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

The periodic components of hunger have been investigated in the spectrum of ultradian and circadian rhythms by means of iterative rhythmometry analysis, a method for resolving harmonic components in time series data. The cyclical scanning has been applied in human subjects with eating disorders associated with leanness, ponderosity and obesity. The sensation of hunger was rhythmometrically resolved into ultradian and circadian components which are peculiar for the group investigated. Harmonic modelling can be used on an individualized basis for group-specific configurations and, on that basis, for unphysiologic patterns. A comparison with the rhythmometric model of healthy subjects may have a practical use in identifying and manipulating behavioural disorders in the propensity to eat.
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PMID:Eating behaviour: investigation on the recursive components of hunger sensation by iterative rhythmometry. 174 6

Causes of obesity include a low resting metabolic rate, environmental factors, family behavior patterns, a poorly developed satiety response and reactive eating due to stress or anxiety. Morbid obesity is characterized by an increased number of adipocytes and a degree of irreversibility. Overeating increases the size of adipocytes; however, once adipocytes achieve their maximal size, proliferation is induced and massive, irreversible obesity may result. A syndrome of restrained eating produced by chronic dieting leads to hunger, frustration and rebound overeating. Treatment may be unsuccessful because of the failure to address specific causes of obesity in individual patients and the use of reducing regimens that are not designed to maintain weight loss. Recognition of the diverse clinical forms of obesity and their different etiologies permits treatment regimens to be more specific, increasing the likelihood of success. Even with this approach, treatment failure is common.
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PMID:Obesity: types and treatments. 172 3

The effectiveness of a new model for the treatment of obesity was studied. This model assumed that obesity was not an eating disorder but a "not eating" disorder. Obese individuals do not have a problem eating, they are overly good at it. Obese individuals have a problem not eating. They experience difficulty or anxiety when they do not eat. The model assumed that removal of anxiety associated with "not eating" would allow obese subjects to lose weight. Wolpe and Lazarus' progressive relaxation techniques were used to decondition anxiety assumed associated with "not eating" in subjects. Inferred anxiety was deconditioned under conditions of "not eating" when imagining hunger, emotions, and cravings. Twenty-five subjects were instructed not to follow a diet after deconditioning but to eat less and be hungry to lose weight. A control group of 10 was instructed to follow a balanced 1000-calorie diet to lose weight. The former group lost a statistically significant amount of weight (7.5% of their body weight) over 11.9 months, while the control group subjects gained 6.5% of their weight. The model appears to be effective for the treatment of some individuals who wish to lose weight, based upon this preliminary study. Replication with other and larger groups is essential.
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PMID:Investigating the impact of deconditioning anxiety on weight loss. 219 Feb 55

During the past 50 years, obesity has increasingly become a problem in Western societies. If low energy output by these individuals (i.e. lack of exercise) cannot be held totally accountable for this problem, then their energy input (i.e. appetite) must play a significant role. There are many elements that give rise to appetite disturbances and their effects on weight gain, weight loss or its maintenance. Previously, it was thought that emotional disturbances led to overeating and overweight; a theory that was supplanted later by the theory that physiological rather than psychological causes were to blame. Today, it is generally believed that appetite is controlled by the interaction of internal (genetic, physiological and chemical) and external (environmental and psychosocial) processes. The role of nutritional and dietary factors in controlling the expression of appetite are particularly important. Thus, appetite (hyperphagia or increased hunger) can be induced by changes in brain neurotransmitters and neuromodulators, altered liver metabolism, adjustments of the nutrient/sensory components of the diet, environmentally applied stressors, the mental and behavioural imposition of dieting and the administration of various psychotropic medications. This review focuses on the role of each of these mechanisms plays in the genesis and maintenance of appetite disturbances; the conclusion of each of these contributions is the same--control of appetite must be achieved in order to treat obesity, and to do this, control must be exerted via regulation of the food supply, cognitive methods, environmental adjustment or by pharmacological tools.
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PMID:Appetite disturbance and the problems of overweight. 219 72

The hypothesis that prandial increases in circulating pancreatic glucagon initiates an important peripheral satiety signal is reviewed. Glucagon administration at the beginning of meals reduces the size of test meals in animals and humans and reduces the size of spontaneous meals in rats. Exogenous glucagon may also interact synergistically with cholecystokinin to inhibit feeding. These appear to be satiety effects because they are behaviorally specific in rats and subjectively specific in humans. Glucagon's pharmacological satiety effect is complemented by compelling evidence for a necessary contribution of endogenous glucagon to the control of meal size: administration of glucagon antibodies increases both test and spontaneous meal size in rats. Under many, but not all, conditions exogenous glucagon's satiety effect appears to originate in the liver and to be relayed to the brain via hepatic vagal afferents. Analysis of the central processing of this signal, however, has barely begun. How glucagon changes are transduced into neural afferent signals also remains an open question. The only hypothesis that has been extensively tested is that stimulation of hepatic glucose production initiates the satiety signal, but this is neither convincingly supported nor clearly rejected by currently available data. It is also not yet clear whether glucagon contributes to some forms of obesity or has potential use as a therapeutic tool in the control of eating disorders. Of the several proposed controls of hunger and satiety, glucagon appears to be one of the most likely to be physiologically relevant. This encourages further analysis of its behavioral characteristics, its neural mechanisms, and its clinical potential.
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PMID:Pancreatic glucagon signals postprandial satiety. 223 10

