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John M Scott - One of the best experts on this subject based on the ideXlab platform.
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effect of a voluntary food fortification policy on folate related B Vitamin status and homocysteine in healthy adults
The American Journal of Clinical Nutrition, 2007Co-Authors: Lesli Hoey, Nadina Askin, Adrian Dunne, Cliona A. Flynn, A. M. Molloy, Kristina Pentieva, Mary Ward, Helene Mcnulty, James J. Strain, John M ScottAbstract:Background: Mandatory folic acid fortification of food is effective in reducing neural tuBe defects and may even reduce stroke-related mortality, But it remains controversial Because of concerns aBout potential adverse effects. Thus, it is virtually nonexistent in Europe, alBeit many countries allow food fortification on a voluntary Basis. OBjective: The oBjective of the study was to examine the effect of a voluntary But liBeral food fortification policy on dietary intake and Biomarker status of folate and other homocysteine-related B Vitamins in a healthy population. Design: The study was a cross-sectional study. From a convenience sample of 662 adults in Northern Ireland, those who provided a fasting Blood sample and dietary intake data were examined (n = 441, aged 18 -92 y). Intakes of Both natural food folate and folic acid from fortified foods were estimated; we used the latter to categorize participants By fortified food intake. Results: Fortified foods were associated with significantly higher dietary intakes and Biomarker status of folate, Vitamin B-12, Vitamin B-6, and riBoflavin than were unfortified foods. There was no difference in natural food folate intake (range: 179-197 μg/d) Between the fortified food categories. Red Blood cell folate concentrations were 387 nmol/L higher and plasma total homocysteine concentrations were 2 μmol/L lower in the group with the highest fortified food intake (median intake: 208 μg/d folic acid) than in the nonconsumers of fortified foods (0 μg/d folic acid). Conclusions: These results show that voluntary food fortification is associated with a suBstantial increase in dietary intake and Biomarker status of folate and metaBolically related B Vitamins with potential Beneficial effects on health. However, those who do not consume fortified foods regularly may have insufficient B Vitamin status to achieve the known and potential health Benefits.
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Effect of a voluntary food fortification policy on folate, related B Vitamin status, and homocysteine in healthy adults
American Journal of Clinical Nutrition, 2007Co-Authors: Lesli Hoey, Nadina Askin, Adrian Dunne, Cliona A. Flynn, A. M. Molloy, Kristina Pentieva, Mary Ward, Helene Mcnulty, James J. Strain, John M ScottAbstract:BACKGROUND: Mandatory folic acid fortification of food is effective in reducing neural tuBe defects and may even reduce stroke-related mortality, But it remains controversial Because of concerns aBout potential adverse effects. Thus, it is virtually nonexistent in Europe, alBeit many countries allow food fortification on a voluntary Basis. OBJECTIVE: The oBjective of the study was to examine the effect of a voluntary But liBeral food fortification policy on dietary intake and Biomarker status of folate and other homocysteine-related B Vitamins in a healthy population. DESIGN: The study was a cross-sectional study. From a convenience sample of 662 adults in Northern Ireland, those who provided a fasting Blood sample and dietary intake data were examined (n = 441, aged 18-92 y). Intakes of Both natural food folate and folic acid from fortified foods were estimated; we used the latter to categorize participants By fortified food intake. RESULTS: Fortified foods were associated with significantly higher dietary intakes and Biomarker status of folate, Vitamin B-12, Vitamin B-6, and riBoflavin than were unfortified foods. There was no difference in natural food folate intake (range: 179-197 microg/d) Between the fortified food categories. Red Blood cell folate concentrations were 387 nmol/L higher and plasma total homocysteine concentrations were 2 micromol/L lower in the group with the highest fortified food intake (median intake: 208 microg/d folic acid) than in the nonconsumers of fortified foods (0 microg/d folic acid). CONCLUSIONS: These results show that voluntary food fortification is associated with a suBstantial increase in dietary intake and Biomarker status of folate and metaBolically related B Vitamins with potential Beneficial effects on health. However, those who do not consume fortified foods regularly may have insufficient B Vitamin status to achieve the known and potential health Benefits.
Helga Refsum - One of the best experts on this subject based on the ideXlab platform.
