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

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I took my GKI on Sunday after getting the Novamax Plus kit that measures both glucose and ketones, and was distressed to learn, despite three+ months of a low-carb diet (and losing 30 pounds,) that I was NOT ANYWHERE NEAR being in ketosis. 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] An early observation by Brünings, recalled by Klement [ 27], deserves to be mentioned. In his study, patients were given a low-carbohydrate diet, which was associated with an insulin injection protocol that aimed to decrease the supply of glucose to tumors. Initially he observed a decrease in tumor sizes, and later a rebound, while feeding patients with a high-fat diet. We now know that insulin elicits the release of somatostatin from delta cells, which decreases glucagon and ketogenesis leading to a probable decrease in BHB and growth of ketone-dependent tumors. However, since Brünings fed patients with a high-fat ketogenic diet, a rebound of tumors took place. Brünings was not aware that somatostatin release triggered by the insulin injections was probably behind the initial reduction in tumors [ 28]. Indeed, somatostatin decreases glucagon and ketogenesis at the beginning of the trial; however, a late rebound of tumors probably occurs when insulin fails to maintain somatostatin release. In time, the decline in somatostatin stops inhibiting glucagon, which then boosts ketogenesis, providing ketones to the tumor [ 29]. In an earlier work on animal cancer models, we observed that octreotide, a somatostatin analog, decreases tumor volumes [ 12].

But having Psa at 0.1 does not mean he has remission. After 4 doses of Lu177 my Psa went from 25 before Lu177 to 0.32 at 12 months later in Nov 2019r, and doctors were amazed, but I have always known that to be due to Xtandi working, because I had begun it in April 2019.

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One should also control the BHB influx. Indeed, once in the cell, BHB has multiple effects; first, it feeds the SCOT pathway; second, it goes to the nucleus, where it inhibits HDAC, favoring the acetylation of histones, which induces the expression of fetal genes. A third effect of intracellular BHB is the activation of NFkB-mediated transcription of inflammatory cytokines Il1B. Indeed, intracellular BHB induces phosphorylation of IKB, liberating the NFkB transcription factor, which moves to the nucleus. Thus, if one inhibits the influx of BHB with compounds such as Syringopine or Syrosingopine from Rauwolfia [ 36] or others such as Quercetin or Epigallocatechin [ 33, 34] tumor cells will starve, since ketolysis should decline, particularly if associated with SCOT and ACAT1 inhibitors. In parallel, the decrease in intracellular BHB stops the inhibition over HDAC, which will deacetylate histones, silencing fetal genes, and elicit a transition to adult genes. Hydroxamic acid HDAC derivatives, which display anticancer effects, are probable SCOT inhibitors, and may be able to starve the tumor. Finally, the decrease in intracellular BHB stops the stimulation of inflammatory cytokines transcription mediated by NFkB, since NFkB remains bound to IkB in the cytosol. Schwartz, L.; Guais, A.; Israël, M.; Junod, B.; Steyaert, J.M.; Crespi, E.; Baronzio, G.; Abolhassani, M. Tumor regression with a combination of drugs interfering with tumor metabolism: Efficacy of hydroxycitrate, lipoic acid and capsaicin. Investig. New Drugs 2013, 31, 256–264. [ Google Scholar] [ CrossRef] [ PubMed] 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]

Dimitrieva-Posocco, O.; Wong, A.C.; Lundgren, P.; Golos, A.M.; Descamps, H.C.; Cramer, Z.; Tian, Y.; Yueh, B.; Eskiocak, O.; Egervari, G.; et al. Beta-Hydroxybutyrate suppresses colorectal cancer. Nat. Commun. 2022, 605, 160–165. [ Google Scholar] [ CrossRef] [ PubMed] 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] 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. Pal, D.; Saha, S. Hydroxamic acid–A novel molecule for anticancer therapy. J. Adv. Pharm. Technol. Res. 2012, 3, 92–98. [ Google Scholar] [ CrossRef] [ PubMed]

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. 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.

Zhang, Y.-F.; Zhang, H.; He, L.; Liu, C.; Xu, Y.; Qian, P.-Y. Butenolide Inhibits Marine Fouling by altering the primary metabolism of three target organisms. ACS Chem. Biol. 2012, 7, 1049–1058. [ Google Scholar] [ CrossRef] [ PubMed] 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] Aslam, M.N.; Bergin, I.; Naik, M.; Hampton, A.; Allen, R.; Kunkel, S.L.; Rush, H.; Varani, J. A multi-mineral natural product inhibits liver tumor formation in C57BL mice. Biol. Trace Elem. Res. 2012, 147, 267–274. [ Google Scholar] [ CrossRef][ Green Version]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. 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.