folic acid and vascular health

From: Doug Skrecky (
Date: Sun May 21 2000 - 04:50:51 MDT

  Wilmink HW. Stroes ES. Erkelens WD. Gerritsen WB. Wever R. Banga JD.
  Rabelink TJ.
  Divisions of Internal Medicine , University Hospital Utrecht, The
  Influence of folic acid on postprandial endothelial dysfunction.
  Arteriosclerosis, Thrombosis &
  Vascular Biology. 20(1):185-8, 2000 Jan.
  Triglyceride-rich lipoproteins that circulate postprandially are increasingly
  being recognized as potentially atherogenic. These particles also have been
  shown to cause endothelial dysfunction. We recently demonstrated that acute
  parenteral administration of folic acid restores endothelial function in vivo
  in patients with increased LDL cholesterol levels. In vitro data suggested
  that this effect could be mediated by a reduction of radical stress. In the
  present study, therefore, we evaluated the effect of an acute oral fat load
  on both endothelial function and oxygen radical production. Next, we studied
  whether 2 weeks of pretreatment with 10 mg folic acid PO could prevent these
  fat-induced changes. We conducted a prospective, randomized,
  placebo-controlled study to evaluate the effect of oral folic acid
  administration (10 mg/d for 2 weeks) on basal endothelial function as well as
  endothelial function on an acute fat load in 20 healthy volunteers 18 to 33
  years old. Endothelial function was assessed as flow-mediated dilatation
  (FMD). Endothelium-independent dilatation was measured after sublingual
  nitroglycerin spray. Oxygen radical stress was assessed by measurement of the
  urinary excretion of the stable radical-damage end product malondialdehyde.
  During administration of placebo, FMD decreased significantly after an acute
  oral fat load, with a median from 10.6% (8.3% to 12.2%) to 5.8% (3.0% to
  10.2%), P<0.05. During folic acid administration, FMD was unaffected by a fat
  load, with a median from 9.6% (7.1% to 12.8%) to 9.9% (7.5% to 14.1%), P=NS.
  The increase in malondialdehyde excretion in the urine after fat loading was
  also prevented during folic acid administration (absolute increase after an
  acute fat load during placebo, 0.11+/-0.1 micromol/L versus folic acid,
  0.02+/-0.1 micromol/L, P<0.05). The response to the endothelium-independent
  vasodilator nitroglycerin remained unaltered throughout the study.
  Pretreatment with oral folic acid prevents the lipid-induced decrease in FMD
  as well as the lipid-induced increase in urinary radical-damage end products.
  Because these observations were made in healthy volunteers with normal folate
  and homocysteine levels, it is suggested that a higher folate intake in the
  general population may have vasculoprotective effects.

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