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

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 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

All large prospective studies (n greater than 20,000) and several smaller studies have found that severe obesity [body mass index (BMI) greater than or equal to 35 kg/m2] is associated with approximately a twofold increase in total mortality and in a severalfold increase in mortality due to diabetes, cerebro-, and cardiovascular disease, and certain forms of cancer. Studies that have not been able to confirm this have been small and/or short term, have failed to control for smoking or early mortality, have controlled for intermediate risk factors in an inappropriate way, or have a reduced internal validity due to misclassification biases. As compared with BMI, abdominal obesity is a stronger predictor of mortality in most studies available. The incidence of sudden death unexplained by autopsy may be up to 40 times higher in severely obese subjects as compared with the general population. A small weight increase since the age of 18 is associated with a decreased risk whereas weight increases greater than 10 kg are associated with an increased mortality. The total mortality ratio for severe obesity decreases from 55 y of age and is not detectable above 80 y of age. Studies lacking adequate control groups indicate that a sustained weight loss may induce a reduced mortality but results from controlled intervention studies are so far not available.
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PMID:Mortality of severely obese subjects. 153 Oct 97

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.
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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

Medical writings on cardiovascular disease focus on intravascular pressures. Tissue pressure is assumed to be essentially atmospheric. Yet, under dynamic conditions of sitting, standing, walking, breathing, and the beating of the heart, significant pressures, both above and below atmospheric, do develop outside of important arteries. These dynamic extra-arterial pressures either decrease or increase the pressure gradients across arterial walls, i.e. the transmural pressures are changed. Physical fitness may either prevent the development of negative extra-arterial pressure or increase positive extra-arterial pressure, thereby protecting important arteries from high effective pressures. Deconditioning, old age, abdominal obesity, and other cardiovascular disease risk factors may do just the opposite, in effect, causing 'localized hypertension' in clinically important arteries. This, in turn, may lead to localized acceleration of atherosclerosis. The correlation of predictions made from this hypothesis with clinical findings is so remarkable that it suggests there is a direct cause and effect relationship between transmural arterial pressure and atherosclerosis. The concept of dynamic extra-arterial pressure seems to solve a number of puzzles and paradoxes in cardiovascular disease, it suggests key measurements that may be predictive of disease, and it offers new ideas for treatment and prevention.
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PMID:Physical fitness, dynamic extra-arterial pressures, and the pathogenesis and distribution of atherosclerosis. 178 17

Risk of cardiovascular events was determined over 24 years of surveillance in relation to general adiposity reflected by relative weight and by regional obesity estimated by skinfolds and waist girth per inch of height. Upper quintile values of relative weight, subscapular skinfolds and waist girth were each associated with increased risks of cardiovascular disease in both sexes. Risk of total cardiovascular events increased with the degree of regional, central or abdominal obesity. Mortality from cardiovascular disease was also increased. Increased relative weight and central obesity were both associated with increased risk factors including cholesterol, blood pressure, glucose and uric acid. Changes in weight were mirrored by changes in risk factors with linear trends over a 15 lb range of weight fluctuations. Subscapular skinfold and the ratio of subscapular-to-triceps skinfold, measures of central obesity, were in either sex also associated with an increased probability of coronary attacks in particular. The subscapular skinfold contributed to CHD risk independent of body mass index (BMI). Multivariate analyses taking all the risk factors into account indicate an independent effect of abdominal obesity on stroke, cardiac failure and cardiovascular and all-cause mortality in men. In women, only the subscapular-to-triceps skinfold ratio independently contributes to CHD, cardiovascular and all cause mortality. Regional obesity appears to be an independent contributor to cardiovascular disease at a given level of general adiposity, its effect only partially mediated through promotion of other known risk factors. These data suggest that cardiovascular disease is as closely linked to abdominal as to general adiposity.
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PMID:Regional obesity and risk of cardiovascular disease; the Framingham Study. 199 75

This review concentrates on recent prospective studies concerning evaluation of the health risk of obesity with special reference to the impact of the distribution of the adipose tissue. Analysis of the data indicates that adipose tissue localized to the abdominal region (especially intraabdominal fat) is associated with an enhanced risk profile including elevated levels of triglycerides and insulin, low levels of high density lipoprotein-cholesterol and elevated blood pressure. Abdominal obesity, determined by the waist/hip ratio, was associated with cardiovascular disease, premature death and non-insulin demanding diabetes mellitus. On the other hand, the total fat mass (measured as body mass index) was positively associated only with non-insulin demanding diabetes mellitus. The androgen/estrogen activity seems to be an important factor for determining the topographical localization of the adipose tissue. The great amount of free fatty acids which may be released from the abdominal fat tissue seemed to be of great pathogenetic importance for the metabolic consequences of abdominal obesity. In conclusion, obesity and the abdominal localization of adipose tissue seem to be two separate entities with different pathogenesis and clinical consequences. The abdominal obesity is the type which is predominantly associated with enhanced health risks. These associations may result in an altered strategy of treatment of the obese population.
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PMID:[Health risks of obesity. Significance of the regional distribution of adipose tissue]. 202 93

The health risks of obesity increase with its severity and reach significance at a weight greater than 20% above optimal, by using life insurance tables, or at a body mass index greater than 27. Risks include hypertension, insulin resistance and diabetes mellitus, cardiovascular disease, hypertriglyceridemia, low high-density-lipoprotein cholesterol, and, in some studies, high total-and low-density-lipoprotein cholesterol. There is an increased mortality from endometrial cancer in women and from colorectal cancer in men. Chronic hypoxia and hypercapnia, sleep apnea, gout, and degenerative joint disease can occur with more severe obesity. The distribution of body fat is directly related to these health risks. Abdominal obesity is more dangerous than gluteal-femoral obesity because the amount of intraabdominal fat seems to determine much of the increased peril; therefore, risks of cardiovascular disease, stroke, hypertension, and diabetes increase with abdominal obesity, even independently of total fat mass.
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PMID:Health implications of obesity. 203 92


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