Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our emphasis in the past has been on disease prevention rather than health promotion. This emphasis served us reasonably well when morbidity was high throughout society and when interventions at the community level were able to achieve massive reductions. It is not faring as well now that the major shared environmental determinants of disease have been controlled. The present situation calls for changes in individual health-related behaviour and individual clinical interventions to achieve comparable progress. As difficult to win as collective commitments to community-level interventions have been, compliance in a free society by often unmotivated persons in numerous individual instances of decision making in daily life is even more difficult. Health promotion offers the promise of a quantum leap in improving the health status of the community by participating in behaviour perceived as not only responsible but appropriate and desirable, providing positive reinforcement rather than anxiety-provoking caution. Favourable social trends, such as physical conditioning and dietary changes may be encouraged through media interventions. There are biological limitations to this approach, however. Many healthful practices confer little benefit on large groups of people and a few may be harmful to selected groups. Vigorous promotion of weight reduction and obesity control, for example, may lead to profound dissatisfaction with body image and to severely self-destructive behaviour among those prone to eating disorders such as anorexia, bulimia, and obsessive eating. Health promotion activities may fit well with social trends but their adverse potential can be aggravated because failure to comply can be penalized by peer disapproval in a way that disease prevention strategies usually are not.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Health promotion in perspective. 269 2

CCK appears to regulate short-term control of food intake by acting as a satiety signal. Larger doses of CCK may decrease food intake by aversive actions (malaise, nausea, cramps), presumably by effects on gastrointestinal motility. In rats and most likely humans CCK is released from the upper intestine after a mixed meal and appears to activate afferent vagal fibers by causing pyloric contraction with resultant gastric distention or directly binding to the gastric afferent vagus which courses to the nucleus solitarius with further projections to the paraventricular nucleus and ultimately the ventromedial hypothalamus. Peripherally released CCK may also bind to CNS receptors in the area postrema overlying the nucleus solitarius. Central nervous system CCK released from the paraventricular nucleus may also exert a satiety effect. The satiety effect of CCK appears to be a physiologic action of the peptide since antibodies to CCK and CCK receptor antagonists can increase food intake. CCK is probably just one of several satiety signals but can cause a profound decrease in food intake when administered exogenously in pharmacologic doses. Administration of exogenous CCK, as well as endogenous CCK released by oral protease inhibitors, can decrease food intake in humans. Studies designed to examine the effect of chronic administration of CCK on food intake will be necessary to determine if the peptide has a role in the management of obesity and bulimia.
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PMID:Role of cholecystokinin in the control of food intake. 269 51

Historically, nutrients and related metabolic signals were considered to control the onset and offset of meals. Recent research has focused upon the roles of peptides found in the gastrointestinal tract and brain as alternate controllers of these processes. During a meal, the gut secretes a variety of peptides as part of the digestive process. Some of these substances, acting as hormonal or as local signals, may also provide information which is relayed to the central nervous system, causing eating to stop and producing the sense of satiety. When administered to animals or people before a meal, exogenous cholecystokinin (CCK), the most studied of the putative satiety peptides, reduces food intake in a dose-dependent manner. Recent findings support the concept that endogenous CCK acts during meals to limit meal size, and evidence is reviewed suggesting a possible pathophysiological role for CCK in bulimia. Adiposity is also regulated via peptide hormones, especially insulin. Insulin is secreted in direct proportion to adiposity, and blood-borne insulin gains access to brain areas important in the regulation of feeding. The administration of insulin into the brain causes reduced eating and weight loss.
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PMID:The regulation of food intake by peptides. 269 89

In most cases, obesity does not stem from a specific psychologic disturbance. Some obese people overeat, as do their family or their socio-professional peers, and this cannot be considered a pathologic behaviour. Many obese patients increase their energy intake when frustrated, anxious, or tired, like many normal individuals who enjoy a better weight regulation. But when obesity increases suddenly and/or severely in these circumstances, and in gross obesity, abnormal feeding behaviour is usually responsible: prandial or, more often extraprandial overeating (nibbling, gorging, binge eating, night eating, excess alcohol, carbohydrate craving). Serotoninergic mechanisms of the latter have focused wide interest. Conflicting situations and/or anxiety are usually a factor in child obesity. Deppreciated self-image and feelings of culpability, partly secondary to obesity itself and dietary failures often contribute to feeding disturbances, sometimes surreptitious, carrying a risk of vicious circle. But weight reduction itself, while improving self image, carries a risk of unmasking depressive tendencies, especially when too quick. Hence the importance of careful and comprehensive management.
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PMID:[Eating disorders and obesity]. 270 54

There is a strong psychosocial prejudice and discrimination against obese persons. Despite this pressure, they show no greater psychological disturbance than normal-weight persons do. Patients with bulimia, distortion of body image and - to a lesser degree - with extreme obesity are an exception to the rule and often require psychiatric help. There is no evidence for an obesity-specific disturbance of personality or of eating behavior. Behavior modification - with or without anorectic agents is still a matter of debate - has been the most successful form of therapy. As dieting carries the danger of psychosocial stress and morbidity its indication has to be carefully considered. With the high attrition rate, low compliance of obese persons and the poor outlook for a permanent therapeutic effect supportive care and guidance of obese patients is the most important and difficult task for the physician.
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PMID:[Psychosocial aspects of obesity]. 274 Nov 30

