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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The metabolic syndrome may be a common phenotype increasing risk for type 2 diabetes and cardiovascular disease. We assessed the prevalence and characteristics of the metabolic syndrome among population-based samples of 3,224 white subjects attending Framingham Offspring Study (FOS) exam 5 (1991-1995) and 1,081 non-Hispanic white and 1,656 Mexican-American subjects attending the San Antonio Heart Study (SAHS) phase II follow-up exam (1992-1996). Subjects were approximately 50% women, aged 30-79 years, without diabetes, and classified with the metabolic syndrome according to criteria for obesity, dyslipidemia, hyperglycemia, and hypertension proposed by the Third Report of the National Cholesterol Education Program's Adult Treatment Panel (ATP III) or the World Health Organization (WHO). We used regression models to estimate rates across ethnic groups and to assess the association of the metabolic syndrome with insulin resistance and predicted 10-year coronary heart disease (CHD) risk. Among FOS white subjects, the age- and sex-adjusted prevalence of the metabolic syndrome was 24% by both ATP III and WHO criteria; among SAHS non-Hispanic white subjects, 23 and 21%, respectively; and among SAHS Mexican-American subjects, 31 and 30%. Rates were highest among Mexican-American women (ATP III, 33%) and lowest among white women (21%). Subjects with the metabolic syndrome by ATP III criteria had higher age-, sex-, and ethnicity-adjusted levels of fasting insulin (11.3 micro U/ml), homeostasis model assessment of insulin resistance (2.7), and predicted CHD risk (11.8%) than those without the syndrome (5.9 micro U/ml, 1.3, and 6.4%, respectively; all P = 0.0001); differences were similar using WHO criteria. We conclude that the metabolic syndrome typically affects 20-30% of middle-aged adults in the U.S. By any criteria, subjects with the metabolic syndrome are more insulin resistant and at increased predicted risk for CHD versus those without the metabolic syndrome.
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PMID:Prevalence and characteristics of the metabolic syndrome in the San Antonio Heart and Framingham Offspring Studies. 1288 36

Although low-density lipoprotein cholesterol (LDL-C) remains the primary target for coronary heart disease (CHD) prevention in the latest guidelines of the National Cholesterol Education Program, many individuals who have CHD do not have substantially elevated LDL-C but have derangement of other lipid fractions, most commonly low levels of high-density lipoprotein cholesterol (HDL-C). In the guidelines, HDL-C is important in risk stratification in primary prevention, influencing the need for and intensity of treatment of LDL-C, and both HDL-C and triglyceride are defined as risk factors for the metabolic syndrome, a secondary target of therapy. Triglyceride level also determines in which individuals non-HDL-C should be a secondary target of therapy. Risk assessment that takes into account the entire lipid profile will identify more high-risk individuals than evaluating LDL-C alone. Some epidemiologic data suggest that instead of measuring the cholesterol in LDL or HDL, measuring their respective apolipoproteins, apolipoprotein (apo) B-100 and apo A-I, may improve CHD risk assessment, and in some observational and interventional studies, ratios of lipids and/or apolipoproteins have been better predictors of CHD risk than levels of any one lipid fraction. Trials of lipid-modifying therapy also suggest that apolipoproteins and ratios may provide improved targets for therapy beyond LDL-C, but optimal values have not been established. Because lipid-modifying therapy affects multiple components of the lipid profile, the effect on all lipid parameters should be considered when selecting the most appropriate agent. Therapies with beneficial effects across the lipid profile would be expected to improve CHD risk reduction.
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PMID:Role of lipid and lipoprotein profiles in risk assessment and therapy. 1289 Nov 89

