Effect of vitamin B-6 deficiency on fasting plasma homocysteine concentrations

Miller, Joshua W.; Ribaya-Mercado, Judy D.; Russell, Robert M.; Shepard, Douglas; Morrow, Frank D.; Cochary, Elizabeth F.; Sadowski, James A.; Gershoff, Stanley N.; Selhub, Jacob

doi:10.1093/ajcn/55.6.1154

Cited by 130 publications

(55 citation statements)

References 40 publications

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“…If the fasting plasma homocysteine concentration could be effectively reduced by vitamin supplementation, it might lessen the morbidity and/or mortality of CAD. Our results were in agreement with previous studies (Brattström et al, 1990;Miller et al, 1992;Ubbink et al, 1994), showing that vitamin B 6 supplementation did not affect homocysteine concentration. In addition, an unexpected finding was that fasting homocysteine levels slightly, although not significantly, increased in the placebo group during the study.…”

Section: Discussionsupporting

confidence: 94%

“…In contrast, some studies showed that vitamin B 6 had no effect on fasting plasma homocysteine concentration. Miller et al (1992) indicated that total fasting plasma homocysteine concentrations were not initially elevated in vitamin B 6 -deficient humans and rats. Brattström et al (1990) studied homocysteine metabolism in 72 patients with occlusive arterial disease.…”

Section: Introductionmentioning

confidence: 97%

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Folic acid and vitamin B12 are more effective than vitamin B6 in lowering fasting plasma homocysteine concentration in patients with coronary artery disease

et al. 2004

Eur J Clin Nutr

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Objective: To investigate whether vitamin B 6 supplementation had a beneficial effect on lowering fasting plasma homocysteine concentrations in coronary artery disease (CAD) patients. Design: A single-blind intervention study. Setting: The study was performed at the Taichung Veterans General Hospital, the central part of Taiwan. Subjects: A total of 50 subjects were identified by cardiac catheterization to have at least 70% stenosis of one major coronary artery. In all, 42 patients successfully completed this study. Interventions: Patients were randomly assigned to one of five groups and treated with a daily dose of placebo (n ¼ 8), 5 mg vitamin B 6 (n ¼ 8), 10 mg vitamin B 6 (n ¼ 8), 50 mg vitamin B 6 (n ¼ 9), or 5 mg folic acid combined with 0.25 mg vitamin B 12 (n ¼ 9) for 12 weeks. Main outcome measures: Nutrient intakes were recorded by using 24-h diet recalls when patients returned to the cardiology clinic before the intervention (week 0) and at week 12. Vitamin B 6 status was assessed by direct measures (plasma pyridoxal 5 0 -phosphate) and indirect measures (erythrocyte alanine and aspartate aminotransaminase activity coefficient). Fasting plasma homocysteine, serum folic acid, and vitamin B 12 were measured. Results: Fasting plasma homocysteine concentration did not respond to high or low doses of vitamin B 6 when compared with a placebo treatment after 12 weeks of supplementation. The mean fasting plasma homocysteine concentration, however, decreased significantly after 12 weeks of folic acid combined with vitamin B 12 supplementation (P ¼ 0.047). Further, within group, mean fasting plasma homocysteine concentration was nonsignificantly increased by 25.5, 16.2, and 18.3% in placebo, 10 mg/day and 50 mg/day vitamin B 6 supplemented groups, respectively; whereas folic acid combined with vitamin B 12 supplementation significantly reduced fasting plasma homocysteine concentration by 32% (Po0.001). Conclusions: Our results indicate that vitamin B 6 supplementation alone is less effective than folic acid combined with vitamin B 12 in lowering plasma homocysteine concentrations in CAD patients.

