Wellness Fasting and Hyperketosis
DOI:
https://doi.org/10.17140/DROJ-2-e007Abstract
Ketoacidosis is sometimes a lethal complication of diabetes mellitus.1-3 Ketone bodies are considered to be the toxic elements of ketoacidosis. Wilder3 considered that the threshold of ketogenesis (i.e. the maximal ratio compatible with the oxidation of the ketogenic compounds) was reached when the number of ketogenic molecules just equaled the number of glucose molecules. Each glucose molecule being ketolytic for 2 molecules of acetoacetic acid, the ratio is 2:1. As the glucose concentration exceeds 3 mM in the blood, 3-6 mM of ketone bodies in the blood would be considered to reach hyperketosis. Ketogenic food containing a high proportion
of fat has been successfully used to treat epileptic fits resistant to medication.4 In a typical epilepsy diet, fat accounts for 90% of the energy intake. Such meals bring about changes in the enterobacterial flora.5
References
Stojanovic V, Ihle S. Role of beta-hydroxybutyric acid in diabetic ketoacidosis: A review. Can Vet J. 2011; 52(4): 426-430. Web site. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058661/. Accessed September 24, 2016.
Laffel L. Ketone bodies: A review of physiology, pathophysiology and application of monitoring to diabetes. Diabetes Metab Res Rev. 1999; 15(6): 412-426. doi: 10.1002/(SICI)1520-7560(199911/12)15:6<412::AID-DMRR72>3.0.CO;2-8
Wilder RM, Winter MD. The threshold of ketogenesis. J Biol Chem. 1922; 52: 393-401. Web site. http://www.jbc.org/con-tent/52/2/393.short. Accessed September 24, 2016.
Kang HC, Chung DE, Kim DW, Kim HD. Early- and late- onset complications of the ketogenic diet for intractable epilepsy. Epilepsia. 2004; 45(9): 1116-1123. doi: 10.1111/j.0013-9580.2004.10004.x
Chu DM, Antony KM, Ma J, et al. The early infant gut microbiome varies in association with a maternal high-fat diet. Genome Med. 2016; 8(1): 77. doi: 10.1186/s13073-016-0330-z
Watanabe S, Hirakawa A, Aoe S, Fukuda K, Muneta T. Basic ketone engine and booster glucose engine for energy production. Diabetes Res Open J. 2016; 2(1): 14-23. doi: 10.17140/DROJ-2-125
Cahill GF Jr. Fuel metabolism in starvation. Ann Rev Nutr. 2006; 26: 1-22. doi: 10.1146/annurev.nutr.26.061505.111258
Goldblatt MW. Observation on the effect of various carbohydrates on the ketosis of starvation in human subjects. Biochem J. 1925; 19: 948-958. Web site. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1259284/. Accessed September 24, 2016.
Hirakawa A, Watanabe S, Tanaka K. Koda’s fasting therapy: Energy balance and intestinal bacterial flora. Adv Food Technol Nutr Sci Open J. 2015: 1(5): 112-123. doi: 10.17140/AFTNSOJ-1-120
Aagaard K, Petrosino J, Keitel W, et al. The human microbiome project strategy for comprehensive sampling of the human mi-crobiome and why it matters. FASEB J Off Publ Fed Am Soc Exp Biol. 2013; 27: 1012-1022. doi: 10.1096/fj.12-220806
Vael C, Verhulst SL, Nelen V, Goossens H, Desager KN. Intestinal microflora and body mass index during the first three years of life: An observational study. Gut Pathog. 2011; 3(1): 8. doi: 10.1186/1757-4749-3-8
Tuohy K, Rio DD. Diet-Microbe Interactions in the Gut: Effects on Human Health and Disease. 1st ed. CA, USA: Elsevier; 2014.
