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Are You Low Carb, Very Low Carb, Or Ketogenic?

Written by Wellness Club on July 1, 2017 – 8:09 am -

Are We Still Standing Behind Our Low Carb Diet Advice?

Nurse Mark says:

Every now and then someone writes us with what they really hope will be a "Gotcha!" that will simultaneously demonstrate their genius and place our ignorance on display for all the world to see.

Most of the time it is obvious that these folks have either spent far too much time studying at The University of Google, or that they have a particular agenda and "axe to grind" with their questions or comments.

We are not quite sure which of those is the case with the following letter we received since it is a little disjointed and hard to understand with its lack of punctuation and grammar. However, we think that the writer is taking us to task for favoring a Very Low Carbohydrate Ketogenic Diet.

An "Anonymous" writer recently asked:

"It’s 2017 lol do you still stand by the ‘carbs are bad for you’ ex-trend?
You know your articles written by some ‘doctors’ who got their degrees in some third-rated universities looks like word play on middle school science combined with things people promise in elections, right?"

(Here’s a request from us to you: If you are going to write us to tell us why we are wrong about something, please supply some supporting evidence and references – not just "everybody knows", or "I saw it on the internet." Real, actual citations like you will find at the end of all our scientific articles will be appreciated and will help support your case. Oh, and insults rarely achieve anything positive in swaying opinions – remember how well that recent "Basket of Deplorables" comment worked out…)

Dear Anonymous,

Welcome back from your year-long meditation retreat in the Himalayas! I can only assume that you have been in a cave the past year without television or internet connection. You are right, it is 2017.  And we stand by our recommendation of a ketogenic diet now more than ever.

Not only do we stand by our low carb dietary advice, we are finding more and more conventional scientific and clinical research and studies in the medical news every day that tells us that Dr. Myatt has been on the right track for 28 years. We recommend not just ‘low carb’ – but an out-and-out Very Low Carbohydrate Ketogenic Diet (VLCKD). I’ll let the Ketogenic Diet guru, Dr. Myatt, get you up to speed on the most recent science.

Dr. Myatt says:

Do we still stand by the low carb (ketogenic) diet in 2017?  You Betcha!  Evidence confirming the many health benefits of a VLCKD continues to unfold by the day. The use of a ketogenic diet is actually becoming well known in conventional medicine. Here’s what science shows to date.

For weight loss:

For weight loss, ketogenic diets have performed as well or better than low calorie/high carb diets. (1-4) The ketogenic diet is more effective than a low calorie diet for those with insulin resistance (IR), non-alcoholic fatty liver disease (NFLD), atherogenic dyslipidemia (AD) – a blood fat profile that predisposes to coronary artery disease. Many overweight and obese individuals exhibit one or more of these problems. (5)

Many people find a ketogenic diet easier to stick with to than a low calorie diet because of the appetite-curbing effect of ketosis. A ketogenic diet has a stimulating effect on our appetite control hormones. Ketones may also have a direct appetite-suppressant action. Staying on a ketogenic diet will keep ghrelin (the hunger hormone) and appetite levels low as long as the dieter stays in ketosis A VLCKD causes a reduction in lipogenesis (fat cell creation) and increased lipolysis (fat cell "burning").
A VLCKD reduces the resting respiratory quotient and gives the body greater metabolic efficiency in consuming fats.

Because the ketogenic diet contains higher protein intakes than the S.A.D. (Standard American Diet), muscle tissue is typically well-preserved while weight is lost. Increased metabolic costs of gluconeogenesis (the process of making glucose from protein) and the thermic effect of proteins means that a VLCKD makes the body use more energy to process the food it takes in.

