Vitamin Supplementation Reduces Blood Homocysteine Levels

Heijer, Martin den; Brouwer, Ingeborg A.; Bos, Gerard M.J.; Blom, Henk J.; Put, N.M.J. van der; Spaans, Anja; Rosendaal, Frits R.; Thomas, Chris M.G.; Haak, H. L.; Wijermans, P. W.; Gerrits, W. B. J.

doi:10.1161/01.atv.18.3.356

Cited by 143 publications

(41 citation statements)

References 31 publications

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“…In one study, healthy subjects were given a multivitamin supplement containing 0.4 mg/day of hydroxicobalamin, 5 mg of folic acid, and 50 mg of pyridoxine (den Heijer et al, 1998); the results demonstrated a 49% reduction in the basal median value of Hcy, among individuals with the 677TT genotype. In another study, a similar response could only be detected among subjects with hyperhomocysteinemia, who were carriers of the polymorphism 677C4T, who had taken the supplements over 4 weeks, and these had either normal or elevated levels of vitamin B 12 (D'Angelo et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…Developing recommendations combining folic acid supplementation with other B vitamins, particularly B 12 may be preferable. Available evidence indicates that combined supplementation enhances the reduction of hyperhomocysteinemia in individuals with a deficiency of both vitamins (den Heijer et al, 1998), and probably reduces the risk of spontaneous abortion among MTHFR 677TT and transcobalamin 776GG carriers (Zetterberg et al, 2003). However, more important is the fact that folic acid supplementation alone is likely to mask a deficiency in vitamin B 12 (Obeid et al, 2002) and consequently hampers the possibility of correcting the levels of Hcy.…”

Section: Discussionmentioning

confidence: 99%

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Dietary and genetic determinants of homocysteine levels among Mexican women of reproductive age

et al. 2006

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Objective: To evaluate the independent and joint effects of dietary folate, vitamin B 12 consumption and methylenetetrahydrofolate reductase (MTHFR) polymorphisms (677C4T and 1298A4C) on the circulating folate and homocysteine (Hcy) levels among Mexican women of reproductive age. Design: A cross-sectional, population-based study. Subjects: The first 130 healthy non-pregnant women (aged 16-34 years) who agreed to participate in a reproductive cohort in Morelos, Mexico. Main outcome measurements: Dietary intakes of vitamin B 12 and folate were estimated using a semiquantitative food frequency questionnaire. MTHFR 677C4T and 1298A4C polymorphisms were ascertained using the PCR-based method. Serum levels of Hcy and folate were determined using high-performance liquid chromatography and radioimmunoassay, respectively. Results: Genotype frequencies for the MTHFR 677C4T polymorphism were 21.5% (CC), 52.3% (CT) and 26.2% (TT) among Mexican women. Of the population, 22% had the MTHFR 1298AC genotype, while no individual carried the 1298CC genotype. We observed an increased level of Hcy among carriers of the 677TT genotype, compared to carriers of the 677CC genotype. The highest level of Hcy was observed among MTHFR 677TT carriers with low B 12 intake (o2.0 mg/day), which resulted with a significant interaction (P ¼ 0.01).

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Dietary and genetic determinants of homocysteine levels among Mexican women of reproductive age

et al. 2006

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“…Recent intervention studies have shown that a similar reduction in plasma tHcy can be accomplished by far smaller supplements, 500 mg (den Heijer et al, 1998;Brouwer et al, 1999a, b). We found that in regular users of > 300 mg supplementary folic acid per day (mean 513 mg) the mean plasma tHcy concentration was 28% lower compared to non-users.…”

Section: Discussionmentioning

confidence: 99%

Folate intake, plasma folate and homocysteine status in a random Finnish population

Alfthan

Laurinen²,

Valsta³

et al. 2003

Eur J Clin Nutr

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Objective: To assess the folate status of Finnish adults using plasma folate and homocysteine as biomarkers and to evaluate dietary and supplementary folate intakes. Materials and methods: Plasma folate, vitamin B 12 and total homocysteine (tHcy) were determined in a random sample of 643 subjects aged 25 -74 y living in the Helsinki area. The methylenetetrahydrofolate reductase (MTHFR)-genotypes were analyzed from a subsample (n ¼ 394). Dietary intake data by 24 h recall and use of vitamin supplements were collected. Results: Plasma folate was normal ( ! 5 nmol=l) in 99% of subjects and optimal ( ! 8 nmol=l) in terms of a minimum tHcy in 90%. Mean plasma folate of non-supplement users was 13.7 and 12.9 nmol=l and tHcy 11.3 and 9.2 mmol=l for men and women, respectively. Elevated tHcy ( > 14 mmol=l) was found in 11% of subjects. Homozygote frequency for MTHFR genotype TT was 5.0% and their plasma tHcy was 14.8 mmol=l compared to the mean of the other subjects, 10.5 mmol=l, P < 0.05. The mean dietary folate intake was 241 mg=day (29 mg=MJ of energy) for men and 205 mg=day (33 mg=MJ) for women, respectively. The main dietary sources of folate were vegetables 12%, wholemeal ryebread 11%, fruits 10%, and potato 10%. Regular supplement users (n ¼ 97) received on average 207 mg folic acid per day from supplements. Conclusions: The folate status of Finnish adults seems to be adequate according to energy adjusted folate intake, plasma folate and homocysteine. The MTHFR homozygote frequency was low compared to other countries. Regular use of supplementary folic acid less than 300 mg increased plasma folate, but supplemental folic acid over 300 mg was required to lower tHcy values significantly.

