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Folate and homocysteine
1Department of Clinical Biochemistry, Institute of Clinical Science, Royal Victoria Hospital, Queen's University Belfast, Belfast, UK.
Insights
High homocysteine levels are linked to cardiovascular disease risk. Supplementing with folate and B vitamins lowers homocysteine and improves blood vessel function, but clinical trial results are pending.
Area of Science:
- Cardiovascular Medicine
- Nutritional Biochemistry
- Renal Medicine
Background:
- Hyperhomocysteinaemia is an independent risk factor for cardiovascular disease (CVD).
- Elevated plasma total homocysteine is observed in renal impairment, potentially as a consequence of CVD.
- Plasma total homocysteine may promote CVD via effects on endothelial function and coagulation.
Purpose of the Study:
- To explore the role of hyperhomocysteinaemia in cardiovascular disease.
- To investigate the impact of B-group vitamins and genetic factors on homocysteine metabolism.
- To assess the efficacy of vitamin supplementation on homocysteine levels and endothelial function.
Main Methods:
- Epidemiological studies identified hyperhomocysteinaemia as a CVD risk factor.
- Analysis of factors influencing plasma total homocysteine, including renal function, B-group vitamins (especially folate), and gene polymorphisms.
- Review of studies on vitamin supplementation and its effects on homocysteine and endothelial function.
Main Results:
- Folate and B-vitamin supplementation effectively reduces total plasma homocysteine levels.
- Vitamin supplementation has been shown to improve endothelial function.
- The precise impact of these interventions on cardiovascular morbidity and mortality requires further clinical trials.
Conclusions:
- Hyperhomocysteinaemia is a significant risk factor for cardiovascular disease.
- B-group vitamins, particularly folate, play a crucial role in homocysteine metabolism and cardiovascular health.
- Further clinical trials are necessary to confirm the cardiovascular benefits of homocysteine-lowering therapies.
Abstract:
Hyperhomocysteinaemia has been identified from epidemiological studies as an independent risk factor for cardiovascular disease. Plasma total homocysteine is elevated in renal impairment, which may be a consequence of cardiovascular disease. However, it is also likely that plasma total homocysteine promotes cardiovascular disease, particularly through effects on endothelial function and coagulation pathways. It is influenced by complex interactions between B-group vitamins, especially folate, and polymorphisms in various genes involved in homocysteine metabolism. Supplementation with folate and other B-group vitamins effectively lowers total plasma homocysteine and improves endothelial function. The results of clinical trials to assess effects on cardiovascular morbidity and mortality are awaited.