1. Patients launch $1.27 million crowdfunding campaign for ME/CFS gut microbiome study.
    Check out the website, Facebook and Twitter. Join in donate and spread the word!
Join the National PR Campaign for ME: Power to the Patient (P2tP)
Have you had enough of all the neglect and abuse of ME/CFS patients? Gabby Klein says now is the time for a National PR Campaign for ME/CFS to impress a change. Join the Patient Revolution to restore power to ME patients ...
Discuss the article on the Forums.

B-12 - The Hidden Story

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by Cort, Jul 26, 2009.

  1. soulfeast

    soulfeast Senior Member

    Messages:
    410
    Likes:
    44
    Virginia, US
    Folic Acid

    Thanks, Freddd. I think you are probably right about the Thorne. They told me their product is from merk but would not reveal if it is the patented metafolin. I have not had the obvious die off, detox effect from it like I did with the metagenics products. If the Deplin site is right, there the MTHFr conversion or lack there of takes place between 5 methyl THF and the production of l- methyl. Metafolin is supposed to be l-methyl as is the deplin product, which I am assuming is and all are metafolin. OK. So that would probably mean that MTHFr is at least slow even though I have heterogenous mutations (I think every MTHFr gene yasko tests, I am hetero on).

    What do you think about a potential need for folicin? I know yasko includes some in as does Rich.

    B Right has folic acid.. I know Rich does not use folic acid and yasko limits i feel pretty certain because the folates compete with each other and that potentially FA will block the active forms from cells. What do you think of this idea?

    You are dosing metafolin much higher, so thats different as well. What do you think of the lower doses of about 300mcg 5-methyl THF (0r really l- methyl) and 100 folicin?
     
  2. soulfeast

    soulfeast Senior Member

    Messages:
    410
    Likes:
    44
    Virginia, US
    B12s

    Thanks Freddd. More questions. :-D

    What do you think about the role of hydroxo in scavenging NO?

    That makes sense when focusing on the CNS and repairing damage. Esp given your stats on how much hydroxo is converted to methyl. Do you have a source for that or this based on experience?

    My symptoms started neuro, not with fatigue or pain, rather buzzing and zapping. This could be lyme but Im not so sure. Most "activity" is in my spinal cord. It feel whacky off like a puppet wire is keeping it together and not very well. I started having very bad neuropathy, more horrible creepy sensations than pain, though pain is sometimes a relief from the creepy feelings. I have gait issues that come and go and the bottom of my feet will feel numb (I guess numb is the best way to describe it.. like I cant feel teh ground properly) and I have problems walking. My lower spine and hips are pretty bad off at times too.

    So I am wondering if I need methyl B12. I am also wondering how this plays with my COMT++,++ status and probable mercury toxicity. Do you have any thoughts on these scenerios?

    As for your dosing. Makes sense how you ramped up. I am wondering if you take 3 shots a day.. sounds like you are.. does it leave the system that fast? Have you checked your MTR, MTRR status? I am homogenous for MTR++ and I dont know how I made it as long as I did (40 years) being a vegetarian for 23 years, bearing two children and nursing while pregnant and into toddler years.

    Lastly, my MMA urine was 10.. thats not that bad is it? If I have degeneration in my spinal column due to b12 deficiency, why not a higher MMA?

    Thank you, Freddd, for any attempt you can make to plow though this post.
     
  3. soulfeast

    soulfeast Senior Member

    Messages:
    410
    Likes:
    44
    Virginia, US
    Amino Acids

    Thanks, again, Freddd. Do you see glutathione as a problem and how do these two cancel out the active forms? I think I really need glutathione. At least particularly with hydroxo...

    When I was able to tolerate glut IV, it took away my neuropathy as long as I kept it up, which I didnt. It came back... then after starting the simplifed/yasko (with very limited methyl folate to none because of the detox effect and using folicin instead.. I had a detox reaction that scared me and have not used glut since. This happened with the nasal spray I was using as well. But, i want to try transdermal because I remember how it made everything ok in the past.

    Do you know if you were low on amino acids? I think the methylation cycle may very well sap up AA in some way. I think homocysteine is needed to help active folic stay in cells. Low methionine was implicated in the low homocysteine (though I think there are more ways to achieve low homocysteine?). The same article stated that B12 deficiency was contrued by the cells to be low methionine. ??

    AAs also fuel the methylation cycle ??
     
  4. Freddd

    Freddd Senior Member

    Messages:
    4,545
    Likes:
    913
    Salt Lake City
    Hi Soulfeast,

    Deplin is Metafolin. There are several brands of prescription forms of Metafolin with various doses and with various additional forms. There is also Metanx with Metafolin, p5p and methylb12 for homocysteine reduction.


    What do you think about a potential need for folicin? I know yasko includes some in as does Rich.

