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What are people's thoughts and doses of adb12?

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by dbkita, Jan 11, 2013.

  1. dbkita

    dbkita Senior Member

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    My question is in the title. But specifically (and all theory aside please) what do you feel it does for you clinically whether in a positive or a negative way.

    Personally I find a 1/4 tablet of adb12 (Source Naturals Dibenzocide) every day to produce some odd effects. Like weird metallic taste, sometimes initial fatigue but wired at night, increased sensation of thirst, etc.

    I am doing better on 1/8th tablet I think, but I still wonder if every day is too much.

    How much do people on these forums take? Does it help you? How? Does it hurt you? How? What brands, etc.

    Those who reply can debate the theory but I have looked at a lot of that and I understand it for the most part.

    I am more interested in clinical results.

    Thanks ahead of time.
  2. Phred

    Phred Senior Member

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    Hi dbkita,

    You and I have discussed privately the metallic taste and dry mouth I had. I'm quite certain it was from something other than the adb12 I take. I take the 1/4 tab of Source Naturals Debnzocide every day. I've been doing this for several weeks now. The metallic taste I had was only for a few days and has since gone. I'm still taking my adb12. So for me, that metallic taste was definitely something else. Unless the adb12 is working in conjunction with something else I dropped to make that taste. Don't know.

    It doesn't interfere with my sleep. The first couple of times I took it (although I took a whole tab at once about once a week) it made me more wired.

    I'm quite certain it is responsible for the muscle mass I have developed. I remember wondering, many months ago, where the hell all my calf muscles had gone. I've done nothing different in the past few months, but noticed I suddenly had my calf muscles back. I also have some bicep and tricep muscles starting. I have not lifted one weight to get those. I'm not even doing the banquet work I once did, so there really is no reason for the muscles to be developing now. But I gotta say I'm happy they are.

    Oh, and the muscles didn't start developing until I started taking the adb12 daily. Hope that answers the questions you asked. :)
    Phred
    Michael likes this.
  3. pela

    pela

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    I took a whole Source Naturals daily for some time with good results. I cut back to half a tablet daily because I thought I should, and had less energy as a result. I am currently taking half a capsule of Anabol Naturals Dibencoplex daily with about the same result as a whole Source Naturals. Sometimes a whole Anabol. No adverse effects of any kind. No metallic taste, no jitteriness, although initially I needed extra potassium. I think I was really deficient! I also am gaining muscle but I am not sure if this is due to the ADB12 or due to the fact that my body is making much better use the the thyroid hormones I take. I atttribute the better conversion of thyroid to B12. I've been on Freddd's protocol for about 8 months.
  4. dbkita

    dbkita Senior Member

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    What thyroid meds do you take Pela and what dose? Just curious.

    Also how much mb12 and methyfolate?
  5. LaurieL

    LaurieL Senior Member

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    I started the methylation protocol in 2010 to current. I used the recommended supplements at that time when I started, Solgar methylfolate, Jarrow methylcobolamin, and Country Life Dibencozide. Prior to my beginning, I was and had been supplementing the recommended supportives, also to current. I also took the recommendations of Freddd, to start each one separately to observe reactions.

    I started with the methylfolate, and at that time my decision was based purely on my history of folate inhibiting antibiotics I have been on and off of for most of my life. Two weeks after starting the methylfolate, I added the Country Life dibencozide.

    I am also one in which needs high doses daily. I can tell you exactly what it did/does for me. I believe if I remember correctly, it was two days after I started, and I was driving at night. I was floored at my vision. It was like a filter had been lifted, and colors became very bright to me and the lines were very sharp. It was very overwhelming at the time.

    I remember just sitting at a stoplight while the green light came on, and just staring at it. It was so green and so bright. (I don't do that anymore...hehe) But two years later I am still amazed that I just didn't notice it. After a few months, I had to stop the Country Life brand, as I discovered that the folic acid it contained was affecting my menstrual cycle. It stopped. Don't get me wrong, I didn't mind that aspect, but it was abnormal. I switched to Source Naturals 8.6 mgs, and I still take it daily. My body demands it, insists on it, and does well with this.

    Methylation was the beginning of my journey. It has not been the end.

    Lauriel
    Seewell likes this.
  6. dbkita

    dbkita Senior Member

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    So let me make sure .. you take 8.6 mgs of adb12 daily sublingually? Just checking.

