Morning all, what’s the difference between
Serum Holotranscobalamin conc
Serum vit B12 in simple terms 😂
I’m arguing (politely) with the Drs and need to be armed with facts and noticed my b12 results are : holo trans (66pmol/l) and serum B12 (327ng/l) both taken AFTER loading doses 3 months earlier. But taken at different times. (Wether different labs do different B12 testing?) so I’m not sure which one is the B12 I need and the other is “useless” B12 (am I making sense-it’s early 😂)
I meant B12 in heading 🙈
Dont know if this is of any help but just found a post by Gambit one of the (administrator's ) holo-T is known as active B12 in the UK. Some areas of nhs do it but don't think all do. 🤔
Your right Bumblebee02 it's too early to get my head around. 🤔
Have you googled it ? My heads not withit this morn.
How do you argue politly ? I just say it as it is. 😱
Just had a coffee so heads more awake, take a look at this.........
ncbi.nlm.nih.gov/pmc/articl...
I hope it helps. 😘
It's a bit testicle ( op's I mean technical ) 🤣
I’ve googled it but can’t make any sense out of it.
There’s no clear layman’s terms on anywhere I’ve looked.
Politely arguing is my speciality. 😂
We shouldn't have to battle like this just to receive the appropriate treatment. My Dr has just rechecked my B12 after 2yrs of being on injections !
What a numpty when it's obvious my levels will be high . 😵💫
total serum B12 measures all B12 in your blood. Active/holo-T measures just the B12 that is bound to the protein that allows it to be transported into cells. In general it is about 20% of serum B12 - which is the case with your results above, which is why, in general it doesn't matter which test you have.
serum B12 is only accurate to 20% - holo-T is a bit more accurate.
However, both tests are difficult to interpret as they only tell you what is happening in your blood - not what is actually happening with the B12 once it is in your cells - and people vary a lot in the level that is right for them because of differences in efficiency in the way B12 is processed in your cells.
Without an absorption problem the levels are regulated by stores in the liver and levels will be pretty constant over time. This means that the test - if used to monitor and identify drops in levels - is good for identifying an absorption problem. However, after a loading dose - because people vary so much in how quickly excess B12 is removed - it is difficult to determine if drops are just excess being removed, or evidence of an absorption problem so the test isn't recommended after loading doses. It is also possible for the serum B12 to be bound to proteins that actually make them inaccessible to humans - which would be an advantage of the holo-T test at this point ... but it still doesn't tell you, from a single test, if your levels are right for you or falling because you have an absorption problem, or just falling because you still have excess B12.
thank you so much Gambit62, that made it perfectly understandable. Much appreciated. Thank you again.
This one's easy for an old hand like me, but understanding the answer might not be!
Vitamin B12 is measured by a variety of methods. Common to these methods is that the B12 is separated from the binding proteins [in old terms, 'Transcobalamins'] and the free B12 is now able to be assayed. The binding proteins are the important bit here. 'Active' B12 is the fraction that is bound to a minor fraction of the transcobalamins; around 25% of the total or thereabouts. So, it would be reasonable to expect that the Active fraction would be around 25% of the total, although it's going to be a bit different in every individual.
Much of the excess circulating, injected free B12 is assumed to be excreted in around 24 hours, because the transcobalamins have become saturated. [This was a crucial bit in the Schilling Tests].
However, the actual methods used to detect the Vitamin B12 in the assay will vary, and the method used, and the manufacturer involved, will mean that you can't simply compare 'Active' and 'Total' to expect [Active/Total] to give a reliable ratio of the proportion of the two transcobalamins involved. Likewise, in your case, the 'Active' is reported in Molar concentration whereas the 'Total' is shown as Mass concentration.
Suggesting that 'Total B12' could be described as 'Useless B12' has just undermined much of my life's work in the laboratory, so I'm a bit offended. Most folks who are monitored for B12 levels are monitored using 'Total B12' rather than the 'Johnny Come Lately' so-called 'Active B12'. It seems to work for them, although the manufacturer of the 'Active B12' methodology might not agree with me.
Two transcobalamins?
Scratching my head, there's possibly more than 2, but certainly two, and short of digging out textbooks, I'll stick at two! Which is why we've got the 'Active' and the rest. But the extraction process of the B12 assays releases the B12 from the carriers, by dropping the pH, and converting the freeB12 to Cyanocobalamin in the first assay I performed. We made up all of the reagents so had a better idea of what was happening. Incidentally, that was a Microbiological Assay using Lactobacillus Leichmannii, and that needs B12 to grow, but that's another story entirely.
Hey FlipperTD.
It is my understanding there are two main transporters Intrinsic Factor and transcobalamin though others are known. The first transports the B12 from the stomach lining to the blood and the second from the blood to the cells.
There's a transcobalamin III, but information on it is scarce....
my B12 transport primer mentions it briefly:
healthunlocked.com/pasoc/po...
Thank you for that!
Three that I've read of: TC1, TCII, TCIII.
"....The proteins referred to in older literature as R-binder, TC1 or TCIII are collectively named haptocorrins .... "
[Advances in the Understanding of Cobalamin Assimilation and Metabolism: E V Quadros]
" As a matter of fact, three to 5h after entering the enterocyte, the cobalamin appears in the portal blood bound to transcobalamin II (TCII), a specific protein secreted unidirectionally across the basolateral surface of the enterocyte."
[Cobalamin Deficiency: Clinical Picture and Radiological Findings : C. Briani et al]
It seems that, since 80% of cobalamin is bound to TC1 and TCIII - whose role in cobalamin metabolism remains unknown (clearance of analogues + ?) - the main focus in research rests with the 20% of cobalamin binding with TCII to deliver rapidly to target tissues (rapid since it's half-life is given as 6-9 min). Well, fair enough.
Transcobalamin III rarely gets any mention in research.
"If vitamin B12 is ingested in its free (or non-protein bound form), it will bind to a carrier protein known as R-binders or transcobalamin 1 that is secreted by both the salivary glands in the oropharynx and the gastric mucosal cells within the stomach. The free vitamin B12 ingested by mouth will remain in the bound form with an R-binder until it reaches the second segment of the duodenum in the small intestine ........ the pancreas will secrete additional protease, which will then degrade the R-binders holding onto the vitamin B12. It is at this point that the vitamin B12 will bind to (or complex with) intrinsic factor for the remainder of its journey to the ileum of the small intestine for absorption ...... The absorbed vitamin B12 then binds to transcobalamin II where approximately 50% of the vitamin B12 will be delivered to the liver and the remainder will be delivered to other tissues."
- No mention of TCIII there !
[The mechanism of Absorption of Vitamin B12 (cobalamin) in the GI Tract : Evidence-Based Medicine: Consult]
"Much of the excess circulating, injected free B12 is assumed to be excreted in around 24 hours"
I have wondered about this, in terms of frequency of injections. If most of the injected cobalamin is excreted in 24 hours, and the natural storage in the liver is not usable because the liver feeds B12 into the stomach, where the natural transport system leading to cells is broken, how can an injection frequency of 1 per month, or as infrequent as 1 per 3 months, effectively supply the needed amounts of B12 to the cells?
Thanks for any help with this question.
Oh dear... this get more complicated. I've read statements that 'the natural storage in the liver isn't usable' but I suspect it's more complicated than that, because when PA strikes, we only seem to realise when all the B12 stores are exhausted. But it's outside my sphere of 'expertise' such as it is! There's no doubt that some folks survive very well on one every three months.
Low Vit b12 and Ferritin. Possibly PA?
What to do next? 
B12 serum levels and IFA test?
Help with blood test results
