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

Persons 45.4 kg (100 lb) or more above desirable weight have exponential increases in mortality and serious morbidity compared with normal persons. The presence of a complication or an independent coronary risk factor along with obesity increases the mortality further. Among the "threshold conditions" that appear at a critical level of body weight (60% or more above desirable weight), the most important are sudden unexplained death, ventilatory disorders, circulatory congestion, and functional limitations in activities of daily living. Recent epidemiologic data on extreme obesity and data on cardiac dysfunction show impaired quality of life in young, morbidly obese patients. Because of the malignant nature of morbid obesity and the inability to achieve and maintain sufficient weight reduction by non-surgical means, surgery is justified in this population.
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PMID:Morbid obesity and related health risks. 406 22

642 persons without respiratory and circulatory diseases were selected from 1087 steel mill workers. The examined persons were classified according to the intervals of relative body mass. The relations between spirometric parameters (VC and FEV1) and degree of obesity were studied. For each interval the equations of multiple regression were calculated, taking into account the dependence of VC and FEV1 on age, height and present body mass. The numeric factor from the equation of multiple regression of coefficient describing the dependence of VC on the present body mass was positive in 90-114% and 115-124% intervals but negative in 125-134% and 135% of body mass. In case of FEV1 the negative factor of the same coefficient was not negative until 135% of body mass. A positive correlation of VC and FEV1 with the present body mass in the whole population was shown. If the group of obese persons was formed on the basis of Wot anthropometric index (which included skinfolds thickness, present body mass and height), significantly lower values of VC and FEV1 were found in comparison to non-obese counterparts. For the persons with morbid obesity a new method of calculation of predicted VC and FEV1 values was presented. The equation of multiple regression used for this purpose takes into account the dependence of spirometric values on age and Wot index.
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PMID:[Effect of obesity on the ventilatory capacity of the respiratory system. II. Reference spirometry values of VC and FEV1 for overweight males]. 406 89

Although often coexisting in the same patient, obesity and essential hypertension exert disparate cardiovascular effects. An excess of adipose tissue augments cardiac output, stroke volume, and left ventricular filling pressure, expands intravascular volume, and lowers total peripheral resistance. In contrast, essential hypertension in a non-obese patient is associated with a contracted intravascular volume, high total peripheral resistance, and normal cardiac output, but increased left ventricular stroke work due to high afterload. Left ventricular adaptation will consist of eccentric hypertrophy in the obese (irrespective of arterial pressure) and concentric hypertrophy in the non-obese hypertension patient. The combination of obesity and hypertension burdens the heart with high preload and high afterload, thereby greatly enhancing the risk of congestive heart failure. Peripheral resistance and intravascular volume may be normal in mildly hypertension obese patients because of the mutually antagonising effects of the increase in arterial pressure and the increase in body weight. The fall in arterial pressure associated with weight loss seems to be caused by a decrease in adrenergic activity which leads to a fall in cardiac output without change in vascular resistance. Obesity hypertension may be the result of an inappropriately raised cardiac output in the presence of a relatively restricted arterial capacity due to the low vascularity of adipose tissue. In morbid obesity increased blood viscosity may contribute to the raised arterial pressure.
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PMID:Cardiovascular effects of obesity and hypertension. 612 45

Hepatic damage resembling alcoholic hepatitis has been described after jejunoileal bypass surgery for morbid obesity, but has not been previously reported as a complication of gastric partitioning operations (gastric bypass and gastroplasty). A patient who developed an alcoholic hepatitislike clinical picture 8 mo after gastroplasty is described, suggesting that malnutrition superimposed on obesity may be responsible for the injury in both settings. Reversal of the gastroplasty was associated with clinical and biochemical improvement.
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PMID:Liver injury with alcoholiclike hyalin after gastroplasty for morbid obesity. 619 39

Literature on liver morphology in untreated obesity reveals varying prevalences of various pathological findings. The purpose of this literature study was to summarize and evaluate the published observations and to discuss discrepant findings. A complete search was aimed at utilizing bibliographic methods including a computerized survey. Forty-one original articles were included, comprising information on liver morphology in 1515 morbidly obese patients. Liver biopsy was considered normal in 12 per cent of the cases. The most frequent abnormality reported was fatty change, present in 80 per cent of the biopsies. Portal inflammation was also common (33 per cent). Fibrosis, mainly portal or periportal, was observed in 29 per cent. Cirrhosis, however, involved only 3 per cent. Study of relationships between the degree of liver change and certain possible pathogenetic factors (eg degree and duration of obesity, age, sex, alcohol consumption, diabetes mellitus) does not point towards a single causal factor. Co-influence of additional pathogenetic factors are likely in the development of liver changes in morbid obesity.
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PMID:Liver morphology in morbid obesity: a literature study. 637 41

