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Methionine Synthase

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by Thewonders92, Sep 2, 2017.

  1. Thewonders92

    Thewonders92

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    There appears to be overwhelming evidence that (MS) is in fact a cuproenzyme, leaving me kind of scratching my head at its exclusion or antagonism in any methylation programs, specifically those involving B12/Folate.

    Keep in mind that a long standing copper deficiency results in copper toxicity by nature of coppers role in the body. Blood tests are inconclusive on this matter as high copper in blood serum can be an indicator of any level of inflammation, infection or oxidative stress in the body. A liver biopsy is the only reliable method of determining copper status in the body.

    https://www.ncbi.nlm.nih.gov/pubmed/10350650

    Copper deficient rats saw a 21% reduction in (MS) activity.
    Copper deficient rats saw elevated hepatic 5-methyltetrahydrofolate and homocysteine concentrations.

    https://www.ncbi.nlm.nih.gov/pubmed/17513393
    Copper deficient rats saw a significant decrease in plasma homocysteine.
    Copper deficient rats saw down regulation in BHMT function (MS shortcut).
    Trimethylglycine (Betaine) lowers homocysteine substantially.
    Copper deficient rats saw increased amounts of gluathione.
    This is in contrast to longstanding copper deficiency which eventually leads to increased homocysteine. Shortterm loss of homocysteine through the transulfuration will lead to longterm (MS) dysfunction.

    https://www.ncbi.nlm.nih.gov/pubmed/18472229
    Copper deficient myleopathy is strikingly similar to subacute combined degeneration (SCD) of which B12 is involved.

    http://m.pnas.org/content/101/12/4234.full
    There is indication in a rare case of s-adenosyl-homocysteine hydroylase deficiency that copper dysregulation exists between homocysteine to methinionine, and not pre-homocysteine.
    Ceruloplasmin and copper levels were found to be normal in the case of 30 and 150x fold increases to AdoMet and AdoHcy respectively.
    A lowered demand for homocysteine recycling appears to spare copper.

    http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0076209
    Homocysteine directly antagonizes serum copper levels, preventing the healthy functioning of cuproenzymes.

    Copper, as it appears to be essential to the functioning of methinione synthase, could in a time of infection or stress, be spread far too thin in the body to adequately break down homocysteine, leading to an eventual antagonism of copper, creating a deficiency state alongside a toxic state. Inadequate copper supply will hinder the (MS) enzyme, preventing the breakdown of homocysteine, further increasing the need for copper to break down homocysteine, further impairing cuproenzyme activity until eventually (MS) has lost function creating an exponentially worsened state of copper deficiency in the body.

    Ceruloplasmin is copper dependant and is required to remove copper from the body (histidine seems to serve this same function very well), in cases where ceruloplasmin is impaired, copper will build up in tissues. Increasing the demand for Zinc to create (MT), impairing zinc functions throughout the body, eventually lowering CuZnSOD and causing extreme oxidative stress throughout the body, depleting essential minerals everywhere through a cascading effect.

    In a histidine deficient state, our secondary carrier and eliminator of copper from the body is also impaired, thus a copper and histidine deficient state over a period of time eventually guarantees high oxidative stress, impaired copper function, copper deficiency and toxic levels of copper in the body, impaired zinc function, and overall incredibly impaired methylation cycle.

    Lacking Histidine (powerful metal carrier) SOD, MT and Cp will allow heavy metals to run rampant the body, leading to increased accumulation. These metals also antagonize copper and zinc.

    It seems to me that if a person has been on a methylation protocol for several months and isn't getting better they should consider what methinionine synthase is fundamentally.

    Supplementing or refeeding copper will not correct this deficiency and is incredibly dangerous, as it will reactivate many enzymatic functions that have been shut down or slowed down over time, resulting in an even higher need for copper without any adequate way of removing it afterwards. I'm doing research on carnosine, that's in the general forum if you'd like to these a look, but I've been curious about it in regards to methylation for a while and figured I'd do a quick bit of research on it in regards to methylation.

    My current idea for rebalancing copper and zinc in the body is through the use of Carnosine (histidine is absolutely required for all essential mineral functioning and transportation in the body, including MT, SOD and ceruloplasmin, as well as the chelation of free copper from the body), a balanced diet including copper at adequate levels, TMG at dosages ranging from 3-12 grams per day to temporarily offset the need of copper in (MS) when TMG can do a good enough job meanwhile, and obviously plenty of water and rest.

    I don't believe driving (MS) with folate and b12 is safe in as copper deficient state, though I'm not giving treatment advice here, just outlining my current research.
     
    Last edited: Sep 2, 2017
  2. Thewonders92

    Thewonders92

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    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2671677/
    A study involving the dangers of copper deficiency alongside elevated homocysteine.
    They actually seem to be working under the high serum copper=/=Copper deficiency model, but the results are still the same. They did note that it was interesting how the results came in, I don't really understand the disconnect.

    A copper deficient diet alongside high homocysteine results in high pressure aortic ruptures, copper repletion in rats at the human equivalent of 6mg daily has been shown to significantly treat heart disease in mice.

    Homocysteine also antagonizes and lowers the functioning of cuproenzymes, understanding this makes the idea of forcing methylation through high dose folate and b12, without adequate copper to sustain (MS) function, as well as impaired health globally and lack of cuproenzymatic function could result in severe heart problems. Noted are prolonged QT intervals, arrythmia and pressure buildup damaging arterial lining. I have noticed that some folks who are pushing their methylation cycle end up with general heart issues, or even have to quit because of it, I'm not sure if anyone involved with methylation protocols has had a heart attack though.

