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For these reasons, an Initial Regulatory Flexibility Analysis is not required for the proposed Special Requirements for REHs

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Homocysteine and Cardiovascular Disease Homocysteine mediates adverse effects on the blood vessels through diverse pathways: homocysteine isoforms directly damage the blood vessel walls11 interactions between homocysteine and low-density lipoprotein (LDL) cholesterol contribute to subendothelial plaque genesis3 post-translational modifications of LDL particles, promoting the formation of foam cells and plaque progression12 increased peroxide production and reduced glutathione peroxidase activity increase endothelial cell damage13 reduced nitric oxide availability results in vasoconstriction11 activation of monocytes leads to cytokine secretion and inflammation3,14 platelet activation and aggregation, reduced thrombomodulin expression, depressed protein-C activity, and tissue plasminogen activator cause dysregulation of the coagulation system.3,15,16 Hyperhomocysteinemia is also associated with impaired hepatic capacity to synthesize apoA-I, thereby lowering HDL particle concentrations.17 Although the association between Hcy and vascular disease is widely recognized, elevated Hcy has also been associated with the following disorders and diseases: Deficiency of folic acid or vitamins B6/B12 : Elevated homocysteine levels are most commonly caused by low levels of one or all of these B vitamins