NeuroTalk Support Groups - STICKY - The Vitamin B12 Thread:

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- - STICKY - The Vitamin B12 Thread: (https://www.neurotalk.org/peripheral-neuropathy/85103-sticky-vitamin-b12-thread.html)

If you are not converting some of the Bs to active form, they may show up in the serum as high.

B6 must be activated to P5P. (riboflavin is used for this conversion)
B12 is activated to methylcobalamin
Folic acid is converted to methylfolate.

There are genetic errors that prevent this conversion. You inherit them. They are called MTHFR polymorphisms and I explain it earlier on in this thread.

A doctor came on to another thread here about them recently...
take a look: I have read 10% of people have this, but he claims new info at 30%:
http://neurotalk.psychcentral.com/post663808-20.html

Metanx is an RX vitamin with all 3 activated B's in it. That is what that thread is discussing...generic and OTC versions.

folate level high, Why??

I have pn from schwanomas removed from my spinal cord at L4-5/S-1. I have a bad left leg and foot.

My endocrinologist did a workup a week ago of blood work and my folate level was over 20 and considered high. I have been trying to find out what this means.

Any help would be greatly appreciated.

CTYankee3

High folate accompanies low B12. It may also be high if you are not converting folic acid in the body to its active form,
methylfolate. The folic acid builds up therefore. And your tissues may be starved for the active form.

Getting a homocysteine test will reveal more.
People with the genetic failure MTHFR polymorphisms cannot make active vitamins for the body to use, from those taken in pill form or from enriched foods. Many foods today are enriched with folic acid, so that may read high in some people.
People with the MTHFR gene polymorphism typically develop elevated homocysteine as they age.

Just read the B12 thread. Thanks to all for this very important discussion.

Question re this statement: "Low B12 actually damages nerves, the myelin that insulates them is maintained by B12 and other nutrients. Myelin damage also shows up as numbness/tingling and peripheral nerve pain."

I have small fiber neuropathy. As I understand it, the nerves affected are not myelinated. Will B12 improve my condition?

Thanks.

Mrs D will come along with the technical info for you, but I can say, yes it does help. I have small fiber/sensory neuropathy, and I have been taking B12 for 6 yrs. It does help, greatly slowed the progression of my neuropathy, then started healing in some areas.

Yes, B12 has other functions too in the cell itself.

This link explains this complex molecule pretty well.
http://en.wikipedia.org/wiki/Vitamin_B12

scroll down to "functions", and you will see other uses of B12 besides maintaining the myelin sheath (which is composed of fatty acids).

I often find it amazing that such a tiny amount of this one substance can affect us so globally!

Thanks for these responses.

Now, I have a concern about folate/folic acid. For many years, I have been taking a reputable multiple vitamin with 1000 mcg of "Folate (= Folic Acid +Folacin)." After finding this site, I added in 800 mcg Folic Acid (Solgar brand). Is is dangerous for me to be taking folic acid in such high doses?

There is a thread where I bring this new problem up...and a doctor came on with additional information:

http://neurotalk.psychcentral.com/sh...ghlight=Metanx

It is long, but I think worth reading carefully.

Until about a year or so ago, the common thought was folate was good for everyone. Then young women started using high dose folate for preventing spina bifida in their babies. Then, some new data emerged that some of these high dose patients were showing up with colon cancer at a young age.

According to the doctor who comes on that Metanx thread, it is the "unactivated" folate that may be to blame. But still the research is not firm on that.

I stopped recommending high dose folate over a year ago, because the subject remains murky.

Folate has been pushed and even added to US foods, in the hopes of reducing heart disease/stroke which may be caused by elevated homocysteine levels.

I would keep your total folate consumption down to 800mcg a day, until this data clarifies.

Methylfolate is available now thru Solgar at 400 and 800mcg doses. It was off the market for a while, because Merck, who holds the patent for making it, wanted to control it and make more $$ off the RX versions. But it now has returned to OTC status. So if anyone is really concerned, using it instead of folic acid regular type, may be a better intervention. But there are no guarantees yet.

