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Query: UMLS:C0311277 (abdominal obesity)
 2,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Separate lines of evidence suggest that abdominal obesity, insulin, and renin are independent risk factors for coronary heart disease. Since insulin levels are higher in abdominally obese subjects and may enhance renin and aldosterone production, these risk factors may not be entirely independent. Moreover, the renin-angiotensin system may contribute to insulin resistance. These observations suggest that some inconsistencies in the literature regarding the effects of salt restriction on insulin may be explained by baseline anthropometric and metabolic differences in the subjects studied. To examine these issues, 29 volunteers with a range of risk factors were studied after 1 week each on isocaloric 20 and 200 mmol/day NaCl diets. Measurements included ambulatory blood pressures, plasma renin and aldosterone, and responses to oral glucose and intravenous insulin. Subjects were divided into three groups based on a composite score reflecting the risk factor cluster associated with abdominal obesity and hyperinsulinemia. The nine subjects with the highest scores had significantly greater values for renin and aldosterone on both the high and low salt diets than the nine subjects with the lowest scores. Fasting insulin and triglycerides, the insulin response to oral glucose, and plasma aldosterone all rose significantly more with salt restriction in the high than in the low risk subjects. Plasma renin activity also tended to increase more on the low salt diet in the high risk group. Ambulatory blood pressures were greater on the low than the high salt diet only in the high risk group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renin and aldosterone are higher and the hyperinsulinemic effect of salt restriction greater in subjects with risk factors clustering. 782 51

Hypertension and atherosclerosis are highly prevalent disorders which contribute substantially to the burden of premature morbidity and mortality at significant cost to the economy. Hypertension, abdominal obesity and risk factor clustering represent complex regulatory disorders which probably reflect an interaction of multiple genetic and environmental factors. Information has been summarised which indicates that fish oil, obtained either as a dietary supplement or by the consumption of more fish products, represents a relatively simple and comparatively inexpensive dietary intervention which may lower BP, especially in combination with a low salt diet, and favourably alter multiple risk factors in the cluster. This summary also indicates that multiple significant gaps in our knowledge about fish oil remain. Closing these gaps through further clinical and basic research may lead to greater acceptance and more appropriate therapeutic use of fish oil for health maintenance and disease prevention.
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PMID:Is there a role for dietary fish oil in the treatment of hypertension? 788 88

Obesity can result in alterations in cardiac structure and function even in the absence of systemic hypertension and underlying organic heart disease. Increased total blood volume creates a high cardiac output state that may cause ventricular dilatation and ultimately eccentric hypertrophy of the left (and possibly the right) ventricle. Eccentric left ventricular (LV) hypertrophy produces diastolic dysfunction. Systolic dysfunction may ensue due to excessive wall stress if wall thickening fails to keep pace with dilatation. This disorder is referred to as obesity cardiomyopathy. The presence of systemic hypertension in obese individuals facilitates development of LV dilatation and hypertrophy. Congestive heart failure may occur in such individuals, and may be attributable to LV diastolic dysfunction or to combined LV diastolic and systolic dysfunction. The sleep apnea/obesity hypoventilation syndrome occurs in 5% of morbidly obese individuals and is potentially life-threatening. Treatment of obesity cardiomyopathy consists of weight loss, salt restriction, and diuretics. Digitalis and vasodilators may be useful in selected cases. Central obesity is probably a risk factor for the development of coronary heart disease. Alterations in lipid and insulin metabolism may facilitate development of coronary heart disease in obese patients.
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PMID:Obesity and the heart. 836 92

Central obesity is a strong predictor of higher prevalence of diabetes, hypertension and coronary artery disease among Indian immigrants to Britain. To test this hypothesis in Indians, 1569 adults, between 25 and 64 years of age, from 750 randomly selected households (representative of 0.52 million population of Trivandrum city, Kerala) were selected for this study. The response rate was roughly 95% and the sample consisted of 1497 individuals (737 males and 760 females). The survey methods included dietary diaries for 7-day food intake record, blood pressure measurements using a mercury sphygmo-manometer and anthropometric measurements. The prevalence rates of hypertension between 25 and 64 years was 189/1000 (95% confidence limits 85-360) and between 45 and 64 years was 335/1000 (95% confidence limits 210-460) which is higher than in Western populations. The prevalence was higher in males than females in the younger age groups and comparable in both sexes in the upper age groups. The prevalence of central obesity was significantly higher among male (77.2 vs. 48.9%) and female (84.0 vs. 51.4%) hypertensives compared to non-hypertensive subjects; however, mean body weight, body mass index and waist-hip ratio (WHR) were lower among Indian men compared to a British comparison group. Thus, comparison of Indian men with Britons showed that obesity, salt and alcohol intake, sedentariness, smoking and dietary fat intake do not explain the cause of higher prevalence of hypertension among South Indian men from Kerala.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diet, central obesity and prevalence of hypertension in the urban population of south India. 852 15

