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The relationship between overweight and cardiovascular disease was a matter of debate for many years. Recent studies have demonstrated that obesity defined as body mass index of 30 kg/m2 or higher is associated with an exponential increase of cardiovascular complications. This effect is largely mediated by the induction of established risk factors such as dyslipidemia, hypertension and type 2 diabetes mellitus. Recently, there is growing evidence that the occurrence of most complications of obesity depends not only on the degree of overweight but also on the pattern of body fat distribution. Many data suggest that the anatomical localization of body fat is more important for the risk of developing complications than the adipose tissue mass per se. An abdominal, upper-body type of fat distribution, which can be easily determined by the measurement of waist and hip circumferences (waist/hip ratio = WHR), is also a confirmed risk factor for metabolic disturbances, hypertension and atherosclerosis, independent of body weight. However, the clinical appearance of these disturbances is frequently associated with the development of obesity. This network of metabolic disorders and their vascular complications is termed "metabolic syndrome" or "syndrome X" (Table 2). Abdominal obesity is now known to be closely associated with the metabolic syndrome and is regarded to represent its readily recognizable phenotypic feature. The components of the metabolic syndrome are characterized by varying forms and degrees of insulin resistance. It is assumed that insulin resistance, defined as diminished biological response to the action of insulin, represents the primary defect or at least the common pathogenetic link between these disturbances.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Abdominal obesity and coronary heart disease. Pathophysiology and clinical significance]. 771 76

The metabolic syndrome usually goes along with abdominal obesity: diabetes type II, hypertension, dyslipidemia, and gout are often associated. The common characteristic is the resistance to insulin action. Reasons for the metabolic syndrome are--besides a genetic determination--overnutrition, physical inactivity, and alcohol consumption. Therefore, a causal therapy aims at the elimination of these factors. Consequently, the non-pharmacological therapy of the metabolic syndrome should be emphasized. The most important treatment is the reduction of body weight in the presence of obesity which is relevant for almost 90% of the patients. Body weight can rapidly be diminished by hypocaloric diets. Both, conventional reducing diets or formula diets may be used for weight reduction. Total fasting should not be performed for several reasons. For minor weight reduction or weight maintenance following a period of rapid weight loss with a hypocaloric diet, increased physical activity also lowers weight or prevents relapsing. Aims of therapeutical procedures are the elimination or amelioration of insulin resistance and subsequently the diseases of the metabolic syndrome. Both methods, reducing diet and physical training, act on various factors related to insulin resistance. For example, hypocaloric diets activate thyroxine kinase of the insulin receptor and reduce glucose and insulin in plasma. Physical training reduces not only insulin and glucose in plasma but also free fatty acids in addition and increases capillary density in skeletal muscle. Using the glucose clamp technique, diets and training are equally effective in improving glucose metabolism. Compared to these non-pharmacological methods drugs are less convincing. Since the non-pharmacological treatment implies behavioral changes with regard to nutrition, physical activity and alcohol consumption, simple instructions are not sufficient. Usually long-lasting changes in life style are necessary in order to achieve health improvement. Therefore, health care programs on individual or social basis are required in order to improve nutrition and increase physical activity. However, long-acting effects are difficult to achieve in adults; more promising is the prevention of insulin resistance.
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PMID:[Non-pharmacological therapy of metabolic syndrome]. 771 78

We examined whether the association of regional fat distribution with stress, defined in terms of vital exhaustion, and depression varies according to the total amount of body fat accumulation in healthy middle-aged men (n = 64). Regional fat distribution was measured using the waist-to-hip circumference ratio (WHR), and the total amount of body fat accumulation was measured using the body mass index (BMI). The results indicate that WHR in lean men was associated with characteristics contrary to those in moderately obese men. In lean men WHR tended to be associated with a high level of stress, while in moderately obese men an association was found with a low level of stress and a low level of depressive symptomatology. The present results support the suggestion that there is a difference between abdominal obesity at different degrees of generalized obesity, and they are likely to further our understanding about the differing risk for cardiovascular disorders posed by abdominal obesity in lean men compared to abdominal obesity in moderately obese men.
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PMID:Association of stress and depression with regional fat distribution in healthy middle-aged men. 773 33

Type IIB muscle fibres are among the most insulin-insensitive muscle fibres and are not adapted to oxidation of fat during muscle work. The first characteristic of this type of muscle fibre most probably reflects or contributes to further development of insulin resistance contribute to further perpetuation of obesity and to the channeling of excess free fatty acids to the liver followed by secondary deterioration of its function. The impaired functioning of the liver is epitomized, among other changes, by impairment of insulin extraction. The increasing hyperinsulinaemia is followed by inhibition of synthesis of specific proteins such as carrier proteins for transporting testosterone (sex hormone binding globulin, SHBG). This results in an increased free testosterone concentration which induces androgenization in women and may further increase insulin insensitivity in abdominal obesity in women. The poor capillarization and changed muscle morphology in spite of great interindividual variety is observed in several pathological conditions characterised by insulin sensitivity (stroke, PCO, hypertension, diabetes, obesity). It is suggested that, in addition to the previous concept of the main role of intraabdominal adipose tissue, even muscles and liver are also important organs contributing to the pathogenesis and development of the metabolic syndrome.
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PMID:Role of muscle morphology in the development of insulin resistance and metabolic syndrome. 783 Dec 32

