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Cholesteotoma question?

Discussion in 'Educating Doctors' started by Jack Kruse, Dec 1, 2017.

  1. Jack Kruse

    Jack Kruse Administrator

    Q: Dr. Jack Kruse I've been reading about ear cholesteatomas and endoplasm reticulum and mithocondrial stress, do you have any comment on that?? Thanks.

    ANS: Yes, It is very complicated. nnEMF and blue light increase the deuterium fractionation of tissues. Well if you are arounf a lot of nnEMF your ear pays deep attention to this because of how the reflex arc of acoustics works in the brain. You can read about this here: https://www.jackkruse.com/cpc-14-tinnitus-quantum-view-point/

    I always ask people with this disease about occupation and habits and if they have had tinnitus or a Bell's Palsy. I have never found one patient where this was not true. nnEMF is why I ask because it stimulate growth in the middle ear skin via reflex. You have to know how the acoustic reflex works. Inicdent light forms the afferent loop. This means humans use light to hear as the link above shows. As the nnEMF destroys the reflex arc it allows the middle ear skin to begin to collect massive amounts of deuterium and this stimulates the growth of the middle ear epithelium. Cholesteatoma is a mitochondrial disease and not a genetic one that is mediated thermodynamically by volume changes due to deuterium fractionation in the epitympanum. Throughout the history of oncology research, in both the conventional and alternative cancer research realms, there has been a cause and effect relationship that has been largely ignored. The ability of a cell to divide, whether it be a malignant (CA) or non-malignant cell (cholestetoma), is highly dependent on cell volume (deuterium fraction in tissue growing), as well as membrane potential (DHA).

    The collagen tensegrity system is piezo and flexoelectric and releases and absorbs light from the sun diurnally, and this is why cell volume and cancer are related; so when you lose energy and charge in a cell, the cell, mitochondria and nuclear membrane enlarges and the signal heads to the ER via the other mitochondrial membrane to stimulate translation. The temporal sequence of the enlargement inside a cell is the critical difference. Mitochondrial morphology is one of the earliest changes because of changes in how electrons and protons are used in the matrix. Cells that are cycling (dividing), progress through the following phases: G1 (Gap 1) – this is the phase where the cell is preparing for the next phase, which is the S phase, or DNA Synthesis phase. Once DNA synthesis is complete, the cell enters the G2 phase (G 2), where it prepares to enter the final phase, called the M phase, or mitosis.

    During mitosis, the cell divides into 2 cells. The cell volume is at its smallest at G1, and gradually increases its volume until it reaches its largest volume in the M phase. This should be intuitive, because the cell must become large enough to divide and then support two cells. This process is stimulated by TCA intermediates loaded with deuterium in this ear disease because nnEMF stimulate deuterium absorbtion in the middle ear. Cholesteatomas are more aggressive and have associated bony and ossicular erosive changes and arise from specific locations in the middle ear because of the volume changes in skin cells. The typical pars flaccida type cholesteatoma arises in the epitympanum. When MRI is used (rare cause CT is better) we can see sigal change in the fat signals when we vary MRI parameters. This is strong evidence for the presence of high deuterium in this area because of its kinetic isotope effect on imaging. It affects image intentsity compared to H+ fat. Deuterium has double the atomic weight the spin effect is the real problem in the middle ear. The numbers on its magnetic moment destroy chemical flux in any system via changes of the TCA cycle in the middle ear from the nnEMF effect of collecting deuterium in this region. This collection of deuterium leads to tissue swelling which stimulate the cell cycle to get to the mitosis phase and skin cells are expert at making ketatin and cholesterol. So the chronic swelling of the cell volumes there turn out the RER and make tons of the stress lipid cholesterol and it is loaded with deuterium. This is a progrowth action because of how volume is controlled. The interesting thing is that young living systems use deuterium (insulin/GH) to retain deuterium to stilmulate growth as we develop. Plants do the same to their fruits because they want birds to eat the fruit to spread the seeds. the fruit is designed to stimulate the birds growth and the growth of the seed to germinate. This is why understanding the nuanace of it is critical fro those interested in biology. Right now bio-chemists are impotent to get that nuance and why everyone has no clue about the etiology of this disease. It mimics cancer and I just did a webinar December 2017 on the mechanism. You might want to watch it at some point.
    WalterNL, Alex97232, JanSz and 2 others like this.
  2. Josh Rosenthal

    Josh Rosenthal Charter member of Purple Angels Club

    is the MRI collimation that you use to see deuterium pre picture or after formatting? IE... can an MRI be reformatted afterwards to see this effect?
    Paleodocteur likes this.
  3. Jack Kruse

    Jack Kruse Administrator

    Each D control's the T1 relaxation of 96 H+ atoms so the density and intensity changes is what I look for. I also look for the changes in muscle, bone and liver if I have a L spine scan.
    Paleodocteur and JanSz like this.

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