posted
On mega doses of B12 and my body will not hold on to it. Shots and tablets. Anybody else have this??
Posts: 22 | From East Quogue, New York | Registered: Feb 2011
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Razzle
Frequent Contributor (1K+ posts)
Member # 30398
posted
Some cannot convert cyanocobolamin (the most common form of B12 found in supplements/shots) into the active and useful forms (hydroxycobolamin, methylcobolamin)...the solution is to try the active forms instead.
I personally am unable to absorb B12 in any form orally (sublingual or swallowed), so I have to get shots.
I also find I need to change which form I'm getting from time to time. I've gotten side-effects from cyano-B12, but not from methyl-B12.
You should also get checked for parasites (genova is a better lab for this than the usual labs most MD's use) because some parasites "use up" B12...
Good luck,
-------------------- -Razzle Lyme IgM IGeneX Pos. 18+++, 23-25+, 30++, 31+, 34++, 39 IND, 83-93 IND; IgG IGeneX Neg. 30+, 39 IND; Mayo/CDC Pos. IgM 23+, 39+; IgG Mayo/CDC Neg. band 41+; Bart. (clinical dx; Fry Labs neg. for all coinfections), sx >30 yrs. Posts: 4167 | From WA | Registered: Feb 2011
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Methylcobalamin, Hydroxocobalamin, Cyanocobalamin, or Adenosylcobalamin?
As per a researcher I kept in touch with, I think he said that he thinks B12 (cobalamin) may be robbed by toxins in some people (in much more complicated lingo). I'm really not sure if I got that correct as I can't find the source.
Are they monitoring your levels? How do you know your body is not holding on to it? I had to push 25 mg/cc of methylcobalamin with folate and p5p to get my body to accept it, and then the effects were profound.
Large dosages of prescription Folate (such as Deplin) can really help push detoxification hard as well, but should be taken with B12.
For injections, make sure you use a reputable compounding pharmacy, and not some random compounding pharmacy near you. There can be quality issues since "active" forms (such as methylcobalamin) aren't very stable. For an example, you can't expose methylcobalamin to light, and you always keep the vial refrigerated.
I used methylcobalamin compounded WITH preservative (benzyl alcohol).
Hope you get things figured out.
Posts: 967 | From A deserted island without internet access | Registered: Sep 2009
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quote:To the best of my current understanding, all the cobalamin forms except glutathionylcobalamin can be hijacked by toxins. There are still some parts of B12 metabolism that have not been sorted out completely by the researchers in this field, but here's a synopsis of what is believed to be known at this point:
When various forms of B12 are taken orally via food or ordinary oral supplements (not sublingually, transdermally, liposomally or by injection) in a normally operating digestive system, all the forms of B12 are separated from protein by acid in the stomach, and are bound to haptocorrin. In the early part of the small intestine, the haptocorrin is broken down, and the B12 forms are bound to intrinsic factor, which is produced by the parietal cells of the stomach. In the last part of the small intestine (the terminal ileum) there are receptors for intrinsic factor, and it is drawn into the cells lining the intestine (enterocytes), together with the forms of B12 that are bound to it. The enterocytes transfer the B12 forms to transcobalamin, which is carried in the blood to the various cells of the body. The cells have receptors for transcobalamin, and they draw it into lysosomes inside the cells. In the lysosomes, the transcobalamin is broken down, and the forms of B12 are freed. They are passed from the lysosomes into the cytosol, and their beta ligands are removed. These include hydroxo-, methyl-. and adenosyl-. At this point the B12 is just cobalamin. The cobalamin is then passed either to methionine synthase in the cytosol or into the mitochondria. The fraction that is passed to methionine synthase is methylated by SAMe to become methylcobalamin and it supports the methylation cycle. The fraction that passes into the mitochondria is converted to adenosylcobalamin, and it supports methylmalonyl-CoA mutase.
It has been proposed that during its metabolism in the cytosol of the cells, B12 is normally chaperoned by proteins over its entire pathway to formation of the B12 coenzyme forms. There is evidence that glutathione is involved in this chaperoning process, by formation of glutathionylcobalamin, which protects cobalamin from reacting with toxins during its transition from the initial form that was absorbed to its final coenzyme form, either methylcobalamin or adenosylcobalamin. But the details of this process are still not totally elucidated. I have hypothesized that this need for chaperoning is the reason why depletion of glutathione leads to loss of B12 function, and thus a partial block of the methylation cycle as well as a partial block of the methylmalonate reaction, which causes methylmalonate to rise in the urine organic acid tests.
Note that all forms of B12 that are taken by the ordinary oral route are normally treated the same way. Their individual ligands are removed, and then the two coenzyme forms of B12 are produced as needed by the cells. Because of this, the intake form of B12 are all vulnerable to hijacking, if there is not enough glutathione to protect the intermediate cobalamin.
