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Henry C. McGill, Jr, MD; C. Alex McMahan, PhD

JAMA. 2003;290:2320-2322.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

For more than 50 years, it has been known that atherosclerosis begins in childhood and progresses through adolescence and young adulthood to cause coronary heart disease (CHD) in middle age and later.¹ Although previously considered an inevitable consequence of aging, atherosclerosis is now thought to be caused by a number of genetic-environmental interactions. Risk factors, including intervening variables (eg, elevated levels of low-density lipoprotein cholesterol [LDL-C]) and environmental exposures (eg, cigarette smoking) predict the incidence of CHD in adulthood and are associated with advanced atherosclerotic lesions. A vast body of knowledge about the molecular and cellular biology of atherosclerosis now provides plausible mechanisms for a causal relationship among risk factors, atherogenesis, and clinical CHD.

For years, debate raged about whether modification of risk factors in adults, particularly lowering serum cholesterol levels, would reduce risk of CHD. The answer to that question . . . [Full Text of this Article]

Author Affiliations: Southwest Foundation for Biomedical Research, San Antonio, Tex (Dr McGill); and Department of Pathology, The University of Texas Health Science Center at San Antonio (Drs McGill and McMahan).

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