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B Vitamins

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Graeme J Hankey – 1st expert on this subject based on the ideXlab platform

  • B Vitamins for stroke prevention
    Stroke and vascular neurology, 2018
    Co-Authors: Graeme J Hankey

    Abstract:

    Supplementation with B Vitamins (vitamin B9(folic acid), vitamin B12 and vitamin B6) lowers Blood total homocysteine (tHcy) concentrations By aBout 25% and reduces the relative risk of stroke overall By aBout 10% (risk ratio (RR) 0.90, 95% CI 0.82 to 0.99) compared with placeBo. Homocysteine-lowering interventions have no significant effect on myocardial infarction, death from any cause or adverse outcomes. Factors that appear to modify the effect of B Vitamins on stroke risk include low folic acid status, high tHcy, high cyanocoBalamin dose in patients with impaired renal function and concurrent antiplatelet therapy. In regions with increasing levels or estaBlished policies of population folate supplementation, evidence from oBservational genetic epidemiological studies and randomised controlled clinical trials is concordant in suggesting an aBsence of Benefit from lowering of homocysteine with folic acid for prevention of stroke. Clinical trials indicate that in countries which mandate folic acid fortification of food, folic acid supplementation has no significant effect on reducing stroke risk (RR 1.05, 95% CI 0.90 to 1.23). However, in countries without mandatory folic acid food fortification, folic acid supplementation reduces the risk of stroke By aBout 15% (RR 0.85, 95% CI 0.77 to 0.94). Folic acid alone or in comBination with minimal cyanocoBalamin (≤0.05 mg/day) is associated with an even greater reduction in risk of future stroke By 25% (RR 0.75, 95% CI 0.66 to 0.86), whereas the comBination of folic acid and a higher dose of cyanocoBalamin (≥0.4 mg/day) is not associated with a reduced risk of future stroke (RR 0.95, 95% CI 0.86 to 1.05). The lack of Benefit of folic acid plus higher doses of cyanocoBalamin (≥0.4 mg/day) was oBserved in trials which all included participants with chronic kidney disease. Because metaBolic B12 deficiency is very common and usually not diagnosed, future randomised trials of homocysteine-lowering interventions for stroke prevention should proBaBly test a comBination of folic acid and methylcoBalamin or hydroxocoBalamin instead of cyanocoBalamin, and perhaps vitamin B6.

  • B Vitamins in stroke prevention: time to reconsider.
    Lancet Neurology, 2017
    Co-Authors: J. David Spence, Qilong Yi, Graeme J Hankey

    Abstract:

    Summary B vitamin therapy lowers plasma total homocysteine concentrations, and might Be a Beneficial intervention for stroke prevention; however, cyanocoBalamin (a form of vitamin B12) can accelerate decline in renal function and increase the risk of cardiovascular events in patients with impaired renal function. Although early trials did not show Benefit in reduction of stroke, these results might have Been due to harm in participants with impaired renal function. In patients with diaBetic nephropathy, cyanocoBalamin is harmful, whereas B Vitamins appear to reduce cardiovascular events in study participants with normal renal function. Our meta-analysis of individual patient data from two large trials of B vitamin therapy (VISP and VITATOPS) indicates that patients with impaired renal function who are exposed to high-dose cyanocoBalamin do not Benefit from therapy with B Vitamins for the prevention of stroke (risk ratio 1·04, 95% CI 0·84–1·27), however, patients with normal renal function who are not exposed to high-dose cyanocoBalamin Benefit significantly from this treatment (0.78, 0·67–0·90; interaction p=0·03). The potential Benefits of B vitamin therapy with folic acid and methylcoBalamin or hydroxycoBalamin, instead of cyanocoBalamin, to lower homocysteine concentrations in people at high risk of stroke warrant further investigation.

