Methyl b12
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Methyl B12: Therapeutic Potential and Mechanisms
Methyl B12 and Autism Spectrum Disorder (ASD)
Clinical Improvements in ASD Symptoms
Methyl B12 has been investigated for its potential to improve symptoms in children with Autism Spectrum Disorder (ASD). A randomized, placebo-controlled trial involving 57 children with ASD demonstrated that methyl B12 significantly improved clinician-rated symptoms as measured by the Clinical Global Impressions-Improvement (CGI-I) score. The study found a positive correlation between clinical improvement and increased plasma methionine levels, decreased S-adenosyl-l-homocysteine (SAH), and improved S-adenosylmethionine (SAM) to SAH ratios, indicating enhanced cellular methylation capacity1.
Biomarker and Behavioral Responses
Another study explored the effects of methyl B12 on behavioral measures and biomarkers in children with autism. Although no significant mean differences in behavior tests or glutathione status were observed between the treatment and placebo groups, a subset of children showed clinically significant improvements. These responders exhibited increased plasma concentrations of glutathione (GSH) and an improved redox ratio of reduced to oxidized glutathione (GSH/GSSG), suggesting that methyl B12 may alleviate symptoms in a specific subgroup by reducing oxidative stress2.
Methyl B12 and Immune Function
Modulation of T-Cell Activity
Research has shown that methyl B12 can modulate immune function, particularly T-cell activity. In vitro studies revealed that methyl B12 enhances the proliferative response of T cells to concanavalin A (Con A) and autologous B cells at suboptimal concentrations. Additionally, methyl B12 was found to potentiate the activity of helper T cells for immunoglobulin synthesis and significantly enhance the induction of suppressor cells in Con A-activated cultures, indicating its role in augmenting regulatory T-cell activities3.
Methyl B12 in DNA Methylation and Epigenetics
Impact on DNA Methylation
Vitamin B12, including its methylated form, plays a crucial role in DNA methylation processes. Studies have shown that maternal and newborn vitamin B12 concentrations are associated with DNA methylation at multiple CpG sites in offspring blood. These methylation changes have been linked to various health outcomes, including birth weight, gestational age, and childhood cognitive skills7. Furthermore, B12 supplementation has been found to influence the methylation of genes associated with Type 2 diabetes, providing an epigenetic explanation for the association between disordered one-carbon metabolism and metabolic diseases8.
Neuroprotective Effects
In experimental models of pneumococcal meningitis, vitamin B12 demonstrated neuroprotective effects by modulating hippocampal DNA methylation. B12 treatment attenuated hippocampal apoptosis and restored global DNA methylation levels. The study suggested that B12's neuroprotective action is mediated through methyl-dependent epigenetic mechanisms, highlighting its potential in reducing neuroinflammation and promoting neuronal survival10.
Conclusion
Methyl B12 shows promise in various therapeutic applications, particularly in improving symptoms of ASD, modulating immune function, and influencing DNA methylation and epigenetic regulation. While clinical improvements have been observed in specific subgroups, further research is needed to delineate the mechanisms and identify biomarkers for response to methyl B12 treatment.
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Most relevant research papers on this topic
Randomized, Placebo-Controlled Trial of Methyl B12 for Children with Autism.
Methyl B12 treatment improved clinician-rated symptoms of autism in children, correlated with improvements in methionine metabolism and cellular methylation capacity.
RCT
Rigorous Journal
Highly CitedPilot study of the effect of methyl B12 treatment on behavioral and biomarker measures in children with autism.
Methyl B12 treatment may improve behavioral symptoms in a subgroup of children with autism, possibly by reducing oxidative stress, but overall results show it is ineffective.
RCTHighly CitedEffects of methyl-b12 on thein vitro immune functions of human T lymphocytes
Methyl-B12 can modulate lymphocyte function by enhancing regulatory T-cell activities, but does not enhance T-cell proliferation.
In Vitro StudyAnaerobic bacteria need their vitamin B12 to digest estrogen
Anaerobic bacteria need vitamin B12 for growth and energy production, and its deficiency can lead to a variety of health issues.
Methylation by methyl vitamin B12
Methyl vitamin B12 can transfer methyl groups to various metals, with two different reaction paths involved, involving acid-base and oxidation-reduction reactions.
Vitamin B12, folate, and the methionine remethylation cycle—biochemistry, pathways, and regulation
Vitamin B12 and folate play crucial roles in cellular metabolism and regulation of methylation-dependent reactions, with recent advances in understanding their regulation.
Highly CitedA meta-analysis of epigenome-wide association studies on pregnancy vitamin B12 concentrations and offspring DNA methylation
Maternal and newborn vitamin B12 concentrations are associated with DNA methylation in offspring blood, potentially impacting child health outcomes like birth weight, gestational age, and cognition.
Meta-AnalysisVitamin B12 supplementation influences methylation of genes associated with Type 2 diabetes and its intermediate traits.
B12 supplementation influences the regulation of metabolically important Type 2 diabetes-associated genes through methylation of miR21, providing a novel epigenetic explanation for the association between disordered one carbon metabolism and diabetes risk.
Observational StudyVitamin B12 deficiency
Vitamin B12 deficiency can lead to serious clinical consequences, and diagnosis and management require careful consideration of individual factors and dietary habits.
Systematic Review
Very Rigorous JournalHighly CitedVitamin B12 is neuroprotective in experimental pneumococcal meningitis through modulation of hippocampal DNA methylation
Vitamin B12 shows neuroprotective effects in an infant rat model of pneumococcal meningitis by modulating hippocampal DNA methylation and reducing apoptosis.
RCT
Animal StudyRigorous Journal