    Rich made a convincing argument for it recently. I'm going to include it on my next order and give it a try. I definitely have folate problems and they have continued much worse every since I tried the glutathione precursors. I have to take 4000mcg in 5 doses in order to achieve the same effect I used to get from 800mcg, and that changed suddenly and hasn't reverted.

    I had folate deficiency symptoms all my life including while taking folic acid. They didn't clear until a few days after starting just 400mcg of Metafolin and with increasing benefit to 800mcg. That remained satisfactory until I took the glutathione precursors which plunged me into folate deficiency starting within a few hours. I then spent 6 months in "glutathione detox" which had all the symptoms of mostly folate deficiency with a little b12 deficiency thrown in after I researched it on the internet. I upped my folate to 4800mcg daily divide in 2 doses and then I had mb12 and separately adb12 startup symptoms all over again. All the induced deficiency symptoms were 90% gone in 4 days though some problems lingered for 9 more months until they finally went away one day as suddenly as they came on.

    B Right has folic acid.. I know Rich does not use folic acid and yasko limits i feel pretty certain because the folates compete with each other and that potentially FA will block the active forms from cells. What do you think of this idea?

    I would avoid folic acid if the supplements that worked would allow that but at present they don't. Howver, I have noticed no interference in absorbtion at all though I have seen the the theoretical statement that it could.

    You are dosing metafolin much higher, so thats different as well. What do you think of the lower doses of about 300mcg 5-methyl THF (0r really l- methyl) and 100 folicin

    I think that the dose that gets rid of all deficiency symptoms and gives maximum benefits is the right dose. In my own case that has changed and it might change again.
     
  5. Freddd

    Freddd Senior Member

    Messages:
    4,545
    Likes:
    913
    Salt Lake City
    That makes sense when focusing on the CNS and repairing damage. Esp given your stats on how much hydroxo is converted to methyl. Do you have a source for that or this based on experience?

    I have seen that repeated so often in so many places, concerning how much can be absorbed via IF and transported via HTC2 and thereby subject to conversion, that I can't give you any specific source. I also can't vouch for the numbers as I have no way of verifying them. What is demonstrated over and over is that a person can go from hycbl to methylb12 and/or adb12 and have all sorts of startup symptoms from unfullfilled needs no matter how long they are on hycbl. In fact it appears that the longer a person is on hycbl the more severe some mb12 and adb12 deficieciency symptoms get and the more severe the startup reaction is correcting those. Hycbl never appears able to fullfill the full need for mb12 and adb12 in the vast majority of people. Instead the majority of people appear to get deeper and deeper in the hole the longer they take it. It works for some symptoms but not the majority of them.

    What do you think about the role of hydroxo in scavenging NO?

    In that role it controls and decreases inflammation. I think that methylb12 is about 100x more effective at reducing inflammation than hycbl. That is based purely on pragmaticly determined effectiveness.

    My symptoms started neuro, not with fatigue or pain, rather buzzing and zapping.

    These are generally very specifcally mb12 deficiency symptoms.

    Most "activity" is in my spinal cord. It feel whacky off like a puppet wire is keeping it together and not very well. I started having very bad neuropathy, more horrible creepy sensations than pain, though pain is sometimes a relief from the creepy feelings. I have gait issues that come and go and the bottom of my feet will feel numb (I guess numb is the best way to describe it.. like I cant feel teh ground properly) and I have problems walking. My lower spine and hips are pretty bad off at times too.

    How long has this been going on? Is it continuing to get worse or has it leveled off or getting better? This is very specifically mb12 deficiency. I used to have similar problems. My feet are no longer dead numb. I have a normal gait back. I have regained normal reflexes. I have motor control of my toes. I can sense where my feet and lower legs are located. These started improving within hours of getting enough methylb12, with cofactors. I had 2 layers of numbness; skin and muscle. The skin sensation came back more easily than the muscles. I spent a couple of weeks on top of a second story roof last summer which I could never have done without the neurological healing I have had from the mb12. A year before I was falling a lot and could never have done that.

    Elsewhere one man, a vegetarian, was able to get up out of a wheel chair becasue of daily hycbl. However, the rest of the healing and getting out of the braces was dependent upon mb12 and adb12. He also needed 30mg/day of mb12, just as I do, to do that. So, if you want to correct your spinal nerve problems with a pragmatically based protocol based on those with the experience of having done so, we can give you the information. A year from now you could be healed to a substantial extent. However, what we have to say will be at odds with many of the theories you appear to embrace.


    So I am wondering if I need methyl B12. I am also wondering how this plays with my COMT++,++ status and probable mercury toxicity. Do you have any thoughts on these scenerios?

    As far as the COMT++ status theory, if it keeps you from doing what is required to heal your feet it might not make sense for you to adhere to it. All sorts of theories abound to fill a void when there is not an effective therapy. Pragmatic results overide theories. Would you want to try something that could heal most all of that?