  • effects of homocysteine lowering with B Vitamins on cognitive aging meta analysis of 11 trials with cognitive data on 22 000 individuals
    The American Journal of Clinical Nutrition, 2014
    Co-Authors: Robert Clarke, Jane Armitage, Sarah Lewington, Derrick A Bennett, Sarah Parish, Murray Skeaff, Simone J P M Eussen, Catharina Lewerin, David J Stott, Graeme J Hankey

    Abstract:

    Background: Elevated plasma homocysteine is a risk factor for Alzheimer disease, But the relevance of homocysteine lowering to slow the rate of cognitive aging is uncertain. OBjective: The aim was to assess the effects of treatment with B Vitamins compared with placeBo, when administered for several years, on composite domains of cognitive function, gloBal cognitive function, and cognitive aging. Design: A meta-analysis was conducted By using data comBined from 11 large trials in 22,000 participants. Domain-Based z scores (for memory, speed, and executive function and a domain-composite score for gloBal cognitive function) were availaBle Before and after treatment (mean duration: 2.3 y) in the 4 cognitive-domain trials (1340 individuals); Mini-Mental State Examination (MMSE)–type tests were availaBle at the end of treatment (mean duration: 5 y) in the 7 gloBal cognition trials (20,431 individuals). Results: The domain-composite and MMSE-type gloBal cognitive function z scores Both decreased with age (mean 6 SE: 20.054 6 0.004 and 20.036 6 0.001/y, respectively). Allocation to B Vitamins lowered homocysteine concentrations By 28% in the cognitive-domain trials But had no significant effects on the z score differences from Baseline for individual domains or for gloBal cognitive function (z score difference: 0.00; 95% CI: 20.05, 0.06). Likewise, allocation to B Vitamins lowered homocysteine By 26% in the gloBal cognition trials But also had no significant effect on end-treatment MMSE-type gloBal cognitive function (z score difference: 20.01; 95% CI: 20.03, 0.02). Overall, the effect of a 25% reduction in homocysteine equated to 0.02 y (95% CI: 20.10, 0.13 y) of cognitive aging per year and excluded reductions of .1 mo per year of treatment. Conclusion: Homocysteine lowering By using B Vitamins had no significant effect on individual cognitive domains or gloBal cognitive function or on cognitive aging. Am J Clin Nutr 2014;100: 657–66.

Helene Mcnulty – 2nd expert on this subject based on the ideXlab platform

  • The BVitamins
    Sustainable Nutrition in a Changing World, 2017
    Co-Authors: James J. Strain, Catherine F. Hughes, Kristina Pentieva, Mary Ward, Leane Hoey, Helene Mcnulty

    Abstract:

    It is likely that future scenarios will see trends toward a reduced consumption of animal-Based foods and increased consumption of fruit and vegetaBles. This chapter reviews the metaBolic roles, essentiality, deficiency symptoms and food sources of each of the BVitamins and identifies how trends towards improving environmental sustainaBility could impact on B-vitamin status.

  • emerging roles for folate and related B Vitamins in Brain health across the lifecycle
    The Proceedings of the Nutrition Society, 2015
    Co-Authors: C Mcgarel, James J. Strain, Kristina Pentieva, Helene Mcnulty

    Abstract:

    Nutrition plays a fundamental role in supporting the structural and functional development of the human Brain from conception, throughout early infancy and extending into later life. A growing Body of evidence suggests that folate and the metaBolically related BVitamins are essential for Brain health across all age groups, owing to their specific roles in C 1 metaBolism and particularly in the production of S -adenosylmethionine, a universal methyl donor essential for the production of neurotransmitters. Emerging, though not entirely consistent, evidence suggests that maternal folate status throughout pregnancy may influence neurodevelopment and Behaviour of the offspring. Furthermore optimal B-vitamin status is associated with Better cognitive health in ageing. Of note, a recent clinical trial provided evidence that supplementation with folic acid and related BVitamins over a 2-year-period reduced gloBal and regional Brain atrophy, as measured By MRI scan in older adults. In terms of potential mechanisms, the effects of these BVitamins on cognitive health may Be independent or may Be mediated By nutrient–nutrient and/or relevant gene–nutrient interactions. Furthermore, a new area of research suggests that the in utero environment influences health in later life. Folate, an important cofactor in C 1 metaBolism, is indirectly involved in DNA methylation, which in turn is considered to Be one of the epigenetic mechanisms that may underlie fetal programming and Brain development. The present review will explore the evidence that supports a role for folate and the related BVitamins in Brain health across the lifecycle, and potential mechanisms to explain such effects.