Using recently updated guidelines to evaluate and manage lipid disorders is discussed. Coronary heart disease (CHD) is a costly chronic condition associated with significant morbidity and mortality. Epidemiologic data further indicate that dyslipidemia and associated conditions, which may lead to CHD, are grossly undertreated. In 2001, the third National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP III) released updated guidelines for the evaluation and treatment of lipid disorders. Significant changes to the updated guidelines include designation of a CHD risk equivalent category identifying patients who require aggressive management, recommendation of Framingham-based CHD risk assessment in patients with multiple risk factors, revised target levels for several of the lipids and lipoproteins, and criteria for the identification of patients with the metabolic syndrome. Low-density lipoprotein cholesterol (LDL-C) continues to be the primary target of therapy. In addition, non-high-density lipoprotein cholesterol (HDL-C) is now defined as a secondary treatment target in patients with hypertriglyceridemia. Increased emphasis is placed on the metabolic syndrome, low HDL-C levels, and the presence of multiple and emerging risk factors in guiding the intensity of therapy. The NCEP ATP III guidelines acknowledge challenges in implementing and maintaining patient adherence to both lifestyle changes and pharmacotherapy regimens and provide strategies for increasing treatment success. Implementation of these new guidelines will likely enhance identification, management, and treatment success rates among patients at risk for CHD in the United States.
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PMID:Role of the National Cholesterol Education Program Adult treatment panel III guidelines in managing dyslipidemia. 1290 Oct 24

The use of niacin, alone and in combination, for the treatment of dyslipidemia in patients with or at risk for coronary heart disease (CHD), is discussed. Cardiovascular risk is independently predicted not only by high levels of low-density lipoprotein cholesterol (LDL-C), but also low levels of high-density lipoprotein cholesterol (HDL-C) and elevated triglycerides. Moreover, we now understand that LDL particle size and number are associated with differing levels of atherogenicity. Metabolic syndrome, increasingly being recognized as a marker for elevated cardiovascular risk, is associated with atherogenic dyslipidemia characterized by low HDL-C, high triglycerides, and small, dense LDL particles. Controlled clinical studies have shown that niacin therapy effectively increases HDL-C and lowers triglyceride and LDL-C levels while causing a shift toward larger, less atherogenic LDL particles. Niacin, alone or in combination, prevents progression and promotes regression of coronary atherogenic lesions and significantly reduces CHD-related morbidity and mortality. Statin monotherapy causes modest increases in HDL-C and decreases triglycerides, while more potently reducing LDL-C. Combinations of lipid-modifying agents may better address the full spectrum of lipoprotein abnormalities in some patients. Investigations have shown that combining statin therapy with niacin results in additive improvement in the major lipids and lipoproteins and improves clinical outcome. With recently broadened treatment recommendations, it seems likely that combination therapy will be increasingly deemed the appropriate choice for addressing a range of lipid abnormalities.
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PMID:Advances in the understanding and management of dyslipidemia: using niacin-based therapies. 1290 Oct 26

With an evolving landscape of a growing number of obese and/or type 2 diabetic patients in our affluent population, the metabolic syndrome has become a major issue because of its impact on cardiovascular disease risk. In this regard, although it is appropriate to aim at a better glycaemic control in type 2 diabetic patients, hyperglycaemia does not appear to be the main culprit responsible for the markedly increased cardiovascular disease risk in this population. Rather, studies have suggested that a cluster of metabolic abnormalities, which includes an atherogenic dyslipidaemic state, an impaired glucose/insulin homeostasis, and a pro-thrombotic and inflammatory profile, substantially increases the risk of coronary heart disease in type 2 diabetic patients in a manner which is partly independent of glycaemic control. These results imply that in order to reduce the risk of atherosclerotic macrovascular disease in type 2 diabetic patients, physicians need not only to focus on a better glycaemic control but also to improve the features of the metabolic syndrome. As a consequence, in order to evaluate the clinical benefits of pharmacotherapy in type 2 diabetic patients, we need to quantify the impact of any pharmacological intervention beyond glucose control. In this context, metformin has been shown to not only contribute to a better glycaemic control but also to induce some weight loss (especially in the visceral depot) which may contribute to the improvement of the features of the metabolic syndrome. Thus, metformin treatment may represent a relevant element of an integrated lifestyle modification-pharmacotherapy to prevent not only type 2 diabetes but also cardiovascular disease.
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PMID:Potential contribution of metformin to the management of cardiovascular disease risk in patients with abdominal obesity, the metabolic syndrome and type 2 diabetes. 1450 1

