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

An investigation of dietary restraint during adolescence was conducted in two phases. First, two school classes of 12- and 14-year-old girls completed a restraint questionnaire. Second, the functional nature of the restraint scores was assessed in 24 girls from each age group using a procedure previously shown to lead to overeating in restrained adults. A wide distribution of restraint scores was found, with restrained individuals present in both age groups. Restraint was found to be functional, predicting higher food consumption in a taste test after imagining eating highly palatable foods. Hunger ratings were elevated by the imagination procedure, although the extent of this increase was similar for both restrained and unrestrained girls. The girls' body weight index was significantly correlated with degree of restraint. The existence and breakdown of restraint at this young age is regarded with concern, particularly in view of the links between dieting and eating disorders.
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PMID:Dietary restraint in young adolescent girls: a functional analysis. 274 55

The relapse prevention model has recently been applied to the treatment of obesity in order to explain why people stop practising caloric restriction and hence stop losing weight. This study attempted to identify environmental, affective and physiological variables characterizing 'high risk' situations that lead individuals to either overeat or eat unplanned meals, thereby violating the rules of dietary abstinence. Thirty-five individuals (5 male; 30 female) at least 20 percent above ideal body weight were instructed to keep a continuous record of their eating behavior during a 10-week behavioral weight loss program. Each eating episode was entered into the computer as a separate behavioral observation resulting in 3066 usable observations. Log-linear analysis of multidimensional contingency tables was used to fit Markov chains to the data in order to examine whether dietary slips (overeating; unplanned eating) could be predicted from the following antecedents or pairs of antecedents: meal, people, place, mood, and hunger. Antecedents found to be associated with conditional probabilities 25 percent greater than the unconditional probabilities for unplanned meals and overeating (very much; some) are reported. Three basic categories of high-risk situations emerge: positive social interactions, negative emotions, and physiological craving. Individual differences were observed in the unconditional probabilities of the target behaviors, in exposure to high-risk situations, and in impulsive eating in response to meal, people, place, and hunger.
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PMID:Identification of high-risk situations in a behavioral weight loss program: application of the relapse prevention model. 274 34

It was hypothesised that the hunger-enhancing effects of exposure to the sight and smell of palatable food would disinhibit eating in restrained eaters (self-reported dieters). In two experiments exposure to palatable food stimuli led to increases in motivational (hunger) ratings and salivation, and was followed by overeating in restrained subjects compared with the control condition (no food during exposure) and a condition in which nonpreferred food was presented during the exposure phase. The food intake of unrestrained subjects, on the other hand, was reduced following exposure to palatable food in the first experiment. This shows that breakdown of dietary restraint can be induced by food stimuli even when the food does not constitute a preload. Mere exposure to the sight and smell of palatable food is sufficient to precipitate loss of dieting motivation. The effects of exposure on hunger and salivation were, in general, unrelated to food intake or degree of dietary restraint. Therefore, changes in hunger do not appear to directly mediate increased food intake in dieters. Instead, it is tentatively suggested that anxiety resulting from exposure to liked food may play a role both in disinhibiting eating and suppressing salivation in restrained subjects.
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PMID:Breakdown of dietary restraint following mere exposure to food stimuli: interrelationships between restraint, hunger, salivation, and food intake. 278 22

A 17-year-old adolescent had a recurrent episode of somnolence and morbid hunger (Kleine-Levin syndrome) three years after a first attack, from which he had spontaneously recovered. He was treated with 50 mg daily of clomipramine for the somnolence accompanied by disturbance of attention and memory. Under this treatment he developed thymoleptic symptoms with polyphagia, logorrhea and hyperactivity. Placed on a trial dose of at first 600 mg, then 400 mg carbamazepine daily the abnormal findings disappeared within a few days, and there has been no recurrence after some months. It is postulated, based on the observations of this case, that the Kleine-Levin syndrome, presumably a functional hypothalamic disorder, is closely related to the endogenous psychoses.
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PMID:[Kleine-Levin syndrome. The provocation of manic symptoms by an antidepressant and a therapeutic trial of carbamazepine]. 279 6

Results of a number of studies have suggested that hyperinsulinemia and resultant hypoglycemia are part of a sequence of responses that can lead to hunger and to sugar-induced hyperphagia. However, it is argued in the present paper that neither hyperinsulinemia, hypoglycemia, nor any other factor per se is solely responsible for the hyperphagic effect of sugar or any other feeding effect. Also, the present paper emphasizes the need for caution in attempting to evaluate the role of a given factor in sugar-induced hyperphagia, or any other feeding effect, by eliminating the factor of interest. I have reviewed evidence indicating that the elimination of preabsorptive insulin, which may mediate sugar-induced hyperphagia, actually potentiates other factors that may mediate the same effect.
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PMID:Sugar-induced hyperphagia: is hyperinsulinemia, hypoglycemia, or any other factor a "necessary" condition? 305 64