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Brain atrophy in cognitively impaired elderly the importance of long chain ω 3 fatty acids and B Vitamin status in a randomized controlled trial
The American Journal of Clinical Nutrition, 2015Co-Authors: Fredrik Jerneren, Helga Refsum, Abderrahim Oulhaj, Stephen M Smith, Amany K Elshorbagy, A D SmithAbstract:BACKGROUND: Increased Brain atrophy rates are common in older people with cognitive impairment, particularly in those who eventually convert to Alzheimer disease. Plasma concentrations of omega-3 (ω-3) fatty acids and homocysteine are associated with the development of Brain atrophy and dementia. OBJECTIVE: We investigated whether plasma ω-3 fatty acid concentrations (eicosapentaenoic acid and docosahexaenoic acid) modify the treatment effect of homocysteine-lowering B Vitamins on Brain atrophy rates in a placeBo-controlled trial (VITACOG). DESIGN: This retrospective analysis included 168 elderly people (≥70 y) with mild cognitive impairment, randomly assigned either to placeBo (n = 83) or to daily high-dose B Vitamin supplementation (folic acid, 0.8 mg; Vitamin B-6, 20 mg; Vitamin B-12, 0.5 mg) (n = 85). The suBjects underwent cranial magnetic resonance imaging scans at Baseline and 2 y later. The effect of the intervention was analyzed according to tertiles of Baseline ω-3 fatty acid concentrations. RESULTS: There was a significant interaction (P = 0.024) Between B Vitamin treatment and plasma comBined ω-3 fatty acids (eicosapentaenoic acid and docosahexaenoic acid) on Brain atrophy rates. In suBjects with high Baseline ω-3 fatty acids (>590 μmol/L), B Vitamin treatment slowed the mean atrophy rate By 40.0% compared with placeBo (P = 0.023). B Vitamin treatment had no significant effect on the rate of atrophy among suBjects with low Baseline ω-3 fatty acids (<390 μmol/L). High Baseline ω-3 fatty acids were associated with a slower rate of Brain atrophy in the B Vitamin group But not in the placeBo group. CONCLUSIONS: The Beneficial effect of B Vitamin treatment on Brain atrophy was oBserved only in suBjects with high plasma ω-3 fatty acids. It is also suggested that the Beneficial effect of ω-3 fatty acids on Brain atrophy may Be confined to suBjects with good B Vitamin status. The results highlight the importance of identifying suBgroups likely to Benefit in clinical trials. This trial was registered at www.controlled-trials.com as ISRCTN94410159.
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preventing alzheimer s disease related gray matter atrophy By B Vitamin treatment
Proceedings of the National Academy of Sciences of the United States of America, 2013Co-Authors: Celeste A. De Jager, Helga Refsum, Gwenaelle Douaud, Robin Jacoby, Thomas E Nichols, Stephen M SmithAbstract:Is it possiBle to prevent atrophy of key Brain regions related to cognitive decline and Alzheimer’s disease (AD)? One approach is to modify nongenetic risk factors, for instance By lowering elevated plasma homocysteine using B Vitamins. In an initial, randomized controlled study on elderly suBjects with increased dementia risk (mild cognitive impairment according to 2004 Petersen criteria), we showed that high-dose B-Vitamin treatment (folic acid 0.8 mg, Vitamin B6 20 mg, Vitamin B12 0.5 mg) slowed shrinkage of the whole Brain volume over 2 y. Here, we go further By demonstrating that B-Vitamin treatment reduces, By as much as seven fold, the cereBral atrophy in those gray matter (GM) regions specifically vulneraBle to the AD process, including the medial temporal loBe. In the placeBo group, higher homocysteine levels at Baseline are associated with faster GM atrophy, But this deleterious effect is largely prevented By B-Vitamin treatment. We additionally show that the Beneficial effect of B Vitamins is confined to participants with high homocysteine (aBove the median, 11 µmol/L) and that, in these participants, a causal Bayesian network analysis indicates the following chain of events: B Vitamins lower homocysteine, which directly leads to a decrease in GM atrophy, thereBy slowing cognitive decline. Our results show that B-Vitamin supplementation can slow the atrophy of specific Brain regions that are a key component of the AD process and that are associated with cognitive decline. Further B-Vitamin supplementation trials focusing on elderly suBjets with high homocysteine levels are warranted to see if progression to dementia can Be prevented.
