P2P, or not P2P, that is the question
As the 16 January, 2015 deadline for responding to the controversial P2P draft report draws near, and in the interests of balance and representing the whole community, Phoenix Rising presents two differing views on how to react. Today, Clark Ellis flags up important content to...
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. surfbh

    surfbh

    Messages:
    8
    Likes:
    0
  2. Vegas

    Vegas Senior Member

    Messages:
    575
    Likes:
    717
    Virginia
    Good information. Thanks for posting. I have had similar experiences with Betaine. A little is fine; a lot is counterproductive. I think the same can be said for NAC, and I doubt small amounts are going to be harmful. Nevertheless, I agree that the NAC is not a vital component and should be used very carefully; getting the methylation process back on line should achieve much better results. Also, while I don't think NAC (at least in relatively low doses) actually interferes with methylation per se, it definitely mobilizes "stuff," as evidenced by the consistent symptomatic response--brain fog and fatigue. I just assumed that the mobilization of toxins reduced availability of the glutathione. Methylation protocols certainly require one to find the right balance between stimulating the chemical processes too little versus too much. Too little and you don't make any progress, too much and the glutathione deficits can cause short term regression of core symptoms and obviously intolerable detox superimposed on that. I feel like intermittent large doses have been helpful despite the intense detox, but I speculate that one would have to reach a certain condition (perhaps commensurate with glutathione status) before such an aggressive approach should be undertaken. Of course this is a relative term since large doses to me represents 2-3 mg of sublingual methyl. How long did it take you to work up to those dosages of methyl and adenosylcobalamin?
     
  3. surfbh

    surfbh

    Messages:
    8
    Likes:
    0
    We actually quit caffeine (took 1-2 pills a day for years) and quit Zyrtec-D with (pseudoephedrine) the day we started Methyl B-12. And we had NO problems. Started with 4-6mgs a day sublingual MB12. A week later we received Source Naturals Dibencozide (adenysylcobalamin) and started taking 20mgs a day. Right now we take 10 mgs Dibencozide + up to 2 mgs more in their Coenzymated B Complex, 5mgs Jarrow MethylB12 and 1 mg MethylB12 shot per day. We also have MethylMate nasal spray but don't use it right now. Just got the Carnitine Fumurate, 500mgs seems stronger than a few grams of Acetyl Carnitine to me. Anyways, just started not even 4 weeks ago, worst part is sometimes a little brainfog! Take care of that with DMSA though. My best suggestion is to add the Source Naturals CoEnzymate B Complex sublingual. I have given some to several friends and they all wind up ordering it right away.
     
  4. bluezone

    bluezone

    Messages:
    8
    Likes:
    0
    Can someone please help me as I seem to have unknowingly raised my glutathione levels by taking dhea 10mg for 3 days. Whilst my brain fog and all of my mcs symptoms seems to have disappeared, I am once again getting horrible b12 deficiency symptoms. Only recently have I discovered that dhea raises glutathione. Ive now stopped taking the dhea and looking for a way to lower my dhea. Ive tried injecting myself for three weeks now with methylcobalamin 5mg/ml with very little success. Does anyone have any bright ideas? The other problem I seem to be having is sourcing some methylcobalamin in the UK; I have found a source, but it is extremely expensive:(((. Finally I take 4800mcg of folate along with my b12 shot; is that the right amount to take? Should I take the folate on an empty stomach and wait 30mins before I inject??? Any answers to any of these questions will really be helpful!!!
     
  5. cigana

    cigana Senior Member

    Messages:
    832
    Likes:
    537
    UK
    Hi,

    For those of you (Vegas?) who seem to get a reaction to NAC it might be worth considering CPn infection.

    There are a bunch of PWC's on a UK forum who have made significant improvement by treating this, their forum poll gives as impressive results as the Methylation and B12 protocol polls on this forum.

    The (long) thread is here: http://www.foggyfriends.org/forum/showthread.php?18001-I-am-cured

    They get "detox" reactions from taking NAC as it somehow treats the CPn.