To determine the prevalence of coronary risk factors and coronary heart disease (CHD) in rural Rajasthan, 1150 randomly selected individuals in a cluster of villages in central Rajasthan have been studied. These included 805 men and 345 women. The prevalence of various coronary risk factors in the whole group were: Smoking 488 (42.4%); Diabetes (history): 5(0.4%); Alcohol intake: 146 (12.7%); Sedentary lifestyle: 797 (69.3%); Stressful life events: 48 (4.2%); Hypertension (BP > or = 140/90) 152 (13.2%); obesity (BMI > or = 27 Kg/M2): 194 (10.9%); and Truncal obesity (waist:hip > or = 0.93): 20.8%. The overall prevalence of CHD was 46.1/1000. Patients with CHD had a higher prevalence of male sex (67.9 vs 51.5%); educated persons (30.2 vs 28.8%); businessmen (13.2 vs 10.2%); smoking (47.2 vs 40.5%); sedentary lifestyle (75.5 vs 62.3%); stressful life events (7.5 vs 4.8%); and hypertension (26.4 vs 14.8%). On the other hand, persons without CHD had higher prevalence of alcohol intake (10.8 vs 7.5%); regular prayers (23.1 vs 22.6%); physically active lifestyle (37.7 vs 24.5%); obesity (13.6 vs 6.9%), and truncal obesity (21.0 vs 20.0%). The following risk factors emerged significant on statistical analysis (Odds ratio, 95% confidence intervals): male sex (1.99, 1.04 to 3.7); hypertension (2.04, 1.01 to 4.09); male smokers (1.80, 1.28 to 4.09); and sedentary lifestyle (1.86, 1.01 to 3.59). This study shows a low prevalence of CHD in rural population which is however more than previously reported studies from India.
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PMID:Coronary heart disease and coronary risk factor prevalence in rural Rajasthan. 783 42

Two long and broad streams of medical literature, from the 1950's to date, have established the existence of two unrelated abnormalities of androgen production in women with breast cancer. One is the genetically determined presence of subnormal production of adrenal androgens (i.e. DHEA and DHEAS) in women with premenopausal breast cancer and their sisters, who are at increased risk for breast cancer. The other is excessive production of testosterone, of ovarian origin, in subsets of women with either premenopausal or postmenopausal breast cancer and women with atypical breast-duct hyperplasia, who are at increased risk for breast cancer; along with the hypertestosteronism, there is frequently chronic anovulation in the premenopausal patients. The combination of ovarian hypertestosteronism and chronic anovulation is characteristic of the polycystic ovary syndrome and is also frequently seen in women with abdominal ("android") obesity; both PCOS and abdominal obesity are known to be characterized by high risk for postmenopausal cancer. The elevated testosterone levels and the increased levels of insulin, IGF-I, and IGF-II that are seen in PCOS and abdominal obesity could favor the development of breast cancer in several ways, all of which have been demonstrated experimentally: binding of testosterone to cancer cells bearing testosterone receptors, with direct stimulation; intratissular aromatization of testosterone to estradiol, with stimulation of estrogen-sensitive cells; stimulation of the production of epithelial growth factor (EGF) by testosterone, with direct mitogenic effect of EGF on cancer cells; stimulation of aromatase by insulin and IGF-I; direct mitogenic stimulation of cancer cells by insulin, IGF-I, and IGF-II; and stimulation by IGF-I and IGF-II of the intratissular reduction of estrone to estradiol. Since PCOS is probably largely genetically determined, and abdominal obesity may also be, the hypertestosteronism of these conditions may represent a second genetically determined hormonal risk factor for breast cancer.
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PMID:Abnormal production of androgens in women with breast cancer. 784 May 9

