Bread fortification with folic acid, vitamin B12, and vitamin B6 in Hungary

The Lancet ◽  
1998 ◽  
Vol 352 (9135) ◽  
pp. 1225 ◽  
Author(s):  
Andrew E Czeizel ◽  
Zoltan Merhala
Keyword(s):  
Folic Acid ◽  
Vitamin B12 ◽  
Vitamin B6

scholarly journals Blood homocysteine, folic acid, vitamin B12 and vitamin B6 levels in psoriasis patients

TURKDERM ◽  
2017 ◽  
pp. 92-97
Author(s):  
Meltem Uslu ◽  
Neslihan Şendur ◽  
Ekin Şavk ◽  
Aslıhan Karul ◽  
Didem Kozacı ◽  
...  
Keyword(s):  
Folic Acid ◽  
Vitamin B12 ◽  
Vitamin B6

scholarly journals Plasma Vitamin B6 Vitamers before and after Oral Vitamin B6 Treatment: A Randomized Placebo-controlled Study

2003 ◽  
Vol 49 (1) ◽  
pp. 155-161 ◽  
Author(s):  
Mustafa Vakur Bor ◽  
Helga Refsum ◽  
Marianne R Bisp ◽  
Øyvind Bleie ◽  
Jorn Schneede ◽  
...  
Keyword(s):  
Folic Acid ◽  
Vitamin B12 ◽  
Vitamin B6 ◽  
Oral Treatment ◽  
Prolonged Treatment ◽  
Controlled Study ◽  
Plasma Vitamin ◽  
Additional Increase ◽  
Before And After ◽  
B Vitamin

Abstract Background: Vitamin B6 has attracted renewed interest because of its role in homocysteine metabolism and its possible relation to cardiovascular risk. We examined the plasma B6 vitamers, pyridoxal 5′-phosphate (PLP), pyridoxal (PL), pyridoxine (PN), and 4-pyridoxic acid (4-PA) before and after vitamin B6 supplementation. Methods: Patients (n = 90; age range, 38–80 years) undergoing coronary angiography (part of the homocysteine-lowering Western Norway B-Vitamin Intervention Trial) were allocated to the following daily oral treatment groups: (A), vitamin B12 (0.4 mg), folic acid (0.8 mg), and vitamin B6 (40 mg); (B), vitamin B12 and folic acid; (C), vitamin B6; or (D), placebo. EDTA blood was obtained before treatment and 3, 14, 28, and 84 days thereafter. Results: Before treatment, PLP (range, 5–111 nmol/L) and 4-PA (6–93 nmol/L) were the predominant B6 vitamers identified in plasma. During the 84-day study period, the intraindividual variation (CV) in patients not treated with vitamin B6 (groups B and D) was 45% for PLP and 67% for 4-PA. Three days after the start of treatment, the increases in concentration were ∼10-, 50-, and 100-fold for PLP, 4-PA, and PL, respectively. No significant additional increase was observed at the later time points. The PLP concentration correlated to the concentrations of 4-PA and PL before treatment, but not after treatment. The PL concentration correlated with 4-PA before and after treatment. Conclusions: Vitamin B6 treatment has an immediate effect on the concentrations and the forms of B6 vitamers present in plasma, and the changes remain the same during prolonged treatment. Our results suggest that the B6 vitamers in plasma reflect vitamin B6 intake.