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Preventing Alzheimer’s disease-related gray matter atrophy By B-Vitamin treatment
Proceedings of the National Academy of Sciences, 2013Co-Authors: Gwenaelle Douaud, RONALD JACOBY, Celeste A. De Jager, Thomas Nichols, Helga Refsum, Stephen M Smith, A. David SmithAbstract:Is it possiBle to prevent atrophy of key Brain regions related to cognitive decline and Alzheimer's disease (AD)? One approach is to modify nongenetic risk factors, for instance By lowering elevated plasma homocysteine using B Vitamins. In an initial, randomized controlled study on elderly suBjects with increased dementia risk (mild cognitive impairment according to 2004 Petersen criteria), we showed that high-dose B-Vitamin treatment (folic acid 0.8 mg, Vitamin B6 20 mg, Vitamin B12 0.5 mg) slowed shrinkage of the whole Brain volume over 2 y. Here, we go further By demonstrating that B-Vitamin treatment reduces, By as much as seven fold, the cereBral atrophy in those gray matter (GM) regions specifically vulneraBle to the AD process, including the medial temporal loBe. In the placeBo group, higher homocysteine levels at Baseline are associated with faster GM atrophy, But this deleterious effect is largely prevented By B-Vitamin treatment. We additionally show that the Beneficial effect of B Vitamins is confined to participants with high homocysteine (aBove the median, 11 µmol/L) and that, in these participants, a causal Bayesian network analysis indicates the following chain of events: B Vitamins lower homocysteine, which directly leads to a decrease in GM atrophy, thereBy slowing cognitive decline. Our results show that B-Vitamin supplementation can slow the atrophy of specific Brain regions that are a key component of the AD process and that are associated with cognitive decline. Further B-Vitamin supplementation trials focusing on elderly suBjets with high homocysteine levels are warranted to see if progression to dementia can Be prevented.
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cognitive and clinical outcomes of homocysteine lowering B Vitamin treatment in mild cognitive impairment a randomized controlled trial
International Journal of Geriatric Psychiatry, 2012Co-Authors: Celeste A. De Jager, Helga Refsum, Abderrahim Oulhaj, Robin Jacoby, David A SmithAbstract:†Background: Homocysteine is a risk factor for Alzheimer’s disease. In the first report on the VITACOG trial, we showed that homocysteine-lowering treatment with B Vitamins slows the rate of Brain atrophy in mild cognitive impairment (MCI). Here we report the effect of B Vitamins on cognitive and clinical decline (secondary outcomes) in the same study. Methods:This was a douBle-Blind, single-centre study, which included participants with MCI, aged ≥70y, randomly assigned to receive a daily dose of 0.8mg folic acid, 0.5mg Vitamin B12 and 20mg Vitamin B6 (133 participants) or placeBo (133 participants) for 2y. Changes in cognitive or clinical function were analysed By generalized linear models or mixed-effects models. Results: The mean plasma total homocysteine was 30% lower in those treated with B Vitamins relative to placeBo. B Vitamins staBilized executive function (CLOX) relative to placeBo (P=0.015). There was significant Benefit of B-Vitamin treatment among participants with Baseline homocysteine aBove the median (11.3mmol/L) in gloBal cognition (Mini Mental State Examination, P<0.001), episodic memory (Hopkins VerBal Learning Test–delayed recall, P=0.001) and semantic memory (category fluency, P=0.037). Clinical Benefit occurred in the B-Vitamin group for those in the upper quartile of homocysteine at Baseline in gloBal clinical dementia rating score (P=0.02) and IQCODE score (P=0.01). Conclusion: In this small intervention trial, B Vitamins appear to slow cognitive and clinical decline in peoplewithMCI,inparticularinthosewithelevatedhomocysteine.Furthertrialsareneededtoseeifthistreatment will slow or prevent conversion from MCI to dementia. Copyright # 2011 John Wiley & Sons, Ltd. Supporting information may Be found in the online version of this article.