Research has demonstrated that obesity is far more complex than simply eating too much. Although the individual who is only modestly overweight is probably guilty of overindulgence, the grossly obese individual is the victim of a far more complex disorder with genetic, metabolic, psychosocial, and perhaps central nervous system malfunctions all interacting in a poorly understood fashion. The medical consequences of morbid obesity are considerable and demand the patient's and the physician's attention. This article discusses pathogenesis, consequences, and approaches to treatment.
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PMID:Obesity. Pathogenesis, consequences, and approaches to treatment. 647 86

Vigorous respiratory therapy can prevent the development of postoperative pulmonary complications which occur with increased frequency after upper abdominal surgery. Obesity poses an additional risk factor. To study the effects of postoperative chest percussion with postural drainage (CPT), 53 consecutive patients undergoing Roux-en-Y gastric stapling procedures for treatment of morbid obesity were randomized to two groups. Both received identical postoperative respiratory care, except the study group received additional CPT. It was concluded that the addition of CPT to patients without prior chronic lung disease undergoing upper abdominal surgery caused patient discomfort, increased hospital cost, and failed to affect the incidence of postoperative pulmonary complications.
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PMID:Postoperative chest percussion with postural drainage in obese patients following gastric stapling. 649 53

To understand how genetic and environmental factors could interact to lead to different types of obesity, a simple hypothetical model is examined involving two genes and one environmental factor. Separate and interactive effects are illustrated. The confounded expression of distant phenotypes and advantages of studying phenotypes close to immediate gene products are explained. The appearance of population frequency distribution curves for level of obesity are illustrated for five different situations simulating actual data behaving according to the hypothetical model. Six suggestions are given as a practical approach to characterizing morbid obesity: (1) describe the frequency distribution of morbid obesity by age and sex in the general population; (2) obtain accurate family history data from obese probands, spouses, and controls; (3) contrast results of metabolic studies between obese probands with and without a family history of obesity; (4) obtain metabolic screening data from close relatives of selected obese probands and controls; (5) study special settings (twins, adoption, migration, race); (6) when justified, perform extensive pedigree studies using metabolic evaluations, linkage markers, and carefully prepared computer model testing. Careful collection of family history data is explained in detail and is proposed as an important and relatively inexpensive tool that should be part of any study of human obesity.
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PMID:The role of genetic analyses in characterizing obesity. 651 11

Forty-six patients with obesity exceeding 75% (according to Natvig's tables) were subjected to gastroplasty which after 12 months had resulted in an average weight loss of 32 kg. Preoperatively, serum levels of triglycerides, total cholesterol, and LDL cholesterol were significantly raised, while HDL cholesterol was significantly lower than in non-obese controls. One year after surgery, mean serum triglyceride levels had normalized while mean HDL cholesterol had increased steadily to levels not different from those in the non-obese controls. Regarding total cholesterol and estimated LDL cholesterol, no significant changes were recorded. It is concluded that gastroplasty affects serum lipid patterns in obese patients in a fashion quite different from that caused by jejunoileal bypass operations. As the incidence of coronary heart disease is known to be inversely related to serum HDL cholesterol, gastroplasty may offer an additional advantage over jejunoileal shunt operations in improving the long-term prognosis in morbid obesity.
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PMID:Serum lipid changes after gastroplasty for morbid obesity. 652 54

The long-term ingestion of a fat-rich diet caused severe obesity in adult rats. Severe obesity developed in these animals without them having to increase caloric intake. Evidence for this comes from the observation that voluntary intake averaged 36,113 +/- 410 calories/rat per 60 wk for rats eating a high-fat diet (42% of calories from fat) compared to a value of 36,125 +/- 500 calories/rat per 60 wk for those eating a diet of Purina chow. Despite a similar caloric intake, carcass fat averaged 51 +/- 1% for rats eating the fat-rich diet but only 30 +/- 1% body fat for control animals eating the low-fat diet of Purina chow. These results indicate that a fat-rich diet does not always cause rats to overeat. Further, they clearly demonstrate that severe obesity can develop in the absence of hyperphagia provided the animals eat a fat-rich diet. Finally, a correlation coefficient of r = 0.76 between body weight and lean body mass was obtained for the Purina chow-fed rats and that of r = 0.66 was obtained for the fat-fed rats.
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PMID:Effect of dietary fat on food intake, growth and body composition in rats. 653 99


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