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

Liver-function tests measured routinely in hypertensive patients attending the Glasgow Blood Pressure Clinic were abnormal in 15-8% of men and 6-2% of women. The patients studied appeared to be representative of the whole clinic population. Liver dysfunction was related to alcohol consumption, heavy body-weight, male sex, young age, and higher diastolic blood-pressure. It is suggested that alcohol and obesity were the principal causal factors and that fatty infiltration of the liver was the probable pathology. Liver dysfunction was unrelated to treatment. Alcohol use was found to be heavy in 12% of male patients attending the clinic, and this was probably an underestimate. The possibility that alcohol abuse may have a causal role in hypertension needs further study.
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PMID:Liver dysfunction in hypertension. 6 96

Our review focuses on low density lipoprotein (LD lipoprotein) and very low density lipoprotein (VLD lipoprotein) in their roles as transporters of cholesterol and triglyceride and as factors contributing to premature arteriovascular disease. We describe the clinical manifestations of the common, primary hyperlipoproteinemias--that is, hyper-beta-lipoproteinemia, combined hyperlipoproteinemia, hyper-pre-beta-lipoproteinemia, and sporadic hyperlipoproteinemia--and discuss the variations in lipoprotein structure and metabolism that occur in these diseases. Based on an understanding of the physiologic control of lipoprotein metabolism, it is possible for the physician to alter the concentrations of LD lipoprotein and VLD lipoprotein by selecting a course of therapy appropriate to the specific disease. We describe the effects of obesity, diet, insulin, ethanol, estrogens, and the drugs clofibrate, nicotinic acid, and cholestyramine.
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PMID:The common hyperlipoproteinemias: an understanding of disease mechanisms and their control. 18 30

1. Male rats were injected daily for 5 days with 0.15m-NaCl, corticotropin, cortisol or l-thyroxine and the rates of glycerolipid synthesis were measured in the livers after intraportal injection of [(14)C]palmitate and [(3)H]glycerol. 2. Injection of all three hormones decreased the rates of body-weight gain. 3. Cortisol treatment increased the weight of the liver relative to body weight. 4. Thyroxine treatment increased the relative rate of triacylglycerol synthesis from [(3)H]glycerol and decreased the relative accumulation of (3)H and (14)C in diacylglycerol. It did not significantly alter the accumulation of these isotopes in phosphatidate nor the activity of the soluble phosphatidate phosphohydrolase in the total liver. However, this activity increased by 1.5-fold when expressed relative to the soluble protein of the liver. The increased triacylglycerol synthesis appears to be related to a general increase in the turnover of fatty acids in the liver. 5. Treatment with cortisol and corticotropin increased the relative rate of triacylglycerol synthesis from [(3)H]glycerol, decreased the accumulation of (3)H in phosphatidate and increased the flux of both isotopes from phosphatidate to diacylglycerol. This appeared to be caused by the increased activity of the soluble phosphatidate phosphohydrolase that was observed in the livers of the cortisol-treated rats. 6. It is proposed that cortisol could be directly or indirectly involved in increasing the activity of hepatic phosphatidate phosphohydrolase in starvation, diabetes, laparotomy, subtotal hepatectomy, liver damage, ethanol feeding and in obesity. This enzyme adaptation could contribute to the potential of the liver to increase its synthesis and accumulation of triacylglycerols or to secrete very-low-density lipoproteins.
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PMID:The effects of cortisol, corticotropin and thyroxine on the synthesis of glycerolipids and on the phosphatidate phosphohydrolase activity in rat liver. 21 53

