Plasma Vitamin B12, Supplementation and Mortality

We measured methylmalonic acid (MMA) in plasma and succinate in the rumen during the depletion of sheep to a state of severe cobalt deficiency and repletion by various forms of supplementation. Groups of 10, cobalt-deficient weaners were allocated to one of 4 treatments: no supplement, 0.1 or 4.0 mg/day of cobalt as a solution of CoSO4.7H2O per os, or intramuscular vitamin B12. Plasma concentrations of MMA were elevated above the normal range (5 µmol/L) after 35 days on the cobalt-deficient diet, before a reduction in feed intake and while liveweights were still increasing. In all 3 supplemented groups of sheep, plasma vitamin B12 concentrations increased to normal levels within 10 days of supplementation (P < 0.001). Plasma MMA concentrations were reduced to normal levels within 10 days with vitamin B12 supplementation but took 31 days with oral cobalt supplementation (P < 0.001). Plasma MMA concentration in the unsupplemented group continued to rise and remain high for the duration of the experiment and did not show the peak and decline to levels indistinguishable from cobalt adequate levels as observed by others. Rumen succinate concentrations were elevated within 6 days of sheep being introduced to a cobalt-deficient diet and in the unsupplemented sheep remained elevated for the duration of measurement. This rise in rumen succinate was seen at a wider range of cobalt intakes than previously reported. In both oral cobalt treatments, vitamin B12 concentrations increased (P < 0.001) and succinate concentrations decreased (P < 0.001) in the rumen to normal levels within 6 days of supplementation. However, the vitamin B12 provided to the sheep by injection was not recycled to the rumen to any effective degree, as demonstrated by the persistence of high rumen succinate concentrations. The ability of the vitamin B12-supplemented sheep to maintain higher rates of wool growth than deficient sheep, while still exhibiting elevated succinate concentrations in the rumen, demonstrates that overcoming the blockage of the methylmalonyl CoA mutase pathway in the rumen is not essential for restoring metabolic pathways such as those responsible for wool growth. This work contributes to the knowledge of plasma MMA and rumen succinate as useful indicators of functional cobalt status and cobalt intake in sheep.

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Vitamin B12 Deficiency an Unusual Cause of Fever: A Case Report

International Journal of Innovative Research in Medical Science ◽

10.23958/ijirms/vol04-i02/563 ◽

2019 ◽

Vol 4 (02) ◽

Author(s):

Shyama . ◽

P. Kumar ◽

Surabhi .

Keyword(s):

Bone Marrow ◽

Vitamin B12 ◽

Unusual Case ◽

Vitamin B12 Deficiency ◽

Bone Marrow Aspiration ◽

Microcytic Anemia ◽

Peripheral Smear ◽

Erythroid Hyperplasia ◽

B12 Deficiency ◽

Vitamin B12 Supplementation

Introduction: An unusual case of a 19 year old female, presenting with fever, pallor and hepatosplenomegaly for one month. She had microcytic anemia on peripheral smear examination but her bone marrow aspiration & biopsy revealed a hypercelluar marrow with megaloblastic erythroid hyperplasia. Resolution of fever within 48 hours of Vitamin B12 supplementation, initiated in view of the megaloblastic bone marrow picture & low serumVitamin B12 level, suggests a causal association. Conclusion: Vitamin B12 deficiency seems to be an unusual cause of PUO (Pyrexia of unkown origin) which should be ruled out in every case of PUO.

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Faculty Opinions recommendation of Randomized multicenter investigation of folate plus vitamin B12 supplementation in schizophrenia.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.718027511.793483264 ◽

2013 ◽

Author(s):

Jorge Ciprian-Ollivier ◽

Martin Puricelli

Keyword(s):

Vitamin B12 ◽

Vitamin B12 Supplementation

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Long-term Effect of Folic Acid and Vitamin B12 Supplementation on Fracture Risk and Cardiovascular Disease: Follow-up Study of B-PROOF Trial (P24-031-19)

Current Developments in Nutrition ◽

10.1093/cdn/nzz044.p24-031-19 ◽

2019 ◽

Vol 3 (Supplement_1) ◽

Cited By ~ 1

Author(s):

Sadaf Oliai Araghi ◽

Jessica C Kiefte-de Jong ◽

Suzanne van Dijk ◽

Natasja van Schoor ◽

Lisette CPGM de Groot ◽

...

Keyword(s):

