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methylation/apoptosis/caspases

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by determined, Dec 30, 2011.

  1. determined

    determined Senior Member

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    I am curious about something. People with CFS have been shown to have higher than normal levels of apoptosis (programmed cell death). According to the methylation hypothesis, many genes may not have the appropriate methyl groups to ensure appropriate silencing. So it makes sense to me that the TNF levels would be higher than normal and therefore stimulate apoptosis.......however, what bothers me is that the process of apoptosis relies on caspases, which are cysteine-containing. If cysteines are in short supply due to methylation cycle problems, how do the cells find enough to maintain these high levels of apoptosis? I have not been able to find out how many cysteines are required for the caspases......anyone?
     
  2. Valentijn

    Valentijn Activity Level: 3

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    I thought the problem was a shortage of apoptosis, resulting in more messy cell deaths instead of neat and tidy ones.
     
  3. Freddd

    Freddd Senior Member

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    Hi Determined,

    I don't have any specific answers to your questions. Lack of vitamin E causes a higher rate of red blood cell death as seen in jaundiced newborns. However nobody seems to be interested in pointing this out to ladies who have second and third jaundiced babies after a first one. Lack of vitamin mb12/adb12 is one reason for reproductive failure. Lack of methylb12 and adb12 is another cause of reproductive failure. Lack of methylb12 and methylfolate are being investigated as causes of multiple cancers for faulty DNA transactions in cell reproduction as well as the delayed maturity of red cells resulting in elevated MCV. Lack of adb12 can cause lack of repair and growth of muscles as can lack of mb12/methylfolate for a different reason. Epithelial tissue in the body can develop lesions from the mouth and lips to the anus and everything in between. It causes tissue problems in the entire muscosa which breaks down if enough mb12/methylfolate is not present to allow for the rapid cell division needed to maintain these tissues in a harsh environment. Lack of mb12 can lead to neuron death. Lack of adb12 in the neural mitochondria leads to neurological damge. Lack of either leads to demyelination of nerve cells. As far as I can see it is impossible for a person to not have funtioning methylation in the presence of mb12/methylfolate. Use of anything else makes methylation an iffy proposition dependent upon complicated chains of enzyme based reactions with lots of failure points possible. It requires ATP and an enzyme to convert hydroxycbl/cyanocbl to methylfolate. If adb12 is lacking and the ATP isn't getting made then there is not conversion of these inactive cobalamins to the active ones including adb12 needed to make the ATP in the first place. The ability of mb12/adb12/methylfolate to be effective rests upon the support of many vitamins, minerals and l-carnitine fumarate as well as other things. The most limiting factors almost always are adb12/mb12/methylfolate.
     
  4. determined

    determined Senior Member

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    Hmmm, Valentijn, do you remember where you read that there is less apoptosis? Here is the article that says there is more:

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770396/

    Thanks, Fredd.....I have found mB12 and methylfolate to be very helpful. I am still taking tiny, tiny doses that don't really seem able to do much, since the dose is so small, but I am sure that they are! Thanks again for steering me to the mB12.
     
  5. Valentijn

    Valentijn Activity Level: 3

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    http://www.sciencedirect.com/science/article/pii/S0090122997945128:
    So maybe some types of white blood cells (neutrophils) are experiencing more apoptosis, while others (lymphocytes) experience less.
     
  6. determined

    determined Senior Member

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    Cool, valentijn, thanks. It's confusing and I'm in over my head right now...I'm sure it is very complicated, as usual with this illness.
     

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