MY BATTLE AGAINST CANCER: Survivor protocol : foreword by Thomas Seyfried

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MY BATTLE AGAINST CANCER: Survivor protocol : foreword by Thomas Seyfried

MY BATTLE AGAINST CANCER: Survivor protocol : foreword by Thomas Seyfried

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Quite a few drugs for cancer are developed from non natural substances. Many thousands of natural chemicals were tried and tested before the first chemo drug came along, and Docetaxel was derived from Yew tree sap. Maybe its made in a lab now.

Wilson, B.R.; Bogdan, A.R.; Miyazawa, M.; Hashimoto, K. Siderophores in iron metabolism: From Mechanism to therapy. Trends Mol. Med. 2016, 22, 1077–1090. [ Google Scholar] [ CrossRef][ Green Version] Halestrap, A.P. The Monocarboxylate Transporter Family—Structure and Functional Characterization. IUMB Life 2012, 64, 1–9. [ Google Scholar] [ CrossRef] As I watched the Pca spread in scans get worse, the number of bone mets has increased, and I have many little ones not making PsMa hence Lu177 or Ac225 won'k, but Ra may work, but mean extension of lifetime of Ra223 is 4 months, but then men seeking Ra223 have tried all other things and have very high Psa, maybe 600, or 10 times what mine is. Muri, E.M.F.; Nieto, M.J.; Sindelarand, R.D.; Williamson, J.S. Hydroxamic Acids as Pharmacological Agents. Curr. Med. Chem. 2002, 9, 1631–1653. [ Google Scholar] [ CrossRef]Personally I have no problem with eating well and supplements and fasting but what works for the occasional person does not usually work for the masses. Otherwise we would all be doing well. I have tried everything you can think of in the alternative medical world. For my disease all it did was hurt my savings. I think diet is a no brainer and a healthy plant based diet is the way to go but all these other claims are either anecdotal or supported by very low level evidence with very small numbers of patients (therefore a low power study). Just because you can find an article on PubMed does not mean it is a good study. I think that is a major problem on this forum and others that people post links to “studies” but they really don’t know how to critically analyze them well. The conclusion is where everyone jumps to but in reality the methods is the most important part of any study. I’ve been a doc for 20 years and it took a long time for me to be confident in how I interpret a study. I truly believe the guy (no pun intended) is legit as he doesn’t sell anything and you see how his body has changed over the past two years (white hair became grey, went from heavy set to skinny, etc…) and he also makes all of his documents (MRI, Scans, etc…) available for all to view on Google Drive. Aside from having tried Zitiga for 2 months shortly after his diagnosis and having to stop because he was getting ulcers and other side-effects, he’s had no treatment like radiation, surgery or chemo. He still has his prostate intact, but he did get his testicles removed surgically shortly after stopping Zitiga because his doctor told him that this would lower his testosterone and maybe help him survive a little longer. He did not mind doing so because he thought he was going to die anyway. Al Batran, R.; Gopal, K.; Capozzi, M.E.; Chahade, J.J.; Saleme, B.; Tabatabaei-Dakhili, S.A.; Greenwell, A.A.; Niu, J.; Almutairi, M.; Byrne, N.J.; et al. Pimozide Alleviates Hyperglycemia in Diet- Induced Obesity by inhibiting Skeletal Muscle Ketoneoxidation. Cell Metab. 2020, 31, 909–919. [ Google Scholar] [ CrossRef] We have seen quite a few iterations of the extreme starvation approach to cancer management in Medical Hypotheses and elsewhere. Those who have written about it have high technical knowledge and they appear to believe that there is justification in moving forward with animal testing.

We have seen that saturated fatty acids of 16 carbons, accompanied by high-fat diets, stimulate AMP deaminase. The resultant decrease in AMP inhibits AMP kinase, canceling its inhibitory action over ACC, which is activated. This boosts the fatty acid synthesis pathway, while malonyl-CoA turns off the fatty acid degradation into acetyl-CoA. If DAG decreases (and converts to TAG) it will not stimulate PKC. Thus, the CPI 17 inhibitor of PP1 does not form, and the phosphatase dephosphorylates and activates PK and PDH, opening the glycolytic supply of acetyl-CoA. On the contrary, if DAG increases (following the action of Growth hormone, for example) PKC is stimulated, forming the CPI 17 inhibitor of PP1, which maintains the phosphorylation of PK and PDH. Since both the fatty acid and glycolytic acetyl-CoA supplies are closed, tumor cells must then use ketone bodies from the liver to create their acetyl-CoA. Bonuccelli, G.; Tsirigos, A.; Whitaker-Menez, D.; Pavlides, S.; Pestell, R.G.; Chiavarina, B.; Frank, P.G.; Flomenberg, N.; Howell, A.; Martinez-Outschoorn, U.E.; et al. Ketones and lactate “fuel” tumor growth and metastasis. Cell Cycle 2010, 9, 3506–3514. [ Google Scholar] [ PubMed] If using fasting as a strategy to lower glucose and glutamine, I was told that it takes 2 days to deplete glutamine levels and another 2 days to really start killing cancer cells. So, perhaps your fasts weren't long enough in duration. Prof Seyfried indicates that after 14 days he has not seen any cancer surviving in the patients he has been studying. I am gearing up to try a 4-7 day fast soon and hoping that will be enough.

Nelson, D.C.; Riseborough, J.A.; Flematti, G.R.; Stevens, J.; Ghisalberti, E.L.; Dixon, K.W.; Smith, S.M. Karrikins discovered in smoke trigger Arabidopsis seed germination by a mechanism requiring GibberellicAcid synthesis and light. Plant Physiol. 2009, 149, 863–873. [ Google Scholar] [ CrossRef][ Green Version] Guy Tenenbaum is a youtuber that I’ve been following for the past 10 months but I’ve watched every video that he’s put out over the past 2 years to document his journey. Having Psa 0.1 is 10 times the low level accurately measured here, and plenty of men have Psa 0.01 after an RP, maybe for 4 years, then Psa starts to rise, and their Long Fight begins. Considering the highly disappointing results from the TAILORX breast cancer study (specifically 85% of women with early breast cancer ( those with an identifiable genetic signature) received no benefited from traditional preventative treatments. How can metabolic therapies that have shown the success noted above now not be aggressively funded and researched?



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