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Quick Silver Pilot Scooter
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Image by Don Johnson 395
P-51 Mustang – QuickSilver
The P-51 Mustang is an American single-seat fighter aircraft that the Allied Forces used during World War II and the Korean War. In addition to being economical to produce, P-51’s were fast and highly durable aircraft.
The QuickSilver Mustang 51 HY, “The Resurrected Veteran”, is the result of a fourteen-year reconstruction program. The pain scheme is a flying celebration of this nation’s veterans, and those who give the ultimate sacrifice.

The P-51 Mustang is an American single-seat fighter aircraft that the Allied Forces used during World War II and the Korean War. In addition to being economical to produce, P-51’s were fast and highly durable aircraft.
The QuickSilver Mustang 51 HY, “The Resurrected Veteran”, is the result of a fourteen-year reconstruction program. The pain scheme is a flying celebration of this nation’s veterans, and those who give the ultimate sacrifice.

With Vance Breese at the controls, who was one of the most famous test pilots in his day, the XP-51 reached 382 mph, exceeding the P-40’s top speed by 25 mph.5 The P-51 was an immediate success and it even outperformed the Spitfire.6 Unique to the P-51 was the laminar flow wing design which was developed by the US National Advisory Committee for Aeronautics (NACA). Contemporary aircraft wings featured a wing cross-section with maximum thickness about a fifth of the way across the wing from the leading edge, with most of the camber on the top of the wing. The laminar flow wing, in contrast, has its maximum thickness well aft from the leading edge, and has almost as much camber on top as on the bottom. This feature reduced turbulent flow across the wing, thereby, reducing drag and increasing speed and range. Drag was also reduced by positioning a ventral radiator underneath the rear of the fuselage, to present the smallest possible fuselage cross section. The British Purchasing Commission was enthusiastic about the plane, and confirmed a production order for 320 Mustang Is. This was later increased by 300 for NA-83s, which differed only in minor details; the British designation was Mustang IA.7 Powered by the 1,100 hp Allison V-1710-39 (F3R) engine, the airplanes performance was only impressive up to 15,000 ft. However, performance would be dramatically improved once the airframe was matched with the Rolls-Royce Merlin engine. This is not to say that the Allison wasn’t a good engine as it performed very well on the Lockheed P-38. The problem with the Allison had more to do with the USAAF’s heavy reliance on turbosupercharging. This requirement was impossible to meet for all aircraft, due to a shortage of metal alloys, such as tungsten. There was some experimentation with turbosupercharged P-40s by designer Donaldson R. Berlin and these planes outperformed the Spitfire and Messerschmitt Bf 109.8

With the limitations for fighter duties due to the Allison engine, nevertheless, the Mustang had good ground attack potential, and its high speed at low altitude, made it ideal for tactical reconnaissance. To enhance altitude capabilities, a mockup was devised in England to use the Rolls-Royce Merlin engine in the P-51 airframe. One concept was to locate the new engine behind the cockpit, but this idea was rejected and the Merlin was mounted in the conventional position in the nose. Four airframes were adapted in England to take the Merlin engine. These four planes known as Mustang Xs had deep intakes below the engine for carburetor air. The results of the British tests were passed on to North American. In the meantime, North American had undertaken a similar conversion project and was building two Packard Merlin-powered Mustangs. Level speed improvement was increased 51 mph, to 441 mph. The airframes were strengthened to accommodate the extra power, the ventral radiator was deepened, and the carburetor intake was moved from above the nose to below, to accommodate the Merlin updraft induction system.11 Even before the Army’s Merlin powered Mustangs had flown, The US Army ordered 2,200 of the more powerful fighters. For a short time, this model was designated P-78, then redesignated as P-51B. 25 P-51Bs and 275 P-51Cs were given the British designation Mustang III. The California Mustangs were known as the P-51B-NA and the Dallas, Texas facility produced the P-51C-NT.12 The Merlin-powered P-5lB and its Dallas-built twin, the P-51C, began operations in December 1943.
A further improvement to the Mustang was introduced when a graceful teardrop canopy was installed to eliminate the dangerous blind area created by the faired cockpit. First tested on two P-51Bs, they became standard on the P-51D and all later models. 280 P-51Ds were given the RAF designation Mustang IV. The P-51D became the version produced in the greatest quantities, 7,954 being completed. The P-51D model carried six .50 cal. machine guns instead of the four mounted in the P-51Bs. Other refinements, such as moving the wing forward slightly and providing for rocket launchers, were included. The first P-51Ds types were delivered without dorsal fins, but this feature was added to compensate for keel-loss when the bubble canopy was adopted.
Later developments to the P-51 series included the final production type, the P-51H with several changes which made it the fastest production variant with a maximum speed of 487 mph at 25,000 feet. Five hundred fifty-five P-51H’s were delivered before VJ Day out of an original order for 1,445 machines.13

