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Fighting Cancer as Metabolic Disease Using Ketogenic Diet

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  • Fighting Cancer as Metabolic Disease Using Ketogenic Diet


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    According to the World Health Organisation, the probability of being diagnosed with cancer during lifetime is 21.5%. That is, every fifth person at some point personally faces this disease.

    In the United States, the probability of dying from cancer today is almost the same as it was 50 years ago.

    This means that 70 years of experience in the use of chemotherapy, the discovery of the structure of the DNA molecule in 1953, and even Richard Nixon's "War on cancer" declared in 1971 almost did not produce results. Unfortunately, we have not yet learned how to effectively treat cancer.

    Since progress in cancer treatment has been delayed for decades, in recent years, more and more scientists and just concerned enthusiasts suspect that we are looking for answers not where they are.

    We will have to go into a little more detail, but below I will tell you why slowly but surely, experts are returning to the consideration of cancer as a disease of cell metabolism.





    The link between sugar and cancer

    It is surprising how few people know that back in 1921, the German scientist Otto Warburg discovered the most interesting difference between cancer cells and healthy ones. Healthy cells get 90% of their energy using oxygen (aerobic respiration of the cell).

    And almost all cancers, regardless of the type and location of the tumor, the main part of the energy is obtained by fermentation of glucose without oxygen (anaerobic respiration of the cell).

    Yes, cancer cells love sugar, because they can't eat anything else. 10 years later, Otto Warburg received the Nobel prize for this discovery, and the phenomenon of atypical metabolism of cancer cells was later called the "Warburg Effect".





    Aerobic and anaerobic cell respiration

    To generate energy, cells can use two methods of respiration: aerobic, using oxygen, and anaerobic, that is, without oxygen. It is believed that anaerobic respiration of cells is the oldest mechanism developed by the first microorganisms on Earth in conditions when there were no green plants yet, and there was almost no oxygen in the atmosphere.

    Glucose is processed into pyruvic acid (glycolysis) when it enters the body's cell. After that, in the case of aerobic respiration, this acid is sent to the mitochondria (the powerhouse of cells) and produces energy (ATP) using oxygen.

    And in the case of anaerobic respiration, it is processed into ATP by fermentation outside the mitochondria, in the cytoplasm of the cell, with the production of lactic acid as a by-product.

    The most obvious illustration is training. When you walk, your muscles mostly get enough oxygen and "breathe" by burning glucose, fat, or ketones. And with a sharp load, such as a sprint, the energy produced by the mitochondria is no longer enough, and then the muscles compensate for the lack of energy anaerobically, fermenting glucose.

    The lactic acid produced in this case in large quantities accumulates and causes unpleasant sensations that do not pass until you rest.



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    Warburg himself said: "Cancer, unlike other diseases, has countless secondary causes. But even for cancer, there is only one primary cause. The prime cause of cancer is the replacement of the respiration of oxygen in normal body cells by a fermentation of sugar."
    [2].

    Strange, but this property of cancer cells still even experts pay very little attention. This is despite the fact that one of the most accurate methods of research and diagnosis of cancer, PET scanning, works precisely due to the use of features of the Warburg effect.

    By the mid-twentieth century, cancer researchers had stopped paying attention to Warburg's discovery. Although he remained a highly respected scientist, he was not particularly listened to in the field of oncology, perhaps because they believed that a biochemist with his knowledge of metabolism only delves into side effects.

    The true answer to the question of what cancer is was to study DNA — the molecule in which all the information about life and death is encoded, and this information only needs to be extracted from there. However, it still doesn't work out very well.





    Cancer is caused by spontaneous cell mutations. Or not?

    Now, as 50 years ago, the so-called Mutational theory of carcinogenesis (MTK) is generally accepted. According to it, cancer is a disease in which a single cell that has undergone a series of genetic mutations has disabled the mechanism of self-destruction and started to divide uncontrollably, creating its own clones, and forming a tumor (this is called proliferation).

