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Published on: July 9, 2015
Hyperhomocyst(e)inemia
Key1
1University of Minnesota Medical School and Minnesota Vascular Diseases Center, Box 480 Mayo, Harvard St. at East River Road, Minneapolis, MN 55455, USA.
Insights
High homocysteine levels (hyperhomocysteinemia) may increase cardiovascular risk. While low vitamin intake is a common cause, further research is needed to confirm if vitamin supplementation effectively prevents atherosclerotic disease.
Area of Science:
- Cardiovascular Science
- Nutritional Science
- Epidemiology
Background:
- Hyperhomocysteinemia is increasingly recognized as a risk factor for atherosclerotic disease across arterial circulations.
- It is also associated with an increased risk of venous thromboembolism.
- Low dietary intake of vitamin B6 and folic acid is the primary cause of elevated homocysteine levels.
Purpose of the Study:
- To investigate whether hyperhomocysteinemia itself or other effects of vitamin deficiency contribute to cardiovascular risk.
- To determine the efficacy of vitamin supplementation in preventing atherosclerotic disease through prospective randomized studies.
Main Methods:
- Prospective epidemiologic studies are underway to address the relationship between homocysteine and cardiovascular risk.
- The need for prospective randomized trials to evaluate vitamin supplementation for primary and secondary prevention of atherosclerotic disease is highlighted.
Main Results:
- The precise role of hyperhomocysteinemia versus vitamin deficiency in cardiovascular risk remains an unresolved question.
- Evidence from ongoing studies is crucial for clarifying the causative factors.
Conclusions:
- Lifestyle modifications and vitamin supplementation to lower homocysteine are recommended as safe interventions.
- Definitive evidence is required before advocating treatments with higher potential toxicity for hyperhomocysteinemia.
- Further research, particularly randomized controlled trials, is essential to establish clinical benefits.
Abstract:
Hyperhomocyst(e)inemia is under scrutiny as a novel risk factor for atherosclerotic disease in the coronary, cerebral, and peripheral arterial circulations. It also appears to be a risk factor for venous thromboembolism. Low dietary intake of vitamins B(6) and folic acid is the most prevalent cause of hyperhomocyst(e)inemia. A critical unresolved question is whether hyperhomocyst(e)inemia itself, or alternatively some other effect of low vitamin levels, is the true determinant of excess cardiovascular risk. This issue is currently being addressed by prospective epidemiologic studies. There is also an urgent need for prospective randomized studies to determine whether vitamin supplementation is beneficial in the primary or secondary prophylaxis of atherosclerotic disease. In the meantime, lifestyle modifications and vitamin supplementation to reduce plasma homocysteine levels can be recommended, because these are innocuous interventions that may well prove to be beneficial. Until there is definitive evidence that treatment of hyperhomocyst(e)inemia does in fact alter clinical outcomes, however, other therapies that possess the potential for greater toxicity cannot be justified.
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