Adenosylcobalamin

[Banana94]

Hi all

Where do you buy/odere pure Adenosylcobalamin??
On iHerb its only in combination with Folic Acid which i dont want.
Seekinghealth.com has it only in combination with methlcobalamin??
Any other websites which ship to Europe?
Thx

 

[PinkPanda]

www.detoxpeople.eu in the UK has a wide array of supplements. They also ship to other european countries, you might have to ask if they ship to yours.
Three adenosylcobalamin products came up in the search.

 

[Learner1]

According to this, its not very stable in pill form.

https://www.globalhealingcenter.com/natural-health/adenosylcobalamin-4-facts-know/

The kind he recommends, though, has methylcobalamin. I did find this one, though, and Seeking Health has a similar product:

https://www.vitacost.com/country-life-active-b-12-dibencozide-3000-mcg-60-sublingual-lozenges

I have a huge need for B12 and an excellent ND helping me, but he's mainly had me on methylB12 with some hydroxo B12 and only a tiny bit of adenoB12.

I'm curious, why do you only want adenoB12?

 

[Tammy]

Check out www.metabolics.com ........they have an excellent adenosyl..........without any additives.

 

[Hip]

Adenosylcobalamin is also known as dibencozide, in case you want to Google search.

 

[alicec]

According to this, its not very stable in pill form.

I've never come across this claim before. I did a quick google and could find nothing to support the notion and since so many other claims in that article are wrong I wouldn't place much credence on this one either.

The incorrect claims include -

1) dietary sources of B12 are in the hydroxycobalamin form. Actually, while this form is common (probably at least in part because this form is the result of the action of light on the methyl and adenosyl forms), the adenosyl form is even more common, while methyl is predominant in some foods - see this study.

2) whatever form is ingested, the body will convert it to methylcobalamin. It is true that methylcobalamin is the dominant form in the blood but within the cell, B12 is converted to both the methyl and adenosyl forms as needed and adenosyl appears to be the dominant intracellular form.

3) the citric acid cycle fails without the conversion of methylmalonyl CoA acid to succinylCoA (the reaction for which adenosylB12 acts as co-factor). It is true that if this reaction fails completely (such as in some rare genetic diseases) there are severe consequences, mainly because accumulating methylmalonic acid is toxic. The absence of the reaction however doesn't stop the citric acid cycle since this pathway is used only for processing odd-chain fatty acids which are minor forms and a few amino acids; even-chain fatty acids, carbohydrate and most amino acids feed into the citric acid cycle independently of this reaction and keep the cycle going.

 

[Learner1]

whatever form is ingested, the body will convert it to methylcobalamin

Thanks for your post.

I'm still wondering why people are going to extra effort to find AB12, when MB12 is easier to find.

 

[alicec]

Thanks for your post.

I'm still wondering why people are going to extra effort to find AB12, when MB12 is easier to find.

Of course the bit you quoted from my previous post was the bit I was pointing out was incorrect - the statement about all forms being converted to methylB12 is not true.

Some people report a different response to these different active forms. On the face of it, it shouldn't matter since the upper axial ligand (methyl, adenosyl, hydroxy etc) is removed once B12 is taken into the cell and methyl and adenosyl B12 reformed as they are needed.

This is the standard or defined B12 trafficking pathway but there is suggestive evidence that alternative, undefined pathways exist. Possibly, particularly when relatively large amounts of supplemental vitamin are taken, these alternative pathways can be important and explain the different response to the different forms - though this is speculation.

 

[Valentijn]

I'm still wondering why people are going to extra effort to find AB12, when MB12 is easier to find.

Effective marketing from quacks.

 

[Learner1]

Effective marketing from quacks.

That's not really an appropriate comment. Please keep such snarky comments to yourself.

My understanding has been the same as @alicec is saying, that AB12 and MB12 are reformed as needed. I was hoping that someone might have a little more info about the pathways she mentioned, and if there is a situation where someone was unable to use MB12 and could therefore only use AB12.

