What question did this study set out to answer?

To review the relationship between elevated homocysteine levels, MTHFR genetic mutations, and the risk of arterial and venous thrombosis, as well as the utility of vitamin supplementation.

May 16, 2005Circulation

Homocysteine and MTHFR Mutations

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Authors

LVLiz VargaLoughborough University ASAmy C. SturmThe Ohio State University Wexner Medical Center CMCaron P. MisitaUniversity of North Carolina at Chapel Hill

Discussion

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Implication

Review describes clinical risks of hyperhomocysteinemia and MTHFR variants, suggesting homocysteine level rather than genotype dictates management.

Key Points

To review the relationship between elevated homocysteine levels, MTHFR genetic mutations, and the risk of arterial and venous thrombosis, as well as the utility of vitamin supplementation.
Narrative clinical review summarizing the pathophysiology, testing protocols, and dietary or genetic causes of hyperhomocysteinemia.
Synthesized findings from published clinical trials and meta-analyses examining MTHFR variants (C677T and A1298C) and B-vitamin interventions.
Elevated homocysteine is associated with approximately a twofold increase in the risk of coronary artery disease and venous thrombosis.
Although supplementation with folic acid, vitamin B6, and vitamin B12 effectively reduces homocysteine levels, randomized trials show no reduction in recurrent vascular events or blood clots.
MTHFR genetic variants do not independently elevate cardiovascular or thrombotic risk when baseline homocysteine levels remain within the normal range.

Cite This Study

Varga et al. (2005) studied this question.

synapsesocial.com/papers/6aa8b47457fd01e647ef733e https://doi.org/10.1161/01.cir.0000165142.37711.e7

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May 16, 2005Circulation

Homocysteine and MTHFR Mutations

View Full Paper

Ask AI

Bookmark

Authors

LVLiz VargaLoughborough University ASAmy C. SturmThe Ohio State University Wexner Medical Center CMCaron P. MisitaUniversity of North Carolina at Chapel Hill

Discussion

Member takes

Implication

Review describes clinical risks of hyperhomocysteinemia and MTHFR variants, suggesting homocysteine level rather than genotype dictates management.

Key Points

To review the relationship between elevated homocysteine levels, MTHFR genetic mutations, and the risk of arterial and venous thrombosis, as well as the utility of vitamin supplementation.
Narrative clinical review summarizing the pathophysiology, testing protocols, and dietary or genetic causes of hyperhomocysteinemia.
Synthesized findings from published clinical trials and meta-analyses examining MTHFR variants (C677T and A1298C) and B-vitamin interventions.
Elevated homocysteine is associated with approximately a twofold increase in the risk of coronary artery disease and venous thrombosis.
Although supplementation with folic acid, vitamin B6, and vitamin B12 effectively reduces homocysteine levels, randomized trials show no reduction in recurrent vascular events or blood clots.
MTHFR genetic variants do not independently elevate cardiovascular or thrombotic risk when baseline homocysteine levels remain within the normal range.

Cite This Study

Varga et al. (2005) studied this question.

synapsesocial.com/papers/6aa8b47457fd01e647ef733e https://doi.org/10.1161/01.cir.0000165142.37711.e7

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