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

Although they comprise only a small portion of the neurons in the region, cholinergic interneurons in the dorsal striatum appear to play an important role in the regulation of various appetitive behaviors, in part, through their interactions with mesolimbic dopamine (DA) systems. In this review, we describe studies that suggest that the activity of cholinergic interneurons in the nucleus accumbens (NAc) and cholinergic projections to the ventral tegmental area (VTA) affect feeding behavior. In vivo microdialysis studies in rats have revealed that the cessation of a meal is associated with a rise in acetylcholine (ACh) levels in the NAc. ACh activation will suppress feeding, and this is also associated with an increase in synaptic accumulation of ACh. Further, we discuss how, in addition to their role in the ending of a meal, cholinergic interneurons in the NAc play an integral role in the cessation of drug use. Another cholinergic system involved in different aspects of appetitive behavior is the projection from the pedunculpontine nuclei directly to the VTA. Activation of this system enhances behaviors through activation of the mesolimbic DA system, and antagonism of ACh receptors in the VTA can reduce drug self-administration. Finally, we discuss the role of accumbens ACh in both drug and palatable food withdrawal. Studies reveal that accumbens ACh is increased during withdrawal from several different drugs of abuse (including cocaine, nicotine and morphine). This rise in extracellular levels of ACh, coupled with a decrease in extracellular levels of DA, is believed to contribute to an aversive state, which can manifest as behaviors associated with drug withdrawal. This theory has also been applied to studies of overeating and/or "food addiction," and the findings suggest a similar imbalance in DA/ACh levels, which is associated with behavioral indications of drug-like withdrawal. In summary, cholinergic neurons play an important role in the modulation of both food and drug intake, as well as the aversive aspects of food- and drug-related addictive behaviors.
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PMID:Cholinergic modulation of food and drug satiety and withdrawal. 2246 12

Palatable foods lead to overeating, and it is almost a forgone conclusion that it is also an important contributor to the current obesity epidemic - there is even talk about food addiction. However, the cause-effect relationship between taste and obesity is far from clear. As discussed here, there is substantial evidence for altered taste sensitivity, taste-guided liking and wanting, and neural reward processing in the obese, but it is not clear whether such traits cause obesity or whether obesity secondarily alters these functions. Studies with calorie restriction-induced weight loss and bariatric surgery in humans and animal models suggest that at least some of the obesity-induced alterations are reversible and consequently represent secondary effects of the obese state. Thus, both genetic and non-genetic predisposition and acquired alterations in taste and reward functions appear to work in concert to aggravate palatability-induced hyperphagia. In addition, palatability is typically associated with high energy content, further challenging energy balance regulation. The mechanisms responsible for these alterations induced by the obese state, weight loss, and bariatric surgery, remain largely unexplored. Better understanding would be helpful in designing strategies to promote healthier eating and prevention of obesity and the accompanying chronic disease risks.
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PMID:Modulation of taste responsiveness and food preference by obesity and weight loss. 2252 12

Diets high in saturated fats are linked to health problems and impairments in cognitive function in humans. Recent evidence suggests that exposure to a high-fat diet can impair rats' ability to appropriately inhibit responding to stimuli that are reinforced in some circumstances but not in others. Here, we examined the effects of exposure to a high-fat diet on the context-specific renewal of extinguished responding. Rats first received pairings of a noise stimulus with a food reinforcer. After 14 days of exclusive access to either a high-fat or a matched control diet, rats received nonreinforced presentations (extinction) of the noise in either the same context in which they were trained or a different context. Finally, responding to the noise was evaluated in the original training context in all rats. In control rats, substantial renewal was observed; that is, responding was greater if extinction was conducted in a context different from that of training and testing. Renewal was significantly less robust in rats fed the high-fat diet despite evidence that they were at least as sensitive to context change as control rats. Implications of these results for models of relapse and treatments for phobias, addiction, and overeating are discussed.
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PMID:The effect of high-fat diet on extinction and renewal. 2254 66

Increased availability of tasty, energy-dense foods has been blamed as a major factor in the alarmingly high prevalence of obesity, diabetes, and metabolic disease, even in young age. A heated debate has started as to whether some of these foods should be considered addictive, similar to drugs and alcohol. One of the main arguments for food addiction is the similarity of the neural mechanisms underlying reward generation by foods and drugs. Here, we will discuss how food intake can generate reward and how behavioral and neural reward functions are different in obese subjects. Because most studies simply compare lean and obese subjects, it is not clear whether predisposing differences in reward functions cause overeating and weight gain, or whether repeated exposure or secondary effects of the obese state alter reward functions. While studies in both rodents and humans demonstrate preexisting differences in reward functions in the obese, studies in rodent models using calorie restriction and gastric bypass surgery show that some differences are reversible by weight loss and are therefore secondary to the obese state.
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PMID:Food reward in the obese and after weight loss induced by calorie restriction and bariatric surgery. 2261 27

