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)

The relationships between nutrition and immune defence in man are poorly understood. The clinical situations of nutritional origin involving immune deficiency: protein energy malnutrition (marasmus and kwashiorkor), nutritional disorders in developed countries, anorexia, obesity, mineral salt and vitamin deficiencies, hypercholesterolemia and alcoholism are reviewed.
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PMID:Clinical status of nutritional origin involving immune deficiency. 212 54

Eating disorders among adolescents in the United States constitute the most frequent nutritional problems in this age group, and their prevalence appears to be increasing. A causal relationship of television viewing to obesity is strongly suggested for children and adolescents. Perhaps as much as 25% of the recent increase in obesity among adolescents may be attributable to increases in television viewing. Associations between television viewing and anorexia and bulimia are less explicit than they are for obesity. Nonetheless, because children and adolescents spend more time viewing television than they do in any activity other than sleep, the world shown on television may acquire a greater reality than the world that is experienced. The low frequency of obesity among televised characters, combined with the frequent food-related references that are contained in both commercials and programming, may promote unrealistic conclusions regarding eating and body weight. Television reflects a cultural contradiction by promoting food consumption and leanness. In this context, bulimia may be viewed as an adaptive response, because only bulimics can eat everything they wish and remain thin.
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PMID:You are what you eat--what you eat is what you are. 230 99

Two cases of idiopathic hypothalamic dysfunction (one boy and one girl) are reported. Symptoms of hypothalamic dysfunction were noted by the age of 2 years: initial polyphagia and obesity with subsequent anorexia and emaciation were observed in one patient. Thermoregulation and thirst disorders, recurrent accesses of hypernatremia, acrocyanosis and profuse sweating were present. Impaired growth and delayed puberty in one case, and in the other hypogonadism, absence of growth hormone and gonadotrophins release in response to provocative stimuli were observed as well as abnormal thyroid stimulating hormone response to thyrotropin releasing hormone with hyperprolactinemia. Magnetic resonance imaging showed structural lesion in the lateral part of the lentiform nucleus in one case. Treatment with naltrexone, an opiate antagonist, had little if any effect.
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PMID:[Hypothalamic dysfunction. 2 cases: the contribution of nuclear magnetic resonance, therapeutic trial of naltrexone]. 266 35

Anorectic agents constitute the most widely used supportive drug treatment in obesity as well as that most often prescribed. A large number of substances have been proposed for this purpose, and some have been found to be reasonably effective, while others exhibiting side effects which forbid their use, as thyroid hormones and diuretic agents. There are other substances with properties that might justify their use, such as ballast preparations, some antidepressive agents, and a few compounds acting principally on the gastrointestinal tract. Of current interest are substances furthering thermogenesis, but for the time being these remain in the realm of pure research. The anorectic agents usually available bring about a weight loss of about 0.5 lb (0.230 kg) per week more than prescription of a placebo, though only over a limited period of time. Once the drug is discontinued, weight regain is the rule and it appears even that association of an anorectic agent to behavioural therapy might have an unfavourable effect on maintenance of the weight loss. Their use is therefore difficult to justify except in the rare cases where a short-term reduction in weight is desired or in patients suffering from an illness linked to their overweight. Differences in eating habits observed with amphetamines compared with fenfluramine and its dextrorotatory isomer dexfenfluramine suggest that these compounds could play a supportive role in the management of obese patients along with the dietetic training and changes in eating habits which are still fundamental to the medical treatment of obesity.
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PMID:[Drug treatment of obesity]. 266 70

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

This minireview deals with the possible roles of monoamines in feeding and feeding disorders. The introduction sketches the results of earlier studies with local drug injections and selective neurotoxins which provided pharmacological evidence that monoamines can influence food intake and body weight. A table summarizing this evidence is used to list monoamine changes that could underlie anorexia or hyperphagia. It is apparent that abnormalities in the monoamines, along with their cotransmitters, could cause many forms of feeding disorder. It is proposed as a working hypothesis that several varieties of hyperphagia leading to obesity have a common element. This common factor is a change in excitability of a lateral hypothalamic reinforcement system as manifested in self-stimulation at a stimulation-bound feeding site. Understanding this feeding reward-aversion system helps us understand hyperphagia and anorexia. The neurochemistry of reward and aversion involves the monoamines. This paper focuses on dopamine and serotonin. The data support the hypothesis that dopamine systems projecting to the nucleus accumbens and other forebrain areas from the mid-brain ventral tegmental area (VTA) are important for approach and positive reinforcement in ingestive behavior and self-stimulation. Serotonin is hypothesized to facilitate satiety and inhibition of feeding reward in the hypothalamus. The next section abstracts our recent experiments that measured pharmacological and physiological release of the monoamines in the hypothalamus and nucleus accumbens during ingestive behavior and self-stimulation. In vivo microdialysis in freely moving rats suggested the following: (1) Norepinephrine was released in the paraventricular nucleus during the active, feeding period of the circadian cycle. (2) The serotonin metabolite 5-HIAA also increased in the PVN at the same time if there was food to eat. (3) Amphetamine infused into the lateral hypothalamus (LH) by reverse dialysis increased synaptic dopamine, norepinephrine, and serotonin. (4) The anorectic drug d-fenfluramine increased synaptic serotonin in the LH and also increased the dopamine metabolite DOPAC, suggesting that serotonin and dopamine in the LH might contribute to fenfluramine-induced satiety. Local d-fenfluramine injection into the LH or local infusion by reverse dialysis again increased serotonin and decreased 5-HIAA and interfered with local dopamine metabolism as reflected in decreased DOPAC and HVA. (5) Tryptophan, a serotonin precursor, given systemically at an anorectic dose, increased extracellular serotonin in the LH, but this effect was only detectable in food-deprived rats. This was seemingly pH independent (between 5.8 and 8). The passage other cations through CFo is strictly suppressed (even at pH 8 and with 300 mM NaCl in the medium).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Microdialysis studies of brain norepinephrine, serotonin, and dopamine release during ingestive behavior. Theoretical and clinical implications. 269 87

