This first article in the starve cancer series is quite instructive. I had no idea that glucose levels could be brought down to the levels reported in the article. I have seen the tumor responses to fairly modest reduction in glucose in mice models; one can only guess what might happen if glucose levels were brought down to the extent imagined in the article. 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. Kashan, A. Biological roles and therapeutic potential of hydroxyl-carboxilic acid receptors. Front. Endocrinol. 2011, 2, 1–12. [ Google Scholar] 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?

Bernstein, B.A.; Richardson, T.; Amundsen, C.H. Inhibition of Cholesterol biosynthesis and Acetyl-CoA synthetase by bovine Milk and Orotic acid. J. Dairy Sci. 1977, 60, 1846–1853. [ Google Scholar] [ CrossRef] [ PubMed] Glucose and ketone bodies are the two major sources of nutrients for cells. When food is scarce, a mobilization of nutritional reserves in several organs will liberate or synthesize these nutrients. Fasting and starvation elicit the release of catabolic hormones: glucagon from the endocrine pancreas, epinephrine and cortisol from adrenals. These hormones act on different organs: glucagon for the liver, muscle adipose tissues and liver for the others. Catabolic hormones trigger glycogenolysis in liver and muscle, making glucose available; these hormones will activate the synthesis of glucose through neoglucogenesis in the liver, while muscle proteolysis provides amino acids that support the process. On the other hand, tissues responding to anabolic hormones, insulin and insulin-like growth factor (IGF) will take up glucose. Glycolysis leads to pyruvate, recovering part of the energy of glucose. Then, mitochondrial oxidative metabolism takes over. This process is energetically more efficient than glycolysis, extracting energy through the citric acid Krebs cycle, which is coupled with the respiratory electron transport chain. The citric acid cycle begins with the conversion of pyruvate into acetyl-CoA by an enzyme pyruvate dehydrogenase (PDH), controlling the glycolytic entry in oxidative metabolism. Cassim, S.; Vučetić, M.; Ždralević, M.; Pouyssegur, J. Warburg and Beyond: The Power of Mitochondrial Metabolism to Collaborate or replace Fermentative Glycolysis in Cancer. Cancers 2020, 12, 1119. [ Google Scholar] [ CrossRef] [ PubMed] So many anti-cancer benefits to fasting could occur; e.g., reduction in lactate, improved immune control, glucose reduction ... . 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]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] 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] 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] 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. 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]

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.Mazurek, S.; Eigenbrodt, E. The tumor metabolome. Anticancer Res. 2003, 23, 1149–1154. [ Google Scholar] [ PubMed] 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] 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. 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] 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]