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Discussion in 'Mitochondrial Rx' started by Jack Kruse, Sep 16, 2021.

  1. Jack Kruse

    Jack Kruse Administrator

    The uricase mutation in humans increases our risk for cancer growth.
    Recent studies suggest that fructose, as well as its metabolite, uric acid, have been associated with increased risk for both cancer incidence and growth. Both substances are known to cause oxidative stress to mitochondria and to reduce adenosine triphosphate (ATP) production by blocking aconitase in the Krebs cycle. The uricase mutation that occurred in the Miocene epoch has been reported to increase serum uric acid and to amplify the effects of fructose to stimulate fat accumulation.

    Chronic elevated uric acid links to metabolic syndrome in humans


    Is it a thrifty gene or a collateral effect?

    Uric acid does have a neuroprotective benefit and few seem to know about as well.

    Uric acid regulates NLRP3/IL-1β signaling pathway and further induces vascular endothelial cells injury in early CKD through ROS activation and K+ efflux.
    JanSz and John Schumacher like this.
  2. I always find it entertaining to watch researchers hunt for genetic pathways for (name the cancer) with the intent to find a drug inhibitor to a proposed cascade of snip gene transcripts.

    My current understanding is: cancer has three root pathways
    • Metabolic dysfunction - including all glycation end products
    • Viral mutation - including gene editing by nature or man's industrial chemical products
    • ATP dysfunction - including toxic waste removal/overload
    Last edited: Sep 16, 2021
    JanSz likes this.
  3. Jack Kruse

    Jack Kruse Administrator

    John Schumacher likes this.
  4. The inhibition of complex 1 decreases NADH oxidation, proton pumping across the inner mitochondrial membrane and oxygen consumption rate, resulting in lower proton gradient (Δψ) and reduction of proton-driven ATP synthesis from ADP and inorganic phosphate (Pi).

    Complex I inhibition causes an energy deficit and can lead to adverse changes in the status of the mitochondrial [NADH]/[NAD+] pool and increased reactive oxygen species production, causing widespread damage.

    mTOR signaling pathway and mTOR inhibitors in cancer: progress and challenges -
    The relationship between mTOR and tumors. Overactivation of mTORC1 can promote tumor formation, proliferation, and metastasis, while mTORC2 can regulate the expression of mTORC1 through the mTORC2/AKT/TSC/Rehb pathway. Pathway 1: The extracellular growth signals and intracellular LKB1 mutations activate mTORC1, which reduces the ubiquitination of histone H2A and H2A after DNA damage by phosphorylating RNF168. This can lead to damage to DNA repair and promote the formation of tumors. Pathway 2: The ubiquitination of Rheb reduces Rheb activity by promoting Rheb binding to TSC2. The down-regulation of Rehb reduces the activation of mTORC1, leading to the inhibition of tumor growth. Pathway 3: TRAF2 and Otud7B respectively regulate mTORC1/2 activity by up-regulating or down-regulating the ubiquitination level of G beta L of mTORC2. TRAF2 enhanced the activity of mTORC1 and inhibited the activity of mTORC2. Although down-regulation of mTORC2 expression inactivates the AKT/TSC/Rehb/mTORC1 pathway, overall mTORC1 activity is enhanced. However, Otud7B has the opposite effect on TRAF2. Pathway 4: Mutated Ras binds mTOR and MAPKAP1 of mTORC2 to promote mTORC2 expression. The up-regulation of mTORC2 promotes tumor proliferation through the AKT/TSC/Rehb/mTORC1 pathway. Pathway 5: Deletion of the PTEN gene induces the expression of B7-H1 to increase tumor progression and invasion. Pathway 6: The PI3K/PTEN/AKT/mTOR pathway is involved in the invasion and metastasis of liver cancer by up-regulating MMP-9.

    Bottomline: mTOR inhibitors can inhibit tumor cell growth; however, their unable to induce tumor cell death.

    When the mitochondrial ATP dysfunctions, reduction in its energy output is not healthy for the human.
    Last edited: Oct 5, 2021
    ND Hauf likes this.
  5. JanSz

    JanSz Gold

    Done in the Memorial Sloan Kettering, Manhattan NYC
    9/29/2005 first thigh surgery (nothing after surgery, no chemo, no radiation, nothing).
    7/23/2020 second thigh surgery (nothing after surgery, no chemo, no radiation, nothing).
    Doctor said
    slow-growing tumor, see you in 15 years

    What say you, what precautions to take? @Jack Kruse @DrEttinger @John Schumacher

    The current diagnosis is the same as the one in 2005.
    Last edited: Oct 5, 2021
    John Schumacher likes this.
  6. @JanSz - you may already be doing these things, here's some thoughts:

    Turn up your redox mitochondrial respiration:
    • N-Acetyl L-Cysteteine
    • R-Alpha Lipoic Acid
    • COX pathway - Dihydromyricetin
    • Tauroursodeoxycholic Acid
    Clean up "dead" material
    • Enzyme Defense by Enzymedica
    • MucoStop by Enzymedica
    • Serrapeptase
    Note: above are taken on an empty stomach

    Ancient minerals
    • Micro-Boost by Beam Minerals
    Note: It's an alkaline mineral form of Fulvic and Humic​

    Do not fry or "char-burn" your food !
    • Glycation is not your friend - RAGE: Receptors for advanced glycation end products
      which make methylglyoxal and glyoxal.
    • The results? -> including Ox-LDL end products the building blocks for tumors. ox-LDL concentrations start from oxidation, manifesting into the most aggressive tumor phenotypes.

    Ox-LDL binding to LOX-1 increases ROS formation and NO release reduction, alternatively it can activate the PI3K/AKT/GSK3β cascade. The activation of both pathways results in the triggering of transcription factors associated to epithelial to mesenchymal transition (EMT-TFs) and of NF-kB. The NO release reduction can also activate the inflammatory signaling (IL-6, IL-8, and IL-1β). The final result is the activation of hypoxia pathways (VEGF, HIF-1α) and the enhancement of mesenchymal markers expression (MMP-2 and MMP-9). The outcome of all these processes determines cell transformation, angiogenesis, and the epithelial to mesenchymal transition.

    Tracking your history:
    Age 28-30 (1970) start of GERD (my current guess, my (potassium RBC) must have been hitting an important low
    Age 40 (1980), got a new house and double beds (adjustable). Sleep on an incline, bad sleeping but less GERD, less anti-GERD chemicals
    Age 50 (1990), starting hitting a wall, not being able to hold urine for 6-7 hrs (job requirement)(prostate growth must have reached an important set point
    Age 55 (1995), started having erection problems
    Age 57 (1997) quit working, found very low testosterone, good E2, (LH did not give a shit about my low testosterone), my pituitary abandoned me)
    Age 60 (2000) Poliquin's explanation convinced me to eat Betaine HCL. Miracle work (but based on mistaken assumption as I have recendly found based on @DrEttinger support​
    Last edited: Oct 5, 2021
    JanSz likes this.

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