Abstract
Elevated homocysteine (HCY) is a risk factor for a variety of vascular and neuropsychiatric pathologies. Although long recognized as a contributor to disease, and as an amino acid that is destructive to cell integrity and DNA, agents that were developed specifically to lower homocysteine were not available until very recently. Those agents are mainly composed of B vitamins in their metabolized forms, as they function as coenzymes in the pathway of homocysteine degradation. It is no surprise that hyperhomocysteinemia is most often the result of low B6, B9, or B12 levels; however, blood levels may not always reflect levels in the central nervous system (CNS), where HCY metabolism is most critical. HCY levels may also be normal in the periphery but not reflect CNS levels, where vascular, neuronal, and DNA damage is occurring. This article discusses the basics of HCY, its proposed mechanisms of toxicity, and the clinical consequences of hyperhomocysteinemia. [ Psychiatr Ann . 2015;45(9):463–468.]
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