The 'hunger-mimetic' model is a prominent explanatory account of benzodiazepine-induced hyperphagia. A salient feature of food deprivation (hunger) in laboratory animals is 'finicky' eating, or an enhanced reactivity to the palatability of food. If the hunger-mimetic model is correct, a similar finicky pattern of increased eating should be observed both in hungry (food-deprived) rats and in benzodiazepine-treated, hyperphagic rats. Two groups of rats were matched on measures of ad lib baseline intake of both a highly palatable food (sweetened condensed milk) and a food low in palatability (milk adulterated with 37.5 mg% quinine). Subsequently one group was placed on a moderate food deprivation schedule while the second group was maintained on ad lib food but was injected (IP) with 5 mg/kg chlordiazepoxide (CDP) 30 min prior to food presentation tests. Single-bottle tests indicated that while the food deprived animals exhibited a greater augmentation of eating when given the high-palatability food, the animals pretreated with CDP exhibited an indiscriminate elevation of eating across both foods. Similarly, on two-bottle choice tests the food-deprived rats exhibited an enhanced preference for the high-palatability food, whereas the CDP-treated animals did not change from baseline food preference. These results fail to support the hunger-mimetic model of benzodiazepine-induced hyperphagia. Alternative models based on a perseverative, disinhibitory action of benzodiazepines are discussed.
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PMID:Benzodiazepine-induced hyperphagia: a test of the hunger-mimetic model. 317 82

Three experiments were conducted to characterize the time course of amphetamine's effects on food consumption using procedures that would allow both decreases and increases in eating to be evident relative to control levels. In Experiment 1 we measured eating over 12 postinjection hr in rats. Orderly changes in within-day temporal patterns of eating over the 12 days of amphetamine administration suggest the role of conditioned adaptive processes. In Experiment 2, animals were not presented food until 2 hr after drug administration. Initial anorexia and subsequent hyperphagia were produced by repeated administration of amphetamine. Experiment 3 assessed both within-day and over-day changes in body weight and food consumption and showed that in addition to the drug's anorectic effect, amphetamine also reduces body weight via other mechanisms. In interpreting tolerance to anorectic drugs, it is necessary to evaluate such changes in body weight that indicate shifts in hunger that occur over days as well as shifts in within-day temporal patterns of eating that indicate the presence of conditioned adaptive changes. It is proposed that these two adaptive mechanisms account for pharmacodynamic tolerance.
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PMID:Amphetamine's effects on food consumption and body weight: the role of adaptive processes. 339 54

We studied eating behavior in two non-overlapping cohorts of consecutive patients electing gastric bypass surgery for obesity: 100 patients one year after operation and 60 patients three years afterward. Information was obtained through structured interviews and from office charts. Eating behavior was compared with previously collected data on 232 morbidly obese adults and 174 adults of normal weight. Despite an average weight loss of 100 lb (45 kg), there was little evidence of disturbed eating patterns among gastric bypass patients. Significantly fewer gastric bypass patients than morbidly obese comparison subjects reported frequent hunger, overeating, guilt about eating, or food preoccupation. Gastric bypass patients reported less preoccupation with food than did the normal-weight comparison subjects.
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PMID:Eating behavior after gastric bypass surgery for obesity. 361 24

There is increasing evidence that peptides in the brain are important in the control of food intake. Administration of opioid and CCK peptides have elicited hunger and satiety, respectively. To evaluate the interaction of these peptides and their role in the central nervous system, concentrations of met-enkephalin were measured in the hypothalamus of rats following peripheral administration of CCK; in addition, effects of feeding and fasting and obesity were studied. In CCK- vs. saline-injected rats met-enkephalin concentrations were decreased in the paraventricular nucleus (PVN), suprachiasmatic nucleus (SC), supraoptic nucleus (SON), dorsomedial hypothalamus (DMH) and ventromedial hypothalamus (VMH). In fed compared with fasted rats met-enkephalin concentrations were higher in the anterior hypothalamus (AH) and lower in the SC; in obese compared with lean rats, concentrations were higher in the AH, PVN, SC, SON, DMH, lateral hypothalamus and VMH. These results show that peripheral injections of CCK can decrease concentrations of met-enkephalin in the brain and suggest a mechanism by which these peptides may interact to influence behavior. In addition, the findings support the hypothesis that the hyperphagia which is typical of obese rats may be due to increased concentrations of met-enkephalin.
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PMID:Changes in brain met-enkephalin concentrations with peripheral CCK injections in Zucker rats. 371 42

Early studies of hypothalamic function found that damage to the ventromedial hypothalamus (VMH) resulted in marked overeating but inferior performance in food-motivated tasks, leading several investigators to conclude that hyperphagic VMH animals were actually less hungry than normal animals. However, numerous studies have since demonstrated that under certain conditions VMH-damaged animals will work as hard or harder for food, and consume as much or more of an unpalatable diet, than normal animals. A review of these experiments suggests that most of the deficits in food-motivated behavior are the result of two dysfunctions, one obesity induced, and the other a direct result of the lesion that can be greatly alleviated by preoperative adaptation. Explanations of the VMH paradox are also examined, and it is concluded that most are too narrow in scope, generally ignoring the fact that obesity and preoperative adaptation have similar effects on thirst- and some avoidance-motivated behaviors. It is proposed that the impaired performance of VMH-lesioned animals in food-reinforced tasks is largely the result of obesity- and lesion-induced dysfunctions that are not specific to either hunger- or thirst-motivated behaviors.
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PMID:A re-examination of the ventromedial hypothalamic paradox. 699 90


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