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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #61340
Title: HIGH DOSE ASCORBATE SUPPLEMENTATION FAILS TO AFFECT PLASMA HOMOCYST(E)INE LEVELS IN PATIENTS WITH CORONARY HEART DISEASE

Author
item BOSTOM, ANDREW - RHODE ISLAND HOSP
item YANEK, LISA - MEMORIAL HOSP, RI
item HUME, ANNE - MEMORIAL HOSP, RI
item EATON, CHARLES - MEMORIAL HOSP, RI
item MCQUADE, WILLIAM - MEMORIAL HOSP, RI
item NADEAU, MARIE - TUFTS-HNRCA
item PERRONE, GAYLE - TUFTS-HNRCA
item JACQUES, PAUL - TUFTS-HNRCA
item SELHUB, JACOB - TUFTS-HNRCA

Submitted to: Atherosclerosis
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/1/1994
Publication Date: N/A
Citation: N/A

Interpretive Summary: The purpose of this study was to determine whether high doses of vitamin C would lower the levels of homocysteine in the blood of patients with coronary heart disease. Homocysteine is a protein found in elevated quantities in the blood of people afflicted with coronary heart disease. A randomized, placebo-controlled trial of 12 weeks of high doses (4.5 grams per day) of vitamin C was completed by 44 patients with established coronary heart disease. Though blood levels of vitamin C in supplemented patients were elevated, our results indicate that vitamin C does not have any significant effect on homocysteine levels in blood.

Technical Abstract: 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 significance 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.