The epidemiological patterns for pancreatic and biliary cancers reveal more differences than similarities. Pancreatic carcinoma is common in western countries, although 2 Polynesian groups (New Zealand Maoris and native Hawaiians) have the highest rates internationally. In the United States the disease is rising in frequency, predominating in males and in blacks. The rates are elevated in urban areas, but geographic analysis uncovered no clustering of contiguous counties except in southern Louisiana. The origin of pancreatic cancer is obsure, but a twofold increased risk has been documented for cigarette smokers and diabetic patients. Alcohol, occupational agents, and dietary fat have been suspected, but not proven to be risk factors. Except for the rare hereditary form of pancreatitis, there are few clues to genetic predisposition. In contrast, the reported incidence of biliary tract cancer is highest in Latin American populations and American Indians. The tumor predominates in females around the world, except for Chinese and Japanese who show a male excess. In the United States the rates are higher in whites than blacks, and clusters of high-risk counties have been found in the north central region, the southwest, and Appalachia. The distribution of biliary tumors parallels that of cholesterol gallstones, the major risk factor for biliary cancer. Insights into biliary carcinogenesis depend upon clarification of lithogenic influences, such as pregnancy, obesity, and hyperlipoproteinemia, exogenous estrogens, familial tendencies, and ethnic-geographic factors that may reflect dietary habits. Noncalculous risk factors for biliary cancer include ulcerative colitis, clonorchiasis, Gardner's syndrome, and probably certain industrial exposures. Within the biliary tract, tumors of the gallbladder and bile duct show epidemiological distinctions. In contrast to gallbladder cancer, bile duct neoplasms predominate in males; they are less often associated with stones and more often with other risk factors. In some respects, bile duct and pancreatic tumors are alike. The male predominance of both tumors, an association between cholecystectomy and pancreatic cancer, and other considerations have prompted the notion that the same biliary carcinogens may affect the bile duct, ampulla of Vater, or, by reflux, the pancreatic duct. Various epidemiological and interdisciplinary approaches are needed to further clarify the origins of biliary tract and pancreatic cancers, but nutritional studies hold special promise in laying the groundwork for prevention of these tumors.
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PMID:Cancers of the pancreas and biliary tract: epidemiological considerations. 110 53

Marked fatty liver was found to develop in both KK and KK-Ay (yellow KK) mice when they were allowed free access to a 15% ethanol solution as drinking fluid. The present studies were undertaken to elucidate the characterization of the fatty liver and associated changes. Chemical analysis showed that accumulated lipids were mainly triglycerides, whose fatty acid composition was changed with increases in palmitoleic and oleic acids, indicating augmentation in endogenous lipogenesis. An accumulation of small fat droplets was histologically observed in centrolobular hepatocytes extending to perilobular zones. Among the tested mice of seven strains, only KK and KK-Ay mice developed the ethanol-induced fatty liver, and the latter mice were more susceptible. Growth, food and alcohol intakes, plasma levels of glucose, triglycerides, and immunoreactive insulin were also surveyed during the development of the alcoholic fatty liver. In contrast to high energy diet, ethanol induced neither development of obesity nor exaggeration of diabetic states. A possible correlation between the pathogenesis of the fatty liver and the genetic factor inherited in KK mice is discussed.
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PMID:Induction of fatty liver by ethanol drinking in KK and KK-Ay mice. 115 19

Fluoxetine is a potent and specific inhibitor of 5-HT uptake even after prolonged dosing. Both fluoxetine and norfluoxetine, an active metabolite, have a long plasma half life. The drug is extensively metabolized and undergoes renal elimination. Impairment of renal function, increasing age or obesity do not appear to alter the disposition of fluoxetine, although hepatic impairment predictably decreases the clearance of the drug. Recent data suggests that fluoxetine is an inhibitor of cytochrome P450-II-D6 in man and has been shown to inhibit the metabolism of a number of drugs which are substrates for this isoenzyme. It does not, however, affect the elimination of ethanol and does not enhance the effect of ethanol on psychometric testing. Fluoxetine has no effect on normal blood pressure although mean heart rate is slightly reduced. It does not appear to have a clinically significant effect on pituitary function. Although there is psychometric and EEG evidence to suggest a vigilance enhancing property, fluoxetine does not exhibit stimulant activity of the amphetamine type and has been shown to be well tolerated at doses clinically useful for appetite suppression in extensive clinical trials and widespread clinical use since marketed in 1987 for depressive illness.
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PMID:The human pharmacology of fluoxetine. 133 86

Many studies of age-related cognitive decline have failed to distinguish between usual and successful aging. Although some degree of cognitive impairment is associated with aging, when one looks at average performance, there is great variability among individuals, with many showing little or no deleterious effects of aging on intellectual abilities. Many of the risk factors for dementia and for conditions associated with cognitive impairments can be treated or controlled. Among the preventable causes of cognitive decline are the following: AIDS, Alcohol and drug abuse, Cerebrovascular disease, Exposure to organic solvents or lead, Head trauma, Overmedication, Syphilis. Other conditions that may cause cognitive decline can be controlled or treated: Atherosclerosis, Depression, Diabetes, Emphysema, High blood pressure, Obesity, Sleep disorders, Thyroid dysfunction. In addition, it may be possible to enhance the cognitive performance of even healthy elderly people through changes in diet and lifestyle. Recent data raise the possibility that improved prenatal and perinatal care and greater access to educational opportunities may result in a decreased incidence of dementia in future generations of older adults. Although they are rapidly becoming more numerous, the efficacy of cognitive training programs in preventing or slowing cognitive decline has not yet been demonstrated. Nevertheless, such programs may ameliorate cognitive impairment by reducing the psychiatric disabilities associated with anxiety and depression. The general principle underlying these strategies for limiting cognitive impairment with age is to maximize brain reserve and minimize brain damage.
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PMID:Preventing cognitive decline. 157 76