    As far as mercury, there is a more complete discussion some ways back on this thread. I modeled the effects of mb12 on mercury based on research of clearance of methylmercury from accidental doses in humans. While huge doses (700mg plus injected mb12 at a time) might possibly have caused some rare mercury toxicity problems from converting mercury to methylmercury, normal doses of mb12 daily appear to clear it out at about 1% per day of the mobilized mercury, 50% in 71 days. In about 10 halflife periods of daily mb12 adminstration, about two years, a person would be largely cleared of mercury. 80% of mercury toxicity symptoms are mb12 deficiency symptoms as well. I have come across papers saying that the biggest problem of mercury is that it disables mb12 which is the active form the nervous system needs thereby causing CNS mb12 deficiency problems. Not taking mb12 appears to be much more of a risk than taking it as taking it corrects the deficiency and clears out the mercury. There may be differences of opinion on this. However, if one interpretation allows you to heal in the coming year and the other one doesn't you might want to choose the interpretation that allows you to heal. There are no guarantees. What I am saying goes against 60 years of research with inactive until converted in the body cobalamins such as hycbl and cycbl. The immediately active without conversion cobalamins, mb12 and adb12 are something entirely different.


    Lastly, my MMA urine was 10.. thats not that bad is it? If I have degeneration in my spinal column due to b12 deficiency, why not a higher MMA?

    There are several reasons. For starters MMA detects the failure of ATP being made in the mitochondria by adenosylb12. At the body wide level which is what is needed for a high serum or urinary MMA subacute combined degeneration has nothing to do with ATP generation. Now if were a cerebral spinal fluid MMA that was high, and there are no standards for that and CSF isn't drawn for that reason it still isn't what is normally associated with spinal nerve breakdown. Methylb12 in relatively large doses, ie 30mg/day in 2-4 doses is what causes repair of the spinal nerves. While adb12 is needed for proper fatty acid generation for the myelin, so is omega3 oils and other coffactors. The high dose of mb12 is generally needed because - pick your hypothesis; 1) many of the people have a depressed CSF b12 level because they either exclude cobalamins too well from the CSF and/or excrete too fast or; 2) A higher level of methylb12 upregulates neurological healing or; 3) Some combination of the first two.

    This comes from the mistaken idea that "b12 deficiency" is all one thing. There are two body wide deficiencies, adb12 and mb12 which each has it's own set of distinguishable symptoms. Then the cerebral spinal fluid is insulated from body wide conditions and may have it's own deficiencies whether or not the body does. Each of these, adb12 and mb12 deficiencies has their own separate characteristics. The amount of MMA and homocystein generated in the CNS are not enough to show up as abnormal in the blood or urine and can be detected only with a CSF draw. In the body or CNS the homocystein specifically indicates failure in homocystein to methionine cycle.

    No matter what some research says about the theoretical interchangability of different forms of b12 in most people it doesn't happen to sufficiency. The two immediately effective without transformation forms of b12, adb12 and mb12 are tremendously more effective for most people much more quickly and completely. And again, most people have different effects from each of them no matter what you compare it too and without regard to their hypothecized genetic characteristics.

    As for your dosing. Makes sense how you ramped up. I am wondering if you take 3 shots a day.. sounds like you are.. does it leave the system that fast?


    Yes, I take 3 shots a day. At two per day I can feel it start and stop it's effects and feel the 3 steps forward and 2 steps backwards each day.


    Have you checked your MTR, MTRR status?

    Nope.
     
  6. soulfeast

    soulfeast Senior Member

    Messages:
    410
    Likes:
    44
    Virginia, US
    Thank you Freddd for being so generous with your details and info. Lots for me to think a bout. I have a strong feeling this is methylb12 deficiency. I felt a lot better when I had myers cocktails with methyl.. gait, tremors, creepies gone. I didnt keep it up. It all came back. Then i started the simplified/yasko after which I had a detox reaction (My head felt very woozy and off) from glutatione IV and stopped that. Nasal glut did the same thing.. noticed it right after I took it. It had been going on for weeks then I finally realized it started up right after I sprayed the glut. So I was left with the myers. I had a strange reaction one day.. just felt I was going to pass out all during it (mag chloride should not do this), so I stopped.

    How long? Started 2.5 years ago... well lyme diagnosis was 2.5 years ago.. symptoms building before that and no gait issues, tremors, etc.. just zapping out, slurring of speech a few times. knowing something was very off.. costrochonrtitis which could be from lyme or babs.. also lots of breathelessness, which also is a babs symtom and did improve with medication. I have gone downhill since. Treated 6 months for babesia and lyme. My gut fell apart from that treatment and Ive only sporadically used abx since. Minocycline did help with some neuro symptoms.. really foggy brain, loose thinking.. hard to describe. I do think that mino is also an anti-inflammatory. Higher dose made me worse neurologically (hit the floor depression) and the low dose 50mg twice a day was wonderful. But the symptoms came back very badly after following the mino with 2 weeks of flagyl. Then my symptoms became much much worse (which made me wonder if I cleared the flagyl) and thats when teh gait issues, puppet feeling, etc came in full force. The myers and glut helped. Then came back as stated above. Not sure its all b12 but I think its a huge part of it.