In primary hypertension a mild hyperresponsiveness of hypothalamic, sympatho-hormonal centres to psychosocial stimuli forms a major pathogenetic element, although high salt intake in some subjects may contribute via volume expansion. Hypertension is often associated with another "civilisation" disorder, the metabolic syndrome, defined as abdominal obesity, insulin resistance and dyslipidaemia. According to recent research, the metabolic syndrome has in all likelihood a central neuroendocrine origin in the form of enhanced engagement of the hypothalamic-pituitary-adrenal (HPA) axis. Here the peripheral endocrine perturbations act as triggers for both central obesity and the metabolic abnormalities. The reaction pattern characterising early primary hypertension is identical with, or closely related to, the "defence reaction", while that leading to the metabolic syndrome is similar to that of the "defeat reaction". Both belong to the primitive survival reactions, common to all mammals, though man can control, or at least mask, his outward-behavioural part but not the neuro-hormonal expressions. Animal experiments show how frequent or chronic mental challenges are capable of engaging these limbic-hypothalamic centres, affecting blood pressure regulation as well as endocrine-metabolic regulation. Furthermore, these centres are tightly coupled functionally, and their signals to the periphery often combined. On a long-term basis their engagements appear to be decisive for the development of both primary hypertension and the metabolic syndrome, as suggested by intervention studies. In both these "disorders of civilisation", observations strongly indicate that psychosocial stress, socioeconomic handicaps, lack of exercise, abuse and also psychiatric traits are involved. Such factors, characteristic of current competitive society, probably cause mixed engagements of the two above-mentioned neuro-hormonal patterns, and thereby, with time, primary hypertension and the metabolic syndrome, with end-points such as coronary artery disease, diabetes mellitus type2 and stroke. Susceptibility to such developments is probably enhanced by genetic factors. This overview of recent developments therefore serves to emphasise how both primary hypertension and the metabolic syndrome seem to have a common central origin. Central regulatory factors are often overlooked, partly because it is not realised that limbic-hypothalamic centres are the major regulators of both circulatory and metabolic events, and partly because of the long period of time required before these disease end-points are reached.
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PMID:Hypertension and the metabolic syndrome: closely related central origin? 1085 28

In this paper, the possible reasons for the prevalence of hypertension in the Asia-Pacific region are examined, along with its likely dietary, nutritional and sociocultural causes. This brief survey indicates the need for more comprehensive blood pressure monitoring and surveillance throughout the region. Findings from research conducted in the region and elsewhere suggest that a variety of aetiological factors predict the occurrence of hypertension, most of which are similar to those observed in western populations. However, several lines of research suggest that obesity, abdominal obesity and a number of dietary constituents, in addition to salt. may play relatively greater roles than in western populations. It is argued that hypertension may be prevented via a combination of individual, community and governmental approaches which promote social capital, environmentally sustainable food production and the public health.
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PMID:Diet and hypertension in the Asia-Pacific region: a brief review. 1171 Mar 65

Menopause-related oestrogen deficiency increases the risk of cardiovascular disease (CVD). The presence of abdominal obesity, dyslipidemia, hypertension, fasting hyperglycaemia or impaired glucose tolerance further aggravates the CVD risk imposed by menopause. A detailed personal history should be recorded, covering PCOS, gestational diabetes mellitus, alcohol intake and smoking, as well as a family history of cardiovascular disease. Screening of the a-symptomatic post-menopausal woman should include fasting lipid profile, plasma glucose and liver, renal and thyroid function tests. Serum low-density lipoprotein cholesterol (LDL-c)>130 mg/dL is associated with an increased risk of CVD. Levels of triglycerides (TG)>or=150 mg/dL and high-density lipoprotein cholesterol (HDL-c)<or=50 mg/dL coupled with an increase in small dense LDL and very low-density lipoprotein (VLDL) particles constitute the atherogenic dyslipidemia, which characterizes the metabolic syndrome. In women with previous VTE episodes, screening for thrombophilia is advisable, as well as an estimation of baseline homocysteine and C-reactive protein (CRP). Non-pharmacological intervention should be targeted towards smoking cessation, a low-salt, low-fat, high-fibre diet and increased physical activity.
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PMID:Cardiovascular disease: screening and management of the a-symptomatic high-risk post-menopausal woman. 1614 Apr 82