Now, what about taking high dosages of forms of B12 by the artificial routes (sublingual, transdermal, liposomal, or injection)? If the dosages are high compared to usual RDA-type B12 dosages, which are in the few micrograms range, that is, if they are up to several milligrams, 1000 times higher than RDA-type levels, then the capacity of transcobalamin to bind the B12 in the blood will be overwhelmed. The transcobalamin will be saturated, and it will carry its bound B12 to the cells in the normal way. The B12 in excess of this will be carried in the blood in an unbound state. As far as I know, the behavior of this unbound B12 has not been researched, but based on the experiences of many people, it appears that some of it is able to diffuse across cell membranes and enter cells without benefit of the transcobalamin receptors. Whatever does not enter the cells in this way is extracted from the blood by the kidneys and passes into the urine.
Again, the behavior of unbound B12 forms after they diffuse into the cytosol of the cells has not been researched. However, based on experiences reported, at least some of both methylcobalamin and adenosylcobalamin appear to be able to perform their normal coenzyme functions after entering the cells in this manner. If the dosages are high enough, they can apparently overwhelm the hijacking by toxins sufficiently so that some survives to perform their normal functions. In the case of hydroxocobalamin given by these artificial routes, some apparently enters the cells, and it must be converted to methylcobalamin and adenosylcobalamin inside the cells, even though it did not come in via the transcobalamin mechanism, because the experimental evidence is that it does support the normal coenzyme functions of B12.
If a person has normal cobalamin processing enzymes in their cells, it seems to me that after sufficient detoxication has taken place and glutathione levels have been restored, the hijacking of B12 by toxins will decrease, and the amount of B12 supplementation needed should also decrease. It may take considerable time to get the toxin load down, though, especially if the person has been ill for a long time, and the toxins have built up considerably while the detox system was dysfunctional.
My experience seems consistent with this theory.
Posts: 967 | From A deserted island without internet access | Registered: Sep 2009
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Razzle
Frequent Contributor (1K+ posts)
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posted
Yes, B12 can be depleted by sulfite preservatives (binds directly to the sulfites, and then the sulfite-B12 combination is eliminated through bowels/bladder). B12 also participates in the methylation cycle because it can act as a methyl donor. The methylation cycle is what gives us glutathione, which is a major detox substance produced in the liver.
-------------------- -Razzle Lyme IgM IGeneX Pos. 18+++, 23-25+, 30++, 31+, 34++, 39 IND, 83-93 IND; IgG IGeneX Neg. 30+, 39 IND; Mayo/CDC Pos. IgM 23+, 39+; IgG Mayo/CDC Neg. band 41+; Bart. (clinical dx; Fry Labs neg. for all coinfections), sx >30 yrs. Posts: 4167 | From WA | Registered: Feb 2011
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posted
Wow! Thank you for all the input. I have been deficient for about a year. They had me taking 5000mg sublingual for the last 6 months and now I am taking shots from my primary every week. I had lymes 2 years ago and went on amoxacillan for 2 months. Then they stopped it. Been going slowly downhill since and have been really sick for the past 2 1/2 months. Can't get anyone to listen too me. WTF??? I feel like I am losing my mind. Sorry for venting. Thank you all again.
Posts: 22 | From East Quogue, New York | Registered: Feb 2011
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posted
Wow! Thank you for all the input. I have been deficient for about a year. They had me taking 5000mg sublingual for the last 6 months and now I am taking shots from my primary every week. I had lymes 2 years ago and went on amoxacillan for 2 months. Then they stopped it. Been going slowly downhill since and have been really sick for the past 2 1/2 months. Can't get anyone to listen too me. WTF??? I feel like I am losing my mind. Sorry for venting. Thank you all again.
Murph257
Posts: 22 | From East Quogue, New York | Registered: Feb 2011
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posted
I have low B12 always. It was one of the first things that dr.s found in this quest of this disease.
I'd get a shot one day and be super low the next.
I've lived on B12 shots now for over 10 yrs.
It's the Babs for me... it's in our red blood cells... and thats what I was told by my first llmd in NY that we run low on B12 because of it.
By the way... easier and cheaper if you can give them to yourself.
-------------------- Lyme, Babs, Fry Bug..... Whatever it is, may a treatment be discovered to make us all whole again! Posts: 941 | From AZ-MT | Registered: Oct 2004
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quote:Originally posted by murph257: Wow! Thank you for all the input. I have been deficient for about a year. They had me taking 5000mg sublingual for the last 6 months and now I am taking shots from my primary every week. I had lymes 2 years ago and went on amoxacillan for 2 months. Then they stopped it. Been going slowly downhill since and have been really sick for the past 2 1/2 months. Can't get anyone to listen too me. WTF??? I feel like I am losing my mind. Sorry for venting. Thank you all again.
If you can't get your B12 up with that, you will probably need shots of methylcobalamin (if your genetics allow) or hydroxocobalamin DAILY.
I don't see how once a week could be enough given your experience. I did them myself every single day. And I think it's really less about getting your B12 levels up (though of course that's important), and more about kickstarting your methylation cycle.
Posts: 967 | From A deserted island without internet access | Registered: Sep 2009
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