![]() ![]() The use of elevated fasting insulin alone as a reflection of insulin resistance simplifies the definition, but it also means that patients with T2D cannot be diagnosed as having metabolic syndrome, since fasting insulin may not be a useful measure of insulin resistance in such patients. In this case, insulin resistance is defined by a fasting plasma insulin value that is greater than the 75th percentile. Like the WHO, the EGIR felt that insulin resistance is central to the pathophysiology of the metabolic syndrome, so it also requires it for the definition. In 1999, the European Group for the Study of Insulin Resistance (EGIR) proposed a modification to the WHO definition ( Balkau and Charles, 1999). Because some of the measurements are not performed routinely, for example, euglycemic clamp studies, this definition is not easily applied clinically and does not lend itself as well to large epidemiologic studies, where rapid and simple assessment is important. The WHO definition also allows patients with T2D to be diagnosed with metabolic syndrome if they meet the other criteria. The definition mandates that insulin resistance be present without it, even if all the other criteria were met, the patient would not have metabolic syndrome. The WHO definition was the first to tie together the key components of insulin resistance, obesity, dyslipidemia and hypertension. These include obesity, dyslipidemia, hypertension and microalbuminuria. In addition to this absolute requirement for insulin resistance, two additional criteria have to be met. Finally, euglycemic hyperinsulinemic clamp studies could be used as evidence of insulin resistance. Alternatively, other measures could serve as evidence of insulin resistance, such as an elevated homeostatic model assessment of insulin resistance (HOMA-IR) value, which is proportional to the product of the fasting insulin and fasting glucose level. This could be impaired fasting glucose or impaired glucose tolerance (IGT, defined as a glucose level above a predetermined cutoff, commonly 140 mg/dl, for 120 minutes after ingestion of 75 grams of glucose load during an oral glucose tolerance test). Because insulin resistance was felt to be central to the pathophysiology of metabolic syndrome, evidence for insulin resistance is an absolute requirement in the WHO definition. The World Health Organization (WHO) first developed its definition in 1998 ( Alberti and Zimmet, 1998). ![]() Table 1 summarizes four of the most commonly used definitions of metabolic syndrome. Third, it facilitates epidemiological and clinical studies of pharmacological, lifestyle and preventive treatment approaches.Ĭurrent definitions of metabolic syndrome Second, by considering the relationships between the components of metabolic syndrome, we may be able to better understand the pathophysiology that links them with each other and with the increased risk of CVD. First, it identifies patients who are at high risk of developing atherosclerotic CVD and type 2 diabetes (T2D). ![]() The metabolic syndrome is a clustering of hyperglycemia/insulin resistance, obesity and dyslipidemia. This clustering of some risk factors and their shared responsiveness to lifestyle modifications suggests that they are not independent of one another and that they share underlying causes, mechanisms and features ( Grundy et al., 2005 Kahn et al., 2005). Furthermore, the lifestyle modifications of dietary change and increased physical activity can significantly affect several risk factors simultaneously and, in so doing, reduce the risk of CVD. It has become increasingly clear that certain CVD risks tend to cluster, or occur together. The risk of CVD can be decreased by addressing these individual risk factors, both by lifestyle modifications and, if appropriate, pharmacologic treatment ( National Cholesterol Education Program, 2002). Of these risks, some can be modified – for example, cessation of smoking – whereas others, like genetic predisposition, cannot. Age increases the risk of CVD, as does male gender and post-menopausal hormonal status. These risk factors include a family history of premature coronary disease, hypertension, hyperlipidemia, diabetes and smoking. Physicians and scientists have long known that certain conditions increase a person’s risk of developing atherosclerotic cardiovascular disease (CVD). ![]()
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