Palatability is a hypothetical construct which is needed to account for the hedonic aspects of the taste, smell, flavour, texture, etc. of food. Palatability is influenced by innate factors, but can also be modified by learning. Powerful preferences and aversions can be conditioned by the aftereffects of food ingestion. Despite the common assertion that palatability is enhanced in a state of relative food deprivation, there is evidence to suggest that hunger and palatability act largely independently to determine intake. Accordingly a distinction should be made between the pleasantness of the taste of food (influenced by palatability) and the pleasantness of ingesting that food (influenced by hunger/satiety). Increased palatability appears to be at least part of the explanation of why certain diets promote hyperphagia and obesity. However, the postingestive effects which contribute to the greater palatability of such diets remain to be identified.
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PMID:Why a palatability construct is needed. 236 10

Low-dose human chorionic gonadotrophin (HCG) combined with a severe diet remains a popular treatment for obesity, despite equivocal evidence of its effectiveness. In a double-blind, placebo-controlled study, the effects of HCG on weight loss were compared with placebo injections. Forty obese women (body mass index greater than 30 kg/m2) were placed on the same diet supplying 5,000 kJ per day and received daily intramuscular injections of saline or HCG, 6 days a week for 6 weeks. A psychological profile, hunger level, body circumferences, a fasting blood sample and food records were obtained at the start and end of the study, while body weight was measured weekly. Subjects receiving HCG injections showed no advantages over those on placebo in respect of any of the variables recorded. Furthermore, weight loss on our diet was similar to that on severely restricted intake. We conclude that there is no rationale for the use of HCG injections in the treatment of obesity.
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PMID:Human chorionic gonadotrophin and weight loss. A double-blind, placebo-controlled trial. 240 6

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

The effects of preloads, deprivation, and palatability on the eating behavior of non-dieting lean and obese subjects were studied during laboratory meals, using small solid food units (SFUs) to measure the rate of ingestion over the time-course of the meals. In both weight groups, rate of intake decreased from the beginning to the end of meals. The smaller the preloads and the longer the deprivation interval, the faster subjects ate at the beginning of meals and the higher their hunger ratings were. The longest deprivation interval also increased palatability ratings, meal length, and the total amount that subjects ate. Increasing the palatability of the food increased the rate of intake at the beginning of meals, meal length, and the amount of food that subjects ate. Obese subjects were more sensitive to palatability and less responsive to deprivation than lean subjects. For example, while lean subjects became less discriminating about the palatability of the food at the beginning of meals as deprivation increased, obese subjects did not. The satiation mechanism of obese subjects was also different from lean subjects. For example, obese subjects overate after preloads while lean subjects underate compared to their baselines.
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PMID:Responses of lean and obese subjects to preloads, deprivation, and palatability. 278 66

Of the many factors that influence food intake, there is strong evidence that opioid and CCK peptides, which stimulate feeding and elicit satiety, respectively, are important components that may act in concert to regulate energy balance. Cholecystokinin peptides have been isolated in both the brain and gastrointestinal tract, and changes in concentration in the brain and in plasma have been shown to vary with feeding. Peripherally injected CCK has been shown to elicit satiety in many species, including humans, an effect that may be mediated in the CNS via the vagus. In several species, most notably the sheep, direct injection into the CSF potently decreases food intake. Questions remaining regarding the role of CCK peptides in eliciting satiety include the sites and mechanisms of action. It is unknown whether CCK acts directly on receptors, indirectly on some other parameter, or as a neurotransmitter. Although opioid peptides have also been localized in portions of both the periphery and brain, a specific physiological role for their presence has not yet been determined. Opioid peptides from three families--endorphins, enkephalins, and dynorphins--have been shown to stimulate feeding in various species. They have been active at several opioid receptor types in the CNS, but there is limited evidence to suggest they affect food intake when administered peripherally. In contrast, peripheral injection of opiate antagonists has effectively decreased food intake, an observation that led to the original hypothesis that opioids were involved in the hunger component in the control of food intake and that excess concentrations might be involved in the development of obesity. An increasing body of evidence supports the concept that opioid and CCK peptides may interact to control food intake, but the evidence is more suggestive than conclusive.
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PMID:Role of cholecystokinin and opioid peptides in control of food intake. 286 68


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