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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:368.)
© 2003 American Heart Association, Inc.

Editorials

Is Oxidant Stress a Connection Between Obesity and Atherosclerosis?

Jason D. Morrow

From the Departments of Medicine and Pharmacology, Vanderbilt University School of Medicine, Nashville, Tenn.

Correspondence to Jason D. Morrow, MD, Departments of Medicine and Pharmacology, Vanderbilt University School of Medicine, 526 RRB, 23rd and Pierce Aves, Nashville, TN 37232-6602. E-mail jason.morrow@vanderbilt.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The marked increase in the incidence of overweight and obese persons is recognized as one of the most serious public health issues in the United States. It is estimated that currently >60% of American adults are overweight and 20% are obese.¹ Overweight and obesity are associated with a significantly increased mortality from atherosclerotic cardiovascular disease and other causes.^2–4 Although obesity itself appears to augment the incidence of cardiovascular events, it is also associated with major risk factors for atherosclerosis including hyperlipidemia, diabetes mellitus, hypertension, and the metabolic syndrome.^1,5 How obesity and each of these risk factors are involved mechanistically in atherosclerosis have been areas of intense research but are poorly understood. A panel of experts assembled by the National Institutes of Health recently concluded that the study of mechanisms by which obesity contributes to atherosclerosis should be a high priority.¹ The report by Keaney et al⁶ in this issue of Arteriosclerosis, Thrombosis, and Vascular Biology provides evidence that increased systemic oxidant stress may be an important mechanism by which obesity increases the incidence of atherosclerotic cardiovascular disease.

See pages 365 and 434

Enhanced oxidant stress, occurring either locally in the arterial wall or systemically, is one hypothesis to explain the development and progression of atherosclerosis in humans.^7–9 In particular, oxidative modification of the lipid components of LDL has been hypothesized as causative. LDL is deposited in the vascular wall early in the course of atherosclerotic lesion development where it is oxidized.¹⁰ There is evidence both in vitro and in animal . . . [Full Text of this Article]

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