The Real ME: A Stock Photography Resource for the Media
We’ve all seen them in the news stories about ME/CFS: the guy in a suit at the office, yawning; the beautiful woman sitting at her desk with her immaculate make-up and elegantly coiffed hair, hand to her head and looking slightly pained.
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To all that suffer

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by newradost, Aug 29, 2013.

  1. Freddd

    Freddd Senior Member

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    Salt Lake City
    And you know that how?
     
  2. Violeta

    Violeta Senior Member

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    It's good to find out why you're not supposed to take Vitamin a or Vitamin c while taking MMS.
     
  3. newradost

    newradost

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    Oh my God you are so lost!
    It is not about MMS, even it kill the ropes. The real point here are the rope parasites. They exist and the future will prove it. I have tried many protocols and the only thing working for now is the mms enemas. I haven't drink MMS because it is gross. I'm researching for alternatives. I was going to try Fenbendazole but I found a doctor with 10 years of experience in Africa and hope we are on the right path of curing. I won't tell more at this point.
    The rope parasite is different because in our opinion it is a colony of one-celled parasites that acts like one animal.
     
  4. WoolPippi

    WoolPippi Senior Member

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    I understand, it is about the rope parasites. Which are only just discovered, you áre on the cutting edge of medicine!
    A colony of one-celled parasites, how very interesting! I would not be surprised if such an organism lives in our bodies.

    Various enema's might help to get rid of them, for you and your child the MMS helps, which is great and we will not question this because it is effective and theories are meaningless when there's evidence right there, in the childs behaviour during die off and in the toilet.
    You mention other enema's too (eucalyptus-lemon) so anybody not wanting MMS can try something different.

    Thank you for bringing rope parasites to the attention.
    And sharing a solution that works for you and others in your group.
    Thank you for starting this thread!
     
  5. Violeta

    Violeta Senior Member

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    Don't bother trying the Fenbendazole, because you don't need to kill the rope worm, just need to get it out.

    MMS doesn't kill the rope worm, it just makes it come out, and so you're right, it isn't about the MMS, but some people do try to make all about MMS.

    In whose opinion is the rope worm a colony of one-celled parasites? Why haven't Volinsky and Gubarev taken the time to prove that? Have you looked at pictures of the 5 stages? How do the one-celled parasites work together to change from stage to stage? Why don't Gubarev and Volinsky take one cell from a rope worm and cultivate it? If it's a one-celled parasite surely it will divide and multiply. It cannot reproduce, so why don't they see if it can divide?

    Why are they asking people to send them $300 for genetic testing?

    It doesn't really matter what people think it is or what works to get it out, which is why I wonder why such a big to do is made about it and the MMS. Why do people get so belligerent and down right rude. Saying to someone, "Oh my God, you are so lost," is rude.
     
  6. newradost

    newradost

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    I'm not representing the engineers Volinsky and Gubarev. They have done their job and offered us many optical
    micrographics for future reference. Now the parasitologists need to make a move. I'm sharing the vision of my doctor and my opinion on this. As I say, MMS is the fastest test to show if one is infected. I have lab works proving my theory to some extent and I see many sighs of improvement. But everyone should decide how to live its life.
     
  7. WoolPippi

    WoolPippi Senior Member

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    it is.
    But it's also an utterance of frustration when the discussion focusses on MMS when one wants to alert people to the existence of rope parasites.
    Also, OP has not English as a first language and comes across more staccato in English than in her own language. As do I probably.

    So let's chalk it up to one of those internet forum things, where we cannot see someones face nor hear their voice and we tend to forget things are written by well meaning people. Especially as a brainfogged person I need to remind myself constant of this... "people mean well, people mean well".

    interesting thought that the rope parasite doesn't need to be killed, just needs to get out.
     
    Wayne likes this.
  8. Violeta

    Violeta Senior Member

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    @WoolPippi, sorry, "Oh my God you are so lost is rude", it doesn't matter if English isn't her first language.
     
  9. Wayne

    Wayne Senior Member

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  10. Asklipia

    Asklipia Senior Member

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    Hi @Wayne I was looking at thiamine cures (as you most probably know I am on high thiamine with very good results) when I came across this case study in Germany:
    Non-Hodkins Lymphoma Reversal with Dichloroacetate which gives a good explanation on how it works on the mitochondria. It is interesting that the good results occurred when this was paired with a lot of thiamine, which is also working on the mitochondria.

    "DCA is a by-product of water chlorination [6, 7] that inhibits aerobic glycolysis. It has been used in medicine for over 30 years [8] as an investigational drug to treat severe metabolic disorders such as diabetes and hypercholesterolemia [5, 9] as well as the treatment of congenital lactic acidosis in North American children [10]. The bioavailability [11] and pharmacokinetics [12] of DCA have been well researched over several decades in adults [6], children [13, 14], and animals [15]. As a medicinal, DCA is generally well tolerated from dosages between 10 mg/Kg and 50 mg/Kg, although prolonged exposure is associated with peripheral neuropathy [16]. Its activation of the pyruvate dehydrogenase enzyme (PDH) of the mitochondria decreases glycolysis and reactivates glucose oxidation, a favorable approach to ameliorate lactic acidosis [9].

    Cancer cells predominantly utilize a system of glycolysis for energy instead of the glucose oxidation used by healthy cells. Cancer appears to be a form of intracellular lactic acidosis caused by a block in the oxidation of glucose at the level of PDH (pyruvate dehydrogenase). The glycolysis metabolism of glucose increases cancer cells’ lactic acid and reduces the intracellular pH [7] resulting major shifts in the intracellular biochemistry. Aerobic glycolysis, known as the “Warburg Effect” [17], inactivates mitochondrial respiration which allows cancer cell growth [18]. DCA reverses this glycolysis causing several major detrimental changes in the cancer tumor cells.

    First and foremost DCA inhibits pyruvate dehydrogenase kinase (PDK). PDK blocks pyruvate dehydrogenase (PDH) through its phosphorylation activity. When this kinase is inhibited by DCA, the PDH is reactivated causing the mitochondria to no longer be hyperpolarized, instead the membrane and the mitochondria are depolarized, reactivating the mitochondrial K+ channels which then decreases cytosolic K+. When PDH is inhibited in cancer cells by PDK, an excess cytosolic K+ occurs that inactivates the caspases 3 and 9, important factors in apoptosis. DCA reactivates these caspases along with an increase in H2O2 intracellularly, allowing the release of cytochrome c from the mitochondria. The release of cytochrome c is a major activating step for cell apoptosis as it triggers the caspase cascade [19]. The results of DCA on cancers are seen both in vitro and in vivo. These effects are not seen in normal cells.

    Dichloroacetate’s other major effect on cancer cells is the release of mitochondrial calcium (Ca++). The increase of Ca++ in cancer cells is associated with the increase and proliferation of transcription factors. Calcium also activates ornithine decarboxylase, the rate limiting enzyme in DNA synthesis [20], and the antiapoptosis factor NFAT (nuclear factor of activated T lymphocytes) [21]. When the calcium decreases with the introduction of DCA, the cell is further directed toward apoptosis and a decrease in cell replication. In addition to DCA causing a major shift in the mitochondria, cytoplasm, and cellular membrane [19], the end effect of DCA is a cell cycle arrest in the Gap 1 phase (G1), which also increases apoptosis [22]."

    Be well! :hug:
    Asklipia
     
    Last edited: Oct 22, 2017
    helen1 and Wayne like this.

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