The P-51D with the dorsal fin, represents the most typical Mustang configuration. It had a 37-foot wingspan with an area of 233 square feet and was 32 feet 3 inches long. Height was 13 feet 8 inches. The Packard-built Merlin V-1650-7 was capable of delivering 1,695 hp which provided a speed of 437 mph at 25,000 feet. Weights were 7,125 lbs. empty and 10,100 lbs. normal gross, but an additional 2,000 lbs. could be carried. Internal fuel capacity was 105 gallons, giving a range of 950 miles at 362 miles per hour at 25,000 feet. Armament was six .50 cal. wing-mounted machine guns with a total of 1,880 rounds.
To say the Merlin Mustangs were successful would be an understatement. The P-51 became one of the aviation world’s elite. The total number of 14,819 Mustangs of all types were built for the Army. American Mustangs destroyed 4,950 enemy aircraft in Europe to make them the highest scoring US fighter in the theater. They were used as dive-bombers, bomber escorts, ground-attackers, interceptors, for photo-recon missions, trainers, transports (with a jump-seat), and after the war, high performance racers.

“Ketogene Diäten. Vorsicht bei Verzicht auf Kohlenhydrate“ – eine Klarstellung
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Image by Ketose Portal
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Im Artikel „Ketogene Diäten. Vorsicht bei Verzicht auf Kohlenhydrate“ wird empfohlen, sich nicht ketogen zu ernähren. Wir als Ketoseportal können das natürlich nicht so stehen lassen.

Hier eine Richtigstellung der Fakten:

Dieser Artikel sagt prinzipiell aus, dass

a) kohlenhydratreduzierte Diäten nur helfen bei Epilepsie, alle weiteren Anwendungsfälle sind nicht nachgewiesen

b) ketogene Diäten zu Ablagerungen an den Gefäßen führen mit der Folge von Schlaganfällen oder Herzinfarkten

c) Ketogene Diät führt zu einer erhöhten Harnsäureproduktion und kann somit zu Gicht führen

Der Artikel zitiert als Quellen nur Interviewpartnern wie Professor Georg Wechsler oder Margret Morlo. Wissenschaftliche Studien werden nicht angegeben. Soviel schon mal zur Tiefe der Recherche, die der Journalist da unternommen hat. Vielleicht ist deswegen auch die Kommentarfunktion ausgeschaltet bei dem Artikel.

Schauen wir doch mal, was an den Punkten jeweils an Wahrheit dran ist.

Zu a) kohlenhydratreduzierte Diäten nur helfen bei Epilepsie, alle weiteren Anwendungsfälle sind nicht nachgewiesen

Dass Ketose bei Epilepsie hilft, ist lange nachgewiesen. Außerdem ist seit über 20 Jahren bekannt, dass Kohlenhydratverzehr zum Metabolischen Syndrom, das zusammen hängt mit Herzkrankheiten, Diabetes, Bluthochdruck, etc. Der Verzicht auf Kohlenhydrate könnte also durchaus helfen, diese Krankheiten zu lindern oder sogar zu heilen.

Kohlenhydratreduzierte Diäten helfen nachgewiesenermaßen für


Risiko kardiovaskulärer Krankheiten



Erste Hinweise in Studien gibt es auf eine Wirksamkeit bei



Neurologischen Krankheiten


Außerdem gibt es weitere Anwendungsfelder, die wohl erst in den nächsten Jahren wissenschaftlich nachgewiesen werden, aber schon von Ketanern in Foren diskutiert werden. Einfach mal bei reddit unter /keto suchen.

b) ketogene Diäten zu Ablagerungen an den Gefäßen führen mit der Folge von Schlaganfällen oder Herzinfarkten

(„Es besteht die Gefahr, dass eine nur fettreiche Ernährung zu Ablagerungen an den Gefäßen führt. Die Folge davon können Schlaganfall oder Herzinfarkt sein.“)

Dies beruht auf Ernährungsempfehlungen aus den 60er / 70er Jahren. Es wurde damals angenommen, dass Fett und Cholesterin zuständig ist für eine Verengung der Gefäße. Selbst groß angelegte Studien konnten dies nicht wirklich nachweisen.
Was man jedoch nachweisen konnte, ist, dass der Verzehr von vielen Kohlenhydraten zu mehr ungesunden Cholesterinpartikeln führt. Cholesterin ist nicht gleich Cholesterin. Es gibt unterschiedliche Partikel. Die fiesen kleinen dichten, die zu Ablagerungen an den Gefäßen führen, werden von der Leber aus Kohlenhydraten gebaut.