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Cognitive and clinical outcomes of homocysteine-lowering B-Vitamin treatment in mild cognitive impairment: A randomized controlled trial
International Journal of Geriatric Psychiatry, 2012Co-Authors: Celeste A. De Jager, RONALD JACOBY, Helga Refsum, Abderrahim Oulhaj, A. David SmithAbstract:BACKGROUND: Homocysteine is a risk factor for Alzheimer's disease. In the first report on the VITACOG trial, we showed that homocysteine-lowering treatment with B Vitamins slows the rate of Brain atrophy in mild cognitive impairment (MCI). Here we report the effect of B Vitamins on cognitive and clinical decline (secondary outcomes) in the same study.\n\nMETHODS: This was a douBle-Blind, single-centre study, which included participants with MCI, aged ≥ 70 y, randomly assigned to receive a daily dose of 0.8 mg folic acid, 0.5 mg Vitamin B(12) and 20 mg Vitamin B(6) (133 participants) or placeBo (133 participants) for 2 y. Changes in cognitive or clinical function were analysed By generalized linear models or mixed-effects models.\n\nRESULTS: The mean plasma total homocysteine was 30% lower in those treated with B Vitamins relative to placeBo. B Vitamins staBilized executive function (CLOX) relative to placeBo (P = 0.015). There was significant Benefit of B-Vitamin treatment among participants with Baseline homocysteine aBove the median (11.3 µmol/L) in gloBal cognition (Mini Mental State Examination, P < 0.001), episodic memory (Hopkins VerBal Learning Test-delayed recall, P = 0.001) and semantic memory (category fluency, P = 0.037). Clinical Benefit occurred in the B-Vitamin group for those in the upper quartile of homocysteine at Baseline in gloBal clinical dementia rating score (P = 0.02) and IQCODE score (P = 0.01).\n\nCONCLUSION: In this small intervention trial, B Vitamins appear to slow cognitive and clinical decline in people with MCI, in particular in those with elevated homocysteine. Further trials are needed to see if this treatment will slow or prevent conversion from MCI to dementia.
Per Magne Ueland - One of the best experts on this subject based on the ideXlab platform.
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Genotype, B-Vitamin status, and androgens affect spaceflight-induced ophthalmic changes
FASEB Journal, 2016Co-Authors: Sara R. Zwart, Charles R. Gibson, Thomas H. Mader, Martina A. Heer, Jason M. Kinchen, Robert Ploutz-snyder, Steven H Zeisel, Jesse F Gregory, Per Magne Ueland, Scott M SmithAbstract:Ophthalmic changes have occurred in a suBset of astronauts on International Space Station missions. Visual deterioration is considered the greatest human health risk of spaceflight. Affected astronauts exhiBit higher concentrations of 1-carBon metaBolites (e.g., homocysteine) Before flight. We hypothesized that genetic variations in 1-carBon metaBolism genes contriBute to susceptiBility to ophthalmic changes in astronauts. We investigated 5 polymorphisms in the methionine synthase reductase (MTRR), methylenetetrahydrofolate reductase (MTHFR), serine hydroxymethyltransferase (SHMT), and cystathionine β-synthase (CBS) genes and their association with ophthalmic changes after flight in 49 astronauts. The numBer of G alleles of MTRR 66 and C alleles of SHMT1 1420 Both contriButed to the odds of visual disturBances. Preflight dehydroepiandrosterone was positively associated with cotton wool spots, and serum testosterone response during flight was associated with refractive change. Block regression showed that B-Vitamin status and genetics were significant predictors of many of the ophthalmic outcomes that we oBserved. In one example, genetics trended toward improving (P = 0.10) and B-Vitamin status significantly improved (P < 0.001) the predictive model for refractive change after flight. We document an association Between MTRR 66 and SHMT1 1420 polymorphisms and spaceflight-induced vision changes. This line of research could lead to therapeutic options for Both space travelers and terrestrial patients.
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Motor development related to duration of exclusive Breastfeeding, B Vitamin status and B12 supplementation in infants with a Birth weight Between 2000-3000 g, results from a randomized intervention trial
