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Homocysteine and cardiovascular disease: cause or effect?

L Brattström¹, D E Wilcken

¹Department of Medicine, County Hospital, Kalmar, Sweden. lars.brattstrom@ltkalmar.se

The American Journal of Clinical Nutrition

|August 2, 2000

Summary

Elevated homocysteine levels increase vascular occlusion risk. Folate may offer benefits, potentially through antioxidant effects, especially in patients with chronic kidney disease and vascular disease.

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Area of Science:

Cardiovascular Medicine
Biochemistry
Metabolic Disorders

Background:

Elevated circulating homocysteine is linked to vascular occlusion risk.
Inborn errors cause high homocysteine and thromboembolic disease.
Mild elevation affects 20-30% of atherosclerotic patients.

Purpose of the Study:

Review mechanisms linking homocysteine to vascular effects.
Investigate homocysteine's role in atherosclerosis.
Explore folate's therapeutic potential.

Main Methods:

Literature review of homocysteine metabolism and vascular disease.
Analysis of studies on homocysteine levels, renal function, and atherosclerosis.
Examination of data on methylenetetrahydrofolate reductase polymorphism and cardiovascular risk.

Main Results:

Markedly and mildly elevated homocysteine increase vascular occlusion risk.
Mild hyperhomocysteinemia may be an effect, not a cause, of atherosclerosis, linked to renal decline.
Folic acid shows potential antioxidant effects independent of homocysteine reduction.

Conclusions:

Homocysteine's role in vascular disease is complex, potentially influenced by renal function.
Folate treatment may benefit vascular patients, particularly those with renal insufficiency, via antioxidant pathways.
Further research is needed to clarify homocysteine's causal role and folate's therapeutic mechanisms.

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