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Section: Discussionsupporting

confidence: 94%

Section: Introductionmentioning

confidence: 97%

Folic acid and vitamin B12 are more effective than vitamin B6 in lowering fasting plasma homocysteine concentration in patients with coronary artery disease

et al. 2004

Eur J Clin Nutr

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“…In our study, vitamin B12 and total Hcy were used according to our facilities. Vitamin B6 was not measured in our study given that the main determinants of total Hcy are intakes and plasma concentrations of vitamin B12 and folate, whereas the results regarding vitamin B6 are inconsistent [60,61] .…”

Section: Discussionmentioning

confidence: 77%

Plasma homocysteine and vitamin B12 serum levels, red blood cell folate concentrations, C677T methylenetetrahydrofolate reductase gene mutation and risk of recurrent miscarriage: a case-control study in Spain

Creus

Deulofeu

Peñarrubia

et al. 2013

Clinical Chemistry and Laboratory Medicine

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Background : Hyperhomocysteinemia and methylenetetrahydrofolate reductase (MTHFR) gene mutation have been postulated as a possible cause of recurrent miscarriage (RM). There is a wide variation in the prevalence of MTHFR polymorphisms and homocysteine (Hcy) plasma levels among populations around the world. The present study was undertaken to investigate the possible association between hyperhomocysteinemia and its causative genetic or acquired factors and RM in Catalonia, a Mediterranean region in Spain. Methods : Sixty consecutive patients with ≥ 3 unexplained RM and 30 healthy control women having at least one child but no previous miscarriage were included. Plasma Hcy levels, MTHFR gene mutation, red blood cell (RBC) folate and vitamin B12 serum levels were measured in all subjects. Results : No significant differences were observed neither in plasma Hcy levels, RBC folate and vitamin B12 serum levels nor in the prevalence of homozygous and heterozygous MTHFR gene mutation between the two groups studied. Conclusions: In the present study RM is not associated with hyperhomocysteinemia, and/or the MTHFR gene mutation.

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“…When the transsulfuration pathway is stressed by an oral l -methionine load test, it is sometimes possible to differentiate between heterozygotes and controls by the higher postmethionine load plasma tHcy concentrations in the former group (27,28). In addition, changes in vitamin B-6 status do not affect fasting plasma tHcy concentrations (29,30), while high dose pyridoxine supplementation has been shown to attenuate the post-methionine load plasma tHcy concentrations (31,32).…”

Section: Introductionmentioning

confidence: 99%

The effect of a subnormal vitamin B-6 status on homocysteine metabolism.

Ubbink¹,

Merwe²,

Delport³

et al. 1996

J. Clin. Invest.

226

112

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Homocysteine, an atherogenic amino acid, is either remethylated to methionine or metabolized to cysteine by the transsulfuration pathway. The biochemical conversion of homocysteine to cysteine is dependent upon two consecutive, vitamin B-6-dependent reactions.To study the effect of a selective vitamin B-6 deficiency on transsulfuration, we performed oral methionine load tests on 22 vitamin B-6-deficient asthma patients treated with theophylline (a vitamin B-6 antagonist) and 24 age-and sex-matched controls with a normal vitamin B-6 status. Both groups had normal circulating vitamin B-12 and folate concentrations. Methionine loading resulted in significantly higher increases in circulating total homocyst(e)ine ( P Ͻ 0.01) and cystathionine ( P Ͻ 0.05) concentrations in vitamin B-6-deficient patients compared with controls. 6 wk of vitamin B-6 supplementation (20 mg/d) significantly ( P Ͻ 0.05) reduced post-methionine load increases in circulating total homocyst(e)ine concentrations in deficient subjects, but had no significant effect on the increase in total homocyst(e)ine concentrations in controls. The increases in post-methionine load circulating cystathionine concentrations were significantly ( P Ͻ 0.01) reduced in both groups after vitamin supplementation.It is concluded that a vitamin B-6 deficiency may contribute to impaired transsulfuration and an abnormal methionine load test, which is associated with premature vascular disease. ( J. Clin. Invest. 1996. 98:177-184.) Key words: folate • methionine • coronary heart disease • vitamin B-12 • cystathionine

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Effect of vitamin B-6 deficiency on fasting plasma homocysteine concentrations

Cited by 130 publications

References 40 publications

Folic acid and vitamin B12 are more effective than vitamin B6 in lowering fasting plasma homocysteine concentration in patients with coronary artery disease

Folic acid and vitamin B12 are more effective than vitamin B6 in lowering fasting plasma homocysteine concentration in patients with coronary artery disease

Plasma homocysteine and vitamin B12 serum levels, red blood cell folate concentrations, C677T methylenetetrahydrofolate reductase gene mutation and risk of recurrent miscarriage: a case-control study in Spain

The effect of a subnormal vitamin B-6 status on homocysteine metabolism.

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