Ketosis is a physiological metabolic situation characterised by the increase of ketone bodies (acetoacetate, acetone and 3-hydroxybutyrate) in blood and ECM. These chemical compounds can provide a considerable part of the energy required by the organism in catabolic metabolic situations, such as food shortages, low-carbohydrate diets or increased performance conditions, replacing glucose as the primary energy source.
Over a period of 2.5 million years, ketosis shaped the natural metabolic state of humans. This was a time when fast-food shops and bakeries were not on every corner ready to overload the glucotoxic brain with sugar. Nutritional ketosis, as it is now called in distinction to starvation and fasting ketosis, formed a decisive prerequisite for encephalisation, i.e. for the increase in brain weight and anatomical-physiological brain differentiation in humans, and made this possible in the first place. “Without ketones as a source of energy,” writes Dr Mary Newport, “it is highly unlikely that the human species would still exist, at least not with today’s large brains and high intelligence.” 1
In sugar prison: the history of nutrition
In the following, we want to look at the history of mankind from the perspective of the development of nutrition on the basis of the dominant metabolic situation. From this perspective, I think we can distinguish three major epochs: the Ketogenic Age, the Gluco-centric Age and the Gluco-toxic Age.
The Ketogenic Age came to an end with the Neolithic Revolution at the beginning of the Neolithic period about 12,000 years ago. The wandering wild hunters became sedentary farmers, and there was a slow transition to the use of cereals as a staple food. The triumph of carbohydrates had begun. The long period that followed, from the Neolithic until about 1850, can be called the Gluocentric Age. At the beginning of the 19th century, this epoch was replaced by the start of industrial production of grain and refined sugar. Pastoral pastoralism gave way to so-called “conventional agriculture” (the term is a euphemism), the fatal effects of which have been compounded since the 1970s by the development of transgenic wheat, genetically modified soya and High Fructose Corn Syrup (Monsanto). The period from 1850 to the present can aptly be called the Glucotoxic Age.
While glycolysis, under the dictum of the glucocentric way of thinking, was the first metabolic pathway, the course of which was already considered to have been clarified by the end of the 19th century, it took a lot longer with ketones and protein metabolism. Nevertheless, the basic features of ketone metabolism had already been deciphered between 1946 and 1968 by Peter & Van Slyke (1946), Lynen & Ochoa (1953), Lehninger & Greville (1953) and Campbell & Best (1956)2 and not least by Owen & Cahill (1967)3 at Harvard Medical School. Groundbreaking work on brain metabolism by Cahill, among others, followed. However, the insights gained from this work have still not made it into the textbooks.4
The spectre of ketoacidosis
Another circumstance that hinders the reception of ketosis research is that ketones entered the world stage of medicine together with the urine of diabetics and were for a long time wrongly interpreted as signs of exclusively pathological changes – quasi as substrates of incomplete oxidation. Even today, doctors learn in universities that “fats burn in the fire of carbohydrates”. Doctors, Veech therefore also writes aptly, are only ever afraid of ketoacidosis.
From the point of view of orthodox medicine, ketoacidosis is a life-threatening derailment of the fat metabolism, which can occur above all in type I diabetes, in rarer cases also in alcoholics. With low insulin and high glucagon levels, the ketone level can rise to a life-threatening level of up to 10, sometimes even 25 mmol /l in exceptional cases. In this case, the high blood sugar level prevents the utilisation of the ketones in the tissues. However, if a high blood sugar level inhibits the utilisation of the ketone bodies, then ketoacidosis is, strictly speaking, a derailment of the sugar metabolism, not the fat metabolism. The fat metabolism is only dragged into the abyss by the high glucose level due to the absolute insulin deficiency in type I diabetes. A comparison of the different states of ketosis in Table 1 clearly shows the differences between the wide field of a ketone level achievable by Nutrional Ketosis (NK) and the pathological occurrence of a ketoacidosis.
Ketoadaptation: Using the ketones in the tissues
Nutrional ketosis (NK) occurs physiologically under nutritional and performance conditions in which glucose becomes scarce and insulin levels drop as a result, or fat metabolism gets going enough to convert excess
Acetyl-CoA into ketone bodies, which are then converted back into the tissues for feeding into the citrate cycle. The fact that we eat the most of a nutrient that we actually need the least is one of the fatal aberrations of a society trapped in a sugar prison: “There is,” writes John Brosnan, “strictly speaking, no dietary requirement for carbohydrate. Gluconeogenesis is capable of supplying the body with adequate amounts of glucose.” 5 An NK can therefore also be achieved without starvation if carbohydrates are greatly or very greatly reduced and/or performance is increased accordingly (post-exercise ketosis).
Normally, glucose is also produced from dietary proteins, which is why in our nutritional concept of dr. reinwald metabolic regulation we also use MyAMINO ®, an amino acid preparation that provides almost no nitrogen loss and no glucose (1% compared to up to 84% with plant proteins). This enables us to guarantee an optimal protein supply even in tumours where the classic ketogenic diet would be far too risky (such as pancreatic or liver carcinoma), as MyAMINO ® neither requires peptidases nor burdens the liver or kidneys with nitrogen waste. In this way, it is possible to “fast without fasting”. And it helps to limit the dangers of tumour cachexia.