    More info on CPn in CFS can be found here:

    http://www.cpnhelp.org/chlamydiapneumoniaechronicfatigue

    Best wishes,

    Cig
     
  6. surfbh

    surfbh

    Messages:
    8
    Likes:
    0
    I take both an injectable MB12 and Jarrow MB12 5000. The Jarrow seems just as good, if not better (1 a day) as the 1 mg injection, and much cheaper. If I were you I would try SAM-E to fix your situation, then stop it to see if it is fixed and repeat. Personally, I wouldn't stay on SAM-E unless absolutely necessary.
     
  7. surfbh

    surfbh

    Messages:
    8
    Likes:
    0
    I read this thread in its entirity in two weeks and it's dead? What happened to Freddd? I believe I have something that WILL help his healing.
     
  8. richvank

    richvank Senior Member

    Messages:
    2,716
    Likes:
    787
    Hi, surfbh.

    I don't know why freddd has not been posting lately. I hope he's O.K. He dropped out for an extended period once before, and then came back on. He may still be posting at the WrongDiagnosis forum. I can't say for sure, because I don't monitor that one, but I know that it was one of his main sites for posting in the past.

    It's pretty amazing that you got through this whole thread! That in itself could probably produce CFS!! :)-)

    I hope the methylation treatment continues to help you to improve your health status.

    Best regards,

    Rich
     
  9. kerrilyn

    kerrilyn Senior Member

    Messages:
    246
    Likes:
    2
    If you are trying a methylation protocol why would taking L-Glutamine be discouraged? It is recommended for Leaky Gut, and lists a number of benefits but is not recommended in this thread. I don't think I actually found an answer to that. A couple people mentioned problems taking it.

    Also, can you give me some insight into it and glutamate and excitotoxicity? I found a good link about it but I think I need it dumbed down a bit at the moment. Thanks
     
  10. cfsbear

    cfsbear

    Messages:
    9
    Likes:
    0
    Hi Kerrilyn,

    I think the answer is found on Freddd's updated summary page at the following site:
    http://forums.wrongdiagnosis.com/showthread.php?t=62327

    Here are two relevant sections:

    You might want to reread that entire section even though it has much of the same information as the first post in this thread because it is updated and the first post in this thread is frozen in time.

    CFSBear:cool:
     
  11. Vegas

    Vegas Senior Member

    Messages:
    575
    Likes:
    717
    Virginia
    I've taken glutamine for long periods of time, in moderate dosage, without any adverse effect. I cannot say how much effect glutamine has had on the leaky gut, but I'm certain the methylation protocol has helped immensely. Right now I'm taking whey protein, which of course includes a host of aminos including glutamine. Aside from a mild headache I haven't appreciated any other deleterious sequelae. My experience is of course only a singular experience, and I haven't been using the whey that long, so take it with a grain of salt. Nevertheless, I think the whey powder is giving me more stamina. By the way, I take it with methylcobalamin, and the active folates.

    As for adverse reactions to whey protein, glutamine and other glutathione precursors, I would be interested in hearing what others have experienced. I could certainly see people experiencing unpleasant side effects caused by the sulphur metabolism inefficiencies, but I would surmise that after one gets these pathways working better, one can tolerate the precursors much more easily. This is purely my speculation based upon the fact that my sulfite headaches have diminished over time.
     
  12. richvank

    richvank Senior Member

    Messages:
    2,716
    Likes:
    787
    Hi, kerrilyn.

    I'll take a shot at explaining this, also, for what it's worth.

    First, it's a fact that glutamine is the main fuel for the enterocytes, the cells lining the small intestine. (It's also important for fueling the lymphocytes and the fibroblasts in the body.) Some PWCs report that it helps with their gut issues. Glutamine has been used in large dosages for treating gut problems independent of ME/CFS.

    Other PWCs find that glutamine supplementation causes them problems. I think there are two hypotheses that have been suggested.

    1. Dr. Amy Yasko has suggested that because glutamine is readily converted to glutamate in the body, it can contribute to excitotoxicity, which can be a problem for people with autism and ME/CFS, particularly when they undertake treatment of the methylation cycle partial block.

    In excitotoxicity, the neurons in the brain that have so-called NMDA receptors (one of the types of glutamate receptors, named after N-methyl D-aspartate) become overactivated. The symptoms of excitotoxicity are anxiety, insomnia, a "wired" feeling, and hypersensitivity of the senses. (Actually, NMDA itself is not usually present in the body, but it has been found to be a specific stimulant for this type of glutamate receptor, so that's why the receptor is called the NMDA receptor.) Note that glutamate is the main excitatory neurotransmitter in the brain. Excitotoxicity, if uncontrolled, can cause death of neurons, so it's important to try to limit it.