Genauer gesagt macht die Leber große Fetttropfen, wenn viele Kohlenhydrate gegessen werden. Diese großen Fetttropfen werden in Transportblasen gesteckt. Zusammen bilden Fetttropfen und Transportblase dann die sogenannten LDL Partikel. Diese wandern durch den Körper und geben einen Teil des Fetts ab als Energie an die Zellen. Was übrig bleibt, sind kleine dichte LDL Partikel. Fiese kleine dichte LDL Partikel, die bevorzugt in Gefäßen rumhängen und da Ablagerungen machen.
Wenn wenig Kohlenhydrate da sind, baut die Leber mittelgroße Fetttropfen und legt diese ab in der Transportblase. Dies sind ebenfalls LDL Partikel. Diese mittelgroßen werden aber nie zu kleinen dichten LDL Partikeln, sondern bleiben fluffig. Fluffige LDL Partikel sind unheimlich nett und kuschelig und machen keine Ablagerungen in den Gefäßen.

Kurz gesagt:

Wenig Kohlenhydrate = wenig kleine dichte LDL Partikel
Es sind also Kohlenhydrate, nicht Fett, die Schlaganfälle und Herzinfarkte verursachen.

(Lieber Herr Prof. Wechsler, kennen Sie das Buch „Good Calories Bad Calories“? Wenn Sie mir mehr Studien zeigen können, die darauf hinweisen, dass eine ketogene Ernährungsweise zu Ablagerungen an den Gefäßen führt als Herr Taubes Studien aufführt dazu, dass Kohlenhydrate zu Ablagerungen an den Gefäßen – dann haben Sie hiermit eine persönliche Entschuldigung via Skype und ein persönliches Interview zur Gegendarstellung gewonnen.

Sorry, den Kommentar konnte ich mir nicht verkneifen. Vielleicht weil ich beeindruckt bin, dass Sie einen Professortitel haben. Das heißt, dass Sie viel geforscht und gelesen haben, so einen Titel bekommt man nicht einfach so. Ich wünschte nur, die Forschungsergebnisse zu Low Carb würden zu mehr Ärzten und Professoren durchdringen. Dann würden Menschen wie meine Mama vielleicht nicht fast an Herzproblemen sterben. Oder übergewichtig sein mit Diabetes. Oder mit Erwachsenen-Akne kämpfen. Oder mit Alzheimer. Oder Migräne. Das macht mich wahrscheinlich etwas wütend und daher mein fieser Kommentar. Über ein Interview mit Ihnen würde ich mich trotzdem freuen Herr Professor Wechsler.)

c) Ketogene Diät führt zu einer erhöhten Harnsäureproduktion und kann somit zu Gicht führen

Das ist zum Teil richtig. Bei einer Umstellung von einer Ernährung mit vielen Kohlenhydraten zur ketogenen Ernährung produziert der Körper für mehrere Tage bis Wochen mehr Harnsäure. Danach produziert der Körper genauso viel Harnsäure wie vorher, wenn nicht sogar weniger.

Was genau die zwischenzeitliche Erhöhung der Harnsäure auslöst, ist noch unklar. Es hängt in jedem Fall mit der Umstellung der Energieversorgung des Körpers von Glukose auf Ketone zusammen. Möglicherweise ist das Hirn (braucht am meisten Energie aller Organe im Körper, selbst bei Doofen) verzweifelt, weil es erstmal keine Energie in der gewohnten Form mehr bekommt. Dann baut der Körper etwas Muskelmasse ab und baut die Proteine zu Glukose um. In diesem Prozess entsteht wahrscheinlich die Harnsäure.
Wenn der Körper eine Weile lang nur Ketone als Nahrung hat, gewöhnt er sich daran. Dann funktioniert das Hirn wieder super und ist sogar glücklicher als zuvor, denn es Ketone liefern eine hochwertigere Energie als Glukose.
(Wer jetzt Angst um seine hart trainierten Muskeln hat: auch die leiden nur kurzfristig. Studien haben gezeigt, dass nach kurzer Zeit wieder alles dran ist. Und ja, man kann auf Ketose auch Muskeln aufbauen. Dauert „optisch“ nur länger, weil es reine Muskelmasse ist und keine Fettschicht darauf ist wie beim Muskelaufbau mit Kohlenhydraten.)