A crucial step in the smooth utilisation of ketones in the tissues is going through a process called ketoadaptation. In the literature, this is generally thought to take up to three weeks in adults. Cahill & Aoki demonstrated in the 1980s, using insulin infusion in ketosis, that even in adults blood glucose levels up to 25 mg/dl, in some subjects even up to 20 mg /dl, can be tolerated without neurological deficits if the ketone level is appropriately high (4.5 – 5.0 mmol / l) and the ketolysis capacity is present.6
The transitions between the metabolic states must take place without friction, which they no longer do due to our malnutrition. The reason for the need for ketoadaptation lies in the loss of ketolysis capacity of the tissues, especially the brain, acquired through sugar imprinting. The inability to metabolise ketones without transition is due to the lack of enzymes required for this: the mitochondrial 3-hydroxy-3-methylglutaryl coenzyme A transferases. Remember: infants at the mother’s breast are basically in ketosis. As the responsible therapist, one has to take a breath at this point when one considers how much fat metabolism is in the deadly grip of established medicine and the feed industry. The former attacks the production of cholesterol by inhibiting cytosolic HMGA-CoA reductase via statins, while the latter contributes to damaging the ketolysis capacity of the brain and other tissues via carb overfeeding.
|Nutrition / Status||Ketone level mmol / l|
|moderate KH diet (fasting)||0,1 – 0,5|
|Fasting status several weeks: Starvation ketosis||5,0 – 7,0|
|Very low KH diet below 50 g / day (nutritional ketosis / post-exercise ketosis)||0,5 – 3,5|
|Very low KH diet with MyAMINO® (Therapeutic Ketosis)||1,0 – 8,0|
|Ketoacidosis (insulin insufficiency, type 1 diabetes)||10,0 – 25,0|
The danger of tumour cachexia
The tightrope walk between calorie restriction and the danger of tumour cachexia must be kept carefully in mind. Tumours are enormous nitrogen traps. However, they do not absorb amino acids, but mainly more complex proteins such as albumin, through pinocytosis. Under strict food deprivation, patients with advanced tumours lose about 5 % of their body mass in protein every day. The nitrogen balance of tumour cells is therefore basically positive, in contrast to healthy cells, even with complete abstinence from food. Pure fasting, even if it deprives the tumour of an important part of its nutrition, is always at the expense of the patient. The tumour cannibalises its host, regardless of whether the host eats or not. However, we can avoid this development with the substitution of MyAMINO ®, because as an extremely low-calorie amino acid formula, it reduces the glucose load from dietary proteins and still provides a build-up profile of 99% protein nutritional value. This makes mild to very high ketosis possible with the lowest calorie intake without the risk of disruption, because anabolic processes can be served with the help of MyAMINO ® without at the same time burdening the excretory organs with nitrogen waste from dietary proteins.
Tumour cells absorb 16 times more sugar than healthy tissue. The release of lactate is 24 times higher than normal. Fatty acids are taken up, but the uptake is equal to the release, i.e. the net utilisation is zero. Tumours are capable of de novo lipogenesis via substrate supply from the PPW and glutaminolysis, thus producing fat from sugar and glutamine. Cancer cells, like hepatocytes, are able to produce the enzyme FAS (fatty acid synthase) required for fat synthesis themselves. Ketones are also taken up, but as with FS, more are released, so there is no net utilisation.7
The sensitisation of tumour cells to cytotoxic measures is a “side effect” of ketosis that is now well known and even popular with orthodox physicians. The cancer cell simply runs out of strength to resist chemotherapy. The response rate to gemcita- bin, for example, is significantly increased in ketosis.8 So if a tumour lives primarily on carbohydrates and the body’s own protein, then a nutritional intervention in the sense of a KD or HKD is in any case effective, especially with the nutritional component MyAMINO ®. Every responsible therapist should draw nutritional conclusions from these findings:
- consume as few carbohydrates and simple sugars as possible,
- Protect the body’s own protein with a sufficient supply of dietary protein (MyAMINO ® is recommended because of its unique properties),
- Administer sufficient fats, especially fats with medium-chain fatty acids (such as coconut oil).
- Newport M (2012): Alzheimer vorbeugen und behandeln: Die Keton-Kur. VAK Verlag
- Krebs HA (1961): The Physiological Role of the Ketone Bodies. Biochem. J. 80: 225 ff 3 Owen OE et al. (1967): Brain metabolism during fasting, J Clin Invest. Vol. 46: 1589-95 4 Cahill GF (2003): Ketoacids? Good Medicine? Transactions of the ACCA, Vol. 114
- Brosnan J (1999): Comments on metabolic needs for glucose and the role of gluconeogenesis. Eur. J. Clin. Nutr. Apr; 53 Suppl 1: 107-11
- Cahill GF et al. (1980): Alternate Fuel Utilization by Brain. In: Janet V et al. (Editors): Cerebral Metabolism and Neuronal Function. Wiliams & Wilkins, London
- Holm E (2007): Stoffwechsel und Ernährung bei Tumorkrankheiten: Analysen und Empfehlungen, Thieme Verlag
- Isayev O ( 2014): Inhibition of glucose turnover by 3-bromopyruvate counteracts pancreatic cancer stem cell features and sensitizes cells to gemcitabine. Oncotarget, Jul 15;5(13):5177-89