Three patients are described in whom surgical removal of a craniopharyngioma was followed by extreme hyperphagia resulting in obesity and abnormal food-seeking behavior, including foraging for food, stealing food or stealing money for food. These behaviors resemble those seen in the Prader-Willi syndrome but contrast with those noted in bulimia. This deviant behavior was a major factor in the poor outcome of surgery. Attempts at rehabilitation were unsuccessful.
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PMID:Abnormal food-seeking behavior after surgery for craniopharyngioma. 281 93

Patients with bulimia (binge-purge syndrome) frequently complain that they consume a very restrictive diet to avoid gaining weight. To investigate this claim, 23 hospitalized bulimic patients were assessed daily for body weight, caloric intake, macronutrient diet content, activity measures, and body composition estimates during weight-stable periods. Bulimic patients ate fewer kilocalories per kilogram body weight (22.1 +/- 4.6 kcal/kg) than did age-matched normal women (29.7 +/- 6.5 kcal/kg) but had similar activity levels and body composition. Clinical variables, such as history of laxative abuse, anorexia, or obesity, and physiological characteristics, such as body weight, activity level, or dietary content, could not account for this difference in caloric consumption. Bulimic patients tended to eat a diet lower in fat and higher in protein than did control subjects. These results agree with observations of increased efficiency of caloric utilization in obese patients and support patient complaints of a tendency to gain weight easily.
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PMID:Decreased caloric intake in normal-weight patients with bulimia: comparison with female volunteers. 291 15

Obesity is not a single disease, but a variety of conditions resulting from different mechanisms and associated with various types and degrees of risks. To determine who should lose weight, how much weight should be lost, and how to undertake weight loss, the following types of information are needed: personal-demographic data, developmental patterns, family history, energy balance, body composition/fat distribution, psychological/behavioral measures, endocrine/metabolic measures, complications and associated conditions. Weight reduction should be undertaken by women with morbid obesity, with complications secondary to the obesity, with a strong family history of conditions associated with obesity, or with increased abdomen:hip ratios. In contrast, women who have excess weight localized in the hips and thighs and no personal or family history of associated conditions may not benefit from dietary restriction. Low calorie diets result in adaptive changes, "designed" to prolong survival in the face of famine. These include changes in water balance, metabolic rate, and appetite. Metabolic rate declines, allowing the individual to burn fewer and fewer calories. Each time a woman diets she tends to lose weight less rapidly than the time before. "Restrained eating" predisposes binge eating. Indeed, bulimia rarely occurs in the absence of prior caloric restrictions. Current medical definitions of obesity do not consider these nuances. Existing definitions "over-diagnose" obesity in women, in general, and in older women and nonwhite women, in particular. For example, by existing standards, more than 60 percent of black women more than 45 years of age are considered obese. In contrast, the health risks of similar degrees of obesity are substantially greater for men than for women. Part of the problems lies in the fact that many women have pear-shaped fat distribution,a pattern which is not associated with increased health risks.Current cultural definitions of obesity for women distort the picture even further. In the past 20 years,there has been a progressive decline in the weight-for height of such "culture models" as Playboy centerfold subjects and Miss America contestants. Attempting to achieve such low weights predisposes women to an endless cycle of dieting and regaining, and contributes to the growing problems of eating disorders, including anorexia nervosa and bulimia.
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PMID:Obesity. 312 Feb 16

There is evidence that endogenous opiates are involved in the control of feeding in experimental animals. Several types of experimental obesity are associated with increased opiate production and/or increased numbers and sensitivity of opiate receptors. Research with experimental animals suggests that nutrients, particularly sugar, have an effect on feeding behavior that is mediated by opiates. For instance, the obesity-producing effect of a palatable diet in rodents is blocked by opiate antagonists. Stress induced feeding in rodents leads to preferential sucrose ingestion and is blocked by opiate antagonists and beta-endorphin. The effect of nutrients on the endogenous opiate system of humans is less clear. Clinical experience suggest that carbohydrates (sugar in particular) play a role in binge eating and obesity. Many binge eaters preferentially eat sweets during a binge. Many obese individuals consume more than half of their total daily calories as carbohydrates. Sweet snacking is a frequent behavior at times of stress. Recent evidence suggests that sugar can lead to increased beta-endorphin production in obese subjects.
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PMID:Sugar, opioids and binge eating. 316 88

Though education for healthy body weight traditionally has focused on obesity, the increased incidence of anorexia nervosa and bulimia among young women suggests education also is needed to address the opposite end of the spectrum. Anorexia nervosa and bulimia are complex and multidimensional disorders associated with individual, family, and sociocultural factors. This article examines the cultural pressure for dieting and thinness currently experienced in America and its impact as a possible predisposing factor for developing eating disorders among adolescent females. Literature is reviewed related to the changing American standard of attractiveness for females reflected by 20th century mass media and its subsequent influence on adolescent concerns for dieting and thinness. Preventive strategies are recommended to help adolescents balance the cultural pressure for thinness and their own desires for attractiveness within the larger context of overall good health.
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PMID:Education for healthy body weight: helping adolescents balance the cultural pressure for thinness. 321 26


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