    Why does excitotoxicity often become worse when a person starts methylation treatment? I have a hypothesis for that. First, it's known that normally, after a neuron has exported a glutamate molecule into its junction with another neuron (called a synapse), and the glutamate has done its job by stimulating the other neuron via one of its NMDA receptors, then a neighboring astrocyte (a type of cell in the brain that helps the neurons to do their jobs) imports the glutamate, converts it to glutamine, and exports it back to the first neuron, so that it can be converted back to glutamate and used again to excite the second neuron, as needed. Now, here's the hypothesis: If the astrocyte's mitochondria cannot produce ATP fast enough to power the importation of glutamate and its conversion to glutamine, then too much glutamate will stay in the synapse, and this will keep stimulating the second neuron, producing excitotoxicity.

    So, why would methylation treatment cause a problem for the mitochondria in the astrocytes? I suggest that when methylation treatment is started, more of the homocysteine is converted back to methionine, completing the methylation cycle. However, that means that initially less homocysteine will feed the transsulfuration pathway, which contributes cysteine to make glutathione. So glutathione production, already too low, will actually go lower at first, and this will worsen the oxidative stress temporarily, which will worsen the mitochondrial dysfunction. In the long run, methioniine will rise, and the sulfur metabolism will become more normally regulated, so that the glutathione level will rise, and the mitochondrial function will improve, but in the short term, the mito function gets a little worse.

    Recently I have suggested that it might help to boost glutathione a little in this early stage, such as with one of the liposomal glutathione supplements, or by taking one of the nondenatured whey protein products, if they are tolerated. These include Whey to Health, True Whey, ImmunePro, and RenewPro. I haven't heard from anyone who has tried this, to find out if it actually helps with the excitotoxicity.

    2. freddd has reported on this thread that he and several others have found that adding glutathione or amino acids that go into making glutathione, including glutamine or glutamate, to his protocol, which includes high dosages of methylcobalamin, causes a reversal of the benefits of the treatment, and he does not recommend adding them.

    Here's what I think is going on in that situation: freddd himself has reported that he has an inborn error of metabolism (a genetic defect) involving the intracellular B12 processing enzymes. His cells are not able to use cyanocobalamin or hydroxocobalamin very well to make the coenzyme forms of B12 that the cells need (methylcobalamin and adenosylcobalamin). So he has found that by swamping his body with high dosages of the coenzyme forms via sublingual supplementation or injection, his cells can apparently get enough of these coenzyme forms directly by diffusion from the blood into the cells, so that the normal B12 metabolism is bypassed. Now, when he adds glutathione or the ingredients that help his body to make more glutathione, apparently what happens is that glutathione reacts with the methylcobalamin to form glutathionylcobalamin, and then his cells are not able to convert it back to methylcobalamin. It is known that glutathione will react readily with methylcobalamin, and it is also known that glutathione is normally involved in the B12 metabolism in the cells, at an intermediate step between the normal import of various forms of B12 and its final conversion to the two coenzyme forms. Normally, glutathione performs a protective role for B12 at this intermediate stage. In the GD-MCB hypothesis for CFS, which I've proposed, depletion of glutathione is actually the thing that allows B12 to be hijacked by reacting with toxins, and that is what brings on the partial block in the methylation cycle and ultimately, CFS itself.

    But in freddd's case, and apparently in the cases of several others who have used his protocol. boosting glutathione is actually detrimental. One possible reason is the genetic issue that freddd himself has reported having. Perhaps some others on his protocol have this issue as well. But for people who do not have this genetic problem, I don't think that supplementing glutathione would be detrimental. and may be beneficial, as I've suggested above. The reason I've suggested liposomal forms as something to try is that I think they are more likely to deliver glutathione to the cells with a minimum of raising glutamate than are other approaches. Thus, I think they are more likely to help with the excitotoxicity problem, rather than to make it worse. But so far, I don't have any results as to whether this works.

    I hope this is helpful. I do need to add, as always, that people doing the methylation treatment need to be working with a physician, because in a small number of cases, serious adverse effects have been reported by people trying this treatment.

