Homocysteine: role and implications in atherosclerosis

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Updated: Aug 11, 2026

Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
07:29

Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein

Published on: October 12, 2017

Sasidhar Guthikonda1, William G Haynes

  • 1Department of Cardiology, Bayor College of Medicine, Houston, TX 77584, USA. guthikon@bcm.tmc.edu

Current Atherosclerosis Reports
|March 3, 2006
PubMed

Insights

Hyperhomocysteinemia, linked to B-vitamin deficiencies, accelerates atherosclerosis by increasing oxidative stress and thrombosis. Supplementing folic acid, B6, and B12 can effectively lower homocysteine levels.

Area of Science:

  • Cardiovascular Science
  • Metabolic Disorders
  • Nutritional Biochemistry

Background:

  • Hyperhomocysteinemia is a condition characterized by elevated levels of homocysteine in the blood.
  • It is frequently associated with deficiencies in B vitamins (folic acid, B6, B12), genetic factors, certain medications, and kidney dysfunction.
  • Elevated homocysteine contributes to atherosclerosis via increased oxidative stress, endothelial dysfunction, and promotion of thrombosis.

Purpose of the Study:

  • To review the role of hyperhomocysteinemia in atherosclerosis.
  • To discuss the causes and consequences of elevated homocysteine levels.
  • To outline appropriate diagnostic and therapeutic strategies for hyperhomocysteinemia.

Main Methods:

  • Review of prospective studies and established literature on homocysteine and cardiovascular disease.
  • Analysis of mechanisms by which homocysteine impacts vascular health.
  • Evaluation of current treatment approaches, including vitamin supplementation.

Main Results:

  • Prospective studies indicate that elevated plasma homocysteine levels double the risk of cardiovascular disease and moderately increase cerebrovascular disease risk.
  • Identification of hyperhomocysteinemia is crucial in patients with unexplained or progressive atherosclerosis.
  • Vitamin supplementation (folic acid, B6, B12) is the primary treatment, with betaine and 5-methyl tetrahydro-folate also showing efficacy.

Conclusions:

  • Hyperhomocysteinemia is a significant risk factor for atherosclerosis and cardiovascular events.
  • Prompt identification and treatment with B vitamins are recommended for affected patients.
  • Further randomized outcome trials are needed to guide treatment for moderately elevated homocysteine in individuals without existing atherosclerosis.

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