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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relationships between body fatness, adipose tissue distribution, plasma glucose, insulin levels, lipoprotein levels, and resting blood pressure were studied in 81 men aged 36.0 +/- 3.3 years (mean +/- s.d.) (body mass index (BMI): 27.4 +/- 3.8 kg/m2, percentage body fat: 26.4 +/- 6.6%). Systolic and diastolic blood pressures (BP) were significantly associated with the BMI (r = 0.31, r = 0.33, P < 0.01), the waist circumference (r = 0.33, r = 0.27; P < 0.01) as well as with adipose tissue areas measured by computerized tomography (CT) (0.27 < or = r < or = 0.36, P < 0.01). Furthermore, the relative accumulation of subcutaneous abdominal fat, as estimated by the ratio of abdominal to femoral adipose tissue areas measured by CT, was positively correlated with systolic and diastolic BP (P < 0.01). Fasting plasma insulin level (r = 0.30, P < 0.01) as well as the insulin area measured during an oral glucose tolerance test (0.34 < or = r < or = 0.37, P < 0.01) were significantly correlated with blood pressure. Systolic and diastolic BP were significantly associated with HDL2-cholesterol (C) as well as with the HDL2-C/HDL3-C ratio (-0.24 < or = r < or = -0.34), whereas triglycerides (r = 0.23) and the HDL-C/C ratio (r = -0.23) were significantly correlated with diastolic BP only (P < 0.05). Multivariate analysis indicated that the insulin area was the most important variable associated with blood pressure and that this association was independent of total body fatness and regional adipose tissue distribution. Plasma insulin levels explained 14% and 11% of the variance observed in the systolic and diastolic blood pressures respectively. These results suggest that most of the association between abdominal obesity and high blood pressure is mediated by the hyperinsulinemia and/or the related insulin resistant state.
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PMID:Relation of abdominal obesity to hyperinsulinemia and high blood pressure in men. 133 43

Abdominal obesity is closely associated with risk factors for cardiocerebrovascular disease and NIDDM and the precipitation of these diseases. Together, they seem to constitute a metabolic syndrome where hyperinsulinaemia, insulin resistance, hyperlipidaemia, hypertension, visceral fat accumulation, cardiocerebrovascular disease and NIDDM are the individual constituents. The background to this syndrome might be a primary aberration expressing itself as an increased sensitivity of the hypothalamo-adrenal axis, and subsequent inhibition of sex steroid hormone secretions. This in turn will probably be followed by metabolic derangements, primarily peripheral insulin resistance, as well as by visceral fat accumulation by mechanisms which are partially visualized by recent work in the field. Visceral fat accumulation may then amplify the metabolic aberrations via hepatic effects of excessive concentrations of portal FFA, producing hyperproteinaemia, hyperglycaemia, hyperinsulinaemia and, perhaps, hypertension. The background to the central endocrine aberration remains more speculative, but factors leading to increased cortisol production, including specific stress reactions, tobacco smoking and alcohol may turn out to be important. The tentative conclusion provides a hypothesis for further work, and has recently obtained considerable support from further observations in humans in other than the endocrine and metabolic areas, as well as from studies in experimental animal models, where such factors can be studied under fully controlled conditions, which is not possible in humans for ethical reasons.
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PMID:Regional fat distribution--implications for type II diabetes. 133 83

A male fat distribution pattern with abdominal obesity increases the risk for hypertension and cardiovascular disease, and is closely linked to a number of metabolic aberrations including insulin resistance. Recent observations suggest that changes in the peripheral vasculature may be of pathophysiological importance for the development of hypertension and its associated metabolic disturbances. We therefore investigated the hemodynamic correlates of abdominal obesity. A central fat distribution was found to be associated with a specific hemodynamic profile, characterized by elevated total peripheral resistance and lower cardiac output. In response to sympathoadrenal activation during mental stress, the normal cardiac output-dependent pressor response was reversed into a systemic vasoconstrictor response. There was a direct relationship between degree of abdominal obesity (expressed as waist-hip ratio) and fasting serum insulin. Furthermore, the stress-induced increase in total peripheral resistance correlated positively with fasting serum insulin concentration, whereas there was an inverse relation between serum insulin and cardiac output and heart rate. In a second study, the circulatory responses to stress during physiological hyperinsulinemia were investigated. During hyperglycemic hyperinsulinemia the central hemodynamic response to stress was changed into a systemic vasoconstrictor response. In the forearm the physiological vasodilation during stress was markedly attenuated, suggesting that insulin may have peripheral vascular effects. In conclusion, central obesity is associated with a specific hemodynamic pattern characterized by higher total peripheral resistance and lower cardiac output, and a vasoconstrictor response to psychosocial stress. This hemodynamic response pattern may be related to insulin metabolism.
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PMID:Hemodynamics of the male fat distribution pattern. 134 31