    Moreover, I do not just write "some mutations". Only a few of these mutating genes have been identified, and they are called proto-oncogenes, and they are believed to be activated by exposure to viruses (oncoviruses) or carcinogenic substances.

    But the problem with MTK is that 80% of cancers are still not explained by mutations of specific genes [3], and with those for which these genes are found, everything is also not so obvious. Namely, a mutation of such a gene is not always necessary for the occurrence of cancer. Or vice versa, not all cases of this type of cancer are associated with a mutation of this gene.





    Example of a defining mutation

    For instance, a known mutation called the "Philadelphia Chromosome" is associated with 95% of cases of chronic myeloid leukemia (CML) and about 20% of cases of acute lymphoblastic leukemia (ALL). However, it turns out that 5% of CML and 80% of ALL are not accompanied by this mutation. Moreover, this mutation also occurs in perfectly healthy people [4].


    A stunning project of the National Cancer Institute of the United States, the "Atlas of the Cancer Genome" (ARG), on which great hopes were placed, and during which the genomes of thousands of samples of cancer cells were decoded, did not actually answer what exactly is wrong with these cells.

    The result is, roughly speaking, nonsense: the variety of mutations is too large, and sometimes even within a single tumor (!), and it is extremely difficult to identify with confidence the mutations that are determining. And the number of defining mutations found was too small to explain the strange behavior of these cells.





    The problem with defining mutations

    A 2013 research paper by Bert Fogelstein reviewed the results of ARG over nearly 10 years of efforts to decipher the genome of cancer cells. In the" Dark matter " section of the article, scientists wrote the following [6]:

    "In children's tumors, such as medulloblastoma, the number of determining (driver) mutations is low (from zero to two)… In common adult tumors, such as pancreatic cancer, colorectal cancer, breast and brain cancers, the number of mutated driver genes is between three and six, but some tumors have one or two mutated driver genes. How can this be explained given the generally accepted view of the process of tumor formation and development as requiring several successive genetic changes accumulated over decades?»

    In other words, it was assumed that 5-8 consecutive changes in the driver genes must occur for the formation of a tumor. Instead, we see that in some cases there are fewer than five such changes or none at all.

    This means that there is some additional force that makes cancer cells what they are. This force Fogelstein called "Dark matter" by analogy with unknown matter, which consists of more than 70% of the Universe.

    But even if we assume that there really are a series of mutations that cause cancer, why do these mutations occur so often? Spontaneous mutations are a rare event, and the reasonable question should arise: how do so many people around the world manage to have all these mutations during their lifetime?

    Plus, it turns out that the larger the animal, the greater should be the likelihood of cancer, because it has more cells, each of which is a candidate for mutants. But why then do huge whales live so long and do not die young from cancer? It is still unknown why, and this inexplicable part of the MTK is called the Peto paradox.

    English scientist Richard Peto wrote in 1977:

    "A man has 1000 times as many cells as a mouse... and we usually live at least 30 times as long as mice. Exposure of two similar organisms to the risk of carcinoma, one for 30 times as long as the other, would give perhaps 304 or 306 (i.e., a million or a billion) times the risk of carcinoma induction per epithelial cell. However, it seems that, in the wild, the probabilities of carcinoma induction in mice and in men are not vastly different. Are our stem cells really, then, a billion or a trillion times more "cancerproof" than murine stem cells? This is biologically pretty implausible; if human DNA is no more resistant to mutagenesis in vitro than mouse DNA, why don't we all die of multiple carcinomas at an early age?"

    — "Epidemiology and Multistage Models", 1977[4]


    It turns out, on the one hand, there are tumors where there are too few mutations to cause cancer in its current understanding. On the other hand, there are tumors where there are too many mutations to occur spontaneously.

    Obviously, the theory of mutation as a cause of cancer must be in a precarious state. [7] The conclusion is that mutations are not a cause, but an effect.

    In addition to supporting doubts about the validity of the generally accepted theory, decoding the genomes of cancer cells has shown that it is almost impossible to find effective drugs for the targeted treatment of most types of cancer.