Gorvitovskaia A, Holmes SP, Huse SM. Interpreting prevotella and bacteroides as biomarkers of diet and lifestyle. Microbiome. 2016; 4: 15. doi: 10.1186/s40168-016-0160-7
Hayashi H, Sakamoto M, Benno Y. Fecal microbial diversity in a strict vegetarian as detemined by molecular analysis and cul-tivation. Microbiol Immunol. 2002; 46: 819-831. doi: 10.1111/j.1348-0421.2002.tb02769.x
Kurakawa T, Ogata K, Matsuda K, et al. Diversity of intestinal clostridium coccoides group in the Japanese population, as demonstragted by reverse transription-quantitative PCR. PLOS One. 2015. doi: 10.1371/journal.pone.0126226
Moorkoth D, Nampoothiri KM. Production and characterization of poly(3-hydroxy butyrate-co-3 hydroxyvalerate)(PHBV) by a novel holotolerant mangrove isolate. Bioresour Technol.2016; 201: 253-260. doi: 10.1016/j.biortech.2015.11.046
Robinson AM, Williamson DH. Physiological roles of ketone bodies as substrates and signals in mammalian tissues. Physiol Review. 1980; 60: 143-187. Web site. http://physrev.physiology.org/content/60/1/143. Accessed September 24, 2016.
Newman JC, Verdin E. β-hydroxybutyrate: Much more than a metabolite. Diabetes Res Clin Pract. 2014; 106(2): 173-181. doi: 10.1016/j.diabres.2014.08.009
Delcuve GP, Khan DH, Davie JR. Roles of histone deacetylases in epigenetic regulation: Emerging paradigms from studies with inhibitors. Clin Epigenetics. 2012; 4(1): 5. doi: 10.1186/1868-7083-4-5
Shimazu T, Hirschey MD, Newman J, et al. Suppression of oxidative stress by β-hydroxybutyrate, an endogenous histone deacetylase inhibitor. Science. 2013; 339(6116): 211-214. doi: 10.1126/science.1227166
Youm YH, Nguyen KY, Grant RW, et al. The ketone metabolite beta-hydroxybutyrate blocks NLRP3 inflammasome-mediated inflammatory disease. Nat Med. 2015; 21(3): 263-269. doi: 10.1038/nm.3804
Kesl SL, Poff AM, Ward NP, et al. Effects of exogenous ketone supplementation on blood ketone, glucose, triglyceride, and lipoprotein levels in Sprague-Dawley rats. Nutr Metab (Lond). 2016; 13(1): 9. doi: 10.1186/s12986-016-0069-y
Zhang J, Cao Q, Li S, et al. 3-Hydroxybutyrate methyl ester as a potential drug against Alzheimer’s disease via mitochondria protenction mechanism. Biomaterials. 2013; 34(30): 7552-7562. doi: 10.1016/j.biomaterials.2013.06.043
Cox PJ, Kirk T, Ashmore T, et al. Nutritional ketosis alters fuel preference and thereby endurance performance in athletes. Cell Metabolism. 2016; 24: 256-268. doi: 10.1016/j.cmet.2016.07.010
Floegel A. Low carbohydrate-high protein diets. BMJ. 2012; 344: e3801. doi: 10.1136/bmj.e3801
Fung TT, van Dam RM, Hankinson SE, et al. Low-carbohydrate diets and all-cause and cause-specific mortality: Two cohort studies. Ann Intern Med. 2010; 153(5): 289-298. doi: 10.1059/0003-4819-153-5-201009070-00003
Lagiou P, Sandin S, Weiderpass E. Low carbohydrate-high protein diet and mortality in a cohort of Swedish women. J Intern Med. 2007; e261: 366-374. doi: 10.1111/j.1365-2796.2007.01774.x
Ebe K. Diabetic diet and carobohydrate restricted diet: Safety and risk. Clin Funct Nutriol. 2016; 8(5): 243-246.
Veech RL. The therapeutic implications of ketone bodies: The effects of ketone bodies in pathological conditions: Ketosis, ke-togenic diet, redox states, insulin resistance, and mitochondrial metabolism. Prostaglandins Leukot Essent Fatty Acids. 2014; 70(3): 309-319. doi: 10.1016/j.plefa.2003.09.007
Bonuccelli G, Tsirigos A, Whitaker-Menezes D, et al. Ketones and lactate “fuel” tumor growth and metastasis: Evidence that cancer cells use oxidative mitochondrial metabolism. Cell Cycle. 2010; 9(17): 3506-3514. doi: 10.4161/cc.9.17.12731
Oleksyszyn J. The complete control of glucose level utilizing the composition of ketogenic diet with the gluconeogenesis in-hibitor, the anti-diabetic drug methormin, as a potential anti-cancer therapy. Med Hypotheses. 2011; 77(2): 171-173. doi: 10.1016/j. mehy.2011.04.001
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