Obesity is a multifactorial disease with a marked genetic component. The situation is further complicated by the heterogeneity of obesity demonstrated by the topographical distribution of body fat, e.g. upper body (central) and lower body (gluteal) obesity. Furthermore, the distribution of fat shows a stronger heritable tendency compared with total body fat. Central obesity is characterized by hyperinsulinaemia and insulin resistance, a feature in common with non-insulin dependent diabetes mellitus, hypertension and atherosclerosis. In order to study the molecular genetics of central obesity we have examined 56 severely obese (mean body mass index 40), unrelated British Caucasoid young non-diabetic women for associations of restriction fragment length polymorphism of candidate genes with anthropometric measurements and indices of insulin secretion and resistance. The candidate genes examined were insulin receptor, insulin sensitive glucose transporter and insulin. An association of the class 3 allele of the hypervariable region in the 5' flanking region of the insulin gene was found with upper segment obesity (P = 0.005). Furthermore, the class 3 allele was also associated with fasting hyperinsulinaemia (P = 0.01), stimulated insulin secretion (P = 0.01) and insulin resistance as calculated from the homeostatic model of assessment (HOMA; P = 0.008). No such associations were found with the other candidate genes studied. This data suggests that polymorphisms in the 5' flanking region of the insulin gene may affect expression of the gene and thereby modulate insulin production in severely obese female subjects.
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PMID:Central obesity and hyperinsulinaemia in women are associated with polymorphism in the 5' flanking region of the human insulin gene. 135 60

A public health strategy carries more constraints than a high risk strategy because it targets both low risk and high risk individuals; this requires cautious intervention and hence achieves only a modest reduction in risk. Nevertheless, a modest population-wide fall in the concentrations of atherogenic lipoproteins leads to substantial numbers of preventable heart attacks and deaths. Other strategic considerations are to lower non-lipid cardiovascular risks (hypertension, clotting tendency) and to prevent other diet-related disease (such as cancer) through interventions which lower plasma lipids. The major nutritional changes which achieve this are optimising energy balance, reducing total fats and saturated fatty acids and increasing plant foods which are rich sources of unsaturated fatty acids, fibre and antioxidants. Each of these contributes to optimising the low density lipoprotein (LDL) concentration. Antioxidants (vitamins C and E mainly) may inhibit LDL oxidation. The strategy for lowering plasma triglyceride, especially in the context of atherogenic lipoprotein phenotypes, is mainly through energy balance, reduced saturated fat and alcohol. Correcting overweight especially in those with abdominal obesity, may normalise raised plasma triglyceride, low high density lipoprotein (HDL), abnormal LDL and even glucose intolerance and hypertension, which may be associated. The scientific basis for the lipid optimising effects of the different nutrients will be discussed.
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PMID:Optimising plasma lipids: public intervention versus high risk management. 144 40

Hypertensive obese subjects run an increased cardiovascular risk. Their predominantly abdominal obesity is often associated with hypertriglyceridaemia and insulin-resistant diabetes, and their cardiovascular status is characterized by cardiac hyperdynamics and hypervolaemia responsible for left ventricular hypertrophy and dilatation. Insulin resistance and subsequent hyperinsulinaemia are thought to explain the obesity-hypertension association, the cardiovascular effects observed and the metabolic and cardiovascular complications which might result from this situation. Successful control of both arterial pressure and overweight should contribute to regression of the left ventricular hypertrophy. Simultaneous treatment of abnormalities in carbohydrate and lipid metabolism is also necessary to prevent cardiovascular complications.
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PMID:[Cardiovascular consequences of obesity associated with arterial hypertension]. 146 76