    Best regards,

    Rich
     
  13. Glynis Steele

    Glynis Steele Senior Member

    Messages:
    402
    Likes:
    85
    Newcastle upon Tyne UK
    Hi Rich,

    I hope you don't mind, but I've PM'd you with a recent study where it is stated that d-lactic acid may inhibit the supply of energy from astrocytes to neurons. If anyone else is interested, please let me know and I will post it.

    BW

    Glynis
     
  14. susan

    susan Senior Member

    Messages:
    269
    Likes:
    14
    Gold Coast Australia
    Hi Rich,
    Several in our group have had the Metametrex urine test and being treated by and expert in methylation.....few have improved. One only needed methyl b12...no need for folinic acid but it has made No difference in 8 mths. She has no intrinsic factor. Would you have any suggestions. Would she be lacking the enzymes. Would the urine test reveal that info.

    I am trying a nasal spray of b12/folinic acid as I have developed sensitivities once I get to 1/4 of folinic acid.

    Susan
     
  15. aquariusgirl

    aquariusgirl Senior Member

    Messages:
    1,047
    Likes:
    166
    glynnis, pls post the study. thanks.
     
  16. Glynis Steele

    Glynis Steele Senior Member

    Messages:
    402
    Likes:
    85
    Newcastle upon Tyne UK
    Here are 2 studies, however they are in rat and chick models, not human, and I can only access the abstracts, the articles may be purchased online.

    Increased plasma d-lactic acid associated with impaired memory in rats.
    Hanstock TL, Mallet PE, Clayton EH.

    School of Behavioural, Cognitive and Social Sciences, University of New England, Armidale, NSW 2351, Australia.

    Abstract
    AIM: d-Lactic acidosis is associated with memory impairment in humans. Recent research indicates that d-lactic acid may inhibit the supply of energy from astrocytes to neurons involved with memory formation. However, little is known about the effects of increased hind-gut fermentation due to changes in diet on circulating lactic acid concentrations and memory.

    METHOD: Thirty-six male Wistar rats were fed three dietary treatments: a commercial rat and mouse chow, a soluble carbohydrate based diet or a fermentable carbohydrate based diet. The parameters estimating memory were examined by employing the object recognition test. Physical parameters of fermentation including hind-gut and plasma lactic acid concentrations were examined after sacrifice, either 3 or 21h after feeding.

    RESULTS: Increased fermentation in the hind-gut of rats, indicated by lower caecum pH, was associated with increased plasma l-lactic acid (r=-0.41, p=0.020) and d-lactic acid (r=-0.33, p=0.087). Memory, being able to discriminate between a familiar and a novel object during the object recognition test, was reduced with increasing plasma d-lactic acid (r=-0.51, p=0.021).

    CONCLUSIONS: Memory impairment was associated with alterations in plasma d-lactic acid following the fermentation of carbohydrate in the hind-gut. Further work is still required to determine whether these effects are mediated centrally or via direct connections through the enteric nervous system.



    Inhibition of astrocytic energy metabolism by d-lactate exposure impairs memory




    References and further reading may be available for this article. To view references and further reading you must purchase this article.


    Marie E. Gibbsa and Leif Hertzb, ,

    aDepartment of Anatomy and Developmental Biology, Monash University, Clayton 3800, Australia

    bCollege of Basic Medical Sciences, China Medical University, Shenyang 110001, PR China

    Received 9 July 2007; revised 21 September 2007; accepted 19 October 2007. Available online 26 October 2007.

