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Search for the Ironclad Evidence

Frank B. Hu, MD, PhD

JAMA. 2007;297:639-641.

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

The iron-heart hypothesis first put forth by Sullivan¹ in 1981 suggests that increased body iron stores are a risk factor for coronary heart disease (CHD) and thus that iron depletion through phlebotomy or other means can reduce risk. The hypothesis, which was based on markedly lower incidence of CHD in premenopausal women (who lose iron through menstruation) compared with men and postmenopausal women, is intuitively appealing and seems to be well-grounded in biochemistry.

Iron is an essential mineral and an important component of the oxygen-transporting and storage proteins hemoglobin (in red blood cells) and myoglobin (in muscles).² Conversely, free ferrous iron in the body is a catalyst for the formation of hydroxyl radicals, powerful prooxidants that attack cellular membranes, proteins, and nucleic acids.³ Iron-catalyzed lipid oxidation has been implicated in increased formation of the circulating oxidized form of low-density lipoprotein cholesterol, which is thought to . . . [Full Text of this Article]

Author Affiliations: Departments of Nutrition and Epidemiology, Harvard School of Public Health; and Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass.

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