    The MDs office where I get the IVs from has always used methyl and had good results. They also chelate there.

    If so little hydroxo is converting to methyl and you have a methyl deficiency induced neuro illness, then it doesnt make sense to not use it or at least try. Thats interesting about adenyl helping nerves myelinate. I stopped my sublingual recently.

    I have increased muscle fatigue that has become overwhelming as well as gut dysbiosis, low amino acids UAA, and I do herx pretty hard on abx. Dysautonomia worse, hypreadrenergic.
     
  7. soulfeast

    soulfeast Senior Member

    Messages:
    410
    Likes:
    44
    Virginia, US
    Probably too soon to tell, but I am taking jarrow 1mg sublingual, 3 times yesterday.. am .. no creepies that day. By evening creepies back. Took another, gone. Then went to bed with one in between my cheek and gum.. haha. Woke up with some residue there and no creepies, yet. I have noticed I will have a posotive effect with some therapies that goes away ove a short period of time, so still in experimental mode with this. Remembering how the myers took all this away as well.

    Freddd, do you think there will be a point when you catch up with b12 to the point where your maintenance is lower or do you think you have a genetic glitch that will require you always take this much. Were you ever OK physically? I was OK.. not great lookign back,but able to work out and live my life without problems. I can see now that some emotional issues like panic, OCD might have been the edges fraying biochemically. The OCD is much better, though its hard to tell if the obsessive reasearch has any OCD to it or just will to survive. I can imagine that certain nutrients (given genetic status) and methylation were suboptimally functioning but enough to get by and eventually started sputtering out.

    I am wondering about the high dose metafolin you are taking. Do you think it is possible that you are not only making up for a defiency but also that the b12 and metafolin are lost to scavenging aldehydes and glutamates?
     
  8. Freddd

    Freddd Senior Member

    Messages:
    4,545
    Likes:
    913
    Salt Lake City
    Hi Soulfeast,


    Woke up with some residue there and no creepies, yet. I have noticed I will have a posotive effect with some therapies that goes away ove a short period of time, so still in experimental mode with this. Remembering how the myers took all this away as well.

    It's important to take the cofactors, the other vitamins and minerals etc or healing comes to a halt because you run out of something else.

    Freddd, do you think there will be a point when you catch up with b12 to the point where your maintenance is lower or do you think you have a genetic glitch that will require you always take this much.

    I don't have an answer to all of that. Exccept for the worst damaged areas, the subacute combined degeneration in the cord/brain everything else has gotten pretty much healed. At 62 I'm probably doing at least average physically for my age. As I appear to need the large dose only to promote spinal nerve healing and brain function maintenance, I could probably get along on mb12 5mg sublingual daily plus a a weekly adb12 3mg, if it were not for the CNS/CSF factor. There has been a depressed level of cobalamins found in the cerebral spinal fluid of those with CFS/FMS and Alzheimer's. The Japanese have found that larger amounts of mb12 appear to increase CNS functions with MS and ALS. I had a relatively large response with the first dose at 7.5mg or more and could feel it in my otherwise numb feet. SInce that first dose I have recovered 90% or more of the funtioning in my lower legs and feet.

    It appears that once damaged it either ttakes a long time to heal or function needs a constant high dose to be maintained.

    Since I have at least 2 or more genetic glitches it depends upon which glitch you mean. The inablity to intervconvert doesn't appear to require great quantities, just more than occupies the transport system. If you mean the folic acid to active folate conversion hith found in 50% of people, I do appear to have that as well but it doesn't have much bearing on the b12 ampount.. If you mean the hypothecized glitch possibly causing the low CSF cobalamin level, I appear to have that as well and that is at the heart of the matter. There is a hypothecized glitch in how cobalamin is transported through the blood brain barrier or retained in that space.


    Were you ever OK physically? I was OK

    I was sick a lot. I missed about 1/4 to 1/3 of any given school year. I also was a professional ski partrolman before having my back broken by a guy in a hardware van running a red light. That was the start of a decline. In a few year I devloped FMS. Then some years later I got sick and ended up with CFS at the end of 1987. Nothing at all got anj better for 16 year until May 21, 2003 when I tried my first mb12. While I still have some damage I doing fine on an age adjusted basis, having only some damage from the long tem deficiency. Everything else was healed years ago.

    I am wondering about the high dose metafolin you are taking. Do you think it is possible that you are not only making up for a defiency but also that the b12 and metafolin are lost to scavenging aldehydes and glutamates

    I only needed 800mcg before the glutathione precursors of l-glutamate and NAC. So again I don't know where it is going but the requirements are different for getting the same results.
     