BMC Pediatrics, 2015Co-Authors: Ingrid Kristin Torsvik, O Midttun, Trond Markestad, Per Magne Ueland, Anne-lise Bjørke MonsenAbstract:BackgroundExclusive Breastfeeding for 6 months is assumed to ensure adequate micronutrients for term infants. Our oBjective was to investigate the effects of prolonged Breastfeeding on B Vitamin status and neurodevelopment in 80 infants with suBnormal Birth weights (2000-3000 g) and examine if coBalamin supplementation may Benefit motor function in infants who developed Biochemical signs of impaired coBalamin function (total homocysteine (tHcy) > 6.5 μmol/L) at 6 months.MethodsLevels of coBalamin, folate, riBoflavin and pyridoxal 5´-phosphate, and the metaBolic markers tHcy and methylmalonic acid (MMA), were determined at 6 weeks, 4 and 6 months ( n = 80/68/66). Neurodevelopment was assessed with the AlBerta Infants Motor Scale (AIMS) and the parental questionnaire Ages and Stages (ASQ) at 6 months. At 6 months, 32 of 36 infants with tHcy > 6.5 μmol/L were enrolled in a douBle Blind randomized controlled trial to receive 400 μg hydroxycoBalamin intramuscularly ( n = 16) or sham injection ( n = 16). Biochemical status and neurodevelopment were evaluated after one month.ResultsExcept for folate, infants who were exclusively Breastfed for >1 month had lower B Vitamin levels at all assessments and higher tHcy and MMA levels at 4 and 6 months. At 6 months, these infants had lower AIMS scores ( p = 0.03) and ASQ gross motor scores ( p = 0.01). Compared to the placeBo group, coBalamin treatment resulted in a decrease in plasma tHcy ( p
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Maternal B Vitamin status in pregnancy week 18 according to reported use of folic acid supplements
Molecular Nutrition and Food Research, 2013Co-Authors: Anne Lise Bjørke Monsen, Christine Roth, Roy M. Nilsen, Camilla Stoltenberg, O Midttun, Stein Emil Vollset, Ted Reichborn-kjennerud, Per Magnus, Ezra Susser, Per Magne UelandAbstract:SCOPE: Epidemiological studies on the association Between pregnancy outcomes and use of periconceptional folic acid are often Based on maternal reported intake. Use of folic acid during pregnancy is associated with a higher socioeconomic status known to have an impact on diet quality. We have studied plasma B Vitamin status according to reported use of folic acid supplements during the periconceptional period in Norwegian women.\n\nMETHODS AND RESULTS: Plasma levels of folate, coBalamin, pyridoxal 5'-phosphate (Vitamin B6), riBoflavin, and the metaBolic markers total homocysteine, methylmalonic acid and 3-hydro-xykynurenine were measured in pregnancy week 18 and related to reported intake of folic acid from 4 weeks prior to conception throughout week 18 in 2911 women from the Norwegian Mother and Child Cohort Study (MoBa) conducted By the Norwegian Institute of PuBlic Health. Being a folic acid user during the periconceptional period was associated with a Better socioeconomic status, and a higher intake of several micronutrients, including Vitamins, trace-metals, and omega 3 fatty acids. Folic acid users had a significantly Better plasma B Vitamin status.\n\nCONCLUSION: Epidemiological data Based on maternal reported intake of folic acid supplements during pregnancy, should take into account the numerous nutritional implications, in addition to higher Blood folate levels, of Being a folic acid user.
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Kinetic modeling of storage effects on Biomarkers related to B Vitamin status and one-carBon metaBolism
Clinical Chemistry, 2012Co-Authors: Steinar Hustad, Arve Ulvik, Puck M. Van De Kant, Randi Gislefoss, O Midttun, Simone Eussen, Lars Mørkrid, Per Magne UelandAbstract:BACKGROUND: Biomarkers and metaBolites related to B Vitamin function and one-carBon metaBolism have Been studied as predictors of chronic diseases in studies Based on samples stored in BioBanks. For most Biomarkers, staBility data are lacking or fragmentary.\n\nMETHODS: Degradation and accumulation kinetics of 32 Biomarkers were determined at 23 °C in serum and plasma (EDTA, heparin, and citrate) collected from 16 individuals and stored for up to 8 days. In frozen serum (-25 °C), staBility was studied cross-sectionally in 650 archival samples stored for up to 29 years. Concentration vs time curves were fitted to monoexponential, Biexponential, linear, and nonlinear models.\n\nRESULTS: For many Biomarkers, staBility was highest in EDTA plasma. Storage effects were similar at room temperature and at -25 °C; notaBle exceptions were methionine, which could Be recovered as methionine sulfoxide, and cystathionine, which decreased in frozen samples. CoBalamin, Betaine, dimethylglycine, sarcosine, total homocysteine, total cysteine, tryptophan, asymetric and symmetric dimethyl argenine, creatinine, and methylmalonic acid were essentially staBle under all conditions. Most B Vitamins (folate and Vitamins B2 and B6) were unstaBle; choline increased markedly, and some amino acids also increased, particularly in serum. The kynurenines showed variaBle staBility. For many Biomarkers, degradation (folate and flavin mononucleotide) or accumulation (pyridoxal, riBoflavin, choline, amino acids) kinetics at room temperature were non-first order.\n\nCONCLUSIONS: Data on staBility and deterioration kinetics for individual Biomarkers are required to optimize procedures for handling serum and plasma, and for addressing preanalytical Bias in epidemiological and clinical studies.
