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

Product Information

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. 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] 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. 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]

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] 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]. Quite a few men get Pca which is very weak, and easily defeated by say ADT + EBRT, and I've known men like that. But 2 years of ADT + 70Grey EBRT 1/2 way along was supposed to work, but after quitting ADT to see if it had worked, Psa went up from 0.08 to 8 in 6 months, so I have needed ADT ever since.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. 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] This was a real eye opener for me. Apparently the reduction in recurrence seen in this study is at the same level as that found with chemotherapy. Given this, it is highly discouraging that such a simple metabolic strategy has not been extensively studied before. I would be extremely interested in seeing follow on studies that perhaps extended out the fasting interval to perhaps 24 .. 48 .. 72 .. 240 hours .. . They could also try intermittent fasting such as a paleo zero carb diet with daily ketogenic time restricted feeding. The arrival of continuous glucose monitoring could take the guess work out of diet recall.

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. 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] This book tells my story, the story of a carefree man leaving a happy life in Miami, who suddenly falls into the nightmare of the disease whose just name scares you: cancer. Mine is incurable, or rather all of mine because the prostate, bones and lymph nodes are affected. Despite the terrible prognosis from my oncologists, I have decided that I will not die of cancer. Do you think that's impossible? Yet I should be dead by the time of this writing. The point is, I have never felt this good in years and my latest results point to remission! Konishi, H.; Fujiya, M.; Tanaka, H.; Ueno, N.; Moriichi, K.; Ikuta, K.; Akutsu, H.; Tanabe, H.; Kohgo, Y. Probiotic-derived ferrichrome Inhibits colon cancer progression via JNK-mediated apoptosis. Nat. Commun. 2016, 7, 12365. [ Google Scholar] [ CrossRef]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] 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? 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.