A one-year study of 311 overweight/obese premenopausal women comparing various weight loss diets found the that weight loss over the long-haul (12 months) was better in Atkin’s (a ketogenic diet) than all others compared, as follows:

Atkins solidly beat out the Zone, the Ornish, and the LEARN (55–60% carbohydrate, 10% saturated fat, energy restricted) diets. After 12 months, weight loss in the Atkins group was −4.7 kg compared with −1.6 kg on the Zone Diet, −2.2 kg on the Ornish and −2.6 kg on the LEARN groups. Blood HDL and  triglyceride concentrations were improved more in the Atkins group compared with all other diet groups.(6-7)

Type II Diabetes:

Multiple studies have shown that a ketogenic diet lowers blood sugar and improves glycemic control in type 2 diabetic patients better than a calorie restricted, low glycemic diet. Weight loss was also more substantial in the ketogenic diet group.(8-10)

More participants in the ketogenic diet group were able to discontinue all diabetic medications. (7)

Cardiovascular disease:

A VLCKD lowers both cholesterol and triglycerides in obese patients and increases the size and volume of the low-density lipoprotein molecules, such as triglycerides and LDL ("bad") cholesterol. A ketogenic diet was also found to protect the heart and improve recovery after a heart attack. Compared to a low calorie diet, the ketogenic diet has been seen in numerous studies to lower cardiac risk factors better. (11-14)

In one study of healthy college age male athletes researchers found that while total cholesterol increased in the VLCKD group, it was an increase in HDL (the “good cholesterol) that caused this response and that other values, such as testosterone levels and insulin response, improved significantly in the VLCKD group and the researchers praised the safety of the VLCKD. (104)

Ketogenic diets decrease small LDL particles (the size that causes atherosclerosis) and increases large LDL particles (the kind that doesn’t contribute to atherosclerosis). (15-20)


Having been used clinically since the 1920′s, the role of ketogenic diets in epilepsy treatment is well established. (21-22)


This is a red-hot “emerging” topic. Remember you probably heard it here first.

[Nurse Mark notes: There are so many references and substantiation for use of a ketogenic diet in cancer that Dr. Myatt is writing a book on the subject.]

Here’s the short-course. A ketogenic diet is beneficial in treating cancer by a number of different mechanisms including:

  1. Decreasing the glucose substrate required for cancer cell metabolism. Most tumors express abnormalities in the number and function of their mitochondria. (23-28) Such abnormalities prevent the bioenergetic utilization of ketone bodies, which require functional mitochondria for their oxidation.
  2. Decreasing insulin, a secondary growth factor for cancer cells. (29-30)
  3. Decreasing inflammation. Inflammation acts to promote cancer by altering cell-to-cell communication and delaying local detoxification.(31-41) Metabolic ketosis has significant anti-inflammatory effects. (25, 42-45)
  4. Decreasing ROS production. Reactive Oxygen Species are known to promote cancer (46-48); metabolic ketosis decreases ROS production. (49-52)
  5. Reversing cachexia (the extreme wasting and weight loss of cancer) while simultaneously decreasing tumor weight. (53-55)
  6. Decreasing angiogenesis. (56-57)
  7. Inducing apoptosis. (27,45, 53)
  8. Suppressing the p53 oncogene, the most common point mutation observed in human cancer; more than 50% of all human tumors examined to date have identifiable p53 gene point mutations or deletions. A ketogenic diet has been shown to suppress the p53 oncogene in animal models. (43)
  9. Acting synergistically with chemotherapy and/or specific nutritional supplementation. (58-61)

Ongoing research into the use of ketogenic diets for cancer is very quickly proving that ketosis can have a profound, positive effect on slowing cancer growth even in advanced cancers. (62-82)

Neurological diseases:

Feared neurologic diseases including Alzheimer’s disease, Parkinson’s, brain trauma and Lou Gehrig’s disease (ALS) have all been demonstrated to respond favorably to the metabolic changes created by a ketogenic diet. (83-101)

Other conditions which may benefit from a ketogenic diet include acne (102) and polycystic ovary disease. (103)

In Summary:

Not only is the medical use of ketogenic diets not an “ex-trend” as our questioner believes, it is actually an “emerging” trend that you will continue to hear more and more about. In fact, don’t be surprised if your doctor prescribes a ketogenic diet to you one day soon.