 

[alicec]

Here is a post I wrote on the known intracellular trafficking pathways for cobalamin.

As I note in this post, the statement is always made in reviews that some cobalamin enters the cell by passive diffusion. I have never found any studies which have characterised this path further.

According to the defined pathways, since the upper axial ligand is removed, it shouldn't matter what form is used and indeed, this has been the justification for using cyanocobalamin which is more stable and cheaper to produce.

Interestingly though, from the practice of treating children with genetic defects in B12 metabolism for whom very large doses of supplemental vitamin are required, differences have been found.

In the US and Europe, hydroxycobalamin has become the preferred treatment, rather than cyanocobalamin.

In Asia, particularly Japan where a lot of current research on cobalamin seems to be happening, methylcobalamin is the preferred form.

As far as I have been able to find, the two don't appear to meet - there has never been a trial comparing hydroxy with methyl. Both though appear to be superior to cyano.

Again as far as I have been able to find, the reason for this is unknown but it certainly indicates that there is more to cobalamin processing than we currently understand. Maybe this is part of the reason that some people respond better to some forms than others.

 

[Creachur]

3) the citric acid cycle fails without the conversion of methylmalonyl CoA acid to succinylCoA (the reaction for which adenosylB12 acts as co-factor). It is true that if this reaction fails completely (such as in some rare genetic diseases) there are severe consequences, mainly because accumulating methylmalonic acid is toxic.

The absence of the reaction however doesn't stop the citric acid cycle since this pathway is used only for processing odd-chain fatty acids which are minor forms and a few amino acids; even-chain fatty acids, carbohydrate and most amino acids feed into the citric acid cycle independently of this reaction and keep the cycle going.

Hello AliceC.

I appear to have a type of "methylmalonic acidemia" which I find is much improved when I take adenosylcobalamin but not so improved with methylcobalamin.

I get the impression you have some familiarity with such metabolic diseases.

Of course, in these genetic diseases it's hard to know which specific pathways are disrupted and, unfortunately, this means one cannot always assume normal metabolic processes are taking place.

I believe you mentioned in another thread that in normal metabolism adenosylcobalamin and methylcobalamin can be converted into the other. Do you know if this conversion is normally for trivial amounts? I am trying to understand my strong metabolic preference for adenosylcobalamin and poor conversion would explain why methylcobalamin didn't work very well for me.

Thank you for any advice or help.

 

[alicec]

I appear to have a type of "methylmalonic acidemia" which I find is much improved when I take adenosylcobalamin but not so improved with methylcobalamin.

Of course, in these genetic diseases it's hard to know which specific pathways are disrupted and, unfortunately, this means one cannot always assume normal metabolic processes are taking place. I believe in normal metabolism adenosylcobalamin and methylcobalamin can be converted into the other. Do you know if this conversion is normally for very minor amounts? I am trying to understand my strong metabolic preference for adenosylcobalamin.

Methylmalonic acidemia can result from inherited genetic defects which affect one of the several enzymes involved in processing of B12 within the cell, or simply from B12 deficiency with no inherent problem with these enzymes. The former situation usually results in much more serious problems, though there are degrees of severity even with these inborn errors of metabolism, depending how badly the relevant enzyme is affected by the genetic mutation.

Methylmalonic acid (MMA) accumulates when the enzyme methylmalonyl CoA mutase (MCM, encoded by the gene MUT), which uses adenosylB12 as cofactor, is not functioning well. This enzyme catalyses the transformation of methylmalonyl CoA to succinyl CoA, which in turn feeds into the Kreb's cycle. Methylmalonyl CoA is formed from the breakdown of odd chain fatty acids and some amino acids, which produces MMA, combined with CoA.

When the enzyme is not functioning well and so succinyl CoA is not being formed at a normal rate, increased amounts of the substrate MMA appear in the urine.

