Abstract

Obesity is a growing epidemic. Obesity is not just a cosmetic matter but a serious health problem. Obesity is part of the metabolic syndrome and an established risk factor for type 2 diabetes, cardiovascular disease, and, notably, for myocardial infarction. 1 Mechanistically, the common denominator underlying the metabolic syndrome, the development and progression of systemic atherosclerosis, and ultimately even the acute initiation of myocardial infarction by the rupture of an atherosclerotic coronary plaque is inflammation.2 Apparently, not all obesity is created equal, in that abdominal/visceral adipose tissue is a particular risk factor3 and a particular source of inflammation.4 More specifically, visceral adipose tissue differs from subcutaneous adipose tissue in that visceral adipose tissue produces and secretes cytokines, as well as factors that promote vasoconstriction and thrombosis.5 See accompanying article on page 2063 Clearly, obesity results from an energetic imbalance of caloric intake and expenditure; clearly, also, there is a genetic predisposition to such energetic imbalance through a number of factors that affect energy metabolism, its neuroindocine control, and energy expenditure and its efficiency. The most …

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