1.)  Bueno NB, De Melo IS, De Oliveira SL, et al. Very-low-carbohydrate ketogenic diet v. low-fat diet for long-term weight loss: a meta-analysis of randomized controlled trials. Br J Nutr2013;110:1178–87.
2.)  Santos FL, Esteves SS, Da Costa PA, et al. Systematic review and meta-analysis of clinical trials of the effects of low carbohydrate diets on cardiovascular risk factors. Obes Rev2012;13:1048–66.
3.) Tobias DK, Chen M, Manson JE, et al. Effect of low-fat diet interventions versus other diet interventions on long-term weight change in adults: a systematic review and meta-analysis. Lancet Diabetes Endocrinol 2015;3:968–79.
4.) Sackner-Bernstein J, Kanter D, Kaul S. Dietary intervention for overweight and obese adults: comparison of low-carbohydrate and low-fat diets. A meta-analysis. PLoS ONE2015;10:e0139817.
5.) Mansoor N, Vinknes KJ, Veierod MB, et al. Effects of low-carbohydrate diets v. low-fat diets on body weight and cardiovascular risk factors: a meta-analysis of randomised controlled trials. Br J Nutr 2016;115:466–79.
6.) Mark S, Du TS, Noakes TD, et al. A successful lifestyle intervention model replicated in diverse clinical settings. S Afr Med J 2016;106:763–6.
7.)  Gardner CD, Kiazand A, Alhassan S, et al. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the A to Z Weight Loss Study: a randomized trial. JAMA2007;297:969–77.
8.) Westman EC, Yancy WS Jr, Mavropoulos JC, et al. The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on glycemic control in type 2 diabetes mellitus. Nutr Metab (Lond) 2008;5:36.
9.) Hussain TA, Mathew TC, Dashti AA, et al. Effect of low-calorie versus low-carbohydrate ketogenic diet in type 2 diabetes. Nutrition 2012;28:1016–21.
10.) Daly ME, Paisey R, Paisey R, et al. Short-term effects of severe dietary carbohydrate-restriction advice in Type 2 diabetes—a randomized controlled trial. Diabet Med2006;23:15–20.
11.) Bazzano LA, Hu T, Reynolds K, et al. Effects of low-carbohydrate and low-fat diets: a randomized trial. Ann Intern Med 2014;161:309–18.
12.) Yancy WS Jr, Olsen MK, Guyton JR, et al. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Ann Intern Med2004;140:769–77.
13.) Tay J, Brinkworth GD, Noakes M, et al. Metabolic effects of weight loss on a very-low-carbohydrate diet compared with an isocaloric high-carbohydrate diet in abdominally obese subjects. J Am Coll Cardiol 2008;51:59–67.
14.) Feinman RD, Volek JS, Westman EC. Dietary carbohydrate restriction in the treatment of diabetes and metabolic syndrome. Clin Nutr Insight 2008;34:5.
15.) Volek JS, Phinney SD, Forsythe CE, et al. Carbohydrate restriction has a more favorable impact on the metabolic syndrome than a low fat diet. Lipids 2009;44:297–309.
16.) Aude YW, Agatston AS, Lopez-Jimenez F, et al. The national cholesterol education program diet vs a diet lower in carbohydrates and higher in protein and monounsaturated fat: a randomized trial. Arch Intern Med 2004;164:2141–6.
17.) Volek JS, Fernandez ML, Feinman RD, et al. Dietary carbohydrate restriction induces a unique metabolic state positively affecting atherogenic dyslipidemia, fatty acid partitioning, and metabolic syndrome. Prog Lipid Res 2008;47:307–18.