  9. soulfeast

    soulfeast Senior Member

    Messages:
    410
    Likes:
    44
    Virginia, US
    Thank you Freddd. I am taking all the cofactors you listed (second post) except ALA. How much do you take?

    A local friend with spectrum children who have mthfr homogenous polymorphisms was prescribed half a deplin which is 7.5mg of metagfolin for each. They are 6 and 9. This is making me wonder about how much metafolin is needed. I am heterogeneous as are my children. Assuming homogeneous would require more metafolin than hetero.

    That makes sense needing the higher doses for repair. Didnt think of that.

    About the glutathione.. do you think that is large doses that causes a problem (as you experienced) or small doses as well? Glut has to be in the body, so if one is deficient and taking small doses, I am wondering how you think that might effect the methyl b12. I feel pretty certain it is needed for hydroxo. I am also hearing you say that for folks who are methyl defiecient with nerve damage as I think I may be experiencing, that the hydroxo is not going to cut it.

    I did well today taking mg this am around 9:30. Made it until about 6:30 until the creepies set in again. Took another but was talking while it was in and it dissolved too fast, so took another after that. The creepies backed off, but still not feeling as good as I did earlier today.

    Sounds like the best way to know is to keep experimenting and add in the glut transdermal I have and see what happens. ??

    Do you think you were glut deficient, methylation impaired and all is running well at this point save the ongoing nerve repair?

    Thanks, so much, Freddd.

    I would really like to be able to fit all these folate/b12/methylation protocols together in some way that personally makes sense for me.
     
  10. doveman

    doveman

    Messages:
    22
    Likes:
    0
    Hi Freddd

    I don't believe IF is involved with injections or sublinguals, so that's a red herring. Do you have some reason to think that methyl has some additional way of getting into cells other than via TC, that doesn't apply to hydroxy?
     
  11. Freddd

    Freddd Senior Member

    Messages:
    4,545
    Likes:
    913
    Salt Lake City
    Hi Soulfeast,

    A local friend with spectrum children who have mthfr homogenous polymorphisms was prescribed half a deplin which is 7.5mg of metagfolin for each. They are 6 and 9. This is making me wonder about how much metafolin is needed. I am heterogeneous as are my children. Assuming homogeneous would require more metafolin than hetero.

    Very interesting. Right now I am at the same understanding point with Metafolin as I was 6 years ago with mb12 and adb12, just begining. Over at wrong diagnosis on the b12 thread many have found that Metafolin makes a significant difference in effectiveness whether their folate tests measure low or normal or high. Once again the test is not predictive of lack of effectiveness, the same as with mb12 and adb12. Somewhere over half of the people who find immediately active without conversion mb12 and adb12 effective also find that Metafolin enhances the effectiveness. The majority position, of those who have said anything, is to find that they heal better with Metafolin than without whereas folic acid doesn't appear to make any difference. So far the amount is all over the place as it has been for me. Before I messed myself up with glutathione precursors I needed 1/6 of what I needed for the year afterwards.

    About the glutathione.. do you think that is large doses that causes a problem (as you experienced) or small doses as well? Glut has to be in the body, so if one is deficient and taking small doses, I am wondering how you think that might effect the methyl b12.

    My understanding is that the mb12 itself is a ncessary precursor for glutathione to form naturally. The deficit may be secondary to the mb12 deficiency. I would suspect the effects I had are at least somewhat dose related. I don't have any idea what the lower end of the curve looks like. I have had private communications with somebody who was having infusions every couple of weeks and had signiticant improvment when she stopped and started the mb12 and Metafolin instead.

    I would really like to be able to fit all these folate/b12/methylation protocols together in some way that personally makes sense for me

    I'm working on a moderately long definition of b12/folate deficiency piece that might help put things in perspective. In looking at the list of nearly 300 b12 and folate deficiency symptoms and signs, perhaps 1/3 of them come down to a methylation lack. High homocysteine, one of the main markers b12/folate deficiency is a lack of merthylation usually, more rarely p-5-p. Most all of the epithelial and endothelial problems from sore beef-red tongue to inflamed bladder to IBS to inflamed arteries and veins are from poor cell division - DNA replication, which amount to a methylation problem. Whether some of the neurological problems backtrack to methaltion lack or not, I don't know. Rich pointed out the other day that lack of melatonin generation and the attendent sleep disorders backtracks to a lack of methlation.

    So a large percentage of apparantly unrelated symptoms all backtrack to a lack of methylation caused by specifically a lack of methylb12 and methylfolate. I have put forward the opinion prior to this that none of these methylation problems could have happened if people were routinely receiving methylb12 and methylfolate. I called it "methylation exhaustion" six years ago because it actually appears to be inducable by taking cyanocobalamin and folic acid, and hydroxycobalamin isn't any better as it too competes for methyl groups as does cyanocobalamin instead of providing them.