  • BVitamins and Bone in health and disease: the current evidence.
    The Proceedings of the Nutrition Society, 2014
    Co-Authors: Michelle Clarke, James J. Strain, Mary Ward, Leane Hoey, William Dickey, Helene Mcnulty

    Abstract:

    : Osteoporosis, a metaBolic skeletal disease characterised By decreased Bone mass and increased fracture risk, is a growing puBlic health proBlem. Among the various risk factors for osteoporosis, calcium and vitamin D have well-estaBlished protective roles, But it is likely that other nutritional factors are also implicated. This review will explore the emerging evidence supporting a role for certain BVitamins, homocysteine and the 677 C → T polymorphism in the gene encoding the folate-metaBolising enzyme methylenetetrahydrofolate reductase, in Bone health and disease. The evidence, however, is not entirely consistent and as yet no clear mechanism has Been defined to explain the potential link Between BVitamins and Bone health. Coeliac disease, a common condition of malaBsorption, induced By gluten ingestion in genetically susceptiBle individuals, is associated with an increased risk Both of osteoporosis and inadequate B-vitamin status. Given the growing Body of evidence linking low Bone mineral density and/or increased fracture risk with low B-vitamin status and elevated homocysteine, optimal B-vitamin status may play an important protective role against osteoporosis in coeliac disease; to date, no trial has addressed this possiBle link.

Pilar Galan – 3rd expert on this subject based on the ideXlab platform

  • mthfr 677c t genotype modulates the effect of a 5 year supplementation with B Vitamins on homocysteine concentration the su fol om3 randomized controlled trial
    PLOS ONE, 2018
    Co-Authors: Leopold Fezeu, Serge Hercberg, Veronique Ducros, Jeanlouis Gueant, Jeanclaude Guilland, Valentina A Andreeva, Pilar Galan

    Abstract:

    Aims
    To study how MTHFR 677C→T genotype modulates the effect of supplementation with BVitamins on total homocysteine (tHcy) and B-vitamin concentrations.

    Methods
    2381 patients with a personal history of cardiovascular disease were randomly assigned to one of four groups: 1) BVitamins alone (560 μg of 5-methyl-THF, 3 mg of vitamin B6 and 20 μg of vitamin B12), 2) n-3 fatty acids alone (600 mg of EPA and DHA in a 2:1 ratio), 3) BVitamins and n-3 fatty acids, and 4) placeBo. Participants were followed up for 4.7 years. At Baseline and annually thereafter, Biological parameters were assessed. Multivariate and linear mixed models were fit to study the interaction Between BVitamins and MTHFR genotype.

    Results
    Among supplemented participants, concentrations of all three BVitamins increased during the first year (all p<0.0001) across MTHFR genotype categories. tHcy decreased By 26.3% during the first year (p<0.0001), then steadily increased throughout the 5 years (ptrend<0.001). However, at the end of follow-up, that increase was smaller among TT than among CT or CC suBjects (pinteraction<0.02). At Baseline, the difference in tHcy concentrations Between TT homozygous and CC homozygous suBjects was 2.33 μmol/l (p<0.001). After 5 years, that difference was reduced to 1.06 μmol/l and remained statistically significant (p<0.001). Conclusion Participants with the TT genotype exhiBited a lower 5-year decrease in tHcy concentrations following a B-vitamin supplementation than did participants with the CC or CT genotype.