Optimization of folic acid, vitamin B12, and vitamin B6 supplements in pediatric patients with sickle cell disease

2002 ◽  
Vol 69 (4) ◽  
pp. 239-246 ◽  
Author(s):  
Fey P.L. van der Dijs ◽  
M. Rebecca Fokkema ◽  
D.A. Janneke Dijck-Brouwer ◽  
Bram Niessink ◽  
Thaliet I.C. van der Wal ◽  
...  
Keyword(s):  
Folic Acid ◽  
Sickle Cell Disease ◽  
Vitamin B12 ◽  
Sickle Cell ◽  
Vitamin B6 ◽  
Pediatric Patients ◽  
Cell Disease

scholarly journals The role of increased levels of homocysteine in the development of cardiovascular diseases

2006 ◽  
Vol 59 (3-4) ◽  
pp. 143-147 ◽  
Author(s):  
Zoran Ceperkovic
Keyword(s):  
Folic Acid ◽  
Amino Acid ◽  
Cardiovascular Diseases ◽  
Vitamin B12 ◽  
Vitamin B6 ◽  
Heart Diseases ◽  
Daily Intake ◽  
Cholesterol Oxidation ◽  
Total Risk ◽  
Homocysteine Concentration

Introduction. Homocysteine is a sulphur amino acid produced by demethylation of the essential amino acid methionine. Dysfunction of certain enzymes or insufficient intake of nutrients may cause increase of intracellular homocysteine, which is then exported into plasma. Etiopathogenesis of cardiovascular diseases accompanied with higher level of homocysteine. McCully's theory suggests that high levels of homocysteine are associated with cardiovascular diseases, arteriosclerosis and endothelial dysfunction. Harmful effects of homocysteine are associated with LDL cholesterol oxidation, increased production of collagen, lower availability of nitric oxide as well as prothrombotic activity. Reduction of homocysteine levels. The most recent researches show that hyperhomocysteinemia is responsible for about 10% of total risk of cardiovascular diseases. Vitamin BJ2 plays a major role in the remethylation of homocysteine. Reducing the homocysteine concentration in blood by 3 mol/l (with daily intake of 0.8 mg of folic acid) reduces the risk of ishemic heart diseases by 16%, vein thrombosis by 25%, and stroke by 24%. A six-month therapy with folic acid (Img/d), vitamin B12 (400g/d) and vitamin B6 (10mg/d), reduces the frequency of cardiovascular occurrences after successful PTCA. Plasma homocysteine concentration over 12/1 doubles the risk of myocardial infarction. Conclusion. A lack of folates, vitamin B6 and vitamin B12 increases the level of homocysteine and thus increases the risk of cardiovascular diseases. Changes in lifestyle and diet, as well as intake of food supplements, are of great importance in reducing homocysteine levels in plasma and therefore in reducing the occurrence and acceleration of arteriosclerosis. .

scholarly journals Holo-Transcobalamin Is an Early Marker of Changes in Cobalamin Homeostasis. A Randomized Placebo-controlled Study

2002 ◽  
Vol 48 (10) ◽  
pp. 1768-1771 ◽  
Author(s):  
Ebba Nexo ◽  
Anne-Mette Hvas ◽  
Øyvind Bleie ◽  
Helga Refsum ◽  
Sergey N Fedosov ◽  
...  
Keyword(s):  
Folic Acid ◽  
Vitamin B12 ◽  
Vitamin B6 ◽  
Oral Treatment ◽  
Controlled Study ◽  
Control Group ◽  
Oral Vitamin ◽  
Intraindividual Variation ◽  
Early Marker ◽  
B Vitamin

Abstract Background: We examined the effect of oral vitamin B12 treatment on fluctuations in plasma total cobalamin and its binding proteins transcobalamin (TC) and haptocorrin (HC). Methods: Patients (n = 88; age range, 38–80 years) undergoing coronary angiography (part of the homocysteine-lowering Western Norway B-Vitamin Intervention Trial) were allocated to daily oral treatment with (a) vitamin B12 (0.4 mg), folic acid (0.8 mg), and vitamin B6 (40 mg); (b) vitamin B12 and folic acid; (c) vitamin B6; or (d) placebo. EDTA blood was obtained before treatment and 3, 14, 28, and 84 days thereafter. Results: The intraindividual variation for patients not treated with B12 was ∼10% for plasma total cobalamin, total TC, apo-TC, and apo-HC, and <20% for holo-TC and TC saturation. In B12-treated patients, the maximum change in concentrations was observed already after 3 days for total TC (−16%), holo-TC (+54%), and TC saturation (+82%). At this time holo-HC (+20%) and plasma total cobalamin (+28%) showed an initial burst, but had increased further at 84 days. All changes were highly significant compared with the control group (P <0.0001). Conclusions: Oral vitamin B12 treatment produces maximal effects on total TC, holo-TC, and TC saturation within 3 days, whereas maximal increases in holo-HC and plasma total cobalamin occur later. The results support the view that holo-TC is an early marker of changes in cobalamin homeostasis.