    I haven't really tried to separate out the effect of methylfolate from methylb12 and adenosylb12 as they are so closely coupled in the body and the majority of those taking methylb12 also show incremental improvement if not outright startup when they start Metafolin.

    Because of a combination of my history and my genetic status in several areas I can very clearly sense each of the 4 main branches of B12 deficiency and folate deficiency. So something like FMS can be described in terms of CNS deficiency of mb12, body deficiency of mb12, CNS deficiency of adb12 and methylfolate deficiency. With CFS the emphasis is somewhat different with a very strong body deficiency of adb12, a stronger CNS deficiency of adb12 and a lesser body deficiency of methylb12 and a deficiency of methylfolate. I am working on a more exact breakdown on that. However, the centrally mediated neurological differences in FMS, the neurological pain and certain parts of the muscle pain point at a CNS deficiency of mb12 that is not apparant in the CFS. I used to have both. I also has the reverse curvature of the neck and other things characteristic of ME and characteristic of a CNS deficiency of mb12. ALL of the methylation defects appear to stem from a lack of mb12 and methylfolate and do not appear to be possible in their presence.

    I am also hearing you say that for folks who are methyl defiecient with nerve damage as I think I may be experiencing, that the hydroxo is not going to cut it.

    Exactly. Methylb12 is known to promote the neurological healing some how. Everybody I have come across with "idiopathic" neuropathies has shown substantial rapid improvement with mb12 and cofactors. That includes plenty of people who previously took hycbl or cycbl and had already gone as far as those could carry them. For me once the damage was done not even small doses of mb12 stopped it from progressing. I needed the larger neurological healing size doses to promote CNS healing and stop progression.
     
  12. soulfeast

    soulfeast Senior Member

    Messages:
    410
    Likes:
    44
    Virginia, US
    Freddd, Im going back through this thread trying to catch up.

    Could the stocking glove (or whatever its called) feeling be the same as the creepy like feeling I feel that can be around my ankles (and feet can feel like they are very wrong on the ottom.. like they cant feel teh ground right though no sensation in them like creeipes). The same as the creepy like feeling that is in my arms and can be all in my upper back? Sometimes it feels very deep in the muscles and other times it is like a gloving feeling I guess.. so difficult to define these symptoms.

    The glut issue... the glut combines with the Mb12 and converts in backward to the gluta... >> form that hydroxy becomes when it combines with glut as it is supposed to?

    I cannot ignore how the myers took all this away and then it came back. Including the puppet feeling as well as gait issues. I think myers has 5 mg Mb12. This was only once a month but I felt like I needed more.
     
  13. soulfeast

    soulfeast Senior Member

    Messages:
    410
    Likes:
    44
    Virginia, US
    Fredd, did you notice any autonomic nervous system imbalance that cleared up with this therapy and can you remember about when.. what dose, Mb12 and or Ab12 or metafolin?

    Thanks...
     
  14. soulfeast

    soulfeast Senior Member

    Messages:
    410
    Likes:
    44
    Virginia, US
    I have low homocysteine and low methionine. I understand that homocysteine can be created from methionine and I think there is some sort of recycling between the two in that homocysteine recycles back to methionine.. could be wrong about that. Does Mb12 increase methionine? The methylation cycle is complex.
     
  15. doveman

    doveman

    Messages:
    22
    Likes:
    0
    That's just misleading (hopefully not intentionally). As I've told you plenty of times, I had hydroxy injections which cleared up my main symptoms of burning ankles and tingling in the limbs. Taking methyl after that didn't make any noticeable difference to anything that could be described as a neuropathy.

    Mind you, I might turn out to have hyperparathyroidism and the resulting high calcium blood levels can cause nerve/muscle problems. In fact, I read that B6 can increase magnesium retention, resulting in a high magnesium / low calcium ratio leading to severe calcium deficiency, with symptoms such as insomnia, heart palpitations, chest pains, anxieties, depression, mood swings and joint / muscle pains, so it might be a good idea for anyone taking B6 long term to get their magnesium, calcium and parathyroid hormone levels checked.
     
  16. soulfeast

    soulfeast Senior Member

    Messages:
    410
    Likes:
    44
    Virginia, US
    Thanks for the info on b6, doveman.

    B12/folates info as well as role of hydroxy scavenging which may be needed by some:

    http://www.healthyawareness.com/articles/about-vitamins-minerals/about-vitamin-b12.aspx

    "The connection between vitaminB-12 and folic acid is also critical. VitaminB-12 reactivates folic acid. If an individual has low levels of vitamin B-12, severe folic acid deficiency may develop.