    Clinical trial registration
    Current Controlled Trials # ISRCTN41926726.

  • cardiovascular effects of B Vitamins and or n 3 fatty acids the su fol om3 trial
    International Journal of Cardiology, 2013
    Co-Authors: Jacques Blacher, Sébastien Czernichow, F. Paillard, Pierre Ducimetière, Serge Hercberg, Pilar Galan

    Abstract:

    ABstract Background Mechanisms involved in coronary stenosis evolution are different than those involved in clinical events. Because of differential vascular effects, N-3 polyunsatured fatty acids (PUFA) and B Vitamins could have differential effects on different types of cardiovascular clinical events in high-risk patients. Methods We analyzed the effects of n-3 PUFA and of B Vitamins on Both coronary revascularization and on hard coronary events risks in a suBgroup of the SU.FOL.OM3 trial, a randomized, douBle-Blind, placeBo-controlled secondary prevention trial. Data were analyzed according to the intention-to-treat principle, with the use of Cox proportional-hazards models. Results After a mean follow-up of 4.2±1.0years among the 1,863 participants with coronary heart disease, 163 coronary revascularizations were performed, and 95 patients experienced a hard coronary event. Neither treatment with n-3 PUFA, nor treatment with B Vitamins was associated with any significant effect on the occurrence of hard coronary events. Allocation to n-3 PUFA was not associated with any significant effect on coronary revascularization. However, treatment with B Vitamins was associated with a statistically significant 52% increase in the risk of coronary revascularization (multivariate HR: 1.52; 95% CI: [1.11–2.10]; p=0.01). Conclusions Neither n-3 PUFA, nor B Vitamins reduced the rates of hard coronary events and of coronary revascularization. Furthermore, B Vitamins significantly increased the rate of coronary revascularization. Consistent with the findings of previous trials, our results do not support the routine use of dietary supplements containing n-3 PUFA and argue against using dietary supplements containing BVitamins in coronary patients in secondary cardiovascular prevention.

  • Cardiovascular effects of BVitamins and/or N-3 fatty acids: the SU.FOL.OM3 trial.
    International Journal of Cardiology, 2012
    Co-Authors: Jacques Blacher, Sébastien Czernichow, F. Paillard, Pierre Ducimetière, Serge Hercberg, Pilar Galan

    Abstract:

    ABstract Background Mechanisms involved in coronary stenosis evolution are different than those involved in clinical events. Because of differential vascular effects, N-3 polyunsatured fatty acids (PUFA) and B Vitamins could have differential effects on different types of cardiovascular clinical events in high-risk patients. Methods We analyzed the effects of n-3 PUFA and of B Vitamins on Both coronary revascularization and on hard coronary events risks in a suBgroup of the SU.FOL.OM3 trial, a randomized, douBle-Blind, placeBo-controlled secondary prevention trial. Data were analyzed according to the intention-to-treat principle, with the use of Cox proportional-hazards models. Results After a mean follow-up of 4.2±1.0years among the 1,863 participants with coronary heart disease, 163 coronary revascularizations were performed, and 95 patients experienced a hard coronary event. Neither treatment with n-3 PUFA, nor treatment with B Vitamins was associated with any significant effect on the occurrence of hard coronary events. Allocation to n-3 PUFA was not associated with any significant effect on coronary revascularization. However, treatment with B Vitamins was associated with a statistically significant 52% increase in the risk of coronary revascularization (multivariate HR: 1.52; 95% CI: [1.11–2.10]; p=0.01). Conclusions Neither n-3 PUFA, nor B Vitamins reduced the rates of hard coronary events and of coronary revascularization. Furthermore, B Vitamins significantly increased the rate of coronary revascularization. Consistent with the findings of previous trials, our results do not support the routine use of dietary supplements containing n-3 PUFA and argue against using dietary supplements containing BVitamins in coronary patients in secondary cardiovascular prevention.