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Why a Cluster is Truly a Cluster: Insulin Resistance and Cardiovascular Disease

¹ Stanford University School of Medicine, Stanford, CA

^aAddress correspondence to this author at: Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford Medical Center, Falk CVRC, 300 Pasteur Drive, Stanford, CA 94305. Fax 650-725-1599; e-mail greaven@cvmed.stanford.edu.

The first 20% of the full text of this article appears below.

The 2 major definitions of the metabolic syndrome (MetS) are based on disparate views as to the etiology of this diagnostic category. Proponents of the Adult Treatment Panel III (ATP 3) version(1) consider this entity to be "truly is a syndrome," a grouping of atherosclerotic cardiovascular disease risk factors that probably has more than one cause. In contrast, adherents to the International Diabetes Federation (IDF) definition feel that there is a specific cause of their version of the MetS(2), stating that "central obesity is an early step in the etiological cascade leading to the full metabolic syndrome."

I believe the view expressed by the proponents of the ATP III version of the MetS that there is no single "cause" of the components is true at the most simplistic level, but misleading, whereas the notion that abdominal obesity is the "cause" of these components, as expressed by the adherents to the IDF version, can be challenged.

one or multiple causes of the mETs?

The fundamental question is whether there is one root cause that can explain the clustering of the components that comprise the various metabolic conditions thought to indicate the presence of the MetS, not whether any individual component can have more than one cause. It is obvious that any of these individual metabolic abnormalities, e.g., glucose intolerance, high triglyceride (TG) or low HDL cholesterol (HDL-C) concentration, and high blood pressure, can have more than one cause. For example, hypertriglyceridemia can result from a deficiency of lipoprotein lipase and hypertension from renal artery stenosis. Ample evidence exists, however, that insulin resistance and compensatory hyperinsulinemia increase the risk of all of these individual metabolic abnormalities, and I know of no other mechanistic explanation that fulfills that role. The substantial evidence in support of this view cannot be summarized in the context of . . . [Full Text of this Article]

how central is central obesity?

Conclusions

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