The metabolic syndrome (MetS) consists of a constellation of vascular risk factors and metabolic abnormalities comprising (1) centrally distributed obesity; (2) atherogenic dyslipidemia, characterized mainly by elevated triglycerides and decreased high-density lipoproteins; (3) high blood pressure; and (4) hyperglycemia.1 This cluster of highly interrelated factors appears to increase the individual’s risk of vascular disease by promoting the development of atherosclerotic vascular disease and type II diabetes mellitus.2
It is important to recognize that the MetS is a syndrome and not a defined uniform entity. In the effort to introduce the MetS into clinical practice, diverse organizations have used different diagnostic criteria, which may respond to 2 main different conceptual approaches to the syndrome (Table). The first approach focuses on the pathogenesis of MetS and considers insulin resistance as the common physiological abnormality that can lead to the clustering of the mentioned metabolic risk factors and therefore as a main therapeutic target.3–5 The second approach responds to a more pragmatic view and has the purpose of identifying people at higher long-term risk for atherosclerotic vascular disease who may deserve clinical intervention to reduce vascular risk.6,7 These distinct conceptual views of the MetS have probably contributed to a lack of certainty regarding its pathogenesis and value as a cardiovascular disease risk marker.8,9 Therefore, for now, we will attempt to follow a comprehensive and pathogenesis-based approach to MetS to make our exposition more intelligible.
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