There is a growing tendency to regard overeating as an addiction, with obesity as its primary symptom. We propose that similar to other addictions, obesity is associated with excessive risk-taking in men, though not in women. To examine this suggestion we conducted two studies, one involving a sample of overweight and normal-weight students, and the other involving obese adults drawn from a dataset of health care clients, and a control sample of normal-weight adults. In both of these studies, we found that overweight and obese men took more risk in a laboratory task than normal-weight men, while overweight and obese women did not differ from normal-weight women in this respect. At the same time, obese women (but not overweight women) displayed higher impulsivity levels than normal-weight women. These findings shed light on the cognitive characteristics of obesity in men, and accent the importance of taking gender into account when developing research paradigms and treatment methods for obesity.
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PMID:Obesity and risk taking. A male phenomenon. 2263 99

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

The relationship between overeating, substance abuse and (behavioral) addiction is controversial. Medically established forms of addiction so far pertain to substance use disorders only. But the preliminary Diagnostic and Statistical Manual for Mental Disorders V (DSM V) suggests replacing the previous category 'Substance-Related Disorders' with 'Addiction and Related Disorders', thus for the first time allowing the diagnosis of behavioral addictions. In the past psychiatrists and psychologists have been reluctant to systematically delineate and classify the term behavioral addiction. However, there is a broad overlap between chemical and behavioral addiction including phenomenological, therapeutic, genetic, and neurobiological aspects. It is of interest to point out that the hormone leptin in itself has a pronounced effect on the reward system, thus suggesting an indirect link between overeating and 'chemical' addiction. Thus, leptin-deficient individuals could be classified as fulfilling criteria for food addiction. In our overview we first review psychological findings in chemical (substance-based) and subsequently in behavioral addiction to analyze the overlap. We discuss the diagnostic validity of food addiction, which in theory can be chemically and/or behaviorally based.
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PMID:Does food addiction exist? A phenomenological discussion based on the psychiatric classification of substance-related disorders and addiction. 2264

Dopamine is widely associated with reward, motivation, and reinforcement learning. Research on dopamine has emphasized its contribution to compulsive behaviors, such as addiction and overeating, with less examination of its potential role in behavioral flexibility in normal, non-pathological states. In the study reviewed here, we investigated the effect of increased tonic dopamine in a two-lever homecage operant paradigm where the relative value of the levers was dynamic, requiring the mice to constantly monitor reward outcome and adapt their behavior. The data were fit to a temporal difference learning model that showed that mice with elevated dopamine exhibited less coupling between reward history and behavioral choice. This work suggests a way to integrate motivational and learning theories of dopamine into a single formal model where tonic dopamine regulates the expression of prior reward learning by controlling the degree to which learned reward values bias behavioral choice. Here I place these results in a broader context of dopamine's role in instrumental learning and suggest a novel hypothesis that tonic dopamine regulates thrift, the degree to which an animal needs to exploit its prior reward learning to maximize return on energy expenditure. Our data suggest that increased dopamine decreases thriftiness, facilitating energy expenditure, and permitting greater exploration. Conversely, this implies that decreased dopamine increases thriftiness, favoring the exploitation of prior reward learning, and diminishing exploration. This perspective provides a different window onto the role dopamine may play in behavioral flexibility and its failure, compulsive behavior.
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PMID:Thorndike's Law 2.0: Dopamine and the Regulation of Thrift. 2290 23

The question of whether (or to what degree) obesity reflects addiction to high-energy foods often narrows to the question of whether the overeating of these foods causes the same long-term neuroadaptations as are identified with the late stages of addiction. Of equal or perhaps greater interest is the question of whether common brain mechanisms mediate the acquisition and development of eating and drug-taking habits. The earliest evidence on this question is rooted in early studies of brain stimulation reward. Lateral hypothalamic electrical stimulation can be reinforcing in some conditions and can motivate feeding in others. That stimulation of the same brain region should be both reinforcing and drive inducing is paradoxical; why should an animal work to induce a drive-like state such as hunger? This is known as the drive-reward paradox. Insights into the substrates of the drive-reward paradox suggest an answer to the controversial question of whether the dopamine system--a system downstream from the stimulated fibers of the lateral hypothalamus--is more critically involved in wanting or in liking of various rewards including food and addictive drugs. That the same brain circuitry is implicated in the motivation for and the reinforcement by both food and addictive drugs extends the argument for a common mechanism underlying compulsive overeating and compulsive drug taking.
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PMID:Dual roles of dopamine in food and drug seeking: the drive-reward paradox. 2304 82

In this paper, we consider the concept of food addiction from a clinical and neuroscientific perspective. Food addiction has an established and growing currency in the context of models of overeating and obesity, and its acceptance shapes debate and research. However, we argue that the evidence for its existence in humans is actually rather limited and, in addition, there are fundamental theoretical difficulties that require consideration. We therefore review food addiction as a phenotypic description, one that is based on overlap between certain eating behaviours and substance dependence. To begin, we consider limitations in the general application of this concept to obesity. We share the widely held view that such a broad perspective is not sustainable and consider a more focused view: that it underlies particular eating patterns, notably binge eating. However, even with this more specific focus, there are still problems. Validation of food addiction at the neurobiological level is absolutely critical, but there are inconsistencies in the evidence from humans suggesting that caution should be exercised in accepting food addiction as a valid concept. We argue the current evidence is preliminary and suggest directions for future work that may provide more useful tests of the concept.
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PMID:Is food addiction a valid and useful concept? 2301 94


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