Arteriosclerosis, Thrombosis, and Vascular Biology. 1997;17:1157-1162
© 1997 American Heart Association, Inc.
Articles |
The Effects of Folic Acid Supplementation on Plasma Total Homocysteine Are Modulated by Multivitamin Use and Methylenetetrahydrofolate Reductase Genotypes
From the Oregon Regional Primate Research Center, Beaverton (M.R.M., D.L.H., B.U.), Providence St Vincent Hospital (M.R.M., R.A.G., P.C.B., C.R.H., P.H.A.) and the Oregon Health Sciences University, Portland (M.R.M., P.B.D., D.L.H., R.A.G., P.C.B., C.R.H.), Ore; The Johns Hopkins University, Baltimore, Md (F.J.N.); Fox Chase Cancer Institute, Philadelphia, Pa (W.D.K., Q.R.L.); and Carle Foundation Hospital, Urbana, Ill (D.S.).
Correspondence to M.R. Malinow, MD, Scientist, Oregon Regional Primate Research Center, 505 NW 185th Ave, Beaverton, OR 97006. E-mail malinowr{at}ohsu.edu
Abstract Elevated concentration of plasma total homocysteine (tHcy) is a common risk factor for arterial occlusive diseases. Folic acid (FA) supplementation usually lowers tHcy levels, but initial tHcy and vitamin levels, multivitamin use, and polymorphisms in the gene for 5,10-methylenetetrahydrofolate reductase (MTHFR) may contribute to variability in reduction. We tested the effects of a 3-week daily intake of 1 or 2 mg of FA supplements on tHcy levels in patients with and without coronary heart disease (CHD) who were analyzed for the C677T MTHFR mutation. Prior multivitamin intake and baseline vitamin and tHcy levels were also compared with responsiveness to folate supplementation. Both dosages of FA lowered tHcy levels similarly, regardless of sex, age, CHD status, body mass index, smoking, or plasma creatinine concentration. In non–multivitamin users, FA supplements reduced tHcy by 7% in C/C homozygotes and by 13% or 21% in subjects with one or two copies of the T677 allele, respectively; the corresponding reductions were smaller in users of multivitamins. Moreover, T/T homozygotes had elevated tHcy and increased susceptibility to high levels of tHcy at marginally low plasma folate levels, as well as enhanced response to the tHcy-lowering effects of FA. Although other factors are probably involved in the responsiveness of tHcy levels to FA supplementation, about one third of heterogeneity in responsiveness was attributable to baseline tHcy and folate levels and to multivitamin use.
Key Words: homocyst(e)ine • gene mutations • vitamin therapy • arterial occlusive diseases
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