Homocysteine, Iron and Cardiovascular Disease: A Hypothesis
AbstractElevated 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
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Baggott, J.E.; Tamura, T. Homocysteine, Iron and Cardiovascular Disease: A Hypothesis. Nutrients 2015, 7, 1108-1118.
Baggott JE, Tamura T. Homocysteine, Iron and Cardiovascular Disease: A Hypothesis. Nutrients. 2015; 7(2):1108-1118.Chicago/Turabian Style
Baggott, Joseph E.; Tamura, Tsunenobu. 2015. "Homocysteine, Iron and Cardiovascular Disease: A Hypothesis." Nutrients 7, no. 2: 1108-1118.