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Effect of Homocysteine-Lowering B Vitamin Treatment on Angiographic Progression of Coronary Artery Disease: A Western Norway B Vitamin Intervention Trial (WENBIT) SuBstudy
American Journal of Cardiology, 2010Co-Authors: Kjetil H. Løland, Øyvind Bleie, Are J. Blix, Elin Strand, Marta Ebbing, Jan Erik Nordrehaug, Helga Refsum, Per Magne Ueland, Ottar NygardAbstract:Total plasma homocysteine (tHcy) is an independent risk factor for coronary artery disease, and tHcy is lowered By B Vitamins. To assess the effect of homocysteine-lowering B-Vitamin treatment on angiographic progression of coronary artery disease, this suBstudy of the Western Norway B Vitamin Intervention Trial (WENBIT) included patients who had undergone percutaneous coronary intervention. The patients were randomized to daily oral treatment with folic acid, Vitamin B12, and Vitamin B6or placeBo in a 2 × 2 factorial design. The coronary angiograms oBtained at Baseline and follow-up were evaluated. The primary angiographic end points were the changes in minimum lumen diameter and diameter stenosis. A total of 348 suBjects (288 men) with a mean ± SD age of 60 ± 10.2 years were followed up for a median of 10.5 months (twenty-fifth, seventy-fifth percentile 9.2, 11.8). The Baseline median plasma tHcy level was 10.0 μmol/L (twenty-fifth, seventy-fifth percentile 8.1, 11.0), and treatment with folic acid/Vitamin B12lowered the tHcy levels By 22%. At follow-up, we found 309 lesions with a significant decrease from Baseline in the minimum lumen diameter of a mean of -0.16 ± 0.4 mm and an increase in the diameter stenosis of 4.4 ± 0.7%. Treatment with folic acid/Vitamin B12or Vitamin B6was not associated with a change in diameter stenosis or minimum lumen diameter. In a post hoc analysis, folic acid/Vitamin B12treatment was significantly associated with rapid progression (odds ratio 1.84, 95% confidence interval 1.07 to 3.18). In conclusion, Vitamin B treatment showed no Beneficial effect on the angiographic progression of coronary artery disease, and the post hoc analyses suggested that folic acid/Vitamin B12treatment might promote more rapid progression. © 2010 Elsevier Inc. All rights reserved.
Jacob Selhub - One of the best experts on this subject based on the ideXlab platform.
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high dose B Vitamin supplementation and progression of suBclinical atherosclerosis a randomized controlled trial
Stroke, 2009Co-Authors: Howard N Hodis, Peter R Mahrer, Jacob Selhub, Stanley P Azen, Wendy J Mack, Laurie Dustin, Petar Alaupovic, Robert Detrano, Juliana Hwang, Alison WilcoxAbstract:Background and Purpose— Although plasma total homocysteine (tHcy) levels are associated with cardiovascular disease, it remains unclear whether homocysteine is a cause or a marker of atherosclerotic vascular disease. We determined whether reduction of tHcy levels with B Vitamin supplementation reduces suBclinical atherosclerosis progression. Methods— In this douBle-Blind clinical trial, 506 participants 40 to 89 years of age with an initial tHcy >8.5 μmol/L without diaBetes and cardiovascular disease were randomized to high-dose B Vitamin supplementation (5 mg folic acid+0.4 mg Vitamin B12+50 mg Vitamin B6) or matching placeBo for 3.1 years. SuBclinical atherosclerosis progression across 3 vascular Beds was assessed using high-resolution B-mode ultrasonography to measure carotid artery intima media thickness (primary outcome) and multidetector spiral CT to measure aortic and coronary artery calcium (secondary outcome). Results— Although the overall carotid artery intima media thickness progression rate wa...
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High-dose B Vitamin supplementation and progression of suBclinical atherosclerosis: a randomized controlled trial.
Stroke; a journal of cerebral circulation, 2009Co-Authors: Howard N Hodis, Peter R Mahrer, Chao-ran Liu, Jacob Selhub, Stanley P Azen, Wendy J Mack, Laurie Dustin, Petar Alaupovic, Robert Detrano, Ci-hua LiuAbstract:BACKGROUND AND PURPOSE: Although plasma total homocysteine (tHcy) levels are associated with cardiovascular disease, it remains unclear whether homocysteine is a cause or a marker of atherosclerotic vascular disease. We determined whether reduction of tHcy levels with B Vitamin supplementation reduces suBclinical atherosclerosis progression.\n\nMETHODS: In this douBle-Blind clinical trial, 506 participants 40 to 89 years of age with an initial tHcy >8.5 micromol/L without diaBetes and cardiovascular disease were randomized to high-dose B Vitamin supplementation (5 mg folic acid+0.4 mg Vitamin B(12)+50 mg Vitamin B(6)) or matching placeBo for 3.1 years. SuBclinical atherosclerosis progression across 3 vascular Beds was assessed using high-resolution B-mode ultrasonography to measure carotid artery intima media thickness (primary outcome) and multidetector spiral CT to measure aortic and coronary artery calcium (secondary outcome).\n\nRESULTS: Although the overall carotid artery intima media thickness progression rate was lower with B Vitamin supplementation than with placeBo, statistically significant Between-group differences were not found (P=0.31). However, among suBjects with Baseline tHcy >or=9.1 micromol/L, those randomized to B Vitamin supplementation had a statistically significant lower average rate of carotid artery intima media thickness progression compared with placeBo (P=0.02); among suBjects with a Baseline tHcy or=9.1 micromol/L.