18.) Forsythe CE, Phinney SD, Feinman RD, et al. Limited effect of dietary saturated fat on plasma saturated fat in the context of a low carbohydrate diet. Lipids 2010;45:947–62.
19.) Wood RJ, Volek JS, Liu Y, et al. Carbohydrate restriction alters lipoprotein metabolism by modifying VLDL, LDL, and HDL subfraction distribution and size in overweight men. J Nutr2006;136:384–9.
20.) Volek JS, Sharman MJ, Forsythe CE. Modification of lipoproteins by very low-carbohydrate diets. J Nutr 2005;135:1339–42.
21.) Kessler SK, Neal EG, Camfield CS, Kossoff EH. Dietary therapies for epilepsy: future research. Epilepsy Behav. 2011;22:17–22. [PubMed]
22.) Kossoff E. The fat is in the fire: ketogenic diet for refractory status epilepticus. Epilepsy Curr. 2011;11:88–89. [PMC free article] [PubMed]
23.) Meixensberger J, Herting B, Roggendorf W, Reichmann H: Metabolic patterns in malignant gliomas. J Neurooncol 1995, 24:153-161
24.) Pedersen PL: Tumor mitochondria and the bioenergetics of cancer cells. Prog Exp Tumor Res 1978, 22:190-274.
25.) Seyfried TN, Sanderson TM, El-Abbadi MM, McGowan R, Mukherjee P.: Role of glucose and ketone bodies in the metabolic control of experimental brain cancer. Br J Cancer. 2003 Oct 6;89(7):1375-82.
26.) Fearon KC.: Nutritional pharmacology in the treatment of neoplastic disease. Baillieres Clin Gastroenterol. 1988 Oct;2(4):941-9.
27.) Skinner R, Trujillo A, Ma X, Beierle EA. Ketone bodies inhibit the viability of human neuroblastoma cells. J Pediatr Surg. 2009 Jan;44(1):212-6; discussion 216.
28.) Muti P, Quattrin T, Grant BJ, Krogh V, Micheli A, Schünemann HJ, Ram M, Freudenheim JL, Sieri S, Trevisan M, Berrino F. Fasting glucose is a risk factor for breast cancer: a prospective study. Cancer Epidemiol Biomarkers Prev, 2002 Nov;11(11):1361-8.
29.) Venkateswaran V, Haddad AQ, Fleshner NE, Fan R, Sugar LM, Nam R, Klotz LH, Pollak M. Association of diet-induced hyperinsulinemia with accelerated growth of prostate cancer (LNCaP) xenografts.J Natl Cancer Inst. 2007 Dec 5;99(23):1793-800. Epub 2007 Nov 27.
30.) Borugian MJ, Sheps SB, Kim-Sing C, Van Patten C, Potter JD, Dunn B, Gallagher RP, Hislop TG. Insulin, macronutrient intake, and physical activity: are potential indicators of insulin resistance associated with mortality from breast cancer? Cancer Epidemiol Biomarkers Prev. 2004 Jul;13(7):1163-72.
31.) Khan G.: Epstein-Barr virus, cytokines, and inflammation: A cocktail for the pathogenesis of Hodgkin’s lymphoma? Exp Hematol. 2006 Apr;34(4):399-406.
32.) Dalgleish AG, O’Byrne K. Inflammation and cancer: the role of the immune response and angiogenesis. Cancer Treat Res. 2006;130:1-38.
33.) Schottelius AJ, Dinter H.: Cytokines, NF-kappaB, microenvironment, intestinal inflammation and cancer. Cancer Treat Res. 2006;130:67-87.
33a.) Wiseman H, Halliwell B: Damage to DNA by reactive oxygen and nitrogen species: role in inflammatory disease and progression to cancer. Biochem J 1996, 313:17-29.
34.) Otani T, Iwasaki M, Sasazuki S, Inoue M, Tsugane S.: Plasma C-reactive protein and risk of colorectal cancer in a nested case-control study: Japan public health center-based prospective study. Cancer Epidemiol Biomarkers Prev. 2006 Apr;15(4):690-5.