Cardiovascular Disease ◽

Folic Acid ◽

Fracture Risk ◽

Vitamin B12 ◽

Homocysteine Level ◽

Fracture Incidence ◽

Total Homocysteine ◽

The Hague ◽

Vitamin B12 Supplementation

Abstract Objectives To investigate the possible effects of the intervention with folic acid and vitamin B12 supplementation on fracture and cardiovascular disease risk: 5–7 years after the end of the intervention period of 2–3 years. Methods Extended follow-up of B-PROOF trial, a multi-center, double-blind randomized placebo-controlled trial designed to assess the effect of 2–3 years daily supplementation with folic acid (400 µg) and vitamin-B12 (500 µg) versus placebo on fracture incidence. Fracture and cardiovascular outcomes were assessed by follow-up questionnaire. Fracture incidence (and a part of cardiovascular disease incidence) was verified by general practitioners (GPs). Results A total of 1298 individuals participated in the second follow-up round. Median age at baseline was 71.0 years [68.0–76.0] for both groups (n = 662 in the treatment group and n = 636 in the placebo group). No effect of the intervention on first osteoporotic fracture and other fracture risk after a follow up of 5–7 years was observed (HR: 0.99, 95% CI: 0.62; 1.59 and HR: 0.77; 95% CI: 0.50; 1.19, respectively) and also not for cardiovascular- or cerebrovascular disease (OR: 1.14; 95%CI: 0.74–1.74 and OR: 1.01; 95%CI: 0.76–1.33, respectively). Significant interaction for total homocysteine level was observed for osteoporotic- and any fracture (P = 0.10 and 0.06 resp.), which indicated a significantly lower risk of fracture in the intervention group with higher total homocysteine level. Conclusions This study does not support a prolonged effect of supplementation of folic acid and vitamin B12 on fracture risk, or on cardiovascular disease in older individuals with elevated homocysteine concentration. However, B-vitamin supplementation may be beneficial in reducing fractures in individuals with higher total homocysteine levels. Funding Sources The initial B-PROOF study has received funding so far by The Netherlands Organization for Health Research and Development (ZonMw), the Hague; unrestricted grant from NZO (Dutch Dairy Association), Zoetermeer; Orthica, Almere; NCHA (Netherlands Consortium Healthy Ageing) Leiden/Rotterdam; Ministry of Economic Affairs, Agriculture and Innovationn, the Hague; Wageningen University, Wageningen; VUmc, Amsterdam; Erasmus Medical Center, Rotterdam. Supporting Tables, Images and/or Graphs

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Plasma Vitamin B12 Levels, High-Dose Vitamin B12 Treatment, and Risk of Dementia

Journal of Alzheimer s Disease ◽

10.3233/jad-201096 ◽

2021 ◽

Vol 79 (4) ◽

pp. 1601-1612

Author(s):

Johan Frederik Håkonsen Arendt ◽

Erzsébet Horváth-Puhó ◽

Henrik Toft Sørensen ◽

Ebba Nexø ◽

Lars Pedersen ◽

...

Keyword(s):

Vitamin B12 ◽

Vascular Dementia ◽

Cox Regression ◽

Population Based ◽

High Dose ◽

Plasma Vitamin ◽

Hazard Ratios ◽

B12 Deficiency ◽

First Time

Background: It is controversial whether B12 deficiency causes dementia or B12 treatment can prevent dementia. Objective: To assess associations between low plasma (P-)B12 levels, B12 treatment, and risk of Alzheimer’s disease (AD; primary outcome) and all-cause or vascular dementia (secondary outcomes). Methods: We conducted a population-based cohort study using Danish registry data to assess associations between low P-B12 levels, high-dose injection or oral B12 treatment, and risk of dementia (study period 2000–2013). The primary P-B12 cohort included patients with a first-time P-B12 measurement whose subsequent B12 treatment was recorded. The secondary B12 treatment cohort included patients with a first-time B12 prescription and P-B12 measurement within one year before this prescription. For both cohorts, patients with low P-B12 levels (<200 pmol/L) were propensity score-matched 1:1 with patients with normal levels (200–600 pmol/L). We used multivariable Cox regression to compute 0–15-year hazard ratios for dementia. Results: For low P-B12 and normal P-B12 level groups, we included 53,089 patients in the primary P-B12 cohort and 13,656 patients in the secondary B12 treatment cohort. In the P-B12 cohort, hazard ratios for AD centered around one, regardless of follow-up period or treatment during follow-up. In the B12 treatment cohort, risk of AD was unaffected by low pre-treatment P-B12 levels, follow-up period and type of B12 treatment. Findings were similar for all-cause and vascular dementia. Conclusion: We found no associatio1n between low P-B12 levels and dementia. Associations were unaffected by B12 treatment. Results do not support routine screening for B12 deficiency in patients with suspected dementia.

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Does vitamin B12 supplementation improve outcomes for patients taking metformin?

Evidence-Based Practice ◽

10.1097/01.ebp.0000541825.93426.26 ◽

2017 ◽

Vol 20 (9) ◽

pp. E2-E3

Author(s):

Chelsea Carlson ◽

Jenna Ingersoll ◽

Abby Davids

Keyword(s):

Vitamin B12 ◽

Vitamin B12 Supplementation

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The Carriers of Native Vitamin B12 in Normal Human Serum

Clinical Science ◽

10.1042/cs0530453 ◽

1977 ◽

Vol 53 (5) ◽

pp. 453-457 ◽

Cited By ~ 1

Author(s):

C. A. Hall

Keyword(s):

Vitamin B12 ◽

Human Serum ◽

Isotope Dilution ◽

Serum Vitamin ◽

Total Serum ◽

Plasma Vitamin ◽

Isotope Dilution Assay ◽

Dilution Assay ◽

Normal Human ◽

Transcobalamin Ii

1. After fractionation of the vitamin B12-binding proteins of ten normal sera the components containing transcobalamin II and R-type binders of vitamin B12 respectively were studied for endogenous vitamin B12 content by two distinct systems of vitamin B12 assay. 2. The measurements of total serum vitamin B12 by either bioassay with Euglena gracilis or a radioisotope dilution assay agreed closely. 3. The native vitamin B12 carried by transcobalamin II was higher as measured by bioassay than by isotope dilution assay. 4. The presence of the transcobalamin II fraction of human serum altered the key reaction between the binding reagent of the isotope dilution assay, so that this assay failed to measure vitamin B12 quantitatively. 5. Probably, the mean fraction of plasma vitamin B12 carried by transcobalamin II is in the range 20–30%.

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