    Can I ask how much mb12 and methylfolate you are taking as well?
  7. LaurieL

    LaurieL Senior Member

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    Yes. 8.6 mgs of Source Naturals adb12 sublingually. I have a 2000 mcg minimum requirement of methyl b12 daily and my methylfolate requirement has gone down to 800 mcg daily. When I started the methylation protocol those requirements were very much higher. I had a high demand in the beginning and the demand has tapered over time. I had some neurological healing and when that was accomplished, the need wasn't as great, again except for the ad b12.
  8. pela

    pela

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    I was taking T3 only thyroid as I could not convert T4. Now I am taking natural dessicated thyroid which is a T4/T3 combo, with good results.

    I take 8400 mcg of folate. If I lower the dose, I get canker sores. I take 5-6 Enzymatic T B12, and usually I am trying some lesser brand of MB12 as well.
  9. LaurieL

    LaurieL Senior Member

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    When I started, my dosage of methylfolate was 8400 mcg as well. My methyl B12 was through the roof as well, I either had to take 30,000 or 60,000 for noticable change. Between 30,000 and 60,000 there was no noticable difference. Quite a drop aye? (We can talk about overdriving the system some other time as it was my intent)

    I always liked the Jarrow methyl B12 and I got concerned when they changed it. I only noticed it because the color is different and I went through a short lived increase in neuropathy, although that has resolved without my changing the dosage. I am watchful. I also had problems with the acidity and my teeth with the "old" product, so I chewed these into small pieces and then put them up between my gums on my upper deck. This allows the same dosage to diffuse more rapidly than a small tablet over hours. This method worked very well for me. I just can't afford to walk around looking like I am chewing tobacco....or a chipmunk...:/

    We had discussed in the past that the time allowance makes a difference in the bodies ability to absorb and use it. Both occurring together, interdependent. I have been questioned in the past as to kidney insufficiency, and to date, I have none. I was also questioned about my urine color. At those doses it should have been pink, and was and still is not. Hence the questioning of my kidney status.

    Considering the amount of neurological and peripheral neuropathy healing I have gone through, I don't believe my body let those doses go. What stumps me is the demand for high doses of adenosylcobalomin. The rest went way down, but not this one.

    Lauriel
  10. place

    place Be Strong!

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    Laurie's
    You have an interesting story. What was your starting functional level, and what is it now? Is everything resolved?
  11. LaurieL

    LaurieL Senior Member

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    When I first became ill, it was bedridden status. I have slowly climbed the ladder in 7 years. When I started the methylation protocol, I was a 3 to 6 depending on the day. With methylation in place I jumped to 7-9, with 7 being more frequent. And I am now a solid 9. I can't seem to kick the infection. That is my last hurdle. I only believe I am controlling it, and my status would drop if I stopped the supplementation. I do more than just the methylation protocol. I am forever trying to keep my gut/sinuses in line, although it has become much easier of late.
  12. LaurieL

    LaurieL Senior Member

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    I was thinking that perhaps my ACAT +/- status may have an impact on my bodies need for high dose adensylcobalomin?

    Does anyone know right off hand, the multiple pathways that directly need Ad B12?
  13. dbkita

    dbkita Senior Member

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    Adb12 is used in several reactions but one very significant and relevant one is the methymalonyl pathway that enter the Krebs cycle at the succinyl-COA branch. This can prevent pile-ups of the Krebs cycle at AKG (?).

    What happens if you take less adb12? Do you get tired or muscles weaker?

    I don't clearly see the connection to ACAT (Acetyl CoA transferase). You are heterozygote which means you have some functionality. However, Yasko puts high priority on ACAT in her treatment hierarchy and one of the things she uses is adb12. So that too has impact on the Krebs cycle but from the front end.

    How do you respond to benfotiamine, riboflavin, and pantothenic acid since they too are cofactors at the front end of the Krebs cycle. You might also consider 300 mg or so of alpha lipoic acid according to Dr Yasko.
    Lotus97 likes this.
  14. LaurieL

    LaurieL Senior Member

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    Yes, but also neuropathies, numbness, tingling, and then intolerance to cold, sensitivity to bright light, changes in color vision and clarity, malaise, loss of position sense, gait failures, balance, headaches, and.......................

    Yasko has three first priority mutations, 1) SHMT, 2) ACAT, and 3) CBS. I have hetero mutations in all three as an aside.

