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Hyper-homocysteinemia: a novel risk factor or a powerful marker for cardiovascular diseases? Pathogenetic and

Federico Cacciapuoti1

  • 1Department of Internal Medicine, Second University of Naples, Piazza L. Miraglia, Naples, Italy. federico.cacciapuoti@unina2.it

Journal of Thrombosis and Thrombolysis
|January 15, 2011
PubMed

Insights

High homocysteine levels do not directly cause cardiovascular disease. Reduced methylation potential, not elevated homocysteine, appears to be the true cause of cardiovascular diseases (CVD).

Area of Science:

  • Biochemistry
  • Cardiovascular Medicine
  • Nutritional Science

Background:

  • Elevated homocysteine levels are linked to arterial ischemic events.
  • Homocysteine metabolism involves re-methylation and trans-sulfuration pathways, utilizing folic acid and B vitamins.
  • Supplementation with B vitamins and folates aims to normalize plasma homocysteine.

Purpose of the Study:

  • To investigate the direct role of homocysteine in cardiovascular disease (CVD).
  • To identify the actual pathogenic mechanisms underlying CVD.
  • To clarify the relationship between homocysteine, methylation potential, and cardiovascular risk.

Main Methods:

  • Review of existing studies on homocysteine levels, B vitamin supplementation, and cardiovascular events.
  • Analysis of the impact of homocysteine on methylation potential (MP), specifically the S-adenosyl-methionine (AdoMet)/S-adenosyl-homocysteine (AdoHcy) ratio.
  • Examination of proposed pathogenic mechanisms involving DNA hypomethylation and endothelial cell function.

Main Results:

  • Lowering homocysteine levels with B vitamins and folates does not reduce cardiovascular risk.
  • Hyperhomocysteinemia is often a collateral finding in patients with cardiovascular events, not the direct cause.
  • Reduced methylation potential, indicated by decreased AdoMet/AdoHcy ratio, is implicated as the true cause of CVD.
  • Pathogenic mechanisms may involve DNA hypomethylation, affecting cyclin A transcription and endothelial cell growth.

Conclusions:

  • Homocysteine is not directly responsible for cardiovascular diseases.
  • Reduced methylation potential is the likely culprit in CVD pathogenesis.
  • Further human studies are needed to confirm these findings and explore underlying mechanisms.

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