    The hydroxycobalamin can be found a www.Perque.com or it can be ordered through a compounding pharmacy. The body will convert it into the active methylcobalamin and adenosylcobalamin. Large doses of hydroxycobalamin have proved useful in the treatment of both fibromyalgia and chronic fatigue. The reason might be due in part to B12’s ability to mop up excess nitric oxide. Dr. Martin L. Pall hypothesizes that elevated nitric oxide and peroxynitrite may be the common etiology of posttraumatic stress disorder, fibromyalgia, chronic fatigue syndrome and multiple chemical sensitivity. Hypoxia (lack of oxygen) or any traumatic stress can set in motion a vicious cycle that perpetuates the elevated levels of the nitric oxide and peroxynitrite in the body. See www.ImmuneSupport.com/library/showarticle.cfm?ID=2976

    I think Freddd may be right that some people need the Mb12 to heal nerves.
     
  17. soulfeast

    soulfeast Senior Member

    Messages:
    410
    Likes:
    44
    Virginia, US
  18. soulfeast

    soulfeast Senior Member

    Messages:
    410
    Likes:
    44
    Virginia, US
    Very interesting.. its MTHFr (the folic acid genes) that gives non methylated B12 its methyl group. So is methyl b12 that is made in the body borrowing a methyl group from methyfolate???/


    http://www.hbot4u.com/autismdoc2.pdf

    Non-methyl-B12 forms of B12 work well to correct a true B12 deficiency. However,
    their actions are limited because their primary function is to be incorporated into
    the B12 binding site on the methionine synthase molecule. Once they are attached
    to this binding site, it is essentially the same as if they were “locked up in prison
    cell”. Once imprisoned in this manner, they are now dependent on the classical
    interactions of B12 with methionine synthase and methyl-tetrahydrofolic acid
    (MTHF), those actions being to accept the methyl group from MTHF and pass
    this methyl group onward to homocysteine while continually altering the cobalt-
    B12 oxidation/reduction state and repeating the process. “Only methyl-B12 has a
    key to the prison” and therefore is not bound to the prison-B12 rules. Only
    methyl-B12 has the freedom to bypass the need to receive its methyl group from
    MTHF. Only methyl-B12 has its own methyl group to pass onward to
    homocysteine. Therefore only methyl-B12 has the ability to act more quickly and
    more efficiently than other forms of B12.
     
  19. Freddd

    Freddd Senior Member

    Messages:
    4,545
    Likes:
    913
    Salt Lake City

    Hi Doveman,

    I don't believe IF is involved with injections or sublinguals, so that's a red herring

    While what you say is true also, it isn't a red herring. We have no communist fish here. The HTC2 system appears to be sized to be able to handle the amount of cobalamin delivered daily via IF. Until the modern period there was no other way to deliver more to the system than what could be absorbed via HTC1/IF and HTC2. They match quite well. I would be very surprised to see that the HTC2 has 10x the capacity of HTC1-IF. These are the two keyholes that cobalamin has to go through to get to a cell. The third keyhole is the actual type conversion. The estimates of how much can be absorbed via HTC1-IF is considered to be near 100% of the first 10 mcg or so, if everything is working perfectly, decreasing in percentage rapidly as the quantiity available goes up. Above 100mcg or there abouts available tests seem to indicate that it has decreased to the area of 1% via passive absorbtion. There is a lot of disagreement in the literature about the exact numbers but that may merely represent that all these things are on a bell shaped curve. 1mcg distributed in serum accounts for 200pg/ml. It is said that HTC2 makes repeated trips to the absorbed b12 so that it's total capacity at one time does not represent it's total daily capacity. If 97.5% of people have serum cobalamin levels below 1100pg/ml and 20-40% of that is bound in HTC2, that amounts to 220-440pg/ml which equals 1.1-2.2 mcg total at any one time. The total transportable in a day then could be determined by mean round trip time when b12 is availble for loading. There is some suggestion it can bind with unbound cobalamins in the blood but I am not sure that is substantiated.


    Then there is the HTC3 bound cobalamin making the trip to the liver where it is dropped off at the liver to be leaked back into the intestines and selectively reabsorbed again via IF and HTC2. The balance of the serum cobalamin is unbound cobalamin, such as cyanocobalamin which is a preferred excretion form via the kidneys. All unbound cobalamin is fair game for the kidneys. As a smoker you should know that the unbound hycbl you have circulating can directly interact with the cyanide from the tobacco smoke via purely chemical means with the CN replacing the OH thereby detoxifying the cyanide and headed for more rapid excretion via the kidneys where it is NOT subject to reabsorbtion unlike HTC3 bound b12 heading for the liver.

    So we add up all those 3 keyholes from a variety of research, we have 10-30mcg absorbable by HTC1-IF, we have 10-30mcg transportable by HTC2 in a 24 hour period and we have 10-30mcg of stripped cobalamin being converted via enzymes (of limited supply) to the two active cobalamins as needed, adb12 or mb12. All of these line up according to separate research that has been done many times in many ways with different focuses in each study. Together they pretty well establish a channel capacity of 10-30mcg per day. So they all appear to line up as working with the same approximate range which is what would be expected in a system that has evolved over millions of years in every animal of any description. We run on the same mb12/adb12 as most bacteria and almost every animal. I have found one fish identified as not using that pair but that may be old research with the same fault as the original b12 from beef liver studies, accidental cyanide contamination.