    How can I make drugs that hit exactly the target if there are too many of these targets (mutations), even inside a single tumor? [5]





    Example of a targeted drug

    For instance, one of the most effective drugs for the treatment of leukemia is aimed at slowing the production of the BCR-ABL protein by specific mutated genes (the"Philadelphia chromosome", which is described in the box above), since this mutation is present in most forms of leukemia. But other cancers may have more mutations, and they may differ even within the same tumor. This makes it almost impossible to develop targeted imatinib-type drugs for most cancers.

    This may be hard to believe, but given all the controversies at the Mutational theory of carcinogenesis, this theory is still firmly on its feet. Many scientists may be waiting for new discoveries and hypotheses that will expand and complement it, eliminating contradictions.

    But as the history of cancer has shown to date, it is easier to get government or sponsored research funding if the word "genetics" is included in the application.

    So why does cancer occur? Perhaps an improperly functioning DNA "repair" process that allows these mutations to occur more often than they should. [5] But why did the "repairmen" break down? I will say right away that there are no answers yet. But there are hints in the Warburg effect that perhaps the answer is to be found in the strange metabolism of cancer cells.





    Attention to the metabolism in cancer cells

    While the majority of specialists were engaged in MTK, a few continued to study the metabolism of cancer cells. Peter L. Perdersen, a professor of biochemistry at Johns Hopkins University, has devoted much of his work to this, making several important discoveries that confirm and expand the Warburg hypothesis.

    In particular, in 1978, he discovered that the mitochondria (the power plants cells use when breathing with oxygen) of cancer cells are markedly different from the mitochondria of healthy cells.

    There are fewer of them, they look damaged, have an atypical shape, and many other deviations. [8] Apparently, due to defective mitochondria, cancer cells simply cannot get enough energy aerobically.

    He also described the mechanism of the Warburg effect more precisely. A specific enzyme, hexokinase, in cancer cells has significant differences from hexokinase in healthy cells [9]. This altered enzyme lets much more glucose into the cancer cell than if it were a healthy cell, and this explains cancer's appetite for sugar.





    A little more about hexokinase

    Hexokinase exists in different types, and one type, hexokinase 2 (HK2), is unusually common in cancer cells. The role of hexokinase is glucose phosphorylation, i.e. the production of glucose-6-phosphate (G6P), which is the first step in the glycolysis process. It actually regulates the concentration of G6F in the cell and stimulates the delivery of glucose to the cell if the concentration is low.

    When the concentration of G6F is high, glucose intake slows down. So, in cancer cells, this slowing mechanism does not work well, that is, hexokinase 2 launches glucose inside in huge quantities.

    Besides, the concentration of hexokinase 2 in the vicinity of the mitochondria of the cancer cell is much higher than the same indicator in healthy cells.

    At this concentration, it can actively "select" the phosphate residue of ATP produced by the mitochondria, and thus phosphorylate even more glucose, which leads to even greater production of pyruvic acid. Since the mitochondria cannot cope with this amount of pyruvic acid, it can only ferment without oxygen in the cytoplasm.

    These findings gradually bring us closer to understanding the root causes of cancer. Could it be the "broken" mitochondria? What if cells include prehistoric mechanisms of fermentation and proliferation as a defense in response to the partial failure of the main "power plants"?

    If the study of mutations provides almost no answers, why not focus on metabolism? Moreover, the theory of metabolism can provide the answer to the treatment of all or almost all types of cancer, and not one mutation in thousands.





    Cancer cells are not superorganisms. They are seriously ill

    A healthy cell can burn fat and ketones. Cancer can't use them, because its mitochondria are damaged and inactive (fats and ketones can only be burned in the mitochondria). This is their obvious weakness compared to other cells in the body, and it is worth using.