    I believe the connection of ACAT and adenosylcobalamin lies in the final steps of cobalamin synthesis. The propanol side chain and the nucleotide loop that links to the corrin ring. Those with ACAT mutations are also highly correlated with chronic dysbiosis. Something I constantly have to address. I think its this dysbiosis, and either the interference of the synthesis of adenosylcobalamin, or the lack of the bacteria in which are known to produce it, or finally, an overgrowth of bacteria in which steal it.

    Incidently, ad b12 also affects nucleotide assembly. Which is where the SHMT being partially functional could add to my problems, and why so many with ACAT mutations are recommended to supplement nucleotides. Certain bacteria's are known to steal nucleotides for there own use or their metabolites interfere with our own production.

    I believe ACAT interferes with those steps above, and two involve the formation of adenosylcobalamin and then the activation of adenosylcobalamin. What do you think? I am not an expert in this particular area.

    To add....ACAT mutations can result in B12 deficiencies as can a few other mutations. Considering my responses to both forms of active B12, I would say there is something wrong in my adenosylcobalamin side. Whether it be the formation of, or the activation of, I have not been able to determine as of yet.

    It is interesting that you would ask, as these were supportives I found incredibly beneficial prior to my methylation attempts and already had on board when I started. I had to up my B2 in response to inappropriate proteins. I have taken ALA off and on as well. I am currently low dose. Interestingly enough the herbs I found to help control NFkappaB to be queceritin and turmeric a derivative of curcumin, also found beneficial in ACAT mutations.

    As far as the hetero status, I haven't heard of anyone being homozygous, as that would be fatal, early on, manifesting as MMA aciduria. A death sentence if not caught. I am not an expert, and sure would like some input. I like to group think.

    Lauriel
  15. adreno

    adreno 3% neanderthal

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    That's interesting. Would inosine be a good option as a nucleotide supplement for ACAT? Or perhaps RNA? I do not seem to tolerate the adb12 very well, and it doesn't seem to improve my energy either.
  16. adreno

    adreno 3% neanderthal

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    I think this could be why my pyrovate is high? I have ACAT snp, so I guess I'm not converting it well to Acetyl CoA?

    http://dramyyasko.com/wp-content/uploads/2010/06/35-A1-ACAT.pdf

    Wish I understood these things better. I have upped my benfotiamine to 600mg. Can I use pantethine for this (300mg now) or do I need pantothenic acid specifically? I better up my riboflavin also, only at 10mg R5P presently. Already take 300mg R-ALA. Will the AKG help here?
  17. dbkita

    dbkita Senior Member

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    Sorry I should have clarified: I meant I don't see the connection to needing 8.6 grams of adb12 and your heterozygote ACAT mutation in my earlier post.

    I have seen the heartfixer and read Yasko's treatment book and seen some of her online presentations so I understand she has a careful queue priority for treatment.

    I too have chronic dysbiosis but am unaware of any ACAT mutation so while I am not sure the correlation is bi-directional. Gut dysbiosis is quite the menagerie of problems.

    You might ask why a heterozygous ACAT can not by itself be the problem ... well my hypothesis is based on statistics. The same holds for SHMT.

    Basically far too many people are heterozygous for ACAT or SHMT.

    Here is an web site with the observed frequency of ACAT1 rs3741049 SNP (I think this is one Yasko tests).

    http://browser.1000genomes.org/Homo...08010427;v=rs3741049;vdb=variation;vf=2818389

    Note the AG genotype for the first row for ALL (not race specific) is a whopping 24.2. Even the AA homozygote is >4%.

    As a physicist turned bioinfomaticist, that the 24% number is WAY too high to support a severe problem which would then be afflicting large chunks of the population. Hence I would not think a heterozygote for ACAT would be so detrimental if looked at in isolation.

    So I still don't see the connection to ACAT ... though the clinical benefits for you are clear. Can't argue with that :)

    Now for the SHMT SNP (rs1979277).

    The data for that is here:

    http://browser.1000genomes.org/Homo...18232596;v=rs1979277;vdb=variation;vf=1551359

    Now the AG heterozygous genotype is even higher at 33%!

    So the odds of a heterozygous individual for both SHMT and ACAT is about 8%. At 1 in 12 people roughly that is still
    a really large number. Contrast that with someone who is homozygote in both mutations and now you are talking something closer to 0.3%.

