Would an Active B12 result in range, rule out PA ?
My thinking is it should..... but I'm new and I'm not 100% sure of the processes.....
Grateful for any links
Would an Active B12 result in range, rule out PA ?
My thinking is it should..... but I'm new and I'm not 100% sure of the processes.....
Grateful for any links
Active B12 and serum B12 measure the amount of B12 in your blood. Serum B12 is only accurate to 20% and measures all B12. Active B12 is a bit more accurate and looks at B12 bound to the specific protein that allows it to pass through into cells.
Neither test tells you how well your cells are using B12 and as people vary considerably in how efficiently the processes in their cells run, people vary quite a lot in how much B12 they need to transfer to their cells for all the processes to run smooth.
PA is a specific auto-immune condition which results in B12 malabsorption and leads to B12 deficiency.
Active B12 is a better guide than serum B12 as to whether you are currently B12 deficient but as a single point test it won't tell you anything about whether you have a B12 absorption problem - though a series of tests showing declining levels over time would be a good indicator that you have an absorption problem
Thank you that's a really helpful explanation. It has a very complicated journey that B12 doesn't it !
If you're interested to know more about the journey of B12 in absorption and metabolism, you might find this post I wrote useful:
healthunlocked.com/pasoc/po...
I had forgotten about your excellent description of this Technoid. Thanks for referencing it again. Rexz
I just reread your post and wondered yet again that any human absorbs b12 effectively. It is a process which must be subject to so many malfunctions - would there be any evolutionary advantage to it at all?
Regarding (quote) ‘if the circulating B12 exceeds the binding capacity of the blood, the excess is excreted in the urine’ does this then indicate that people with extremely high levels with injections either have an abnormal binding capacity or that b12 binds to other proteins, namely immunoglobulins? (As I have seen suggested)
I've never come across anything that stated in numeric terms , even approximately, what the maximum (normal) B12 binding capacity might be. But extremely high levels with injections is not surprising compared to normal levels of bound B12 since in "normal" conditions, an average maximum of 6-8mcg might be actually absorbed in a day via intrinsic factor, from a dietary average maximum of 30mcg. Compared to 1,000mcg injected directly, even assuming some loss, the injected amount is gigantic (orders of magnitude higher) compared to the normal physiologic processes.
I haven't read anything about B12 binding to immunoglobulins but happy to read up on that if you have something on it.
Although B12 absorption is complex, synthesis of B12 is even worse (36 steps) and only certain types of bacteria (and archea) can do it.
I can’t find links to the papers I read but they reported increased b12 binding capacity or retention in the blood due to creation of antibodies to TC11 (immuno complexes) during hydroxocobalamin therapy. Ralph Carmel was the author of one.
Might have been this one.
Abstract:
"A patient with recurrent pulmonary abscess, weight loss, and alcoholism was found to have extremely high serum vitamin B12 and unsaturated vitamin B12-binding capacity (UBBC) levels. While transcobalamin (TC) II was also increased, most of his UBBC was due to an abnormal binding protein which carried greater than 80% of the endogenous vitamin B12 and was not found in his saliva, granulocytes, or urine. This protein was shown to be a complex of TC II and a circulating immunoglobulin (IgGkappa and IgGlambda). Each IgG molecule appeared to bind two TC II molecules. The reacting site did not interfere with the ability of TC II to bind vitamin B12, but did interfere with its ability to transfer the vitamin to cells in vitro. The site was not identical to that reacting with anti-human TC II antibody produced in rabbits. Because of this abnormal complex, 57Co-vitamin B12 injected intravenously was cleared slowly by the patient. However, no metabolic evidence for vitamin B12 deficiency was demonstrable, although the patient initially had megaloblastic anemia apparently due to folate deficiency. The course of the vitamin B12-binding abnormalities was followed over 4 yr and appeared to fluctuate with the status of the patient's illness. The IgG-TC II complex resembled one induced in some patients with pernicious anemia by intensive treatment with long-acting vitamin B12 preparations. The mechanism of induction of the antibody formation in our patient is unknown. "
from Circulating antibody to transcobalamin II causing retention of vitamin B12 in the blood