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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is now well recognized that insulin resistance and/or hyperinsulinemia are characteristic of a number of common human disease states including obesity, non-insulin dependent diabetes mellitus (NIDDM), essential hypertension, and atherosclerotic cardiovascular disease. More recent evidence suggests that impaired insulin action and elevated levels of circulating insulin may also be present in a substantial proportion of apparently healthy nonobese individuals. Considerable attention is now being focused on the potential long term adverse consequences of elevated circulating insulin levels. In particular, the frequent concurrence of these clinical disorders of carbohydrate metabolism, lipid metabolism, and vascular disease has led to the hypothesis that insulin resistance and the ensuing hyperinsulinemia may be a common pathophysiologic factor in the etiology of these disease states. In this review, we will examine the evidence for this hypothesis with particular attention to the adverse effects of chronic hyperinsulinemia.
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PMID:Hyperinsulinemia and its sequelae. 220 24

Based on postmortem records at the Wayne County Medical Examiners' Office from 1982 to 1986, autopsy results indicated that the deaths of 129 persons aged 20-34 resulted from heart disease: 51 of these deaths were attributed to atherosclerotic cardiovascular disease (ASCVD), 29 to hypertensive cardiovascular disease, 28 to cardiomyopathy, and 21 to other cardiac causes. The majority of the deaths due to ASCVD occurred among men, both black and white, followed by black women, and the incidence increased with age. All of these deaths due to ASCVD were sudden and accounted for all deaths due to ischemic heart disease in this age group among Wayne County residents. Diabetes mellitus, left ventricular hypertrophy, a history of seizures, and the recent ingestion of alcohol were all found to be associated with sudden death from ASCVD in this group. Obesity did not seem to be a significant factor. These data suggest that ASCVD is not rare as a cause of death in young adults and some of the risk factors identified in older subjects also operate in this age group.
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PMID:Atherosclerotic cardiovascular disease and sudden deaths among young adults in Wayne County. 222 Jul 3

Obesity and lipid abnormalities are powerful independent predictors of both diabetes and cardiovascular disease. Nutrition affects the rate of atherogenesis in elderly patients with diabetes. Excess calories worsen glucose tolerance; recent studies relate dietary fats both to serum cholesterol levels within populations and to the development of coronary disease. Dietary and drug interventions for hypercholesterolemia have been found to reduce coronary disease rates. Some nutrients also elevate blood pressure, which further accelerates diabetic atherogenesis. For elderly diabetic patients who are at high risk of atherosclerotic cardiovascular disease, control of diabetes should include--in addition to normalization of blood sugar levels--correction of blood lipids and control of weight and blood pressure.
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PMID:Obesity and nutrition in elderly diabetic patients. 370 87

We evaluated 935 patients for risk factors of cholecystectomy. Factors assessed included reason for cholecystectomy, preoperative laboratory values, sex, age, weight, presence of associated disease, and pathologic findings. Evaluation revealed an overall significant complication rate of 10.50% and a mortality of 1.07%. Risk factors were age over 60 years, hypertension, atherosclerotic cardiovascular disease with prior heart failure, and acute cholecystitis. Incidental cholecystectomy was associated with an increased risk due to concomitant associated disease. Patients with obesity and uncomplicated diabetes had the same risk as the general population.
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PMID:Risk factors for cholecystectomy: analysis of 935 patients. 661 88

Important nutrition concepts will aid primary care/generalist physicians to implement practical aspects of health promotion and disease prevention in their practice, and improve the overall health of their patients. In today's society, chronic diseases that are related variably to overnutrition and dietary excesses or imbalances (obesity, diabetes mellitus, hypertension and atherosclerotic cardiovascular disease, some cancers) warrant knowledgeable diet modifications in high-risk individuals. However, serious nutritional deficiency diseases also still occur (as in alcoholic patients), and instituting appropriate diet and supplements will aid in preventing further morbidity and mortality. Nutrition knowledge changes with new scientific evidence, and the physician must be aware of reliable sources of continuing education and information appropriate for the practitioner and the patient.
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PMID:Nutrition concepts for the primary care/generalist physician. 783 65