The role of alcohol as a risk factor for cerebral infarction and hemorrhage has been assesed in 200 middle-aged and elderly stroke patients and 200 controls matched for age, sex and hospital admission date. Computed tomographic brain scans were done in all but 10 of the stroke patients. Alcohol intake was reckoned on the 12 months preceding hospitalization and expressed in grams daily according to a standard nomogram. The Michigan Alcoholism Screening Test was used for the diagnosis of alcoholism. Cerebral infarction was present in 59% of the stroke patients and cerebral hemorrhage in 9%. The role of alcohol as risk factor for stroke proved to be small (Odds Ratio 1.86) and was practically lost after adjustment for the most common risk factors for cerebrovascular disorders (previous strokes, arterial hypertension, diabetes, obesity and hyperlipidemia). Our findings seem to suggest that alcohol is not an independent risk factor for stroke in the middle-aged and elderly. The data are, however, preliminary and are discussed in the light of methological problems.
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PMID:Cerebrovascular disorders and alcohol intake: preliminary results of a case-control study. 162 76

A total of 789 Japanese male transport service workers between the ages of 35 and 50 were used as subjects in an analysis of daily lifestyle factors related to hypertension. Multiple logistic analysis showed positive dose-response relations between hypertension and age, obesity and alcohol consumption. Age and obesity were factors having a linearly increasing odds ratios for hypertension (including borderline cases and those under treatment). Alcohol consumption of 56 g ethyl alcohol per day or more had an odds ratio about double that of those who did not drink. Smokers had 1/2 the odds ratio of non-smokers. Subjects working a 24-hr shift comprised mostly of standby duty showed a slightly lower rate of hypertension, but it was statistically insignificant.
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PMID:Analysis of factors related to hypertension in Japanese middle-aged male workers. 162 88

Over the last four decades there has been extensive research into the links between diet and coronary heart disease. The most recent literature is reviewed in this position statement. The clinical and public health aspects of the National Heart Foundation's nutrition policy are based on this review. The key points are as follows: 1. Saturated fatty acids A high intake of saturated fatty acids is strongly associated with elevated serum cholesterol and LDL-cholesterol levels and increased risk of coronary heart disease. 2. The n-6 polyunsaturated fatty acids The n-6 polyunsaturated fatty acids (principally linoleic acid) lower serum cholesterol levels when substituted for saturated fats and probably have an independent cholesterol-lowering effect. 3. The n-3 polyunsaturated fatty acids (fish oils) The n-3 polyunsaturated fatty acids reduce serum triglyceride levels, decrease the tendency to thrombosis and may further reduce coronary risk through other mechanisms. 4. Monounsaturated fatty acids Monounsaturated fatty acids reduce serum cholesterol levels when substituted for saturated fatty acids. It is not clear whether this is an independent effect or simply the result of displacement of saturates. 5. Trans fatty acids Trans fatty acids may increase serum cholesterol levels and can be reckoned to be equivalent to saturated fatty acids. 6. Total fat Total fat intake, independent of fatty acid type, is not strongly associated with coronary heart disease but may contribute to obesity. Associations between total fat intake and coronary heart disease are primarily mediated through the saturated fatty acid component. 7. Dietary cholesterol Dietary cholesterol increases serum cholesterol levels in some people and may increase risk of coronary heart disease. 8. Alcohol A high intake of alcohol increases blood pressure and serum triglyceride levels and increases mortality from cardiovascular disease. Light alcohol consumption reduces the risk of coronary heart disease. 9. Sugar The consumption of sugar is not associated with coronary heart disease. 10. Sodium and potassium High salt intake is related to hypertension especially in the subset of "salt-sensitive" people. Potassium intake may be inversely related to hypertension. 11. Overweight and obesity Abdominal obesity increases the risk of coronary heart disease probably by adversely influencing conventional risk factors. 12. Vegetarianism A high intake of plant foods reduces the risk of coronary heart disease through several mechanisms, including lowering serum cholesterol and blood pressure levels.
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PMID:Diet and coronary heart disease. The National Heart Foundation of Australia. 163 Mar 69


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