The importance of the central monoamines NE, DA and 5-HT in ingestive behavior has inevitably resulted in considerable effort being expended in attempting to implicate these monoamines in the mechanism of action of anorectic drugs. The statements that amphetamine-induced anorexia is unlikely to be due to central serotoninergic systems and that central noradrenergic and dopaminergic systems are not implicated in the appetite suppressant effect of fenfluramine are in all probability correct. However, to attribute the ability of drugs to decrease food intake unequivocally to a specific effect on central monoaminergic systems is almost certainly an oversimplification, due to the fact that other putative neurotransmitters, such as GABA and peptides, play a critical role in eating. This can be achieved either directly or by modulating the release of other transmitters. An added complication in attempting to correlate a specific neurochemical process to a behavioral effect, such as anorexia, is the complexity of the central actions of the drug. At best, a predominant but not an exclusive process can be identified. Perhaps the in-built constraint of attempting to correlate a specific neurochemical effect to the desired action of a drug is accountable for the absence of a second generation of centrally acting anorectic drugs. Dramatic progress has been made in elucidating the factors involved in ingestive behavior over the last 5-10 years. This information should, and must, provide the catalyst for more efficacious anorectic drugs because obesity represents one of the few major diseases for which adequate drug therapy does not exist.
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PMID:Neuropharmacology of drugs affecting food intake. 288 62

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

Three studies have been undertaken to investigate why there are individual differences in the response to d-fenfluramine with respect to food intake and hunger in the short term and on body weight loss in the long term. Fenfluramine and norfenfluramine plasma levels have been used as probes to help detect and normalize these variances. In a single dose ranging volunteer study (0, 30, 40, and 60 mg), d-fenfluramine levels were significantly related to caloric intake and hunger rating scales when compared individually, and the slopes of the regression lines showed intersubject variation. These slopes, an index of each subject's response to fenfluramine, appear to be related to both the percentage underweight and more weakly to the percentage overweight. Those subjects at the extremes of weight showed a greater response to a given drug level. In two placebo-controlled 3 month studies (30 mg/day), the variances in weight loss were not explained by steady state drug levels, the percentage overweight, initial weight, duration of obesity, or caloric intake even when weight loss was normalized for differences in drug levels. Age, however, was significantly related to weight loss, with each additional 10 years increasing weight loss by approximately 1 kg. If confirmed, the sensitivity of fenfluramine anorexia may be an objective acute test of the central control of food intake. However, in long term clinical studies, drug levels were only weakly related to weight loss and other undefined factors seem to determine which patients responded better to fenfluramine treatment.
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PMID:Factors that may effect the reduction of hunger and body weight following d-fenfluramine administration. 305 14

Dysfunctional uterine bleeding is classified by the character of the menstrual cycle: ovulatory or anovulatory. Anovulation can occur at any age and is physiologic in the first year or two after menarche and for several years before menopause. Anovulatory cycles are characteristically irregular and marked by prolonged episodes of bleeding unassociated with signs or symptoms of ovulation. Specific causes of anovulation such as hyperprolactinemia, thyroid disease, androgen excess, anorexia, obesity, and excess exercise can be treated specifically; otherwise, therapy depends upon patient goals. Cycle regulation can be affected by monthly courses of progestin, such as medroxyprogesterone acetate (Provera), 10 mg daily for 10 days each month. Contraception and cycle regulation can both be accomplished with oral contraceptives. Fertility, on the other hand, will require ovulation induction. Ovulatory dysfunctional uterine bleeding most prevalent in parous women between the ages of 20 and 40 is associated with regular cycle intervals and premenstrual molimina. Midcycle and perimenstrual spotting can often be treated with observation only, but depending upon patient and/or physician concerns, periodic hormonal suppression is effective. The management of menorrhagia should include the following: (1) exclusion of pathology in the genital tract; (2) reduction in activity during days of heavy flow; (3) the avoidance of aspirin in the week before and on days of flow; (4) nonsteroidal anti-inflammatory drugs; (5) cycle suppression--oral contraceptives, danazol (Danocrine), depo-progestin; (6) luteal phase progestin; and (7) surgical intervention.
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PMID:Dysfunctional uterine bleeding. 305 63


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