Primary hypertension is a frequent polygenic disease with strong genetic and environmental components. During the last decade, evidence has been increasing that insulin resistance as a marker of increased risk for Type 2 diabetes and cardiovascular atherosclerotic disease is present not only in individuals with obesity, Type 2 diabetes and impaired glucose tolerance, but also in the majority of the hypertensive population. Insulin resistance describes a tissue- and pathway-specific defect of glucose metabolism present in the so called 'metabolic syndrome'. Hyperinsulinaemia compensates for insulin resistance, leading to a cluster of undesirable processes predisposing to diabetes, atheroma and, directly or indirectly, hypertension. Candidate mechanisms whereby this metabolic syndrome might lead to hypertension include renal sodium retention, vascular hyperresponsiveness, arteriolar smooth muscle cell proliferation, altered cellular electrolyte transport and composition, stimulation of sympatho-adrenergic activity and growth promoting effects. Insulin per se does not appear to be the cause of elevated blood pressure as frequently seen in insulin-resistant states, but it may act with other factors to promote hypertension and atherosclerotic cardiovascular disease.
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PMID:New aspects of insulin resistance in hypertension. 799 75

Hyperinsulinemia is very much in the spotlight. Debate rages as to its significance and role in the etiology not only of NIDDM, but also other morphological and metabolic risk factors for atherosclerotic cardiovascular disease, including upper-body obesity, dyslipidemia, hypertension, and hyperuricemia. Epidemiological data support a key role for hyperinsulinemia in these disorders but it is far from conclusive except for the fact that hyperinsulinemia and insulin resistance may be present many years before the onset of impaired glucose tolerance and NIDDM, and clearly play a role in their etiology. The thrifty genotype hypothesis provides a plausible basis for a better understanding of how hyperinsulinemia and insulin resistance could lead to glucose intolerance and atherosclerotic cardiovascular disease, but the detailed biochemical mechanisms remain elusive. A role for increased sympathetic nervous system activity, resulting from hypothalamic stimulation as a primary event causing hyperinsulinemia, cannot be excluded as a cause of hyperinsulinemia. The current focus on hyperinsulinemia also has resulted in closer examination of the therapy of diabetes and hypertension, emphasizing the need to avoid hyperinsulinemia in both IDDM and NIDDM individuals because of the putative risk of atherosclerotic cardiovascular disease and hypertension. There is still a paucity of epidemiological data to support a role for hyperinsulinemia in the etiology of hypertension. However, clinical practice already is being influenced by the fact that ACE inhibitors have been shown to reduce insulin resistance in clinical research studies. The research reviewed here, particularly that relating to hyperinsulinemia, insulin resistance, and cardiovascular disease risk factors, has opened new vistas for the treatment and prevention of NIDDM and atherosclerotic cardiovascular disease. Appropriate exercise clearly is associated with improved insulin sensitivity, modification of CVD risk factors, and lower prevalence of NIDDM. Upper-body obesity, the latest culprit in the field, can also be reduced by exercise. Hyperinsulinemia and insulin resistance can be detected in children, adolescents, and young adults. NIDDM can be prevented, but clearly, intervention needs to commence in childhood, and intensive risk factor intervention in subjects with NIDDM can reduce the risk of atherosclerotic cardiovascular disease. It seems paradoxical that prevention of NIDDM and atherosclerotic cardiovascular disease are now possible even though the biochemical and molecular basis of these disorders is not fully understood.
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PMID:Hyperinsulinemia--how innocent a bystander? 829 79