Short-term studies consistently show that raising the carbohydrate content of the diet increases serum triacylglycerol concentrations. As compared with starches, sugars (particularly sucrose and fructose) tend to increase serum triacylglycerol concentrations by approximately 60%. The magnitude of the effect depends on other aspects of the diet, including the total amount of carbohydrate and the types of fat, carbohydrate, and fiber, but definitive studies to describe the dose-response relations are not available. Longer-term studies show that some high-carbohydrate diets are not associated with increased fasting serum triacylgycerol concentrations. However, sedentary subjects with upper-body and visceral obesity who have the metabolic syndrome tend to be at higher risk for hypertriglyceridemia in response to high-sucrose and high-carbohydrate diets; moderate weight loss mitigates the effect. Hyperinsulinemia or insulin resistance may play a role in promoting higher rates of VLDL synthesis and hypertriglyceridemia in obesity, but the mechanisms remain unclear. The effect of fructose in promoting triacylglycerol synthesis is independent of insulinemia, however. In terms of the long-term effects of diets high in sugars on the risk of cardiovascular disease, available epidemiologic evidence indicates no association of sugars or total carbohydrate intake per se, but high dietary glycemic load is associated with higher serum triacylglycerol concentrations and greater risk of coronary heart disease in women. Studies are needed to delineate the independent effects of dietary sugars and glycemic load on serum triacylglycerol concentrations in lean and obese men and women and to determine whether the elevations in fasting and fed concentrations of serum triacylglycerol with high-carbohydrate and high-sugars diets are associated with increased risk of cardiovascular disease.
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PMID:Sugars, hypertriglyceridemia, and cardiovascular disease. 1452 52

Considerable data on the pathophysiology, epidemiology, and treatment of dyslipidemia-induced coronary heart disease (CHD) have accumulated in recent years. These data have been assessed and incorporated into the guidelines of the National Cholesterol Education Program Expert Panel on the Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel [ATP] III). A major focus of the new guidelines is the assessment of the near-term (i.e., 10-yr) risk of experiencing a CHD event and matching the intensity of treatment to this risk. Patients with diabetes and those with a greater than 20% 10-year risk of experiencing a CHD event have been elevated to the risk level of CHD equivalent. The ATP III guidelines also modify several lipid and lipoprotein classifications. A low-density lipoprotein cholesterol (LDL) level below 100 mg/dl is now considered optimum for all individuals. In addition, high-density lipoprotein cholesterol (HDL) and triglyceride cutoff points have been modified to reflect more accurately the risk associated with abnormalities in these lipoproteins. As with the previous guidelines, the primary target of therapy remains LDL. Therapeutic lifestyle changes consisting of diet, weight reduction, and increased physical activity should be included in all treatment regimens. Based on their potent LDL-lowering properties and their proven ability to decrease mortality in a variety of patient populations, statins are generally the first choice for pharmacologic therapy. A secondary target of therapy includes non-HDL goals for patients with high triglyceride levels and the metabolic syndrome, which is characterized by abdominal obesity, elevated triglyceride levels, low HDL levels, and insulin resistance. Management of these secondary targets includes weight reduction and increased physical activity, and treatment of the lipid and nonlipid risk factors. Overall, ATP III represents an aggressive approach to treating dyslipidemia, greatly extending the number of individuals who qualify for treatment.
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PMID:Update on the National Cholesterol Education Program Adult Treatment Panel III guidelines: getting to goal. 1452 36