Since no other metabolic pathway produces MMA, measurement of this metabolite in either serum or urine is also used as a functional test of B12 deficiency.

Specific genetic testing would be needed to determine if a genetic mutation were responsible for the accumulation.

In the post immediately before yours, I gave a link to a detailed post explaining the complexity of intracellular processing of B12 and the different enzymes involved.

I also indicated that according to what is known about this processing, the form of B12 taken shouldn't matter, yet in practice, the form taken has been found to make a difference, at least for the large amounts used in treating children with genetic defects in B12 metabolism.

This suggests alternative pathways for processing B12 which are not understood.

In your own case, you appear to respond better to the adenosyl form. As far as I am aware, the reason for this different response is unknown.

If this form helps you, keep taking it.

 

[Creachur]

@alicec thank you so much for your reply. Your perspective on B12 metabolism is very useful because I've found the research literature on organic acidemias such as MMA can go into specifics without maintaining the big picture.

Also, I'm grateful you mentioned a research paper by Quadros in another thread. I downloaded that paper and, although much of it is beyond my comprehension, the parts I half-understand are excellent such as Quadros's chart of pathways in Fig.1.

It seems many of the details of B12 metabolism are still not fully understood and that surprised me a bit. I personally discovered B12's benefit by sheer chance and I'm now trying to catch up on the theory but I currently have noticeable cognitive difficulties on account of years of untreated illness wreaking its damage.

Thank you, once again.

 

[Galixie]

In the US and Europe, hydroxycobalamin has become the preferred treatment, rather than cyanocobalamin.

I am not sure where you got the impression that hydroxocobalamin has become standard in the US. Cyano is still the most commonly prescribed form here. You can test this by simply walking into any ordinary pharmacy and asking if they even stock hydroxo. Most of them will tell you no. Hydroxo is the form prescribed in most of Europe though.

 

[Learner1]

I am not sure where you got the impression that hydroxocobalamin has become standard in the US. Cyano is still the most commonly prescribed form here. You can test this by simply walking into any ordinary pharmacy and asking if they even stock hydroxo. Most of them will tell you no. Hydroxo is the form prescribed in most of Europe though.

Hydroxo is difficult to find orally and in injectible in the US. I called 25 compounding pharmacies across the US and only 2 could fill a prescription for injectible hydroxo.

Most doctors think cyanocobalamin is the standard version and don't realize that some of us don't use it well, especially if high doses are needed.

 

[Banana94]

My Vit B12 blood level is normal (I know this says nothing) and my MMA is normal.
I feel absolutely nothing by taking MB12 sublingual up to 30mg
HydroxoB12 injections 10mg
AdensoylB12 injections 10mg

It seems Vit B12 does have no effect on me I also tried diffrent brands and took Lithium and other cofactors tol help B12 getting into the cells.
Also by starting Methylation Protocol no improvments. But it also did no harm

Im thingking what else might be wrong?

 

[Banana94]

Hydroxo is difficult to find orally and in injectible in the US. I called 25 compounding pharmacies across the US and only 2 could fill a prescription for injectible hydroxo.

Most doctors think cyanocobalamin is the standard version and don't realize that some of us don't use it well, especially if high doses are needed.

Maybe you could order it from Europe. I ordered it in Belgiuem maybe they ship to the U.S.
There‘s no special pharmacy I just ordered it from a pharmacy found in the internet.

 

[Learner1]

Maybe you could order it from Europe. I ordered it in Belgiuem maybe they ship to the U.S.
There‘s no special pharmacy I just ordered it from a pharmacy found in the internet.

It is available in the US, just a little hard to find.

 

[alicec]

I am not sure where you got the impression that hydroxocobalamin has become standard in the US.

I wasn't referring to general availability, which I know nothing about not living in the US. I was referring to the literature about treatment of children with inborn errors of B12 metabolism.