    Thomas Seyfried, a scientist and author of the famous scientific book "Cancer as a Metabolic disease", and Dominic D'agostino, a scientist who is currently actively studying and popularizing the ketogenic diet, developed a method of cancer therapy, which they called "Press-Pulse", by analogy with the name of one of the theories of the causes of mass extinctions.

    The authors of this theory of extinction assume that the most massive cases of death of living organisms on Earth, like the extinction of the dinosaurs, occurred only when the long-term stress and problems in the ecosystem (Press) was superimposed on a sharp disaster, such as a meteorite fall (Pulse).

    The essence of the Press-Pulse method for fighting cancer: expose cancer cells to constant stress, namely, to deprive them of food (Press), and finish them off with hyperbaric oxygenation (Pulse).

    Fasting and a calorie-restricted ketogenic diet do a good job of depriving cancer cells of food because both trigger ketosis and radically reduce the amount of glucose in the blood - the main food for cancer. Since cancer cells are unable to feed on ketones and fatty acids, healthy cells gain a significant competitive advantage over them.

    It's not just the amount of food for the cells, but also the quality of it. Cancer cells eat mostly glucose and produce a huge amount of reactive oxygen species (these include the more widely known free radicals).

    These are molecules that damage the cell from the inside, reacting with everything they come across. And healthy cells eat ketones and produce much less reactive oxygen species. Not just less than cancer cells, but even less than healthy cells that feed on glucose.

    It turns out that cancer cells are subject to constant increased oxidative stress, and healthy, eating ketones — on the contrary, reduced.

    Cancer cells are weakly resistant to oxidative stress because they produce fewer natural antioxidants (glutathione) that neutralize reactive oxygen species.





    Oxygen and ketones

    Ketones from the point of view of oxidative stress are a very eco-friendly fuel since their processing produces the least amount of reactive oxygen species.

    This is one of the main advantages of ketosis in general because many negative processes are associated with oxidative stress, from difficult recovery after training to aging.

    Even in the state of ketosis, people are much more resistant to oxygen poisoning. Such poisoning occurs, for example, when breathing high-pressure oxygen (when using regenerative scuba gear).

    Their most frequent symptoms are sudden convulsions and loss of consciousness. Thanks to the study of these properties of ketones commissioned by the US Navy special forces, Dominic D'Agostino became interested in the ketogenic diet.

    James Watson, who discovered the structure of the DNA molecule, even suggested that chemotherapy in some cases works not as we thought, but through the mechanism of oxidative stress.

    His hypothesis is that under the influence of many drugs for chemotherapy, and radiation therapy, cancer cells even more actively accumulate molecules of reactive oxygen species, which causes their damage and death [11].

    Due to the fact that healthy cells are better protected from stress in the state of ketosis, and chemo and radiotherapy increase this stress for cancer cells, pre-fasting is a logical addition to traditional methods of treatment.

    Even if fasting itself may not help directly with the treatment of the tumor, it can significantly alleviate the severe side effects of chemotherapy, since healthy cells are better protected. Preliminary research supports this theory [12].

    Since about the 1950s, it became clear that cancer cells can ferment not only glucose but also glutamine, the most common amino acid in the body.

    Glutamine is also involved in many processes directly or indirectly related to tumor growth. Its amount is difficult to regulate through a diet since the body produces enough of it itself, but with a calorie-restricted diet, its activity still decreases.

    In the Press-Pulse method, a drug that suppresses cell processing of glutamine (a glutaminase inhibitor, 6-diazo-5-oxo-L-norleucine) can be added to a calorie-restricted keto diet to increase stress. This drug, although highly toxic, has shown effectiveness in mice, slowing the aggressiveness of metastasis formation [14].

    Since the effective mechanism for killing cancer cells works through oxidative stress, it suggests the idea of exposing weakened cancer cells to even more aggressive oxygen.

    To do this, a hyperbaric oxygenation procedure is used. Theoretically, it can even replace traditional cancer treatments, since it is not as toxic as chemotherapy.