Bei den meisten Menschen ist eine vorübergehende Erhöhung der Harnsäure kein Grund zur Beunruhigung. Menschen, die zu Gicht neigen, sollten sich für eine Umstellung auf jeden Fall ärztliche Unterstützung holen.
Wenn du selbst bisher keine Probleme mit Gicht hattest, aber Verwandte von dir, lieber auch auf Nummer sicher gehen. Eine Begleitung von einem Arzt, der sich mit Ketose auskennt bei der Umstellung ist nie verkehrt.

„Wer sich ketogen ernährt, sollte daher regelmäßig die Harnsäure kontrollieren lassen.“
Damit stimme ich überein. Sicher ist sicher!
Man sollte am besten auch andere Werte messen lassen. Damit man mit eigenen Augen sehen kann, wie Entzündungswerte nach unten gehen, weniger fiese dichte LDL Partikel im Körper sind, der Blutdruck sich normalisiert,… mit anderen Worten: damit du mit eigenen Augen sehen kannst, wie du durch Ketose gesünder und fitter wirst.

Im Gegensatz zum Spiegel, der völlig ohne wissenschaftliche Quellen ausgekommen ist um gegen Ketose zu wettern – hier ein kleiner Auszug von Studien zu Ketose. Die Studien erklären, wie Ketose bei Übergewicht, (Markern für) Herzkrankheiten, Diabetes, Akne, Krebs, PCOS und neurologischen Krankheiten hilft:

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.

Baranano KW, Hartman AL. The ketogenic diet: uses in epilepsy and other neurologic illnesses. Curr Treat Options Neurol 2008; 10: 410–419.

Basu S, Yoffe P, Hills N, Lustig RH. The relationship of sugar to population-level diabetes prevalence: An econometric analysis of repeated cross-sectional data. PLoS One 2013; 8: e57873.

Beck SA, Tisdale MJ. Effect of insulin on weight loss and tumour growth in a cachexia model. Br J Cancer 1989; 59: 677–681.

Bistrian BR, Blackburn GL, Flatt JP, Sizer J, Scrimshaw NS, Sherman M. Nitrogen metabolism and insulin requirements in obese diabetic adults on a protein-sparing modified fast. Diabetes 1976; 25: 494–504.

Blackburn GL, Phillips JC, Morreale S. Physician’s guide to popular low-carbohydrate weight-loss diets. Cleve Clin J Med 2001; 68: 761–766. 768–9, 773–4.

Blank SK, McCartney CR, Chhabra S, Helm KD, Eagleson CA, Chang RJ et al. Modulation of gonadotropin-releasing hormone pulse generator sensitivity to progesterone inhibition in hyperandrogenic adolescent girls–implications for regulation of pubertal maturation. J Clin Endocrinol Metab 2009; 94: 2360–2366.

Boden G, Sargrad K, Homko C, Mozzoli M, Stein TP. Effect of a low-carbohydrate diet on appetite, blood glucose levels, and insulin resistance in obese patients with type 2 diabetes. Ann Intern Med 2005; 142: 403–411.

Bough KJ, Rho JM. Anticonvulsant mechanisms of the ketogenic diet. Epilepsia 2007; 48: 43–58.

Brehm BJ, Seeley RJ, Daniels SR, D’Alessio DA. A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. J Clin Endocrinol Metab 2003; 88: 1617–1623.

Cahill GFJr. Fuel metabolism in starvation. Annu Rev Nutr 2006; 26: 1–22.

Cordain L, Eaton SB, Sebastian A, Mann N, Lindeberg S, Watkins BA et al. Origins and evolution of the western diet: health implications for the 21st century. Am J Clin Nutr 2005; 81: 341–354.

Cordain L. Implications for the role of diet in acne. Semin Cutan Med Surg 2005; 24: 84–91.

Dashti HM, Al-Zaid NS, Mathew TC, Al-Mousawi M, Talib H, Asfar SK et al. Long term effects of ketogenic diet in obese subjects with high cholesterol level. Mol Cell Biochem 2006; 286: 1–9.

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.

DeUgarte CM, Bartolucci AA, Azziz R. Prevalence of insulin resistance in the polycystic ovary syndrome using the homeostasis model assessment. Fertil Steril 2005; 83: 1454–1460.

Eisenstein J, Roberts SB, Dallal G, Saltzman E. High-protein weight-loss diets: are they safe and do they work? A review of the experimental and epidemiologic data. Nutr Rev 2002; 60: 189–200.

