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Nutrients 2015, 7(2), 1108-1118; doi:10.3390/nu7021108

Homocysteine, Iron and Cardiovascular Disease: A Hypothesis

Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, AL 35294, USA
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Received: 23 October 2014 / Accepted: 27 January 2015 / Published: 6 February 2015
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Abstract

Elevated circulating total homocysteine (tHcy) concentrations (hyperhomocysteinemia) have been regarded as an independent risk factor for cardiovascular disease (CVD). However, several large clinical trials to correct hyperhomocysteinemia using B-vitamin supplements (particularly folic acid) have largely failed to reduce the risk of CVD. There is no doubt that a large segment of patients with CVD have hyperhomocysteinemia; therefore, it is reasonable to postulate that circulating tHcy concentrations are in part a surrogate marker for another, yet-to-be-identified risk factor(s) for CVD. We found that iron catalyzes the formation of Hcy from methionine, S-adenosylhomocysteine and cystathionine. Based on these findings, we propose that an elevated amount of non-protein-bound iron (free Fe) increases circulating tHcy. Free Fe catalyzes the formation of oxygen free radicals, and oxidized low-density lipoprotein is a well-established risk factor for vascular damage. In this review, we discuss our findings on iron-catalyzed formation of Hcy from thioethers as well as recent findings by other investigators on this issue. Collectively, these support our hypothesis that circulating tHcy is in part a surrogate marker for free Fe, which is one of the independent risk factors for CVD. View Full-Text
Keywords: iron; homocysteine; cardiovascular disease; methionine; thioether iron; homocysteine; cardiovascular disease; methionine; thioether
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Baggott, J.E.; Tamura, T. Homocysteine, Iron and Cardiovascular Disease: A Hypothesis. Nutrients 2015, 7, 1108-1118.

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