Homocysteine as a risk factor for atherosclerosis
Related Experiment Video
Updated: Oct 17, 2026
Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
Published on: October 12, 2017
M E Temple1, A B Luzier, D J Kazierad
1Infectious Disease & Pediatric Pharmacotherapy, College of Pharmacy, The Ohio State University, Columbus, USA.
Insights
Elevated homocysteine is linked to atherosclerosis. Folic acid, at 650 microg/d, effectively lowers homocysteine levels, but long-term treatment and dietary changes are crucial for managing this risk factor.
Area of Science:
- Cardiovascular Medicine
- Nutritional Science
- Biochemistry
Background:
- Homocysteine is an amino acid linked to cardiovascular disease.
- Hyperhomocysteinemia, or high homocysteine levels, is implicated in the development of atherosclerosis.
- Understanding homocysteine's role is vital for preventing cardiovascular events.
Purpose of the Study:
- To review the role of homocysteine in atherosclerosis pathogenesis.
- To provide recommendations for treating hyperhomocysteinemia.
- To synthesize current evidence on homocysteine and vascular health.
Main Methods:
- Conducted a MEDLINE search (1966-1999) for studies on homocysteine, atherosclerosis, and related vitamins.
- Included studies assessing hyperhomocysteinemia's vascular effects, physiological changes, and clinical outcomes.
- Evaluated studies examining treatment outcomes for hyperhomocysteinemia.
Main Results:
- Elevated homocysteine found in 30-40% of patients with cerebrovascular disease.
- Strong correlation observed between high homocysteine, myocardial infarction risk, and mortality.
- Folic acid (650 microg/d) normalized homocysteine in two weeks; vitamins B6 and B12 were effective only with folic acid.
- Dietary factors, like coffee consumption, correlate with hyperhomocysteinemia, while folate-rich foods may reduce it.
Conclusions:
- Hyperhomocysteinemia is positively correlated with atherosclerosis.
- Folic acid is the primary treatment for hyperhomocysteinemia, with 650 microg/d as a minimum effective dose.
- Further research is needed to assess the impact of treating hyperhomocysteinemia on atherosclerotic morbidity and mortality.
Objective:
To review the role of homocysteine as a risk factor in the pathogenesis of atherosclerosis and to provide recommendations for the treatment of hyperhomocysteinemia.
Data Sources:
A MEDLINE search using key terms such as homocysteine, atherosclerosis, folic acid, vitamin B6, and vitamin B12 was conducted for the time period 1966 through January 1999.
Study Selection:
An article was selected for inclusion in this review if it assessed the relationship and proposed mechanisms of hyperhomocysteinemia on the vasculature, physiologic changes due to hyperhomocysteinemia, and outcomes due to hyperhomocysteinemia, such as morbidity and mortality. In addition, studies that assessed the treatment outcomes of hyperhomocysteinemia were evaluated.
Data Synthesis:
Studies of patients with cerebral vascular disease reveal elevated homocysteine concentrations in 30-40% of patients compared with controls. Many studies demonstrate a correlation between elevated homocysteine concentrations, risk of myocardial infarction, and mortality. In addition, hyperhomocysteinemia and decreased folic acid concentrations have been identified in end-stage renal disease (ESRD) and type 2 diabetic patients, while both concentrations remained normal in healthy controls. Studies using folic acid 650 microg/d reduced homocysteine concentrations to within normal therapeutic range after two weeks of treatment. Studies with vitamins B6 and B12 have demonstrated that the use of either alone is ineffective, but when combined or administered with folic acid, homocysteine concentrations return to normal. All therapies must be given for the lifetime of the patient. In addition, patients must use discretion in their diet, as common beverages, such as coffee, have a strong correlation with hyperhomocysteinemia, while foods high in folic acid, vitamin B6 and vitamin B12 may reduce homocysteine concentrations. Additional prospective studies are needed to determine effects of treatment of hyperhomocysteinemia and various diets on atherosclerotic morbidity and mortality.
Conclusions:
Studies demonstrate a positive correlation between hyperhomocysteinemia and atherosclerosis. The treatment of choice for hyperhomocysteinemia is folic acid. Although the optimal dose is not known, 650 microg/d is the minimum effective dose. To date, no studies have assessed the effects on morbidity and mortality when treating high homocysteine concentrations in atherosclerotic patients.
Related Concept Videos
01:19Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers
These markers indicate stress or strain on the heart muscle:
Natriuretic Peptides (BNP)
Cardiac myocytes produce these hormones in response to ventricular stretching...
01:30Atherosclerosis I: Introduction
01:30Coronary Artery Disease I: Introduction
01:29Cholesterol: Significance and Regulation
Considering cholesterol and...
01:27Atherosclerosis II: Clinical Manifestations and Diagnostic Tests
01:18Lipids: Dietary Sources and Requirements