35) Dobrovolskaia MA, Kozlov SV.: Inflammation and cancer: when NF-kappaB amalgamates the perilous partnership.Curr Cancer Drug Targets. 2005 Aug;5(5):325-44.
36.) Naldini A, Carraro F.: Role of inflammatory mediators in angiogenesis. Curr Drug Targets Inflamm Allergy. 2005 Feb;4(1):3-8.
37.) Ohshima H, Tazawa H, Sylla BS, Sawa T.: Prevention of human cancer by modulation of chronic inflammatory processes. Mutat Res. 2005 Dec 11;591(1-2):110-22. Epub 2005 Aug 3.
38.) Coussens LM, Werb Z.: Inflammation and cancer. Nature. 2002 Dec 19-26;420(6917):860-7.
39.) Stewart JW, Koehler K, Jackson W, Hawley J, Wang W, Au A, Myers R, Birt DF: Prevention of mouse skin tumor promotion by dietary energy restriction requires an intact adrenal gland and glucocorticoid supplementation restores inhibition.Carcinogenesis 2005, 26:1077-1084
40.) Zhu Z, Jiang W, Thompson HJ: Mechanisms by which energy restriction inhibits rat mammary carcinogenesis: in vivo effects of corticosterone on cell cycle machinery in mammary carcinomas. Carcinogenesis 2003, 24:1225-1231.
41.) Patel NV, Finch CE: The glucocorticoid paradox of caloric restriction in slowing brain aging.Neurobiol Aging 2002, 23:707-717.
42.)Gasior M, Rogawski MA, Hartman AL. Neuroprotective and disease-modifying effects of the ketogenic diet.Behav Pharmacol. 2006 Sep;17(5-6):431-9.
43.) Maalouf M, Rho JM, Mattson MP. The neuroprotective properties of calorie restriction, the ketogenic diet, and ketone bodies. Brain Res Rev. 2009 Mar;59(2):293-315. Epub 2008 Sep 25.
44.) Garai J, Lóránd T, Molnár V. Ketone bodies affect the enzymatic activity of macrophage migration inhibitory factor. Life Sci. 2005 Aug 5;77(12):1375-80.
45.) Seyfried TN, Kiebish M, Mukherjee P, Marsh J. Targeting energy metabolism in brain cancer with calorically restricted ketogenic diets. Epilepsia. 2008 Nov;49 Suppl 8:114-6.
46.) Shi DY, Xie FZ, Zhai C, Stern JS, Liu Y, Liu SL. The role of cellular oxidative stress in regulating glycolysis energy metabolism in hepatoma cells. Mol Cancer. 2009 Jun 5;8(1):32. [Epub ahead of print]
47.) Halliwell B. Oxidative stress and cancer: have we moved forward? Biochem J. 2007 Jan 1;401(1):1-11.
48.) Brown N., Bicknell R. Hypoxia and oxidative stress in breast cancer: Oxidative stress – its effects on the growth, metastatic potential and response to therapy of breast cancer. Breast Cancer Res 2001, 3:323-327.
49.) Veech RL: The therapeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism. Prostaglandins Leukot Essent Fatty Acids 2004, 70:309-319.
50.) Veech RL: Metabolic control analysis of ketone and insulin action: Implications for phenotyping of disease and design of therapy. Lecture: The Dynamic and Energetic Basis of Health and Aging Monday, Nov 11 – Wednesday, Nov 13, 2002, The Cloister’s, NIH, Bethesda MD.
51.) Masuda R, Monahan JW, Kashiwaya Y: D-beta-hydroxybutyrate is neuroprotective against hypoxia in serum-free hippocampal primary cultures. J Neurosci Res 2005, 80:501-509.
52.) Bough KJ, Rho JM. Anticonvulsant mechanisms of the ketogenic diet. Epilepsia. 2007 Jan;48(1):43-58.
53.)Beck SA, Tisdale MJ. Effect of insulin on weight loss and tumour growth in a cachexia model. Br J Cancer. 1989 May;59(5):677-81.