    But the danger is there, pushing a cuproenzymes (MS) function to the limit in a copper deficient state will further increase homocysteine and further deplete bioavailable copper, increasing more of a buildup of oxidized copper and oxidative stress without bioavailable copper to manufacture CuZnSOD.

    I want to remind everyone that as simple a source as wikipedia will show you that copper serum testing is pointless and could be taken either way, though for whatever reason this isn't getting through to the majority of medical researchers and family Doctors.
     
    dannybex likes this.
  3. aquariusgirl

    aquariusgirl Senior Member

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    Interesting stuff...& I have only skim read....you should probably email DR Richard Deth @ Nova Southeastern University....world expert in the MS enzyme.


    He always responds .

    I gave thought for a long time that copper & iron dysregulation is at the root of this disease but the testing is lacking
     
    Last edited: Sep 2, 2017
    pamojja likes this.
  4. aquariusgirl

    aquariusgirl Senior Member

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    Also I personally think based on my experience that Mitosynergy copper gets around the issues you are talking about but I would never encourage anyone else to supplement copper.,,,we just don't know enough.


    But I don't think carnosine & TMG is going to do much of anything..,,

    Also did you see my earlier posts ..,Dr Cohen on copper in biofilm? Professor Cooper's copper chelation?
     
    Last edited: Sep 2, 2017
  5. NotThisGuy

    NotThisGuy Senior Member

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    did u ever take normal copper supplements? or did u start with mitosynergy?
     
  6. aquariusgirl

    aquariusgirl Senior Member

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    Only MitoSynergy
     
  7. Thewonders92

    Thewonders92

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    I did yes, I will attempt to make contact with him.

    This does seem very interesting, Mito-synergy I mean, the Niacin binding has me very curious as Niacin is always implicated in overmethylation.

    I'll give it a shot and some research and review it.

    But I'm not really sure how you figure Carnosine will have no result on copper dysregulation. Histidine is required to manufacture most cuproenzymes as well as most mineral dependant enzymes in the body, regardless of whether or not methinionine synthase is a cuproenzyme I would say that carnosine would have some effect on copper metabolism given its metabolite is necessary for copper functioning in the body.

    There's overwhelming evidence to support histidine as both an essential carrier of minerals especially copper, and to chelate and remove them afterwards. I don't know if evidence is even the right word, it's an established medical fact.
     
  8. Thewonders92

    Thewonders92

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    It's a 50/50 chance that you're not in the same boat as myself and Notthisguy in that case, as we are both experiencing pretty severe health effects revolving around copper supplemanation.

    I will try mitosynergy though regardless, it does seem very interesting to me. I'm going to do some research into B3 status and copper, perhaps it's a lack of binding to niacin or some related mechanism that's causing the issues.
     
  9. aquariusgirl

    aquariusgirl Senior Member

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    Yeah I mean I have so much copper stashed away that I will have to chelate. Need heavy hitting solutions
     
  10. Thewonders92

    Thewonders92

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    I'm going to order some today.

    Coincidentally before looking into mitosynergy, I did actually take niacin for the first time today in a few months and have had improved kidney function all day, it's the first time in a week. This does seem very promising.
     
  11. NotThisGuy

    NotThisGuy Senior Member

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    I think I'm gonna order it soon, too.
    Im still left with copper damage, but maybe mitosynergy can resolve this.
     
  12. NotThisGuy

    NotThisGuy Senior Member

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    Its really bad that u split those threads thewonders92.
    It would be easier if everything is in one thread.
     
  13. Violeta

    Violeta Senior Member

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    I followed a group where copper damage was a common concern, and several people tried mitosynergy and their copper problem got worse.
     
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  14. Violeta

    Violeta Senior Member

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    I am looking at copper toxicity/biounavailability again because of post herpetic neuralgia, and I am trying beta alanine and taurine combination, along with small amounts of MegaFood zinc. It's helping the fatigue more than the neuralgia so far. I didn't read this whole thread, I'll do that this evening.
     
  15. NotThisGuy

    NotThisGuy Senior Member

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    why beta alanine and taurine?
     
  16. Violeta

    Violeta Senior Member

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    One controls copper and the other controls zinc, for some reason. I am sorry to be so vague, but every since coming down with shingles my brain is mush.

    Might I ask to all in this thread, I don't know anything about ME, but I just started taking selenomethionine a couple of days ago, I am fairly sure I need selenium, and I had seen that it can be related to sulfur metabolism, but I actually forget what I was going to ask about it. I am rushing to get ready for my first day back at work. If there is anything input that anyone can add, I would be interested.
     
  17. Gondwanaland

    Gondwanaland Senior Member

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    Selenium is needed to convert T4 into T3, and so is copper.

    ETA
     
    Last edited: Sep 6, 2017
  18. Gondwanaland

    Gondwanaland Senior Member

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    I observed that taking carcinine (a modified molecule of carnosine sequesters copper >> worsening of my thinning inguinal joint (copper is needed for cross-linking collagen and carnosine is anti-cross-linking) + my hair gets very white (copper is a co-factor of tyrosinase which generates melanin for hair color)
    http://forums.phoenixrising.me/inde...upps-carnosine-beta-alanine-methylation.50395
     
    Last edited: Sep 6, 2017
    Violeta likes this.
  19. Gondwanaland

    Gondwanaland Senior Member

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    Violeta likes this.
  20. Gondwanaland

    Gondwanaland Senior Member

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