The Better Business Bureau has hundreds of complaints about double-billing and bad supplements from his health supplement store. He’s met with Thomas Seyfried already and here is an interview he’s done with Dr Eric Berg youtube.com/watch?v=uOXom6f... (Not working as expected?) but he’s been interviewed by him more than once. 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]

kimster, I have liked at least on a conceptual level this article https://arxiv.org/pdf/1407.7622.pdf 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. 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.

Author Contributions

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]

medline on Korean Traditional Medicine to fight Gastric, Renal & Lung Tumors and other forms of Cancer: Rhus Verniciflua 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. Apparently some (but not all) cancers can respond quite strongly to glucose lowering. There are a range of strategies that could help to achieve such glucose reduction. For example, even modest overnight fasting helps-- longer fasts could also be tried. For some, even longer fasts could be attempted, though professional medical advice would be necessary at some stage to maintain safety. 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]Kroemer, G.; Pouyssegur, J. Tumor cell metabolism:cancer’s Achilles’ heel. Cancer Cell. 2008, 13, 472–482. [ 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]

The other question I ask myself is whether having the testicles removed might be a better option than ADT even it means no sex for the rest of what could be a longer life. 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] Warburg, O. On respiratory impairment in cancer cells. Science 1956, 124, 269–370. [ 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] 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.

Acknowledgments

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. Wang, K.-L.; Zhang, G.; Sun, J.; Xu, Y.; Han, Z.; Liu, L.-L. Cochliomycin A inhibits the larval settlement of Amphibalanus amphitrite by activating the NO/cGMP pathway. Biofouling 2016, 32, 35–44. [ Google Scholar] [ CrossRef] 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] 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]

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.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. Considering the highly disappointing results from the TAILORX breast cancer study (specifically 85% of women with early breast cancer ( those with an identifiable genetic signature) received no benefited from traditional preventative treatments. How can metabolic therapies that have shown the success noted above now not be aggressively funded and researched? 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]