54.) Tisdale MJ, Brennan RA, Fearon KC. Reduction of weight loss and tumour size in a cachexia model by a high fat diet. Br J Cancer. 1987 Jul;56(1):39-43
55.) Beck SA, Tisdale MJ. Nitrogen excretion in cancer cachexia and its modification by a high fat diet in mice. Cancer Res. 1989 Jul 15;49(14):3800-4.
56.) Zhou W, Mukherjee P, Kiebish MA, Markis WT, Mantis JG, Seyfried TN. The calorically restricted ketogenic diet, an effective alternative therapy for malignant brain cancer.Nutr Metab (Lond). 2007 Feb 21;4:5.
57.) Seyfried TN, Mukherjee P. Targeting energy metabolism in brain cancer: review and hypothesis. Nutr Metab (Lond). 2005 Oct 21;2:30.
58.) Berrigan D, Perkins SN, Haines DC, Hursting SD.: Adult-onset calorie restriction and fasting delay spontaneous tumorigenesis in p53-deficient mice. Carcinogenesis. 2002 May;23(5):817-22.
59.) Marsh J, Mukherjee P, Seyfried TN. Drug/diet synergy for managing malignant astrocytoma in mice: 2-deoxy-D-glucose and the restricted ketogenic diet. Nutr Metab (Lond). 2008 Nov 25;5:33.
60.) Otto C, Kaemmerer U, Illert B, Muehling B, Pfetzer N, Wittig R, Voelker HU, Thiede A, Coy JF. Growth of human gastric cancer cells in nude mice is delayed by a ketogenic diet supplemented with omega-3 fatty acids and medium-chain triglycerides. BMC Cancer. 2008 Apr 30;8:122.
61.) Wargovich MJ, Cunningham JE.:Diet, individual responsiveness and cancer prevention. J Nutr. 2003 Jul;133(7 Suppl):2400S-2403S.
62.) Denley A, Carroll JM, Brierley GV, Cosgrove L, Wallace J, Forbes B, et al. Differential activation of insulin receptor substrates 1 and 2 by insulin-like growth factor-activated insulin receptors. Mol Cell Biol. 2007;27:3569–3577. [PMC free article] [PubMed]
63.) Giovannucci E, Harlan DM, Archer MC, Bergenstal RM, Gapstur SM, Habel LA, et al. Diabetes and cancer: a consensus report. CA Cancer J Clin. 2010;60:207–221. [PubMed]
64.) Rose DP, Vona-Davis L. The cellular and molecular mechanisms by which insulin influences breast cancer risk and progression. Endocr Relat Cancer. 2012;19:R225–R241. [PubMed]
65.) Renehan AG, Frystyk J, Flyvbjerg A. Obesity and cancer risk: the role of the insulin-IGF axis. Trends Endocrinol Metab. 2006;17:328–336. [PubMed]
66.) AA.VV. Research in cancer Science 192562x+xii+xiv.
67.) Warburg O, Wind F, Negelein E. The metabolism of tumors in the body. J Gen Physiol. 1927;8:519–530. [PMC free article] [PubMed]
68.) Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144:646–674.[PubMed]
69.) Warburg O. On respiratory impairment in cancer cells. Science. 1956;124:269–270. [PubMed]
70.) Pelicano H, Xu RH, Du M, Feng L, Sasaki R, Carew JS, et al. Mitochondrial respiration defects in cancer cells cause activation of akt survival pathway through a redox-mediated mechanism. J Cell Biol. 2006;175:913–923. [PMC free article] [PubMed]
71.) Sandri M, Barberi L, Bijlsma AY, Blaauw B, Dyar KA, Milan G, et al. Signalling pathways regulating muscle mass in ageing skeletal muscle. the role of the IGF1-akt-mTOR-FoxO pathway Biogerontology 2013;. e-pub ahead of print 19 May 2013. [PubMed]
72.) Schwertfeger KL, McManaman JL, Palmer CA, Neville MC, Anderson SM. Expression of constitutively activated akt in the mammary gland leads to excess lipid synthesis during pregnancy and lactation. J Lipid Res. 2003;44:1100–1112. [PubMed]
