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

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Warburg, O. On the origin of cancer cell. Science 1956, 123, 309–314. [ Google Scholar] [ CrossRef] [ PubMed] Martinez-Outschoorn, U.E.; Lin, Z.; Whitaker-Menezes, D.; Howell, A.; Sotgia, F.; Lisanti, M.P. Ketone body utilization drives tumor growth and metastasis. Cell Cycle 2012, 11, 3964–3971. [ Google Scholar] [ CrossRef] [ PubMed][ Green Version] Yang, C.H.; Yen, T.L.; Hsu, C.Y.; Thomas, P.A.; Sheu, J.R.; Jayakumar, T. Multi-targeting Andrographolide, a novel NFkB Inhibitor, as a potential therapeutic agent for stroke. Int. J. Mol. Sci. 2017, 18, 1638. [ Google Scholar] [ CrossRef] [ PubMed] Have you looked into Dr Eric Berg’s qualifications to give medical advice regarding cancer, let alone anything? 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.

Gonçalves, J.M.; Barcellos Silva, C.M.; Rivero, E.R.C.; Cordeiro, M.M.R. Inhibition of Cancer stem cells promoted by Pimozide. Clin. Exp. Pharmacol. Physiol. 2019, 46, 116–125. [ Google Scholar] [ CrossRef][ Green Version]I would have to correct the statement of “being cancer free” to being in remission. Since he is 2-3 years into his diagnosis the surgical castration is likely what got him to where he is and my best interpretation is that his particular cancer is very dependent on testosterone at this time. One anomaly I cannot understand though is that his PSA has been at below 0.1 for over a year now and yet he still has a prostate. How is this possible?

Finally, if we limit the ketogenic supply to the SCOT ketolytic pathway it could be useful to preserve the signaling action over the HCA2 receptors, activated by agonists such as niacin.

Acknowledgments

Kashan, A. Biological roles and therapeutic potential of hydroxyl-carboxilic acid receptors. Front. Endocrinol. 2011, 2, 1–12. [ Google Scholar] In general, HDACs, together with other compounds (NO donors), control the embryonic to adult transition for many protein isoforms. This depends, at the epigenetic level, on metabolites formed in glycolytic-ketogenic-ammonotellic fetal metabolism, or metabolites formed in adult oxidative metabolism. In mammals, a series of proteins of the “aquatic fetus” thus adapt to life in an environment with air and gravity [ 9].

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. kimster, I have liked at least on a conceptual level this article https://arxiv.org/pdf/1407.7622.pdf Well, Psa didn't stay at 0.32 for long and whizzed up to 30 last July, so I had 2 more doses Lu177, and Psa went to 7, and I think Xtandi no longer works to do what it is designed to do and so I could not have a 7th dose of Lu177 and now Psa > 60, and rising very fast, and it seems now like I need to have my end stage days planned. 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] 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]There are dozens (hundreds maybe) of debunking videos on YouTube about him from actual qualified medical practitioners. Pournourmohammadi, S.; Grimaldi, M.; Stridh, M.H.; Lavallard, V.; Waagepetersen, H.S.; Wollheim, C.B.; Maechler, P. Epigallocatechin-3–gallate (EGC) activates AMPK through the inhibition of glutamatedehydrogenase in muscle and pancreatic Bcells: A potential beneficial effect in the pre-diabetic state. Int. J. Biochem. Cell Biol. 2017, 88, 220–225. [ Google Scholar] [ CrossRef][ Green Version] 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. Konishi, Y.; Kobayashi, S.; Shimizu, M. Tea Polyphenols inhibit the Transport of Dietary Phenolic Acids Mediated by the Monocarboxylic Acid Transporter (MCT) in Intestinal Caco-2 Cell Monolayers). J. Agric. Food Chem. 2003, 51, 7296–7302. [ Google Scholar] [ CrossRef] [ PubMed] The next two urls are large scale fasting studies that showed that these approaches are quite safe though the studies were not constructed to screen for cancer patients. Water only fasting over prolonged periods does appear to have substantial potential for cancer therapy.

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.

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I think having Cabazataxel now would not work, just like Docetaxel didn't work at all, which would allow Psa to rise much more and then it would be too late to get a big benefit from Ra223, which is usually used here to relieve bone pains.