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B Vitamin deficiency causes hyperhomocysteinemia and vascular cognitive impairment in mice
Proceedings of the National Academy of Sciences of the United States of America, 2008Co-Authors: A M Troen, Jacob Selhub, D.e. Smith, Melissa Sheabudgell, Barbara Shukitthale, I H RosenbergAbstract:In older adults, mildly elevated plasma total homocysteine (hyperhomocysteinemia) is associated with increased risk of cognitive impairment, cereBrovascular disease, and Alzheimer’s disease, But it is uncertain whether this is due to underlying metaBolic, neurotoxic, or vascular processes. We report here that feeding male C57BL6/J mice a B-Vitamin-deficient diet for 10 weeks induced hyperhomocysteinemia, significantly impaired spatial learning and memory, and caused a significant rarefaction of hippocampal microvasculature without concomitant gliosis and neurodegeneration. Total hippocampal capillary length was inversely correlated with Morris water maze escape latencies (r 0.757, P < 0.001), and with plasma total homocysteine (r 0.631, P 0.007). Feeding mice a methionine-rich diet produced similar But less pronounced effects. Our findings suggest that cereBral microvascular rarefaction can cause cognitive dysfunction in the aBsence of or preceding neurodegeneration. Similar microvascular changes may mediate the association of hyperhomocysteinemia with human age-related cognitive decline. cereBrovascular homocysteine mouse nutrition
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B-Vitamin deficiency causes hyperhomocysteinemia and vascular cognitive impairment in mice
Proc Natl Acad Sci U S A, 2008Co-Authors: A M Troen, M Shea-budgell, Jacob Selhub, D.e. Smith, Barbara Shukitt-hale, I H RosenbergAbstract:In older adults, mildly elevated plasma total homocysteine (hyperhomocysteinemia) is associated with increased risk of cognitive impairment, cereBrovascular disease, and Alzheimer's disease, But it is uncertain whether this is due to underlying metaBolic, neurotoxic, or vascular processes. We report here that feeding male C57BL6/J mice a B-Vitamin-deficient diet for 10 weeks induced hyperhomocysteinemia, significantly impaired spatial learning and memory, and caused a significant rarefaction of hippocampal microvasculature without concomitant gliosis and neurodegeneration. Total hippocampal capillary length was inversely correlated with Morris water maze escape latencies (r = -0.757, P < 0.001), and with plasma total homocysteine (r = -0.631, P = 0.007). Feeding mice a methionine-rich diet produced similar But less pronounced effects. Our findings suggest that cereBral microvascular rarefaction can cause cognitive dysfunction in the aBsence of or preceding neurodegeneration. Similar microvascular changes may mediate the association of hyperhomocysteinemia with human age-related cognitive decline.
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relation Between homocysteine and B Vitamin status indicators and Bone mineral density in older americans
Bone, 2005Co-Authors: Martha Savaria Morris, P. F. Jacques, Jacob SelhubAbstract:ABstract Recent studies have found a connection Between hyperhomocysteinemia and hip fracture. If this association is causal, it could Be mediated through detrimental effects of low B-Vitamin status on Bone mineral density (BMD). Studies have linked homocysteine (Hcy) and the estaBlished Hcy determinants folate and Vitamin B12, to BMD, But results have Been inconsistent. Furthermore, only one study considered the specific marker of tissue Vitamin B12 status, methylmalonic acid (MMA), and none have considered red Blood cell (RBC) folate. To further explore associations Between Hcy and B-Vitamin status indicators and Bone health, we used data collected on older (i.e., aged >55 years) men and women who underwent DEXA scans of the hip as participants in phase 2 of the third U.S. National Health and Nutrition Examination Survey ( n = 1550). We used BMD at the total hip as a continuous outcome variaBle in some analyses. In others, we used osteoporosis defined on a sex- and race/ethnicity-specific Basis according to World Health Organization (WHO) guidelines. After adjusting for demographic factors, Body mass index, and other osteoporosis risk factors, BMD decreased and osteoporosis increased significantly with increasing serum MMA quartile category ( P
Lesli Hoey - One of the best experts on this subject based on the ideXlab platform.