Quote:

Originally Posted by mrsD (Post 675716)

Then, some new data emerged that some of these high dose patients were showing up with colon cancer at a young age.

I read this on this site. It is why I raised the question.

Thanks again.

Back in 1999 we were all on the "older format" at BT, some of us that is...;)

rose appeared there with her experience with low B12, and she used to provide the AMA Journal paper by Dr. Chris Snow MD which appeared that year and was a turning point for medicine in this country, for interpreting serum B12 levels. For a while this paper was only available to members of the AMA and it was not online. Rose sent me that article thru the mail, back then as she did for many other posters.

Well, that article is now available online and here is the link to it:
http://archinte.ama-assn.org/cgi/con...ll/159/12/1289

Quote:

As discussed above, patients with Cbl deficiency may have overt neurologic disease in the absence of hematologic findings. Patients with neurologic symptoms and signs and a normal complete blood cell count require a modified diagnostic approach because of several considerations. First, folate deficiency is an unlikely cause of neurologic disease. Second, the neurologic disease of Cbl deficiency may be irreversible if treatment is withheld or delayed; because Cbl therapy is nontoxic, the risk-benefit ratio favors treatment in questionable cases. Finally, an apparent response to therapy (or lack of response to therapy) is less definitive in ruling in or ruling out Cbl deficiency than is the serial measurement of abnormal initial hematologic parameters. Even in patients with a normal complete blood cell count, it may be worthwhile to monitor the MCV after treatment because a significant decline within the normal range provides additional evidence of Cbl deficiency.

An approach to the diagnosis of Cbl deficiency in patients with isolated neurologic findings is outlined in Figure 4. Relevant to the development of this algorithm is a study23 of 419 patients with Cbl deficiency, 12 of whom had serum Cbl levels greater than 148 pmol/L (200 pg/mL). All 12 had elevated levels of serum Hcy and serum MMA. Five patients with normal serum Cbl levels had neurologic disease, and 1 of the 5 had a level greater than 221 pmol/L (300 pg/mL). All 5 patients had a clinical neurologic response to Cbl therapy and normalization of metabolite levels.

(note: picomoles is a European and other country lab report, and we use pg/ml in US-- this link explains how to convert them:
http://neurotalk.psychcentral.com/post627358-43.html )

This article is often quoted in the bibliographies of other papers now, so it is nice to have it to refer to. Some of the information and graphs in it were picked up by AAFP, in their online reference for doctors, in 2003. I gave that link in the first post on this thread, so I won't repeat it here.

Over the years the formulas for oral B12 have changed. I have yet to see the new enhanced absorption one yet, but I understand it is coming. Methyl B12 (bioactive form) oral is available now and it supercedes the cyano (which is not active and is synthetic) by far. Methyl B12 is also available by injection from compounding pharmacies and is mostly used by the autism community, but any doctor can order it.

Also parallel discoveries in pharmaceutical dosage forms and bioavailability about microgram absorption of drugs failing when food is present in the GI tract (esp. fiber) have not yet trickled over to oral B12 recommendations, we often see in papers.
Thyroid and digoxin have been found to not be absorbed when food is present, so now carry the recommendation to take on an empty stomach. Since the oral forms of B12 are in micrograms also, and since they are passively absorbed orally, this recommendation I think should apply to them. Testing for intrinsic factor (the Schilling's test) has been dropped by many labs today. So many doctors and patients have no idea if they have working intrinsic factor or not. The antibody test to parietal cells is sometimes used but it is expensive and often not done either. When intrinsic factor is working, oral B12 will be absorbed better. But when people present with significant neurological symptoms one has to wonder if intrinsic factor is NOT working as it should. So expecting only passive absorption of B12 in the intestine is what we have to go on.
The AAFP link has some nice color illustrations to show how B12 is absorbed ideally, so please check that out.