(Circulation. 2003;107:2632.)
© 2003 American Heart Association, Inc.
Editorials |
From the Cardiovascular Health Research Unit, Departments of Medicine (D.S.S., R.N.L.) and Epidemiology (D.S.S.), and Veterans Affairs Puget Sound Health Care System (D.M.), University of Washington, Seattle, Wash.
Correspondence to David S. Siscovick, MD, MPH, CHRU, 1730 Minor Ave #1360, Seattle, WA 98101. E-mail dsisk@u.washington.edu
Key Words: Editorials fish oils fatty acids, n-3 polyunsaturated diet sudden death
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Clinicians frequently are asked whether dietary fat intake influences the risk of coronary heart disease (CHD). However, many clinicians remain unclear about the role of dietary fat and fatty acids in the occurrence of CHD. The original dietheart hypothesis focused on dietary saturated fat intake, serum cholesterol, and atherosclerosis; and, after more than 3 decades of research, it remains a source of controversy.1 Recent studies have focused on other dietary fatty acids, the n-3 polyunsaturated fatty acids (PUFAs) found in fish oil, and on a specific manifestation of CHD, sudden cardiac death.24 These studies suggest potentially large effects associated with modest dietary intake of n-3 PUFAs, but the findings also seem to conflict with other reports in the scientific literature.5,6 As a result, there is considerable clinical skepticism about the role of dietary fat and fatty acids in efforts to reduce CHD.
See p 2646
The original dietheart hypothesis was characterized by the following syllogism: (1) Dietary saturated fat intake increases serum cholesterol; (2) high serum cholesterol leads to atherosclerosis; and (3) atherosclerosis results in CHD morbidity and mortality. Taken individually, each element of this syllogism is supported by scientific evidence from one or more paradigms, including animal-experimental, genetic, pathological, nutritional, and ecological studies. However, epidemiological studies within populations have failed to consistently support the original dietheart hypothesis. Some have attributed these negative studies to error in the measurement of saturated fat intake and/or a limited range in saturated fat intake within populations. Although a large, clinical primary prevention trial
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