Negative emotions, such as depression and anxiety, have been associated with the development of coronary heart disease (CHD). In multivariate models, negative emotions have predicted CHD outcomes, such as nonfatal myocardial infarction and CHD mortality. Few studies, however, have investigated this relation while controlling for variables associated with the metabolic syndrome or those indicative of sympathetic nervous system activity. We prospectively examined the relation between negative emotions and incident CHD in older men (mean 60.3 +/- 7.9 years) participating in the Normative Aging Study (NAS). Four hundred ninety-eight men who completed the Minnesota Multiphasic Personality Inventory (MMPI) and who participated in a subsequent laboratory assessment were included in the study. All men were not on medication and free of diagnosed CHD and diabetes. Negative emotions were measured by the MMPI Welsh A scale, which is comprised of 39 items measuring symptoms of depression and anxiety. Negative emotion score, sociodemographic characteristics, health behaviors, components of the metabolic syndrome, and stress hormones were used to predict incident CHD over a 3-year follow-up period. During follow-up, 45 CHD events were observed. In unadjusted logistic regression analyses, negative emotions significantly predicted the incidence of CHD (odds ratio [OR] 1.06, 95% confidence interval [CI] 1.01 to 1.10, p = 0.02). After adjusting for potential covariates, negative emotions continued to predict the incidence of CHD (OR 1.06, 95% CI 1.01 to 1.12, p = 0.02) A linear, dose-response relation was observed (chi-square 10.8, degree of freedom 2, p = 0.005): participants who had the highest level of negative emotions experienced the greatest incidence of CHD.
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PMID:Effect of negative emotions on frequency of coronary heart disease (The Normative Aging Study). 1455 63

During the past several decades, obesity has increased substantially, making it a true epidemic and a public health crisis that both health care providers and the public are going to have to face. Currently, 61% of the US population is overweight or obese and therefore at increased risk for a number of diseases that are associated with increased body fat. Indeed, the obesity epidemic already is leading to dramatic increases in type 2 diabetes and the metabolic syndrome. Almost a quarter of the population currently has metabolic syndrome, which places them at high risk for the development of coronary heart disease. The future of the general health of the US population depends on identifying and providing the best treatment and prevention strategies for obesity in the years ahead.
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PMID:The prevalence of obesity. 1456 47

Available evidence clearly indicates a rapid progression in the prevalence of obesity worldwide. As a consequence, there has also been a marked increase in the prevalence of type 2 diabetes all over the world and this chronic metabolic disease is now considered as a coronary heart disease risk equivalent. However, even in the absence of the hyperglycaemic state which characterizes type 2 diabetic patients, non diabetic individuals with a specific form of obesity, named abdominal obesity, often show clustering metabolic abnormalities which include high triglyceride levels, increased apolipoprotein B, small dense low density lipoproteins and decreased high density lipoproteins-cholesterol levels, a hyperinsulinemic-insulin resistant state, alterations in coagulation factors as well as an inflammatory profile. This agglomeration of abnormalities has been referred to as the metabolic syndrome which can be identified by the presence of three of the five following variables: abdominal obesity, elevated triglyceride concentrations, low HDL-cholesterol levels, increased blood pressure and elevated fasting glucose. Post-mortem analyses of coronary arteries have indicated that obesity (associated with a high accumulation of abdominal fat measured at autopsy) was predictive of earlier and greater extent of large vessels atherosclerosis as well as increase of coronary fatty streaks. Metabolic syndrome linked to abdominal obesity is also predictive of recurrent coronary events both in post-myocardial infarction patients and among coronary artery disease men who underwent a revascularization procedures. It is suggested that until the epidemic progression of obesity is stopped and obesity prevented or at least properly managed, cardiologists will be confronted to an evolving contribution of risk factors where smoking, hypercholesterolemia and hypertension may be relatively less prevalent but at the expense of a much greater contribution of abdominal obesity and related features of the metabolic syndrome.
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PMID:[Obesity and cardiovascular disease]. 1461 4


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