Homocyst(e)ine and arterial occlusive diseases
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Updated: Jul 29, 2026

Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
Published on: October 12, 2017
1Oregon Regional Primate Research Center, Beaverton.
Insights
High homocysteine (H(e)) levels are linked to arterial diseases. While vitamin supplements can reverse elevated H(e), their impact on arterial disease progression requires further clinical trials.
Area of Science:
- Biochemistry
- Cardiovascular Medicine
- Nutritional Science
Background:
- Homocysteine (H(e)) is an amino acid linked to cardiovascular, cerebrovascular, and peripheral arterial diseases.
- Elevated H(e) levels are an independent risk factor for atherosclerosis.
Purpose of the Study:
- To discuss mechanisms regulating plasma H(e).
- To explore the association between H(e) and arterial occlusive diseases.
- To examine H(e) relationships with nitric oxide and hemostasis.
Main Methods:
- Review of genetic, physiological, nutritional, and pharmacological mechanisms.
- Discussion of clinical observations linking H(e) to arterial diseases.
Main Results:
- High plasma H(e) levels are frequently observed in patients with arterial diseases.
- Elevated H(e) is an independent risk factor for atherosclerosis.
- High H(e) levels are generally reversible with vitamin supplementation.
Conclusions:
- The association between elevated H(e) and arterial occlusive diseases is well-established.
- Further prospective, placebo-controlled, randomized clinical trials are needed to determine if vitamin supplements can alter the course of arterial occlusive diseases.
Abstract:
Homocysteine is a thiol-containing amino acid resulting from demethylation of methionine. The free and protein-bound forms of the amino acid and derived disulfides are called homocyst(e)ine [H(e)]. Multiple studies have shown elevated H(e) levels in patients with coronary, cerebrovascular, or peripheral arterial diseases; this association is frequent and independent of most other risk factors for atherosclerosis. In the 1993 Frontiers in Medicine Symposium investigators discussed the genetic, physiological, nutritional, and pharmacological mechanisms involved in the regulation of plasma H(e), the association of H(e) with arterial occlusive diseases, and the relationships of H(e) with nitric oxide and haemostasis. High plasma H(e) levels usually can be reversed with vitamin supplements. Whether vitamin supplements will affect the evolution of arterial occlusive diseases needs to be established in prospective, placebo-controlled, randomized, clinical trials.
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