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The Mitochondrial Thermostat (redox)

Discussion in 'Mitochondrial Rx' started by Scompy, Jul 8, 2018.

  1. Scompy

    Scompy Gold

    "Mitochondria and the Future of Medicine", Lee Know, pg.56

    Hey supplementers, read it and weep... might wanna think about being a sunplementer [​IMG]

    MitoAntioxidants.jpg
     
  2. Scompy

    Scompy Gold

    MLP = Maximum Lifespan Potential (humans are rated around 120 years normally)
     
  3. NADme

    NADme New Member

    Its nice that Lee Know makes these assertions, but based on what? It seems to me after 13 years of chasing feathers in the wind as advocated protocols that dead end, that grand assumptions are made at almost every corner of treatment.

    The underpinnings of toxic metals and other toxins and their effects seem to be mentioned in passing, yet never premised as an absolute, as if whatever suggestive protocol will work out of sequence before treating for heavy metals and other toxins.

    By example, I had the last quadrant of Hg, mercury fillings removed from my mouth. My 2000 level zinc dropped to 1063. This was of particular interest because of the effects of AI's and TRT to control a rise in E2. It would appear that the alleviation, which yielded a true zinc that naturally started to rise back to the over 1600 no deficient level in combination with GH feedback loop stabilizing E2 and SHBG has done away with my need to take an AI to control E2.

    The take away is that until removal I thought my zinc levels were solid. The cleaving by the Hg was stopping zinc to synthesize. As applied if mito supplementation is wrong then how does one expect to propel through a soup bowl of toxins?

    As the cite from above reads we are doing more bad than good via supplementation. There are underlying assumptions that require a leap to connect that conclusions, starting with ETOH internal production and external consumption.

    When NAD ratios radically shift and become NADH dominant the electron substrate that effects about 80 cycles takes a huge hit. The lack of converting to aceytlCoA for mito consumption has an effect on P450scc processing of the LDL. I would be interested to know if the inflammatory factor of this excess and ratio imbalance causes the mito bloat Jack references.

    Also, with little research on my part, does that include the effects of C60 on the intracellular as a beyond surface affect of antioxidants on the mito?
     
    JanSz likes this.
  4. Jack Kruse

    Jack Kruse Administrator

    C60 is too big to get past the EZ atomic filter.......another pipe dream.
     
    Scompy likes this.
  5. JanSz

    JanSz Gold

    Summarizing
    The underlying assumptions are that:
    1. the only XYZ that can help must get in thru mitochondrial membrane intact.
    2. nothing is helpful unless it gets inside of mitochondria.

    /
     
  6. Scompy

    Scompy Gold

    Oh bam! I've thought about the buckeyball interactions that could be problematic, if it actually got into the matrix, which also seems like it could have a potential to clog up the ATP synthase if it did, so I never wanted to experiment with it. But if the barrier is already in the cytosol, then ha!
     

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