Association of Plasma Homocysteine and Macular Edema in Type 2 Diabetes Mellitus

2008 ◽  
Vol 18 (2) ◽  
pp. 226-232 ◽  
Author(s):  
E. Aydin ◽  
H.D. Demir ◽  
H. Ozyurt ◽  
I. Etikan
Keyword(s):  
Type 2 Diabetes ◽  
Diabetic Retinopathy ◽  
Folic Acid ◽  
Vitamin B12 ◽  
Macular Edema ◽  
Vitamin B6 ◽  
Serum Vitamin ◽  
Plasma Homocysteine ◽  
Significant Difference

Purpose The aim of this study was to assess the association of macular edema (ME) with plasma homocysteine, vitamin B6, vitamin B12, and folic acid levels in patients with Type 2 diabetes. Methods Sixty-five diabetic subjects with no retinopathy and nonproliferative diabetic retinopathy (NPDR) (no DR, without ME, with ME: 16, 25, 24, respectively), 28 with proliferative diabetic retinopathy (PDR) (with and without ME: 14, 14, respectively), and 19 healthy subjects as control were recruited in this cross-sectional study Plasma homocysteine, vitamin B12, vitamin B6, and folate levels were determined after 8-hour of fasting for all subjects. The levels of serum homocysteine and vitamin B6 were measured using high performance liquid chromatography (HPLC) with fluorescence detection, and the levels of serum vitamin B12 and folic acid were measured by electrochemiluminescence immunoassay. Results When diabetic groups with ME were compared with diabetic groups without ME for homocysteine, vitamin B12, vitamin B6, and folic acid, the only significant difference was detected in homocysteine levels (p=0.001). There was no significant difference between NPDR with ME group compared with NPDR without ME group and no DR group for plasma homocysteine, vitamin B12, vitamin B6, and folic acid (p=0.200, p=0.660; p=0.999, p=0.678; p=1.0, p=0.248; p=1.0, p=0.982, respectively). On the other hand, when PDR with ME group was compared with PDR without ME group, there was only significant difference in homocysteine levels (p=0.023). Conclusions Mild to moderate elevation of homocysteine may explain the role of vascular dysregulation and endothelial dysfunction in patients with DR. The present study suggests hyperhomocysteinemia may be one of the crucial risk factors for development of ME.

scholarly journals Folate, Vitamin B6 and Vitamin B12 Intake in Relation to Hyperuricemia

2018 ◽  
Vol 7 (8) ◽  
pp. 210 ◽  
Author(s):  
Yiying Zhang ◽  
Hongbin Qiu
Keyword(s):  
Folic Acid ◽  
Vitamin B12 ◽  
Lower Risk ◽  
Vitamin B6 ◽  
The United States ◽  
Multivariable Logistic Regression Analysis ◽  
Nutrition Examination Survey ◽  
Dietary Folate ◽  
Health And Nutrition ◽  
Food Folate

