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

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These are my personal choices. 1 cup of V8 juice is good lycopene for a meal, 16 mg. Try to get total daily lycopenes around 50-70mg. watch out for sodim intake. Also consider around 10-20 mg per meal total. I go through a lot of catsup. I want Radium223, but docs don't really know if that will work, and there are not many add on drugs to make it work better.

Warburg, O. On respiratory impairment in cancer cells. Science 1956, 124, 269–370. [ Google Scholar] [ CrossRef] [ PubMed] Poff, A.M.; Ari, C.; Arnold, P.; Seyfried, T.N.; D’Agostino, D.P. Ketone supplementation decreases tumor cell viability and prolongs survival of mice with metastatic cancer. J. Cancer 2014, 135, 1711–1720. [ Google Scholar] [ CrossRef] [ PubMed][ Green Version]

Eigenbrodt, E.; Gerbracht, U.; Mazurek, S.; Presek, P.; Friis, R. Carbohydrate metabolism and neoplasia: New Perspectives for diagnosis and therapy. In Biochemical and Molecular Aspects of Selected Cancers; Prestlow, T.G., Prestlow, T.P., Eds.; Academic Press: Cambridge, MA, USA, 1994; Volume 2, pp. 311–385. [ Google Scholar] 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. 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. Rothemberg, M.L.; Nelson, R.; Hande, K.R. New drugs on the horizon: Matrix MetalloproteinaseInhibitors. Stem. Cells 1999, 17, 237–240. [ Google Scholar] [ CrossRef] [ PubMed] 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.

The production of ketone bodies in the liver requires the mobilization of lipid stores; catabolic hormones trigger lipolysis, which provides fatty acids. These acids enter mitochondria through a carnityl-driven transporter, and the beta-oxidation pathway cuts them into two carbon units, forming acetyl-CoA. Normal liver is ketogenic, converting acetyl-CoA into ketone bodies; no ketolysis takes place in normal liver, which releases ketone bodies such as beta-hydroxybutyrate (BHB) in the blood. Ketolysis will then support the metabolism of tissues responding to anabolic hormones; primarily insulin and IGF. Three enzymes form the ketolytic pathway, which converts BHB into acetyl-CoA. The only specific ketolytic enzyme is (SCOT), the product of the OXCT1 gene. The acetyl-CoA coming from ketone bodies feeds the ketolytic entry into the citric acid cycle. Lee, I.-K.; Han, M.-S.; Lee, M.-S.; Kinm, Y.-S.; Yun, B.-S. Styrylpyrones from the medicinal fungus Phellinusbaumii and their antioxidant properties. Bioorg. Med. Chem. Lett. 2010, 20, 5459–5461. [ Google Scholar] [ CrossRef] [ PubMed] 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. As time passed since 2010, my Psa level has gone up and down and without ADT or add-on drugs or Lu177, I would have died years ago. Schwartz, L.; Abolhassani, M.; Guais, A.; Sanders, E.; Steyaert, J.M.; Campion, F.; Israël, M. A combination of alpha lipoic acid and calcium hydroxycitrate is efficient against mouse cancer models: Preliminary results. Oncol. Rep. 2010, 23, 1407–1416. [ 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] Nearly 3 years after being diagnosed with inoperable metastatic cancer, our patient shows no signs of disease and leads a full and active life.

Klement, R.J. Wilhelm Brünings’ forgotten contribution to the metabolic treatment of cancer utilizing hypoglycemia and very low carbohydrate (ketogenic) diet. J. Tradit. Complement. Med. 2019, 9, 192–200. [ Google Scholar] [ CrossRef] Lithostat acetohydroxamic acid is a typical SCOT inhibitor used to treat bladder stones. Another inhibitor, Pimozide [ 40, 41], used to treat mental diseases, reduces cancer incidence. Several interesting compounds are highlighted in the work of Lissanti’s group, who describe potential SCOT inhibitors, the Mitoketoscine [ 42], through their structural and binding properties. Selecting the best and least toxic derivative for animal cancer models requires collaboration with pharmaceutical groups.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] Israël, M.; Schwartz, L. Inhibition of the ketolytic acetyl CoA supply to tumors could be their “Achilles heel”. Int. J. Cancer 2020, 147, 1755–1757. [ Google Scholar] [ CrossRef] Foster, D.W. Malonyl-CoA: The regulator of fatty acid synthesis and oxidation. J. Clin. Invest. 2012, 122, 1958–1959. [ Google Scholar] [ CrossRef][ Green Version]

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] Liu, R.; Liu, P.; Bi, H.; Ling, J.; Zhang, H.; Zhang, M.; Hu, Y.; Chiao, P.J.; Huang, P.; Liu, J. Malignant transformation by oncogenic K-ras requires IDH2-mediated reductive carboxylation to promote glutamine utilization. Cancer Commun. 2022. Epub ahead of print. [ Google Scholar] [ CrossRef] This first article in the starve cancer series is quite instructive. I had no idea that glucose levels could be brought down to the levels reported in the article. I have seen the tumor responses to fairly modest reduction in glucose in mice models; one can only guess what might happen if glucose levels were brought down to the extent imagined in the article.Fan, J.; Lin, R.; Chen, D.; Xia, S.; Elf, S.E.; Liu, S.; Pan, Y.; Pan, Y.; Xu, H.; Qian, Z.; et al. Tetrameric Acetyl-CoA Acetyltransferase 1 is Important for tumor growth. Mol. Cell 2016, 64, 859–874. [ Google Scholar] [ CrossRef][ Green Version]