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Related Experiment Videos

Homocysteine as a risk factor for atherosclerosis.

M E Temple1, A B Luzier, D J Kazierad

  • 1Infectious Disease & Pediatric Pharmacotherapy, College of Pharmacy, The Ohio State University, Columbus, USA.

The Annals of Pharmacotherapy
|February 11, 2000
PubMed
Summary

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.

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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.

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  • 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.