    At the moment, the mechanism of this procedure in relation to tumor cells is not fully understood, but it is likely that they are even more saturated with active oxygen forms, which increases the probability of death of these cells due to oxidative stress.


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    During the hyperbaric oxygenation procedure, a person is placed in a pressure chamber, the atmosphere of which consists of almost pure oxygen under high pressure, and stays there for some time.

    There is a study by the authors of the Press-Pulse method showing that the use of hyperbaric oxygenation in combination with the ketogenic diet and ketones in the form of food additives significantly slowed down the growth of tumors and metastases in mice, extending their life by two times [13].





    What's next for the metabolic approach to cancer

    The Press-Pulse technique is very promising, but no full-scale human studies have been conducted yet. Also, such methods of treatment today have a small chance of being tried as the main ones.

    They are prescribed only as an addition to traditional treatments. The fact is that the doctor must follow certain prescriptions and protocols issued by authoritative bodies in different countries.

    If the oncologist prescribes hyperbaric therapy and diet instead of chemotherapy or surgery, and the patient does not recover, the doctor may end up in prison.

    On the contrary, if a patient dies despite traditional treatment, the doctor has legally done everything he could. It is obvious that most doctors don't have the motivation to take risks.


    But everything is not so hopeless, and in different clinics around the world, new methods are being tried more and more often. In July 2017, a group of scientists from Turkey, with the participation of the same Thomas Seyfried, published a description of a case of severe stage IV breast cancer with metastases to the abdominal cavity in a middle-aged woman.


    She was prescribed chemotherapy, supported by pre-fasting and insulin injections (to reduce glucose levels), the ketogenic diet, hyperthermic therapy (heating the tumor), and hyperbaric oxygenation. After several months of such treatment, the woman is in remission [15].

    The result is simply amazing, but still, there are too few such studies so far.

    Large-scale studies that would convincingly show the benefits of metabolic therapy would greatly help and give doctors a reason to prescribe new types of treatment.


    But there is a financial issue. It takes a lot of money to conduct human research. In order for someone to invest, they usually have to expect a return on their investment. But if research confirms that Press-Pulse is a very effective technique, then how can it be sold?


    The oxygen chamber is inexpensive and many people produce them, and the ketogenic diet and fasting, for example, are generally free. It turns out that you need to spend a lot of money on the research of such therapy (it will cost millions of dollars), and you will not have to wait for a return on investment, because this therapy can not be sold at a high price.

    Meanwhile, pharmaceutical companies are willing to give a lot of money for research on chemotherapy drugs, because the resulting drugs can be sold for huge sums. For example, treatment with some drugs costs the patient sometimes more than 90 thousand dollars a year. [10].

    Therefore, at the moment, research in this area is mainly funded by non-profit foundations, which, of course, do not have as much money as large pharmaceutical companies.

    Recently, thanks to the increasing interest in the ketogenic diet, there are successful companies that produce products for people who follow it.

    These companies have funds, and it is hoped that they will also participate in the financing (for example, in the scientific work on the Press-Pulse method, a manufacturer of sports nutrition, although not yet "keto", is listed among the sponsors).


    If you have read this article, please do not jump to any conclusions. Fasting, the ketogenic diet, and even hyperbaric oxygenation are not suitable for everyone. For every healing story told, you will also find a tragic story of frustration.


    But the research that has already been done, which we have also written about above, should show serious interest in new methods of treatment, such as Press-Pulse.

    Ignoring the metabolism of cancer cells and focusing only on mutations already seems not only impossible but also irresponsible.

    Cancer is a complex and diverse disease. The number of gaps in our knowledge is still very large, and as they are filled, humanity will surely understand its root causes and find methods of effective treatment.

    But so far all we have is dozens of years with very little improvement in the survival rates of cancer patients.

    Of course, "extremely small improvement" means thousands of lives saved, but for millions of people, cancer still sounds almost like a verdict.

    Perhaps one day this diagnosis will be no worse than a cold. But this will definitely not happen if we simply blindly follow a dogma that has already shown its failure.

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