73.) Klement RJ, Kammerer U. Is there a role for carbohydrate restriction in the treatment and prevention of cancer. Nutr Metab (Lond) 2011;8:75. [PMC free article] [PubMed]
74.) Tisdale MJ, Brennan RA, Fearon KC. Reduction of weight loss and tumour size in a cachexia model by a high fat diet. Br J Cancer. 1987;56:39–43. [PMC free article] [PubMed]
75.) Beck SA, Tisdale MJ. Effect of insulin on weight loss and tumour growth in a cachexia model. Br J Cancer. 1989;59:677–681. [PMC free article] [PubMed]
76.) Ho VW, Leung K, Hsu A, Luk B, Lai J, Shen SY, et al. A low carbohydrate, high protein diet slows tumor growth and prevents cancer initiation. Cancer Res. 2011;71:4484–4493. [PubMed]
77.) Otto C, Kaemmerer U, Illert B, Muehling B, Pfetzer N, Wittig R, et al. Growth of human gastric cancer cells in nude mice is delayed by a ketogenic diet supplemented with omega-3 fatty acids and medium-chain triglycerides. BMC Cancer. 2008;8:122. [PMC free article] [PubMed]
78.) Seyfried BT, Kiebish M, Marsh J, Mukherjee P. Targeting energy metabolism in brain cancer through calorie restriction and the ketogenic diet. J Cancer Res Ther. 2009;5 (Suppl 1:S7–S15. [PubMed]
79.) Zhou W, Mukherjee P, Kiebish MA, Markis WT, Mantis JG, Seyfried TN. The calorically restricted ketogenic diet, an effective alternative therapy for malignant brain cancer. Nutr Metab (Lond) 2007;4:5. [PMC free article] [PubMed]
80.) Schmidt M, Pfetzer N, Schwab M, Strauss I, Kammerer U. Effects of a ketogenic diet on the quality of life in 16 patients with advanced cancer: a pilot trial. Nutr Metab (Lond) 2011;8:54.[PMC free article] [PubMed]
81.) Nebeling LC, Lerner E. Implementing a ketogenic diet based on medium-chain triglyceride oil in pediatric patients with cancer. J Am Diet Assoc. 1995;95:693–697. [PubMed]
82.) Nebeling LC, Miraldi F, Shurin SB, Lerner E. Effects of a ketogenic diet on tumor metabolism and nutritional status in pediatric oncology patients: Two case reports. J Am Coll Nutr. 1995;14:202–208.[PubMed]
83.) Baranano KW, Hartman AL. The ketogenic diet: uses in epilepsy and other neurologic illnesses. Curr Treat Options Neurol. 2008;10:410–419. [PMC free article] [PubMed]
84.) Stafstrom CE, Rho JM. The ketogenic diet as a treatment paradigm for diverse neurological disorders. Front Pharmacol. 2012;3:59. [PMC free article] [PubMed]
85.) Bough KJ, Rho JM. Anticonvulsant mechanisms of the ketogenic diet. Epilepsia. 2007;48:43–58.[PubMed]
86.) Huffman J, Kossoff EH. State of the ketogenic diet(s) in epilepsy. Curr Neurol Neurosci Rep. 2006;6:332–340. [PubMed]
87.) Garriga-Canut M, Schoenike B, Qazi R, Bergendahl K, Daley TJ, Pfender RM, et al. 2-deoxy-D-glucose reduces epilepsy progression by NRSF-CtBP-dependent metabolic regulation of chromatin structure. Nat Neurosci. 2006;9:1382–1387. [PubMed]
88.) Maalouf M, Rho JM, Mattson MP. The neuroprotective properties of calorie restriction, the ketogenic diet, and ketone bodies. Brain Res Rev. 2009;59:293–315. [PMC free article] [PubMed]
89.) Palop JJ, Mucke L. Epilepsy and cognitive impairments in alzheimer disease. Arch Neurol. 2009;66:435–440. [PMC free article] [PubMed]