The health consequences of an adverse body-fat distribution (e.g., android, upper-body, visceral) have only recently concerned the medical community. Ninety years ago, however, actuarial study demonstrated the relationship of body-fat distribution to the mortality experience of insured, North American men. Thirty-four insurance companies pooled their data on males issued life policies between 1870 and 1899. Special classes of risk were defined by weight for height at baseline or by the observation that abdominal girth exceeded the girth of the expanded chest (abdominal obesity). The mortality experience of each risk class was compared to an age-stratified, actuarial table of the period. We present new analyses of these historical data relating specifically to the mortality impact of abdominal obesity. Among 163,567 overweight men, the prevalence of abdominal obesity increased with age and with degree of overweight. Among moderately overweight men, those with abdominal obesity experienced 133% of the expected mortality rate compared to 112% of the expected mortality for those who were not abdominally obese. Severely overweight men with abdominal obesity experienced 152% of the expected mortality compared to 135% of the expected mortality for severely overweight men who were not abdominally obese. We believe this nineteenth-century, acturial study of waist and chest girths was the first demonstration that body-fat distribution can influence longevity. These early actuarial findings, taken with more recent reports, establish that abdominal enlargement, but not necessarily an 'upper-body' fat distribution, constitutes a major health hazard. Future research must establish which abdominal-obesity index best predicts disease outcomes.
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PMID:Abdominal obesity and mortality risk among men in nineteenth-century North America. 786 64

Obesity is frequently associated with a dyslipidaemic state. Several metabolic and epidemiological studies published in the 1980s have, however, emphasized the importance of considering the regional distribution of body fat in the assessment of the health hazards of obesity. The development of imaging techniques such as computed tomography has also allowed it to be established that the fat located in the abdominal cavity, i.e. the visceral adipose tissue, was the critical correlate of the metabolic complications found in abdominal obesity which include insulin resistance and hyperinsulinaemia, glucose intolerance, hypertriglyceridaemia, hypoalphalipoproteinaemia and increased concentrations of dense LDL particles. Furthermore, since several genes are involved in the regulation of plasma lipoprotein-lipid levels and they have been reported to show polymorphism, visceral obesity should be considered as a permissive factor that exacerbates an individual's susceptibility to dyslipidaemia and premature coronary heart disease rather than a primary regulator of the dyslipidaemic state observed in visceral obese patients. Finally, as insulin resistance and the level of visceral adipose tissue are two main correlates of the dyslipidaemic state which characterizes abdominal obesity, treatment should be aimed at reducing visceral fat and improving insulin sensitivity. Prospective studies are clearly warranted to evaluate the potential benefits of such interventions on the incidence of coronary heart disease.
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PMID:Dyslipidaemia and obesity. 798 Mar 50

Recently waist/hip ratio (WHR), a marker of body fat distribution, has been described as a risk factor for cardiovascular disease (CVD). The aim of the present study was to evaluate the influence of body fat distribution on metabolic, haemostatic and haemorheological pattern in premenopausal obese women with different WHR. Fourty premenopausal obese women were subdivided into two groups, matched for age and body mass index (BMI): 20 women with abdominal obesity (WHR = 0.94 +/- 0.02) and 20 women with peripheral obesity (WHR = 0.77 +/- 0.03). Twenty nonobese women were recruited as control group. The abdominal obesity group had significantly higher blood glucose, triglycerides, total cholesterol, Apolipoprotein B and plasma insulin levels and lower high density lipoprotein (HDL) cholesterol and Apolipoprotein A1 levels than the control group. All the haemostatic (figrinogen, Factor VII, plasminogen activator inhibitor (PAI) activity and tissue plasminogen activator (t-PA) antigen (Ag) pre venous occlusion (VO)) and haemorheological parameters (haematocrit, whole blood filterability, blood and plasma viscosity) were significantly higher in the abdominal obesity group as compared to the control group. In contrast, mean values of t-PA (Ag) post VO were significantly lower in abdominal obese women. Moreover positive correlations between WHR and plasma insulin (r = 0.68, p < 0.05), between WHR and fibrinogen (r = 0.63, p < 0.05) and between WHR and PAI pre VO (r = 0.71, p < 0.05) and a negative correlation between WHR and t-PA (Ag) post VO (r = -0.55, p < 0.05) were found.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Coagulation, fibrinolysis and haemorheology in premenopausal obese women with different body fat distribution. 799 33

We examined the effect of the pattern of body-fat distribution on the modification of atherogenic risk factors in obese adolescent girls during weight reduction. During the 6-wk program, which included a mixed diet of 4321 kJ/d and intensive physical exercise, the girls lost 8.5 +/- 2.4 kg and their waist-to-hip ratio (WHR) decreased from 0.86 +/- 0.05 to 0.81 +/- 0.05 (P < 0.01). Significant reductions were observed for total cholesterol, LDL cholesterol, uric acid, fasting insulin, and systolic and diastolic blood pressure. Girls with abdominal obesity (WHR > 0.88) had greater reductions in serum cholesterol, LDL cholesterol, and uric acid than did girls with gluteal-femoral obesity (WHR < 0.81). In a multivariate-regression analysis these differences could be partly explained by the greater weight loss of the girls with abdominal obesity. These results suggest that during weight reduction girls with abdominal obesity exhibit more beneficial changes in the atherogenic-risk-factor profile than do girls with gluteal-femoral obesity, partly because of a greater weight loss.
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PMID:Body-fat distribution and changes in the atherogenic risk-factor profile in obese adolescent girls during weight reduction. 801 38


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