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Modifying Levels of Maternal Dietary Folic Acid or Choline to Study the Impact of Deficiencies on Offspring Health Outcomes
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High- but not low-dose folic acid improves endothelial function in coronary artery disease

S J Moat1, A Madhavan, S Y Taylor

  • 1Department of Medical Biochemistry, University Hospital of Wales, Cardiff, UK.

European Journal of Clinical Investigation
|November 8, 2006
PubMed

Insights

Folic acid (FA) improves endothelial function in coronary artery disease (CAD) patients independently of homocysteine (Hcy) reduction. Higher FA doses enhanced endothelial function, suggesting a novel mechanism involving eNOS dimerization.

Area of Science:

  • Cardiovascular Medicine
  • Nutritional Science
  • Biochemistry

Background:

  • Folic acid (FA) is known to reduce plasma homocysteine (Hcy).
  • The direct impact of FA on endothelial function, independent of Hcy levels, remains unclear in patients with coronary artery disease (CAD).
  • This study investigates the relationship between FA dosage, Hcy reduction, and endothelial function in CAD patients.

Purpose of the Study:

  • To determine if folic acid's improvement of endothelial function in CAD patients is dependent on homocysteine lowering.
  • To examine the dose-dependent effects of folic acid on endothelial function and homocysteine levels.
  • To explore the underlying mechanisms of folic acid's action on endothelial function.

Main Methods:

  • A randomized controlled trial involving 84 CAD patients treated with either 400 µg FA, 5 mg FA, or placebo for 6 weeks.
  • A separate cohort of 44 CAD patients received betaine or placebo.
  • Endothelial function was assessed using flow-mediated dilatation (FMD); in vitro studies used isolated rabbit aortic rings and cultured porcine aortic endothelial cells (PAEC) to investigate FA's effect on endothelial nitric oxide synthase (eNOS) dimerization.

Main Results:

  • Both 400 µg and 5 mg FA significantly increased plasma folate and decreased plasma Hcy.
  • A significant improvement in FMD was observed with 5 mg FA treatment, but this did not correlate with Hcy reduction.
  • No change in FMD was seen with 400 µg FA or placebo; betaine treatment, despite Hcy reduction, impaired FMD.
  • In vitro, FA reversed methionine-induced endothelial dysfunction and promoted eNOS dimerization.

Conclusions:

  • Folic acid dose-dependently improves endothelial function in CAD patients through a mechanism independent of homocysteine lowering.
  • The observed benefits of FA on endothelial function may involve the promotion of eNOS dimerization.
  • These findings suggest a direct vascular protective role for folic acid in CAD.
Abstract

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