    I understand Dr Yasko places these SNPs at high importance in her treatment protocol but she does not do a good job at all imo in her nutrigenomics protocol of distinguishing heterozygote from homozygote in terms of phenotype impact and in genomics that is a HUGE deal. Let's remember she started her protocol with children with autism who probably really are homozygote in one, two or more key SNPs. Even then things can be murky due to all the complexity.

    Do you have a source for the nucleotide direct synthesis link?

    The reason I ask is I know adb2 is directly involved in the synthesis of deoxyribonucleotides (as an intermediate to DNA nucleotides) via class 2 ribonucleotide reductase and 5'deoxy-adb12 but that class is only for bacteria to my knowledge. Eukaryotes use class 1a which uses iron.

    But maybe I am missing something

    Fair enough but again you are heterozygous for ACAT so not sure how that explains it. But I understand what you are saying about the importance of both active forms of B12 (mb12 and abd12) to you ... would just love to know why!

    Remember that the key step to convert the methylene intermediate into 5MTHF is catalyzes by riboflavin-5-phosphate so maybe B2 helped you in other ways as well.

    Quercetin and turmeric are very important as anti-inflammatory agents. If you have read this thread:

    http://forums.phoenixrising.me/inde...min-the-very-large-gorilla-in-the-room.20229/

    you will see there is a link of BH4 and adb12 to lowering inflammation. It was hypothesized that this involves NO
    and its other variants being better modulated. Ironically this suggests that for people with lower BH4 due
    to ammonia issues (CBSers) or people with MTHFR A1298C (like myself) that there may be further compromising
    of BH4 status if adb12 is supplied. But I am not sure it may be BH4 for some that is the rate limiting agent. Not clear.

    Ironically for me on prednisone and medrol, use of quercetin gives me insomnia since it also slows down COMT
    catabolism while maybe over-lowering inflammation = no sleep!

    Have to disagree there. According the data I linked 4.4% of the population is homozygote. That would be the leading cause of mortality in infants / children in the developed world. I am sure it is bad but it suggest homoygote in ACAT1-02 still has some activity.

    -------------------------

    On a separate note remember though that 8.6 grams is not what is absorbed sublingually regardless how long one keeps it under their upper lip. Though based on other forum posts if absorption is an issue, supposedly other posters claim the Anabol diboceplex adb12 works much better than Source Naturals.


    Thought provoking discussion topics you raised though. Most fun on a reply I have had yet. You made me work my bioinformatics "muscles". Thanks :)
    adreno likes this.
  18. dbkita

    dbkita Senior Member

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    What does it do to you when you say you don't tolerate it? This is exactly the type of response I would love detail on.
    I find that not everything with adb12 is roses with me either. Too much seems to mean too much 'wired' mentally later on plus some other things I mentioned above.
  19. dbkita

    dbkita Senior Member

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    Are you heterozygous for the ACAT? If so it would impact your conversion but not maybe as much as to explain your result.

    Other factors can be LDH activity, biotin, TPP (thiamine pyrophosphate), and B5 (pantethine should be fine).

    And yest 10 mg R5p is probably too low.

    Personally 50 mg riboflavin and 50 mg r5p sodium seem a bit too much for me with some overstimulation. But taking only 100 mg riboflavin all at once is not maybe enough since the body's absorption above 30mg in the gut is no longer
    linear and saturates quickly. But given my experience with 50/50 I am reluctant to jump on that yet ...

    Not sure about the AKG yet. It is a krebs cycle component. Have you ever had your Krebs cycle tested? Is there a pile-up?

    My own results from 2010 that I showed Rich Vank were with low normal to low citric acid, cis-aconitic acid, and isocitric acid BUT middle of the range AKG and massively high glutamate (intraconversion and no glutathione drain at that time). But succinic acid was way low and malic acid was undetectable. Rich wasn't sure why that was happening but apparently pile-up at AKG is one of the three choke points. Can't remember the other two off-hand.
  20. adreno

    adreno 3% neanderthal

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    It's hard to say for me exactly, because I have only taken them with mb12 and mthf so they might have contributed to symptoms. I guess I simply feel wired and sort of unstable, like it messes up my electrolyte balance or something. Not really sure, but have decided to avoid for now and focus on the mb12. I am not sure I am really convinced about the importance of adb12, but that is probably because I don't understand the biochemistry, lol.

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