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]. Eliaguov, J.; Gopal, N.; Dixon, A.; Choudhury, M.; Konno, S. Potentiation of Anticancer Effect by Combination of Mushroom extract and Grapeseed extract on human Bladder cancer cells. Cancer Sci. Res. 2021, 4, 1–12. [ Google Scholar] [ CrossRef] Halestrap, A.P. The Monocarboxylate Transporter Family—Structure and Functional Characterization. IUMB Life 2012, 64, 1–9. [ Google Scholar] [ CrossRef]

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