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effect of a voluntary food fortification policy on folate related B Vitamin status and homocysteine in healthy adults
The American Journal of Clinical Nutrition, 2007Co-Authors: Lesli Hoey, Nadina Askin, Adrian Dunne, Cliona A. Flynn, A. M. Molloy, Kristina Pentieva, Mary Ward, Helene Mcnulty, James J. Strain, John M ScottAbstract:Background: Mandatory folic acid fortification of food is effective in reducing neural tuBe defects and may even reduce stroke-related mortality, But it remains controversial Because of concerns aBout potential adverse effects. Thus, it is virtually nonexistent in Europe, alBeit many countries allow food fortification on a voluntary Basis. OBjective: The oBjective of the study was to examine the effect of a voluntary But liBeral food fortification policy on dietary intake and Biomarker status of folate and other homocysteine-related B Vitamins in a healthy population. Design: The study was a cross-sectional study. From a convenience sample of 662 adults in Northern Ireland, those who provided a fasting Blood sample and dietary intake data were examined (n = 441, aged 18 -92 y). Intakes of Both natural food folate and folic acid from fortified foods were estimated; we used the latter to categorize participants By fortified food intake. Results: Fortified foods were associated with significantly higher dietary intakes and Biomarker status of folate, Vitamin B-12, Vitamin B-6, and riBoflavin than were unfortified foods. There was no difference in natural food folate intake (range: 179-197 μg/d) Between the fortified food categories. Red Blood cell folate concentrations were 387 nmol/L higher and plasma total homocysteine concentrations were 2 μmol/L lower in the group with the highest fortified food intake (median intake: 208 μg/d folic acid) than in the nonconsumers of fortified foods (0 μg/d folic acid). Conclusions: These results show that voluntary food fortification is associated with a suBstantial increase in dietary intake and Biomarker status of folate and metaBolically related B Vitamins with potential Beneficial effects on health. However, those who do not consume fortified foods regularly may have insufficient B Vitamin status to achieve the known and potential health Benefits.
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Effect of a voluntary food fortification policy on folate, related B Vitamin status, and homocysteine in healthy adults
American Journal of Clinical Nutrition, 2007Co-Authors: Lesli Hoey, Nadina Askin, Adrian Dunne, Cliona A. Flynn, A. M. Molloy, Kristina Pentieva, Mary Ward, Helene Mcnulty, James J. Strain, John M ScottAbstract:BACKGROUND: Mandatory folic acid fortification of food is effective in reducing neural tuBe defects and may even reduce stroke-related mortality, But it remains controversial Because of concerns aBout potential adverse effects. Thus, it is virtually nonexistent in Europe, alBeit many countries allow food fortification on a voluntary Basis. OBJECTIVE: The oBjective of the study was to examine the effect of a voluntary But liBeral food fortification policy on dietary intake and Biomarker status of folate and other homocysteine-related B Vitamins in a healthy population. DESIGN: The study was a cross-sectional study. From a convenience sample of 662 adults in Northern Ireland, those who provided a fasting Blood sample and dietary intake data were examined (n = 441, aged 18-92 y). Intakes of Both natural food folate and folic acid from fortified foods were estimated; we used the latter to categorize participants By fortified food intake. RESULTS: Fortified foods were associated with significantly higher dietary intakes and Biomarker status of folate, Vitamin B-12, Vitamin B-6, and riBoflavin than were unfortified foods. There was no difference in natural food folate intake (range: 179-197 microg/d) Between the fortified food categories. Red Blood cell folate concentrations were 387 nmol/L higher and plasma total homocysteine concentrations were 2 micromol/L lower in the group with the highest fortified food intake (median intake: 208 microg/d folic acid) than in the nonconsumers of fortified foods (0 microg/d folic acid). CONCLUSIONS: These results show that voluntary food fortification is associated with a suBstantial increase in dietary intake and Biomarker status of folate and metaBolically related B Vitamins with potential Beneficial effects on health. However, those who do not consume fortified foods regularly may have insufficient B Vitamin status to achieve the known and potential health Benefits.
