The Oxford Meeting

by | Dec 5, 2015 | 2 comments

I’m back from the City of Dreaming Spires and dreadful traffic congestion.  I had a two hour meeting with a Professor and one of his colleagues about the problems we, as patients, face in getting treated well.  Prof Y and his colleagues have long been fascinated by the way in which B12 (in its various forms) is absorbed at cell level.  A paper published in September addressed this issue and a copy of it was sent to me via email by another researcher from another university who though I might be interested.  Well I was, because there is this huge problem of patients having their B12 deficiency addressed by injections or other means but still suffering the symptoms of a B12 Deficiency.  The hypothesis that is usually given to explain this is that there must be a problem at cell level – although the patient’s blood B12 is high there must be a problem with the B12 getting into the cell.

I arrived at the Professor’s office and was please to note that he had a copy of my latest book on his desk. These people never cease to amaze me on how patient they are in explaining some extremely complex bio-chemistry.  And that’s what he did using a pencil and a scrap of paper.  He was astonished at the tales that I had to tell about patient’s symptoms and how they deal with them.  And he is convinced the answer lies in “the upper ligand” which apparently is quite important.  Anyway after two hours and some healthy discussion I left with another new member for the Round Table that we host twice a year for researchers who are involved with the society.  I now have to keep him and his colleague informed of any developments and he and she will seek further involvement of the society in their work.

This is such an important development.  It’s so refreshing to be listened to instead of being told that patients must be imagining their symptoms as their B12 status is good.  There must be a very good reason why some patients still experience the symptoms of B12 deficiency even after their B12 deficiency has been addressed and the meeting yesterday has the wonderful potential to provide a scientific explanation of why this is so.

It’s early days but contact has been made and our story has been listened to.  I’ll keep you informed.

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2 Comments

2 Comments

  1. Frank Hollis

    Martyn,

    Thanks for posting this. I’m fascinated by this line of research, for selfish reasons as I find a need IM injections of MeCobalamin once per week. That’s despite having total cobalamin levels off the top of the scale.

    Do you have a link to the abstract? I’ve lost the one you posted to FaceBook a couple of months back.

    I’m going to swap my HOCobalamin injection for a CNCobalamin jab after I’ve seen my GP in a fortnight. It’ll be interesting to see if that works any better.

    Cheers

    Frank

    Reply
  2. Frank Hollis

    Found the abstract – http://www.ncbi.nlm.nih.gov/m/pubmed/25809485/?i=1&from=Gherasim%20C%5BAuthor%5D

    The upper ligand is the methyl/hydroxo/cyano/adenosyl/aquo attached to the cobalamin. The paper is about a mutation in the gene for the enzyme that catalyses the removal of the upper ligand to activate the B12.

    Those with the mutation have impaired dealkylation (removal of the methyl ligand) but decayantion (removal of the cyano ligand) is unaffected. This means that these people may find cyanocobalamin works better than methylcobalamin.

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