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      Metabolic Syndrome in a Screened Worksite Sample: Prevalence and Predictors

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          Relatively limited contemporary information is available about the magnitude of, and factors associated with, the metabolic syndrome in adult men and women. The purpose of our observational study was to describe the prevalence and predictors of the metabolic syndrome in a sample of employed adults attending a worksite cardiovascular screening program. The study sample consisted of 871 men and women between the ages of 21 and 77 years from 6 locations of the parent company. These individuals attended an employer-sponsored cardiovascular screening and wellness program during 2003. A standardized questionnaire was administered to all study participants and a number of different coronary risk factors were measured. Approximately 27% of the study sample was classified as having the metabolic syndrome. Men, persons with a history of hypertension, heart disease, or stroke, sedentary individuals, and those with an increased heart rate and higher levels of C-reactive protein were associated with presence of the metabolic syndrome. A relatively similar risk factor profile was noted in persons without a self-reported history of prior cardiovascular disease. The results of our cross-sectional observational study suggest that the prevalence of the metabolic syndrome is considerable. A number of demographic, comorbid, and other factors are associated with this syndrome. Increased attention to the metabolic syndrome, and modification of predisposing factors, remains of considerable public health and clinical importance.

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          Most cited references 13

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          Banting lecture 1988. Role of insulin resistance in human disease.

           G M Reaven (1988)
          Resistance to insulin-stimulated glucose uptake is present in the majority of patients with impaired glucose tolerance (IGT) or non-insulin-dependent diabetes mellitus (NIDDM) and in approximately 25% of nonobese individuals with normal oral glucose tolerance. In these conditions, deterioration of glucose tolerance can only be prevented if the beta-cell is able to increase its insulin secretory response and maintain a state of chronic hyperinsulinemia. When this goal cannot be achieved, gross decompensation of glucose homeostasis occurs. The relationship between insulin resistance, plasma insulin level, and glucose intolerance is mediated to a significant degree by changes in ambient plasma free-fatty acid (FFA) concentration. Patients with NIDDM are also resistant to insulin suppression of plasma FFA concentration, but plasma FFA concentrations can be reduced by relatively small increments in insulin concentration. Consequently, elevations of circulating plasma FFA concentration can be prevented if large amounts of insulin can be secreted. If hyperinsulinemia cannot be maintained, plasma FFA concentration will not be suppressed normally, and the resulting increase in plasma FFA concentration will lead to increased hepatic glucose production. Because these events take place in individuals who are quite resistant to insulin-stimulated glucose uptake, it is apparent that even small increases in hepatic glucose production are likely to lead to significant fasting hyperglycemia under these conditions. Although hyperinsulinemia may prevent frank decompensation of glucose homeostasis in insulin-resistant individuals, this compensatory response of the endocrine pancreas is not without its price. Patients with hypertension, treated or untreated, are insulin resistant, hyperglycemic, and hyperinsulinemic. In addition, a direct relationship between plasma insulin concentration and blood pressure has been noted. Hypertension can also be produced in normal rats when they are fed a fructose-enriched diet, an intervention that also leads to the development of insulin resistance and hyperinsulinemia. The development of hypertension in normal rats by an experimental manipulation known to induce insulin resistance and hyperinsulinemia provides further support for the view that the relationship between the three variables may be a causal one.(ABSTRACT TRUNCATED AT 400 WORDS)
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            Prevalence of the Metabolic Syndrome Among US Adults

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              Metabolic syndrome with and without C-reactive protein as a predictor of coronary heart disease and diabetes in the West of Scotland Coronary Prevention Study.

              The National Cholesterol Education Program (NCEP) recently proposed a simple definition for metabolic syndrome. Information on the prospective association of this definition for coronary heart disease (CHD) and type 2 diabetes is currently limited. We used a modified NCEP definition with body mass index in place of waist circumference. Baseline assessments in the West of Scotland Coronary Prevention Study were available for 6447 men to predict CHD risk and for 5974 men to predict incident diabetes over 4.9 years of follow-up. Mean LDL cholesterol was similar but C-reactive protein was higher (P<0.0001) in the 26% of men with the syndrome compared with those without. Metabolic syndrome increased the risk for a CHD event [univariate hazard ratio (HR)=1.76 (95% CI, 1.44 to 2.15)] and for diabetes [univariate HR=3.50 (95% CI 2.51 to 4.90)]. Metabolic syndrome continued to predict CHD events (HR=1.30, 95% CI, 1.00 to 1.67, P=0.045) in a multivariate model incorporating conventional risk factors. Men with 4 or 5 features of the syndrome had a 3.7-fold increase in risk for CHD and a 24.5-fold increase for diabetes compared with men with none (both P<0.0001). C-reactive protein enhanced prognostic information for both outcomes. With pravastatin, men with the syndrome had similar risk reduction for CHD as compared with those without (HR, 0.73 and 0.69; pravastatin versus placebo). A modified NCEP metabolic syndrome definition predicts CHD events, and, more strikingly, new-onset diabetes, and thus helps identify individuals who may receive particular benefit from lifestyle measures to prevent these diseases.

                Author and article information

                S. Karger AG
                April 2005
                07 April 2005
                : 103
                : 3
                : 131-136
                aMedical Department, BAE Systems, Nashua, N.H., bAstraZeneca, Wilmington, Del., and cDivision of Cardiovascular Medicine, Department of Medicine, University of Massachusetts Medical School, Worcester, Mass., USA
                83439 Cardiology 2005;103:131–136
                © 2005 S. Karger AG, Basel

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                Page count
                Figures: 1, Tables: 3, References: 29, Pages: 6


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