High dose ascorbate supplementation fails to affect plasma homocyst(e)ine levels in patients with coronary heart disease.
Pharmacologic doses of folate, in the absence of clinical folate deficiency, can reduce plasma levels of the putatively atherothrombotic amino acid, homocysteine (H(e)). Data suggesting that H(e) may accumulate in experimental scurvy prompted us to explore the efficacy of high dose ascorbate supplementation as a H(e)-lowering treatment, in the absence of clinical ascorbate deficiency. A randomized, placebo-controlled trial of 12 weeks of high dose (4.5 g/day) ascorbate supplementation was completed by 44 patients with established coronary heart disease. No significant change in mean fasting total plasma H(e) levels was demonstrable despite a marked increase in mean fasting plasma ascorbate levels amongst those patients randomized to active treatment. Ascorbate supplementation to prevent the development of fasting hyperhomocysteinemia may only be relevant at scorbutic levels of plasma ascorbate.
Bostom
A G
AG
Division of General Internal Medicine, Rhode Island Hospital, Providence.
Yanek
L
L
Hume
A L
AL
Eaton
C B
CB
McQuade
W
W
Nadeau
M
M
Perrone
G
G
Jacques
P F
PF
Selhub
J
J
D001205:Ascorbic Acid / Q000008:administration & dosage / Q000627:therapeutic use*; D003327:Coronary Disease / Q000097:blood* / Q000188:drug therapy*; D006710:Homocysteine / Q000097:blood* / Q000187:drug effects; D006801:Humans
D006710:Homocysteine; D001205:Ascorbic Acid