    Consider that so many things start changing around age 40, the age at which most of a person's effect on evolution ends. Even with all my genetic problems and the near fatal choice of becoming a vegetarian I made it to 40. I had fathered all my children. The b12 recirculation system conserves the rarest resource with amazing efficiency. It extracts miniscule amounts from animal proteins, accumlates it and recycles it, over and over. When we die most of us still have some of the b12 that we were born with. It is the rarest resource. It is the ultimate limiting factor for almost all of our bodies' functions. Our biological structures evolved to make use of 2 forms of b12. It evolved to recycle it and even convert it to and from several intermediate forms within the body, even the form that is normally the preferred waste excretion form post cyanide detox. However, many never have enough for optimum functioning and health. We have enough to survive intermittant starvation situations, seasonal food shortages and periods of vegetarian eating but all that comes at the cost of being able to put off many uses until some time in the future when more becomes available after eating the liver of the animal we just killed, the primative hunter's reward.

    At age 40 or so, stomach acid takes a turn downward in many people. By 65 a good 1/4-1/2 of people are b12 deficienct depending upon the conservative criteria used. By the criteria I would use, having a multitude of the symptoms that respond to active b12s, that number is probably more like 80-90%.


    I give my Amazon green yellow nape parrot some mb12 periodically. He responds noticably, talking more and interacting more. The vet has commented on what perfect beautiful plumage he has for a bird of his age, going on 30. His feet also look much younger. Except for the coloration of a mature mid-life bird, he looks quite a bit younger.



    Do you have some reason to think that methyl has some additional way of getting into cells other than via TC, that doesn't apply to hydroxy?

    There is another way for cobalamins to get into cells, and that is diffusion. For that to work requires a steep enough gradiant between the level in the cell and the level in the serum. Consider that if 1mg, 1000mcg were to appear in the serum instantaneously. That puts the serum level at that intantaneous moment at about 200,000pg/ml. Since it is also being excreted by the kidneys at the same time as it is absorbing into serum the actual peak might be more like 100,000-150,000pg/ml. So from here first it diffuses into the cells and mitochondria. To a lesser extent it diffuses into cerebral spinal fluid.

    The difference is, if hycbl diffuses into cells in excess of the amount of enzymes needed to convert it to one of the two active forms at best it doesn't do anything as it is inactive in and of itself. At worst it hinders the diffusion of the active b12s into the cell by reducing the gradiant. On the other hand if adb12 or mb12 diffuses into cells it can be used immediately unchanged if there is any need for it. Many people have noticed the differerences in startup/onset effects between hycbl and mb12/adb12

    You can demonstrate this effect if you are sensitive to startup/onset effects of both active b12s. You can take the "loading doses" of hycbl and presumably saturate the HTC2 system. At that point take a large dose of adb12 and be aware of all the effects. Then an hour later you can take a methylb12 and be aware of a different set of startup responses. If the hycbl were capable of satisfying all the needs for both active b12s there would be no further effect from mb12 or adb12. That so obviously is not the case with most people who then respond quite specifically to each type of active b12, the effect not blocked by some other form of cobalamin.

    Then at a certain point in the dose increment there is suddenly a new response. This appears to correspond to the diffusion of active b12s inrto the CSF and has a sharp line of demarcation in most people who have that effect. For me that line is >6mg sc and <= 7.5mg sc of mb12 or adb12. It can cause immediate neurological changes which are not apparant with equivalent doses of hycbl.
     
  20. Freddd

    Freddd Senior Member

    Messages:
    4,545
    Likes:
    913
    Salt Lake City
    Hi Soulfeast,


    Non-methyl-B12 forms of B12 work well to correct a true B12 deficiency

    If only that were true. It isn't. It is oft repeated but not true. Unless one defines "true B12 deficiency" as only that which responds well to cycbl or hycbl and ignore 2/3 of the symptoms and 90% of the people with them, which then creates a whole lot of mystery diseases with no treatments. However, those using mb12 for treating autism don't consider autism to be "true b12 deficiency". I have no idea what autism actually consistis of.

    Only methyl-B12 has a key to the prison and therefore is not bound to the prison-B12 rules. Only methyl-B12 has the freedom to bypass the need to receive its methyl group from MTHF. Only methyl-B12 has its own methyl group to pass onward to homocysteine. Therefore only methyl-B12 has the ability to act more quickly and more efficiently than other forms of B12.

    That on the other hand is true as far as it goes. Adenosylb12 also is not bound to the prison b12 rules either. It takes it's actions directly when and where needed without necessity of being changed first.
     

See more popular forum discussions.

Share This Page