My hypothesis is that the antibody that attacks the intrinsic factor and or parietal cell may also bind to B12 rendering it unusable at the cellular level.
That the production of the antibody with regards to amount is unknown and different at different times for the individual and different for each individual. It is known to be in the bloodstream.
That a certain amount of hydroxocobalamin injected into the bloodstream is attached to the antibody and is ineffective to a degree that is unknown and variable.
That those with non cellular B12 function and those that do not recover fully could in fact not have B12 available due to the amount of antibody production in the individual.
It is possible a test could be designed to determine the amount of B12 in the bloodstream or urine that is attached to the antibody.
I sent this hypothesis to the B.H.R. (Bruce) Wolffenbuttel who happens to be a Active Member CluB12 UK. It is a wing and a prayer that anything will be done because of it. More to satisfy my want to have at least tried than expecting any positive action.
At this point this is just a hypothesis which came from my imagination. I have not gone further than; is it contraindicated? No need to speculate until I do that.
I have never posted a hypothesis prior to working with the concept in my head before. I usually only post the trials that came from my hypothesis.
Most hypotheses are abandoned for various reasons and this one may well be abandoned. That will be determined by future work with my imagination if not contraindicated.
To post a hypothesis that would only serve to add complexity would not be something I would do.
I also posted it to express what I mean when I write “Not find what works”, I do not yet understand that process. I seem to be ignorant for reasons unknown to date.
This is just one of many ways I look for my solution. I started with trying to find someone who could treat me successfully. I then looked at standard protocols and chose one that I thought had the highest probability of success based on my evaluation. When that was exhausted I looked at the flaws in the logic used to design the protocols and why those flaws might exist. Usually it is regulatory restraints and old incorrect information or concepts.
I was unlucky that I almost died. I was fortunate that I did not have to wonder if I was B12 deficient as my B12 level was below range of detection.
I posted this for peer review for contradictions. And to share.
Too funny my email was returned. I am guessing as it was on German.
Any suggestions with email address that might have the power/funding to develop the test would be helpful. I am only interested in maybe causing that work to be done with this email. Guessing which individual might act is a matter for fate.
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WIZARD6787
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Don't they just attach themselves to Intrinsic Factor (which surely must be accessible to them and not happening as it is being formed inside cells), and form an IF+antibody unit which is then removed by macrophages or whatever?
Thus IFab numbers would likely rise when IF is appearing in the bloodstream for any reason, And fall after. The cause could be some autoimmune attack on the cells that produce IF.
The antibodies are thought to attack the parietal cells. That is the autoimmune part.
There are no IFab numbers it is a yes or no test hence the 50%
+- false negative.
I am looking for what is not known. There is a reason that is not known that EOD is more effective than other existing protocols and for some of us more than the EOD is effective at preventing pain and suffering.
This what I understand.l believe antibodies do not deactivate vitamin B12. Antibodies are proteins produced by the immune system to identify and neutralize foreign substances such as bacteria and viruses. They generally do not interact with essential nutrients like vitamin B12. Vitamin B12 is a vital nutrient that plays a key role in many bodily functions, including the production of red blood cells and the maintenance of the nervous system. While antibodies can interact with certain molecules and substances in the body, there is no known mechanism by which antibodies can deactivate or neutralize vitamin B12.
There are two types of Intrinsic Factor Antibodies. Type 1 (Intrinsic Factor blocking antibodies) which, blocks the binding site on intrinsic factor for Vitamin B12 and type 2 (Intrinsic Factor binding antibodies) which, target a different site on intrinsic factor and prevent the intrinsic factor-Vitamin B12 complex from attaching to the binding sites in the small intestine.
In my more usual home, I am aware of antibodies to TSH, T4 and T3. A significant impact is on blood test results. But they are usually considered to be rare.
That is my understanding of what is believed to be true.
There is obviously something not understood or those of us that can reduce symptoms with more B12 than EOD do not really heal it is all in our heads. That would be the question I would ask if I thought it had any chance of being considered.
The current understanding of B12 for some of us is has yet to be discovered. Only a solution has been discovered by some.
Thank you all. I have sent the email and I feel better for having done something.
I happen to know a pharmacology professor. Thing is with the current state of the understanding of B12 I do not know how to approach him.
I could make a marble for him and send him a book for general background along with the new guidelines from the UK if and when they are approved.
He is capable of understanding the the EOD is based on it works and that is legitimate. He has the power to test the UK's protocol. In the USA he cannot likely create a more successful protocol due to government restrictions here.
Thing is the UK guidelines are the most effective in the world as far as I know. I find them inadequate but the best. I have no passion for putting effort into at best achieving mediocrity.
Just an idea. I will never have a shortage of things I could do.
I have my own little hypothesis that some people do not retain B12 well, that most of the B12 they digest or have injected into them is quickly excreted in urine, hence the need for more frequent injections. not sure of the mechanisms by which this might be happening.
I would have before contradicted your hypothesis. I would have thought that this would have been discovered with the testing done on retention times.
The retention times often cited as facial are an average. They are quite variable by individual and no testing was done on people specifically that have a DX of B12 deficiency.
So your hypothesis so far as not been contradicted and therefore is a valid hypothesis.
Note: It is known that when experiencing neurological symptoms one of those is increased urination. I and some others have found that supplementing increases urination. No clue if this factors in.
I think any hypothesis is fabulous. We have to think outside the box because too many scientists/researchers are looking inside the box and working only with what they know.
This may be a real foot dragger as we need new ideas to try - clearly for many of us what we know is not enough and not working well enough.
I have hypothesis too and reserve from posting as we always fall on deaf ears
I love that you have started a new idea … fabulous and Thankyou
I wonder if Alfie Thane at Surrey University would be a person to contact. They did the trial we completed. Your hypothesis would explain so much. Thank you WIZARD 6787
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Antibody to transcobalamin ii causing functional B12 deficiency?
One injection per prescription 
Paper preprint: Transcobalamin Receptor Autoantibodies in Central Vitamin B12 Deficiency 