90.) Roberson ED, Halabisky B, Yoo JW, Yao J, Chin J, Yan F, et al. Amyloid-beta/fyn-induced synaptic, network, and cognitive impairments depend on tau levels in multiple mouse models of alzheimer’s disease. J Neurosci. 2011;31:700–711. [PMC free article] [PubMed]
91.) Noebels J. A perfect storm: converging paths of epilepsy and alzheimer’s dementia intersect in the hippocampal formation. Epilepsia. 2011;52 (Suppl 1:39–46. [PMC free article] [PubMed]
92.) Kapogiannis D, Mattson MP. Disrupted energy metabolism and neuronal circuit dysfunction in cognitive impairment and alzheimer’s disease. Lancet Neurol. 2011;10:187–198. [PMC free article][PubMed]
93.) Henderson ST, Vogel JL, Barr LJ, Garvin F, Jones JJ, Costantini LC. Study of the ketogenic agent AC-1202 in mild to moderate alzheimer’s disease: A randomized, double-blind, placebo-controlled, multicenter trial. Nutr Metab (Lond) 2009;6:31. [PMC free article] [PubMed]
94.) Kashiwaya Y, Takeshima T, Mori N, Nakashima K, Clarke K, Veech RL. D-beta-hydroxybutyrate protects neurons in models of Alzheimer’s and Parkinson’s disease. Proc Natl Acad Sci USA. 2000;97:5440–5444. [PMC free article] [PubMed]
95.) Van der Auwera I, Wera S, Van Leuven F, Henderson ST. A ketogenic diet reduces amyloid beta 40 and 42 in a mouse model of alzheimer’s disease. Nutr Metab (Lond) 2005;2:28. [PMC free article][PubMed]
96.) Vanitallie TB, Nonas C, Di Rocco A, Boyar K, Hyams K, Heymsfield SB. Treatment of parkinson disease with diet-induced hyperketonemia: a feasibility study. Neurology. 2005;64:728–730.[PubMed]
97.) Prins ML, Fujima LS, Hovda DA. Age-dependent reduction of cortical contusion volume by ketones after traumatic brain injury. J Neurosci Res. 2005;82:413–420. [PubMed]
98.) Appelberg KS, Hovda DA, Prins ML. The effects of a ketogenic diet on behavioral outcome after controlled cortical impact injury in the juvenile and adult rat. J Neurotrauma. 2009;26:497–506.[PMC free article] [PubMed]
99.) Schwartzkroin PA, Wenzel HJ, Lyeth BG, Poon CC, Delance A, Van KC, et al. Does ketogenic diet alter seizure sensitivity and cell loss following fluid percussion injury. Epilepsy Res. 2010;92:74–84.[PubMed]
100.) Siva N. Can ketogenic diet slow progression of ALS. Lancet Neurol. 2006;5:476. [PubMed]
101.) Zhao Z, Lange DJ, Voustianiouk A, MacGrogan D, Ho L, Suh J, et al. A ketogenic diet as a potential novel therapeutic intervention in amyotrophic lateral sclerosis. BMC Neurosci. 2006;7:29.[PMC free article] [PubMed]
102.) Paoli A, Grimaldi K, Toniolo L, Canato M, Bianco A, Fratter A. Nutrition and acne: therapeutic potential of ketogenic diets. Skin Pharmacol Physiol. 2012;25:111–117. [PubMed]
103.) Mavropoulos JC, Yancy WS, Hepburn J, Westman EC. The effects of a low-carbohydrate, ketogenic diet on the polycystic ovary syndrome: a pilot study. Nutr Metab (Lond) 2005;2:35. [PMC free article] [PubMed]
104.) Silva Jeremy, The effects of very high fat, very low carbohydrate diets on safety, blood lipid profile, and anabolic hormone status. Journal of the International Society of Sports Nutrition 2014 11 (Suppl 1):P39 DOI: 10.1186/1550-2783-11-S1-P39©

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