Atherosclerotic cardiovascular disease is a complex problem involving lipid deposition, pressure, rheologic forces, carbohydrate tolerance and thrombogenesis. The major contributors identified through epidemiologic research include atherogenic personal attributes, living habits which promote them, signs of a compromised coronary circulation and host susceptibility to these risk factors. Of the atherogenic risk attributes, such as blood lipids, blood pressure, glucose tolerance and fibrinogen, each independently contributes to risk, and the risk associated with any one is compounded by the presence of the others. The risk associated with hypertension, hyperlipidemia or diabetes varies widely depending on the level of associated risk factors. Also, at a given level of total cholesterol, risk is greatly affected by the total/HDL cholesterol ratio, which provides a practical means for assessing the two-way traffic of cholesterol. In addition, living habits, such as cigarette smoking or lack of exercise, can independently affect the risk associated with any of the atherogenic traits. These living habits, obesity and diet can also affect the level of atherogenic risk factors and must be taken into account in assessing risk and implementing preventive measures. Finally, preclinical indicators of silent myocardial ischemia greatly augment the risk associated with a poor cardiovascular risk profile. Hence, ECG left ventricular hypertrophy, blocked intraventricular conduction, repolarization abnormalities and abnormal response to exercise on monitoring must be taken into consideration. Optimal risk predictions require a quantitative synthesis of risk factors into a composite estimate. Handbooks, hand calculators and PC software have been devised for office use based on multiple logistic risk formulations. These have been shown to accurately predict disease risk in a variety of American population samples, in elderly as well as young coronary candidates. Preventive management as well as risk estimation should be multifactorial if optimal results are to be achieved. Preventive strategies should include public health measures to alter the ecology so as to shift the distribution of risk factors to a more favorable level, health education to enable people to protect their own health and preventive medicine for high-risk candidates. Greater skill must be developed to carry out such interventions. In selecting drugs to correct hypertension, diabetes and lipid disorders, it is important to choose agents which do not adversely affect the composite risk profile.
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PMID:Long-term epidemiologic prediction of coronary disease. The Framingham experience. 832 76

Childhood obesity is predictive of obesity as an adult, and individual differences in body weight relative to height (body mass index) in adults are important predictors of morbidity as well as mortality from atherosclerotic cardiovascular disease. The observation of strong familial correlations does not ensure that genes are involved in the determination of body mass index, because individuals in families share environments as well as genes. However, several recent studies have found evidence for both additive (polygene) and nonadditive (major gene) components. A question that results from these analyses is--what gene(s) has been inherited that carries an associated risk, most likely mediated by environmental exposures, for obesity? Studies to identify genetic loci linked to familial obesity should add to our understanding of the genetic factors involved in the determination of obesity and may lead to early identification of individuals and families at high risk for the chronic disorders that are associated with obesity.
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PMID:Genetic models of human obesity--family studies. 835 94

Insulin resistance is found in association with obesity, non-insulin-dependent diabetes mellitus, and essential hypertension, which are all risk factors for atherosclerotic cardiovascular disease. Furthermore, hyperinsulinemia has been reported in familial combined hyperlipoproteinemia and endogenous hypertriglyceridemia. Finally, relatively high serum triglyceride and low high-density lipoprotein (HDL) cholesterol concentrations invariably accompany hyperinsulinemia. Whether insulin sensitivity is affected by the isolated presence of high levels of serum low-density lipoprotein (LDL) cholesterol has not been clearly established. We studied 13 subjects with heterozygous familial hypercholesterolemia (FHC) and 15 normocholesterolemic subjects selected to be free of any other known cause of insulin resistance. Thus FHC patients and controls had normal body weight and fat distribution, glucose tolerance, blood pressure, and serum triglyceride and HDL cholesterol concentrations, but were completely separated on plasma LDL cholesterol concentrations (6.05 +/- 0.38 v 3.27 +/- 0.15 mmol/L, P < .0001). Fasting plasma levels of glucose, insulin, free fatty acids (FFA), and potassium and fasting rates of net carbohydrate and lipid oxidation were superimposable in the two study groups. During a 2-hour euglycemic (approximately 5 mmol/L) hyperinsulinemic (approximately 340 pmol/L) clamp, whole-body glucose disposal rates averaged 30.4 +/- 2.3 and 31.1 +/- 3.0 mumol.kg-1 x min-1 in FHC and control subjects, respectively (P = 0.88). The ability of exogenous hyperinsulinemia to stimulate carbohydrate oxidation and energy expenditure and suppress lipid oxidation and plasma FFA and potassium levels was equivalent in FHC and control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin sensitivity in familial hypercholesterolemia. 841 51


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