Obesity has a multifactorial origin. However, although environmental variables undoubtedly play a role in the development of obesity, it is now clear that genetic variation is also involved in the determination of an individual's susceptibility to body fat accumulation. In addition, it is also widely accepted that obesity is not a single homogeneous phenotype. It is also heterogeneous regarding its causes and metabolic complications. The regional distribution of body fat appears to be an important correlate of the metabolic complications that have been related to obesity. Due to their higher accumulation of abdominal fat, men are generally more at risk for the metabolic complications of obesity than women whereas some obese women, with large gluteal-femoral adipose depots may have a cosmetic problem which may not necessarily require medical intervention. Several studies have been conducted to understand the mechanisms by which abdominal obesity is related to diabetes, hypertension and cardiovascular disease. It appears that the increased risk of abdominal obesity is the result of complex hormonal and metabolic interactions. Studies in genetic epidemiology have shown that both total body fatness and the regional distribution of body fat have a significant genetic component. Standardized intervention studies using an identical twin design have shown that individuals that have the same genetic background tend to show similar changes in body fat and in plasma lipoprotein levels when exposed to standardized caloric excess or energy restriction. Finally, although abdominal obesity is a significant risk factor for cardiovascular disease, not every abdominal obese subject will experience metabolic complications, suggesting that some obese individuals may be more susceptible than others. Variation in several genes relevant to lipid and lipoprotein metabolism may alter the relation of abdominal obesity to dyslipoproteinemias. Abdominal obesity should therefore be considered as a factor that exacerbates an individual's susceptibility to cardiovascular disease.
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PMID:Genetic aspects of susceptibility to obesity and related dyslipidemias. 151 6

Recent prospective, epidemiological research has demonstrated the power of an increased waist/hip circumference ratio (WHR) to predict both cardiovascular disease (CVD) and non-insulin dependent diabetes mellitus (NIDDM) in men and women. Obesity, defined as an increased total body fat mass, seems to interact synergistically in the development of NIDDM, but not of CVD. Increased WHR with obesity (abdominal obesity) seems to be associated with a cluster of metabolic risk factors, as well as hypertension. This metabolic syndrome is closely linked to visceral fat mass. Increased WHR without obesity may instead be associated with lift style factors such as smoking, alcohol intake, physical inactivity, coagulation abnormalities, psychosocial, psychological and psychiatric factors. Direct observations show, and the risk factor associations further strengthen the assumption, that abdominal (visceral) obesity is more closely associated to NIDDM than CVD, while an increased WHR without obesity may be more closely linked to CVD than NIDDM. It remains to be established to what extent, if any, an increased WHR in lean men, and particularly in lean women, indicates fat distribution. Other components of the WHR measurement might be of more importance in this connection.
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PMID:Abdominal fat distribution and disease: an overview of epidemiological data. 157 56

Central obesity increases the risk for cardiovascular disease, but little is known about its hemodynamic effects. The aims were to investigate the influence of obesity (as defined by body mass index) and abdominal fat accumulation (as defined by the waist/hip ratio) on hemodynamics at rest and during mental stress. Invasive hemodynamic studies were performed in 20 healthy, normotensive young men (aged 18-22 years) recruited from an unbiased population sample. Their body mass index and waist/hip ratio ranged between 18.5 and 30.2 (mean 24.1) and 0.77 and 0.98 (mean 0.87), respectively. Hemodynamics were related to the two anthropometric indexes by bivariate regression analyses. Cardiac output and stroke volume were positively correlated to body mass index (p = 0.05 and p = 0.005), but inversely to waist/hip ratio (p = 0.01 and p = 0.01). Mental stress augmented the hemodynamic patterns. Total peripheral resistance during stress correlated inversely to body mass index (p = 0.02), whereas high waist/hip ratio was associated with higher systemic vascular resistance p = 0.002). The delta CO/delta MAP ratio, i.e., relative contribution of cardiac output for the stress-induced increase in mean arterial pressure, showed a strong positive association with body mass index (p = 0.004), but was inversely related to the waist/hip ratio (p = 0.002). Serum insulin correlated significantly to the stress-induced change in total peripheral resistance (r = 0.54; p = 0.02), whereas the increase in cardiac output was inversely related to insulin (r = -0.59; p = 0.007). Thus, central obesity is associated with a specific hemodynamic pattern characterized by higher total peripheral resistance, lower cardiac output, and a vasoconstrictor response to psychosocial stress.
Hypertension 1992 Jun
PMID:Relation of central hemodynamics to obesity and body fat distribution. 159 46

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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