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

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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]. 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]

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] 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] 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] Kroemer, G.; Pouyssegur, J. Tumor cell metabolism:cancer’s Achilles’ heel. Cancer Cell. 2008, 13, 472–482. [ Google Scholar] [ CrossRef] Yoshino, M.; Miyajima, E.; Tsushima, K. Kinetics of the interactions of AMP Deaminase with Fatty acids. J. Biol. Chem. 1979, 254, 1521–1525. [ Google Scholar] [ CrossRef]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] 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] 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.

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] This case is unique in that a metabolic-based fasting and ketogenic diet intervention was used as the primary management strategy for a metastatic cancer in the absence of surgery, chemotherapy, or radiotherapy, culminating in a near-complete regression.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. 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] 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. Blatt, J.; Stitely, S. Antineuroblastoma activity of desferoxamine in human cell lines. Cancer Res. 1987, 47, 1749–1750. [ Google Scholar] The Better Business Bureau has hundreds of complaints about double-billing and bad supplements from his health supplement store.

Mi, L.; Zhang, Y.; Su, A.; Tang, M.; Xing, Z.; He, T.; Wu, W.; Li, Z. Halofuginone for cancer treatment: A Systematic review of efficacy and molecular mechanisms. J. Funct. Foods 2022, 98, 105237. [ Google Scholar] [ CrossRef] Okumura, S.; Konishi, Y.; Narukawa, M.; Sugiura, Y.; Yoshimoto, S.; Arai, Y.; Sato, S.; Yoshida, Y.; Tsuji, S.; Uemura, K.; et al. Gut bacteria Identified in colorectal cancer patients promote tumorigenesis via butyrate secretion. Nat. Commun. 2021, 12, 5674. [ 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]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. Warburg, O. On the origin of cancer cell. Science 1956, 123, 309–314. [ Google Scholar] [ CrossRef] [ PubMed] 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. 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] In one of the links below the interesting idea that cancer cells are unable to properly metabolize lactate is introduced. If true, then this could offer a less technically difficult route to glucose withdrawal; simply remove the glucose and add in lactate. Some of the other approaches try to remove glucose from the body but then must find work around for the heart and brain.

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]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. This is exciting! I was wondering whether reports of cancer patients trying prolonged water only fasts might be in the literature. Apparently, recently a report of a 21 day water only fast was reported for a cancer patient which resulted in a long term remission (see the two articles below). There are some caveats here: The type of cancer involved stage IIIa, low-grade follicular lymphoma is highly treatable with current therapies, so one wonders to what extent it is ethical to not first give standard of care. Also this type of cancer appears to have prolonged survival so it is not obvious how effective the diet intervention was. 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]