In spite of a progressive fall in the incidence of traditional risk factors of cardiovascular morbidity (cigarette smoking, high blood pressure, and hyperlipidemia), there is an upward trend in the prevalence of obesity and chronic kidney disease (CKD). Furthermore, there is a strong correlation between body mass indices and the relative risk of progression of CKD. The close biophysiological interaction between obesity and CKD is evident by a similar occurrence of comorbidities including insulin resistance, hyperlipidermia, endothelial dysfunction, and sleep disorders. Truncal obesity is a primary component of metabolic syndrome; unlike peripheral fat, the visceral adipocytes are more resistant to insulin. In addition, lipolysis results in a release of free fatty acid and TG, whereas hypertriglycedemia is potentiated by uremic activation of fatty acid synthase. Hypertriglycedemia and low HDL cholesterol increase the relative risk of progression of CKD. Furthermore, endothelial inflammation and premature atherosclerosis are promoted by hyperhomocysteinemia and oxidation of LDL, both of which are commonly observed in CKD and obesity. Predominance of oxidative stress in both obesity and azotemia stimulate synthesis of angiotensin II, which in turn increases TGF-B and plasminogen activator inhibitor-1, thereby propagating glomerular fibrosis. Furthermore, local synthesis of angiotensinogen by adipocytes, leptin activation of sympathetic nervous system, and hyperinsulinemia contribute to the development of hypertension in obesity and CKD. In addition, increased renal tubular expression of Na-K-ATPase and a blunted response to natiuretic hormones in obesity promote salt and water retention. Glomerular hyperfiltration from systemic volume load and hypertension results in mesangial cellular proliferation and progressive renal fibrosis. In addition, maternal nutritional deprivation increases the incidence of obesity, hypertension, and diabetes in adulthood. Reduced fetal protein synthesis contributes to oxidative glomerular injury and impairment of renal morphogenesis. Thus, kidneys are poorly equipped to handle physiologic stress that may result from the rapid body growth and programmed metabolic dysfunction later in life. Finally, in order to minimize morbidity of obesity-related kidney disease, preventive strategy must include optimal maternal health care, promotion of healthy nutrition and routine physical exercise, and early detection of CKD.
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PMID:The role of obesity and its bioclinical correlates in the progression of chronic kidney disease. 1704 21

Predictors of diabetes and diabetes-related hospitalisations were examined in 15-88-year-old Aboriginal Australians (256 women, 258 men), surveyed in 1988-1989. Linkage to death records and hospitalisations to 2002 allowed proportional hazards or negative binomial modelling. Forty-five men (18%) and 59 women (24%) developed diabetes. Risk of diabetes was predicted positively by waist girth (hazard ratio (HR) 1.08, 95% CI 1.04, 1.13), smoking (HR 2.05, 95% CI 1.23, 3.39) and eating processed meats>4 times/month (HR 1.58, 95% CI 1.05, 2.40) and negatively by lower alcohol intake (HR 0.69, 95% CI 0.49, 0.99), preferring wine (HR 0.13, 95% CI 0.02, 0.97) and eating bush meats>4 times/month (HR 0.34, 95% CI 0.13, 0.90). Hospitalisation was predicted positively by smoking (Incidence rate ratio (IRR) 3.72, 95% CI 1.70, 8.18) and eating processed meats (IRR 1.03, 95% CI 1.01, 1.06), and negatively by exercise>or=once/week (IRR 0.23, 95% CI 0.08, 0.65), eating bush meats (IRR 0.95, 95% CI 0.91, 0.99) and trimming fat from meats (IRR 0.53, 95% CI 0.30, 0.94). Length of hospital stay was predicted positively by eating processed meats (HR 1.76, 95% CI 1.23, 2.53) and added salt (HR 1.52, 95% CI 1.02, 2.26) and negatively by lower alcohol intake (HR 0.90, 95% CI 0.40, 0.92) and exercise (HR 0.66, 95% CI 0.46, 0.95). Central obesity and adverse lifestyle increase risk for diabetes or related hospitalisation among Aboriginal Australians.
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PMID:Predictors of type 2 diabetes and diabetes-related hospitalisation in an Australian Aboriginal cohort. 1753 84


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