scholarly journals Effects of Vitamin B12 Supplementation on Cognitive Function, Depressive Symptoms, and Fatigue: A Systematic Review, Meta-Analysis, and Meta-Regression

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 923
Author(s):  
Stefan Markun ◽  
Isaac Gravestock ◽  
Levy Jäger ◽  
Thomas Rosemann ◽  
Giuseppe Pichierri ◽  
...  

Vitamin B12 is often used to improve cognitive function, depressive symptoms, and fatigue. In most cases, such complaints are not associated with overt vitamin B12 deficiency or advanced neurological disorders and the effectiveness of vitamin B12 supplementation in such cases is uncertain. The aim of this systematic review and meta-analysis of randomized controlled trials (RCTs) is to assess the effects of vitamin B12 alone (B12 alone), in addition to vitamin B12 and folic acid with or without vitamin B6 (B complex) on cognitive function, depressive symptoms, and idiopathic fatigue in patients without advanced neurological disorders or overt vitamin B12 deficiency. Medline, Embase, PsycInfo, Cochrane Library, and Scopus were searched. A total of 16 RCTs with 6276 participants were included. Regarding cognitive function outcomes, we found no evidence for an effect of B12 alone or B complex supplementation on any subdomain of cognitive function outcomes. Further, meta-regression showed no significant associations of treatment effects with any of the potential predictors. We also found no overall effect of vitamin supplementation on measures of depression. Further, only one study reported effects on idiopathic fatigue, and therefore, no analysis was possible. Vitamin B12 supplementation is likely ineffective for improving cognitive function and depressive symptoms in patients without advanced neurological disorders.

Author(s):  
Shyama . ◽  
P. Kumar ◽  
Surabhi .

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.


2019 ◽  
Vol 59 (2) ◽  
pp. 40 ◽  
Author(s):  
Synara Cavalcante Lopes ◽  
Daniel Duarte Gadelha ◽  
Manuela Dias de Carvalho ◽  
Virgínia Oliveira Fernandes ◽  
Renan Magalhães Montenegro Junior

Vitamin B12 is a water-soluble essential micronutrient, required by all the body cells. Its deficiency has been implicated not only in hematological and neurological disorders, but also in many metabolic processes, such as insulin resistance and body composition changes, which have aroused particular interest in recent years. This study reviews the physiology of vitamin B12 from its digestion and absorption to its distribution in tissues, metabolic effects and controversies regarding the diagnosis of deficiency, and to dietary and pharmacological treatments.


2007 ◽  
Vol 7 ◽  
pp. 1649-1657 ◽  
Author(s):  
Ebere C. Anyanwu ◽  
Ijeoma Kanu

A majority of patients with neurological disorders with chronic exposures to toxigenic molds and mycotoxins has vitamin B12 deficiency that is unrelated to dietary insufficiency. Vitamin B12 is a source of coenzymes, and participates in intracellular recycling of methionine, and in methionine synthase reactions. The biochemical processes that lead to B12 depletion and deficiency are not fully understood. This paper examines and assesses various most likely biochemical reasons that could impede upon the normal intracellular functions of vitamin B12 that lead to neurological manifestations. By biochemical implications and derivations, it is most likely that mycotoxins interrupt the structure and function of vitamin B12 through reactive interference with the normal One-Carbon metabolism leading to the observed clinical neurological manifestations such as nerve damage and, demyelination, degeneration of PNS leading to paralysis, progressive peripheral neuropathy, and spinal degeneration.


Sign in / Sign up

Export Citation Format

Share Document