Fauser BC, Tarlatzis BC, Rebar RW, Legro RS, Balen AH, Lobo R et al. Consensus on women’s health aspects of polycystic ovary syndrome (PCOS): the amsterdam ESHRE/ASRM-sponsored 3rd PCOS consensus workshop group. Fertil Steril 2012; 97: 28–38. . e25.

Feinman RD, Fine EJ. Nonequilibrium thermodynamics and energy efficiency in weight loss diets. Theor Biol Med Model 2007; 4: 27.

Fine EJ, Feinman RD. Thermodynamics of weight loss diets. Nutr Metab (Lond) 2004; 1: 15.

Fine EJ, Segal-Isaacson CJ, Feinman RD, Herszkopf S, Romano MC, Tomuta N et al. Targeting insulin inhibition as a metabolic therapy in advanced cancer: a pilot safety and feasibility dietary trial in 10 patients. Nutrition 2012; 28: 1028–1035.

Freedman MR, King J, Kennedy E. Popular diets: A scientific review. Obes Res 2001; 9 (Suppl 1), 1S–40S.

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Gardner CD, Kiazand A, Alhassan S, Kim S, Stafford RS, Balise RR 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. JAMA 2007; 297: 969–977.

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.

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.

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Halton TL, Hu FB. The effects of high protein diets on thermogenesis, satiety and weight loss: a critical review. J Am Coll Nutr 2004; 23: 373–385.

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Hartman AL, Gasior M, Vining EP, Rogawski MA. The neuropharmacology of the ketogenic diet. Pediatr Neurol 2007; 36: 281–292.

Hartman AL, Lyle M, Rogawski MA, Gasior M. Efficacy of the ketogenic diet in the 6-hz seizure test. Epilepsia 2008; 49: 334–339.

Hellerstein MK. De novo lipogenesis in humans: Metabolic and regulatory aspects. Eur J Clin Nutr 1999; 53 (Suppl 1), S53–S65.

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.

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.

Huffman J, Kossoff EH. State of the ketogenic diet(s) in epilepsy. Curr Neurol Neurosci Rep 2006; 6: 332–340.

Jia Y, Hwang SY, House JD, Ogborn MR, Weiler HA, O K et al. Long-term high intake of whole proteins results in renal damage in pigs. J Nutr 2010; 140: 1646–1652.

Johnstone AM, Horgan GW, Murison SD, Bremner DM, Lobley GE. Effects of a high-protein ketogenic diet on hunger, appetite, and weight loss in obese men feeding ad libitum. Am J Clin Nutr 2008; 87: 44–55.

Jornayvaz FR, Samuel VT, Shulman GI. The role of muscle insulin resistance in the pathogenesis of atherogenic dyslipidemia and nonalcoholic fatty liver disease associated with the metabolic syndrome. Annu Rev Nutr 2010; 30: 273–290.

Kapogiannis D, Mattson MP. Disrupted energy metabolism and neuronal circuit dysfunction in cognitive impairment and alzheimer’s disease. Lancet Neurol 2011; 10: 187–198.

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Kessler SK, Neal EG, Camfield CS, Kossoff EH. Dietary therapies for epilepsy: future research. Epilepsy Behav 2011; 22: 17–22.

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McDaniel SS, Rensing NR, Thio LL, Yamada KA, Wong M. The ketogenic diet inhibits the mammalian target of rapamycin (mTOR) pathway. Epilepsia 2011; 52: e7–e11.

Moghetti P, Castello R, Negri C, Tosi F, Spiazzi GG, Brun E et al. Insulin infusion amplifies 17 alpha-hydroxycorticosteroid intermediates response to adrenocorticotropin in hyperandrogenic women: apparent relative impairment of 17,20-lyase activity. J Clin Endocrinol Metab 1996; 81: 881–886.

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.

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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.

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Paoli A, Canato M, Toniolo L, Bargossi AM, Neri M, Mediati M et al. The ketogenic diet: an underappreciated therapeutic option? Clin Ter 2011; 162: e145–e153.

Paoli A, Cenci L, Fancelli M, Parmagnani A, Fratter A, Cucchi A et al. Ketogenic diet and phytoextracts comparison of the efficacy of mediterranean, zone and tisanoreica diet on some health risk factors. Agro Food Ind Hi-Tech 2010; 21: 24.

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Poplawski MM, Mastaitis JW, Isoda F, Grosjean F, Zheng F, Mobbs CV. Reversal of diabetic nephropathy by a ketogenic diet. PLoS One 2011; 6: e18604.

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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.

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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.

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.

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Der Beitrag “Ketogene Diäten. Vorsicht bei Verzicht auf Kohlenhydrate“ – eine Klarstellung erschien zuerst auf Ketoseportal.

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