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“…To date, folic acid doses of 5 to 10 mg per day are currently used. Nevertheless, some data now suggest that a daily administration of folic acid at a dose lower than 1 mg may be adequate to reverse hyperhomocysteinemia (Boushey et al, 1995;Brattström et al, 1998;den Heijer et al, 1998;Rimm et al, 1998). In a recent study, cereal fortification, providing 499 and 665 g of folic acid daily, increased plasma folic acid by 64.8% and 105.7%, respectively, and decreased plasma homocysteine by 11% and 14%, respectively .…”

Section: Vitamin Treatment Of Hyperhomocysteinemiamentioning

confidence: 99%

Impaired Homocysteine Metabolism and Atherothrombotic Disease

Durand

Prost²,

Loreau

et al. 2001

Laboratory Investigation

232

147

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SUMMARY:Based on recent retrospective, prospective, and experimental studies, mild to moderate elevation of fasting or postmethionine-load plasma homocysteine is accepted as an independent risk factor for cardiovascular disease and thrombosis in both men and women. Hyperhomocysteinemia results from an inhibition of the remethylation pathway or from an inhibition or a saturation of the transsulfuration pathway of homocysteine metabolism. The involvement of a high dietary intake of methionine-rich animal proteins has not yet been investigated and cannot be ruled out. However, folate deficiency, either associated or not associated with the thermolabile mutation of the N 5,10 -methylenetetrahydrofolate reductase, and vitamin B 6 deficiency, perhaps associated with cystathionine ␤-synthase defects or with methionine excess, are believed to be major determinants of the increased risk of cardiovascular disease related to hyperhomocysteinemia. Recent experimental studies have suggested that moderately elevated homocysteine levels are a causal risk factor for atherothrombotic disease because they affect both the vascular wall structure and the blood coagulation system. The oxidant stress that results from impaired homocysteine metabolism, which modifies the intracellular redox status, might play a central role in the molecular mechanisms underlying moderate hyperhomocysteinemia-mediated vascular disorders. Because folate supplementation can efficiently reduce plasma homocysteine levels, both in the fasting state and after methionine loading, results from further prospective cohort studies and from on-going interventional trials will determine whether homocysteine-lowering therapies can contribute to the prevention and reduction of cardiovascular risk. Additionally, these studies will provide unequivocal arguments for the independent and causal relationship between hyperhomocysteinemia and atherothrombotic disease. (Lab Invest 2001, 81:645-672).C ardiovascular diseases remain the leading cause of mortality in Western populations. Hyperlipoproteinemia, hypertension, diabetes, obesity, and tobacco smoking are the main risk factors for atherosclerosis and its thrombotic complications. However, these factors alone cannot account for all of the deaths caused by vascular pathologies.As early as 1969, clinical studies conducted in homocystinuric children revealed the importance of severe hyperhomocysteinemia in premature development of atherosclerosis and thromboembolism (McCully, 1983). According to numerous retrospective case-controlled studies, moderate increases in plasma homocysteine, which can be precisely quantitated by high performance liquid chromatography (HPLC), raise the risk for cardiovascular disease 2-fold, after adjusting for classic risk factors. Moreover, up to 20% to 40% of patients with vascular pathologies present moderate to intermediate hyperhomocysteinemia. However, results from prospective studies are inconsistent. Additionally, molecular mechanisms underlying hyperhomocysteinemia-induced vascular diseas...

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Vitamin Supplementation Reduces Blood Homocysteine Levels

Cited by 143 publications

References 31 publications

Dietary and genetic determinants of homocysteine levels among Mexican women of reproductive age

Dietary and genetic determinants of homocysteine levels among Mexican women of reproductive age

Folate intake, plasma folate and homocysteine status in a random Finnish population

Impaired Homocysteine Metabolism and Atherothrombotic Disease

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