To assess the association between intake of folate, vitamin B6, and vitamin B12 with hyperuricemia (HU) among adults from the United States (US), we extracted relevant data from 24,975 US adults aged 20–85 years from the National Health and Nutrition Examination Survey (NHANES) in 2001–2014. All dietary intake was evaluated by 24-h dietary recalls. Multivariable logistic regression analysis was performed to explore the associations after adjustment for confounders. Compared to the lowest quintile (Q1), for males, adjusted odds ratios (ORs) of HU in Q2 to Q5 of folate (dietary folate equivalent, DFE) intake were 0.84 (95% CI, 0.73–0.96), 0.84 (0.73–0.97), 0.72 (0.62–0.84), and 0.64 (0.53–0.77), respectively (p for trend <0.0001). In females, adjusted ORs in Q2 to Q4 of folate (DFE) intake were 0.84 (95% CI, 0.71–0.99), 0.81 (0.68–0.96), and 0.82 (0.68–0.99), with a p for trend of 0.1475. Our findings indicated the intakes of total folate, folic acid, food folate, folate (DFE), vitamin B12, but not vitamin B6, were inversely related to the risk of HU in males. A lower risk of HU with higher intakes of total folate, food folate, and folate (DFE) was found in females, but with no association between intakes of folic acid, vitamin B6, B12, and the risk of HU for females.

scholarly journals Detectable Unmetabolized Folic Acid, and Sufficient Folate and Vitamin B12 Concentrations Are Evident in Canadian Children with Sickle Cell Disease

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1100-1100
Author(s):  
Brock Williams ◽  
Heather McCartney ◽  
Yvonne Lamers ◽  
Suzanne Vercauteren ◽  
John Wu ◽  
...  
Keyword(s):  
Folic Acid ◽  
Sickle Cell Disease ◽  
Vitamin B12 ◽  
Sickle Cell ◽  
Vitamin B6 ◽  
Serum Folate ◽  
High Dose ◽  
Cell Disease ◽  
Median Serum ◽  
B Vitamin

Abstract Objectives Canadian children with sickle cell disease (SCD) are routinely supplemented with high-dose folic acid (1 mg/d), synthetic folate, due to increased erythrocyte production and turn-over in the disease. Folate also plays a vital role in one-carbon metabolism. Impairments in this folate-dependent mechanism can also occur due to secondary B-vitamin (vitamin B2, B6 and B12) deficiencies. The study objective was to determine B-vitamin status in Canadian children with SCD. Methods Serum and plasma samples from children diagnosed with SCD were obtained from BC Children's Hospital BioBank (Vancouver, Canada). Samples were analyzed for folate, vitamin B6, and related metabolites using electrospray ionization-liquid chromatography-tandem mass spectrometry. Vitamin B12 concentrations were analyzed using chemiluminescent immunoassay. World Health Organization cut-offs were used to determine deficiencies of folate (&lt;10 nmol/L) and vitamin B12 (&lt;150 pmol/L), and European Food Safety Authority Panel cut-offs were used for vitamin B6 (&lt;30 nmol/L pyridoxal 5’-phosphate; PLP). Medians with interquartile ranges (IQR) are presented. Results Six individuals (50% male; SCD type: Hgb SS n = 3, Hgb SC n = 2, HbSβ,0-Thal n = 1) were included. Median age of participants was 15 (9, 18) years. Half (50%) of participants were prescribed hydroxyurea (median dose: 21(14, 30) mg/kg/d), and all participants were prescribed 1 mg/d folic acid (adherence data not available). Median serum folate was 55.4 (43.1, 71.9) nmol/L, with levels 3 to 15 times above the cut-off for deficiency. Unmetabolized folic acid (UMFA), unused folic acid in circulation, was detected in all six participants. All participants were vitamin B12 sufficient, with median plasma vitamin B12 of 325 (288, 411) nmol/L. The majority (n = 5; 83%) had sufficient B6 status, with median serum PLP of 39 (36.9, 44.2) nmol/L. Conclusions In this pilot project, there was limited evidence of B-vitamin deficiencies among Canadian children with SCD. Serum folate levels exceeded the cut-off for deficiency by 3 to 15 times, with all participants having detectable levels of UMFA. A randomized clinical trial re-assessing the routine practice of high-dose folic acid supplementation in children with SCD is warranted. Funding Sources Thrasher Research Fund and Rare Disease Foundation.

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