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[Moderate hyperhomocysteinemia and atherothrombosis]
1Instituto Universitario de Ciencias Biomédicas, Fundación Favaloro, Buenos Aires, Argentina. falcon@favaloro.edu.ar
Insights
High homocysteine levels are a risk factor for atherosclerosis. While vitamin supplements can lower homocysteine, their impact on mortality and morbidity needs more research.
Area of Science:
- Cardiovascular Science
- Nutritional Biochemistry
Context:
- Elevated plasma total homocysteine is an independent risk factor for premature atherosclerosis.
- Homocysteine levels are influenced by nutritional, environmental, and genetic factors.
- The precise mechanisms of homocysteine-induced vascular damage, including prooxidative activity, smooth muscle cell proliferation, and endothelial dysfunction, are under investigation.
Purpose:
- To review the role of homocysteine in vascular disease.
- To discuss the impact of nutritional factors, particularly vitamins, on homocysteine metabolism.
- To evaluate the current evidence for vitamin supplementation in managing homocysteine levels and related disorders.
Summary:
- Elevated homocysteine is linked to atherosclerosis, with proposed mechanisms involving oxidative stress and endothelial dysfunction.
- Folate, pyridoxine, and cyanocobalamin are key cofactors in homocysteine metabolism.
- Vitamin supplementation can reduce homocysteine levels, but its effect on clinical outcomes like mortality and morbidity requires further clinical trials.
Impact:
- Vitamin supplementation, particularly folic acid, is recommended for preventing homocysteine-related disorders in North America.
- Further clinical trials are necessary to determine if lowering moderate homocysteine levels reduces atherosclerosis-related mortality and morbidity.
- Understanding homocysteine's role is crucial for developing effective strategies against cardiovascular disease.
Abstract:
Elevated levels of plasma total hornocysteine are now accepted as an independent risk factor for premature atherosclerosis. Nutritional, environmental and genetic factors may contribute to increase the levels of homocysteine. The exact pathogenesis of vascular damage induced by homocysteine is still not completely understood. Various mechanisms have been proposed, including a significant prooxidative activity, a stimulation of smooth muscle cells proliferation and an endothelial dysfunction. Folate, pyridoxine and cyanocobalamin are important cofactors for homocysteine metabolism. In most cases, elevated homocysteine can be reduced by administration of vitamin supplements. It has not yet been demonstrated that reduction in mortality and morbidity can be achieved with these regimens. However, food supplementation with folic acid has been recommended for treatment or prevention of homocysteine-related disorders in the North American population. Appropriate clinical trials are needed to evaluate the effect of lowering moderate homocysteine levels on atherosclerosis.