This post will be my last for the present time on MB12. I will most likely return to this subject at a later date but I do not wish to lose the attention of my readers and so the next post will be on some of the other treatments we use at the clinic. But for today, I wish to focus on what Dr. Neubrander terms “A Really Cool Rat Study”.
So why would he get so excited about a study done on rats and what does it mean for the patient? Since 2002 Dr. Neubrander has been saying the MB12 given in high doses as an injection makes a difference for children with ASD. For several years it was his observations and parent anecdotes as the only confirmation that MB12 could make a difference. That all changed when this rat study came out. Now there is a bit of vindication for justifying the use of MB12 but with a slight drawback; the study did not mention autism. Through this study the benefits of MB12 on nerve and nerve repair is shown and may provide an insight into why it works on autism, but as usual, ‘more study is needed’.
I am including a comment that Dr. Neubrander gives to patients regarding the Okada study.
Please note that at the end of this comment I am including the abstract from a recent publication showing that the methyl analog from the cobalamin “family” (methyl, adenosyl, hydroxy, cyano, glutathionyl, and sulfito cobalamin) is the one that is the most biologically active. What is important to me from the article itself, not the abstract, is that though the methyl form is the most biologically active form, it is short-lived and the authors say that possibly a better delivery system is needed, e.g. “injections”. They also say that greater benefits or benefits at all are seen at the higher doses. I have been saying these exact same things for years — injections and daily shots!
Richard Deth, Ph.D. from Northeastern University in Boston, professor, colleague, and friend of mine dealing with the methylation phenomenon, is a world-renowned researcher in methionine synthase. As you know, methylcobalamin is the form of B12 that works hand-in-glove with methionine synthase. On March 31, 2010, Dr. Deth commented on the Okada article: “Although the article (Okada et al.) is basic science, it does provide some important insights into the effects of methyl-B12 (MeB12) on neurons and how it does it. Using neurons from rats, they showed that MeB12 increases the length of axons, the formation of neurites, and increases resistance to apoptosis. Together these effects indicate a significant role in development of networks among neurons. MeB12 was the best form of cobalamin for doing this, although others had activity, presumably because they were converted to MeCbl. They also showed that the effects of MeB12 reflected increased methylation, and adding SAM had similar, but weaker effects. MeB12 increased activation of the MAP kinase and PI3 kinase signaling pathways, indicating that it mimics the effects of neurotrophic growth factors. Finally, MeB12 improved the repair of transsected nerves as well as improved functional recovery of motor activity, in conjunction with increased myelination. All together a pretty impressive array of effects.“
The abstract on this study I posted below. You can look it up on pubmed, but I am listing it here for your convenience.
Exp Neurol. 2010 Apr;222(2):191-203. Epub 2010 Jan 4.
Methylcobalamin increases Erk1/2 and Akt activities through the methylation cycle and promotes nerve regeneration in a rat sciatic nerve injury model.
Okada K, Tanaka H, Temporin K, Okamoto M, Kuroda Y, Moritomo H, Murase T, Yoshikawa H.
Department of Orthopaedics, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
Methylcobalamin is a vitamin B12 analog and is necessary for the maintenance of the nervous system. Although some previous studies have referred to the effects of methylcobalamin on neurons, the precise mechanism of this effect remains obscure. Here we show that methylcobalamin at concentrations above 100 nM promotes neurite outgrowth and neuronal survival and that these effects are mediated by the methylation cycle, a metabolic pathway involving methylation reactions. We also demonstrate that methylcobalamin increases Erk1/2 and Akt activities through the methylation cycle. In a rat sciatic nerve injury model, continuous administration of high doses of methylcobalamin improves nerve regeneration and functional recovery. Therefore, methylcobalamin may provide the basis for better treatments of nervous disorders through effective systemic or local delivery of high doses of methylcobalamin to target organs. Copyright 2009 Elsevier Inc. All rights reserved.
PMID: 20045411 [PubMed - indexed for MEDLINE]