic learning and motivation processes also shed significant light upon mechanisms underlying drug addiction and maladaptive eating patterns. In this review, we examine the parallels that exist in the neural pathways that process both food and drug reward, as determined by recent studies in animal models and human neuroimaging experiments. We discuss contemporary research that suggests that hyperphagia leading to obesity is associated with substantial neurochemical changes in the brain. These findings verify the relevance of reward pathways for promoting consumption of palatable, calorically dense foods, and lead to the important question of whether changes in reward circuitry in response to intake of such foods serve a causal role in the development and maintenance of some cases of obesity. Finally, we discuss the potential value for future studies at the intersection of the obesity epidemic and the neuroscience of motivation, as well as the potential concerns that arise from viewing excessive food intake as an "addiction". We suggest that it might be more useful to focus on overeating that results in frank obesity, and multiple health, interpersonal, and occupational negative consequences as a form of food "abuse".
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PMID:The contribution of brain reward circuits to the obesity epidemic. 2323 85

Elevated glucocorticoid levels and sign tracking (ST) in Pavlovian conditioning are potential biomarkers of compulsive behaviors such as addiction. As overeating is sometimes viewed as a form of addictive behavior, we hypothesized that murine Pavlovian sign trackers would have a greater propensity to overeat and develop obesity. Using a food reward in the classical conditioning paradigm, we show that ST behavior is a robust conditioned response but not a predictor of eating and growth trajectories in mice, thus challenging the view that the development of obesity and drug addiction depend on identical mechanisms. This interpretation was supported by experiments which showed that overweight mice do not display cross-sensitization to an addictive drug (morphine), and conversely, that overweight morphine-sensitized animals do not overconsume a highly rewarding food. Although the rewarding/motivational effects of both food and drugs of abuse are mediated by similar neurochemical mechanisms, obesity and drug addiction represent a summation of other dysfunctional input and output pathways that lead to the emergence of two distinct disorders, each of which would deserve a specific pharmacotherapeutic approach.
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PMID:Pavlovian conditioning and cross-sensitization studies raise challenges to the hypothesis that overeating is an addictive behavior. 2478 Sep 21

Excess consumption of palatable food has been shown to affect reward-related brain regions, and pharmaceutical treatments for drug addiction may also be effective in treating overeating of such foods. The GABA-B agonist baclofen and opioid antagonist naltrexone have both been used to treat addiction, and have been shown to suppress intake of certain foods. The combination of these drugs has shown to be more effective in reducing alcohol consumption than either drug alone. The present study assessed the effects of naltrexone and baclofen, alone and in combination, on intake of foods comprised of various macronutrients. Male Sprague-Dawley rats were given 12-hr daily access to chow and a fat emulsion, sugar-fat emulsion, or a sugar solution for 21 days. Rats were then administered (intraperitoneal) baclofen-naltrexone combinations (0.1 mg/kg naltrexone and 1.0 mg/kg baclofen, 1.0 mg/kg naltrexone and 1.8 mg/kg baclofen), and naltrexone (0.1, 1.0 mg/kg) and baclofen (1.0, 1.8 mg/kg) alone. The high dose of the baclofen-naltrexone combination reduced palatable food intake in both the fat and sugar-fat groups compared with vehicle, without affecting chow consumption in these groups. Naltrexone showed little significant effects on intake of either palatable food or chow. Baclofen also reduced palatable food intake in the fat and fat-sugar groups, but differences were only noted between the low and high dose. The combination of baclofen and naltrexone may be a useful tool in selectively targeting the consumption of high-fat and sugar- and fat-rich foods.
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PMID:Effects of baclofen and naltrexone, alone and in combination, on the consumption of palatable food in male rats. 2506 13


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