    Abstract
    Bead discrimination learning in day-old chicken was inhibited by bilateral injection into the intermediate medial mesopallium (IMM), a homolog of the mammalian brain cortex, of the poorly metabolized enantiomer of l-lactate, d-lactate. The window of vulnerability extended from 10 min before training to 20 min after training. Unilateral injection 10 min before training inhibited only in the left IMM, whereas 10 min after training injection was only inhibitory if made into the right hemisphere. The pre-training administration caused memory loss from the earliest time tested whereas memory was maintained for another 20 min when d-lactate was injected 10 min post-training. The ability of acetate, an astrocyte-specific substrate, injected into the IMM to counteract the inhibitory effect was tested. Following d-lactate injection 10 min before training, rescue of memory immediately after training was achieved by acetate as long as aspartate, an oxaloacetate precursor, was also present. This suggests that pyruvate carboxylation is necessary for net synthesis of glutamate, which is known to occur at this time [Gibbs, M.E., Lloyd, H.G.E., Santa, T., Hertz, L., 2007. Glycogen is a preferred glutamate precursor during learning in 1-day-old chick: biochemical and behavioral evidence. J. Neurosci. Res., 85, 3326–3333]. However, acetate alone rescued memory 20 min post-training (following d-lactate injection 10 min after training), indicating that pyruvate at this time is used for energy production, consistent with memory inhibition by dinitrophenol. These findings suggest that d-lactate acts by inhibiting uptake of l-lactate into astrocytes (an extracellular effect) or metabolism of pyruvate in astrocytic mitochondria (an intracellular effect). An apparent lag phase between the administration of d-lactate and its inhibition of learning favors the latter possibility. Thus, under the present experimental conditions d-lactate acts as an astrocytic metabolic inhibitor rather than as an inhibitor of neuronal l-lactate uptake, as has occasionally been suggested. Analogously, a rare reversible neurological syndrome with memory deficits, d-lactate encephalopathy, may mainly or exclusively be due to astrocytic malfunction.

    Hope these are useful.

    BW

    Glynis
     
  17. Glynis Steele

    Glynis Steele Senior Member

    Messages:
    402
    Likes:
    85
    Newcastle upon Tyne UK
    Oops, forgot to add that d-lactate encephalopathy is another name for d-lactic acidosis.

    Glynis
     
  18. Lee Ann

    Lee Ann

    Messages:
    84
    Likes:
    9
    Tennessee
    Hello,
    This is such a long thread, I am more confused than ever. I live in a very small town and can not find a pharmacy that compounds methb12. I am using the hydroxb12. It was last year when I was told I was b12 deficient and started the Cb12. The effects were dramatic. At the time, I could only get a shot monthly. Now I have a doctor who prescribed Hb12 every other day. So, is this a waste of time since the Mb12 is supposedly superior? I'm really lost. Thanks
     
  19. velha508

    velha508

    Messages:
    64
    Likes:
    4
    Hi Lee Ann,

    What you want to do is read the active B12 thread - this is where the protocol information is, this thread is for posting questions about that protocol. Read it in it's entirety, many times if necessary, there is a lot of useful information there.

    From my experience, and others, a quality mB12 supplement is better than injections of hydroxyB12. Cb12 is typically not helpful to most and detrimental to many.

    mB12 is very light sensitive and thus manufacturing practices can make a difference in the quality of the supplement - two reliable brands of sublinguals are Enzymatic Therapy and Jarrow Formulas.

    Also, most of us do not get our injectable mB12 from a local pharmacy, due to the sensitivity to light, liquid mB12 very readily turns to hydroxyB12 and proper handling is essential. I use Hopewell Pharmacy in NJ, they ship it to me with a cold pack and I've found their product to be acceptable (been using it daily for 1 year).

    Finally, mB12 is very typically not enough, there are many other important nutrients that come into play in order to heal from CFS, basic vitamins (A, B's, C, D, E, etc.), other active vitamins - B-right, adenosylB12, methylfolate, and some mitochondrial co-factors that can be critical for some (carnitine fumarate, d-ribose, sam-e, etc..)

    Read the information in this link in detail and come back here and post any questions you have.

    Active B12 basics thread:

    http://forums.wrongdiagnosis.com/showthread.php?p=191131&posted=1#post191131


    Don't know why the link isn't working but I copied and pasted it into my browser and it worked that way...

    I followed this protocol for over a year now and I'm doing very well. Can work a full time job, care for young children and still have energy left over to shop and do errands - prior to starting I was on medical leave from work and almost never had any energy to go out of the house, my situation had gotten fairly bad...

    Good Luck,
    Velha
     
  20. CindyWillis

    CindyWillis Senior Member

    Messages:
    110
    Likes:
    53
    I have a bad rash like you described in relation to milk thistle or anything with it in it. If you are taking that, try stopping and see if the rash goes away. When I get the rash it has so far always been an allergic reaction to something I am taking. I try to start things one at a time so I can see which makes me allergic and which don't .
     

See more popular forum discussions.

Share This Page