Dynamic nature of cancer and tissue oxygenation by #89361 ..... Stomach Cancer Forum
Date: 7/26/2008 8:01:45 PM ( 16 y ago)
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Part 1. Cancer and tissue hypoxia
Nobel Laureate, Dr. Otto Warburg, in his article “The Prime Cause and Prevention of Cancer” (1966) wrote, “Cancer, above all other diseases, has countless secondary causes. Almost anything can cause cancer. But, even for cancer, there is only one prime cause. The prime cause of cancer is the replacement of the respiration of oxygen (oxidation of sugar) in normal body cells by fermentation of sugar… In every case, during the cancer development, the oxygen respiration always falls, fermentation appears, and the highly differentiated cells are transformed into fermenting anaerobes, which have lost all their body functions and retain only the now useless property of growth and replication.“ (http://www.alkalizeforhealth.net/Loxygen2.htm).
Do modern scientists have a different opinion? A decade ago Dr. Rockwell from Yale University School of Medicine (USA) studied malignant changes at the cellular level and wrote, “The physiological effects of hypoxia and the associated micro environmental inadequacies increase mutation rates, select for cells deficient in normal pathways of programmed cell death, and contribute to the development of an increasingly invasive, metastatic phenotype” (Rockwell, 1997). The title of this publication is Oxygen delivery: implications for the biology and therapy of solid tumors.
Summarizing the results of numerous studies, a group of biological scientists from University of California (San Diego) chose the following title for their article, The hypoxia inducible factor-1 gene is required for embryogenesis and solid tumor formation (Ryan et al, 1998).
Under normal conditions, even a group of hypoxic cells dies (or is easily destroyed). What about cells in malignant tumours? Researchers from the Gray Laboratory Cancer Research Trust (Mount Vernon Hospital, Northwood, Middlesex, UK) concluded, “Cells undergo a variety of biological responses when placed in hypoxic conditions, including activation of signalling pathways that regulate proliferation, angiogenesis and death. Cancer cells have adapted these pathways, allowing tumours to survive and even grow under hypoxic conditions...” (Chaplin et al, 1986).
There is so much professional evidence about the fast growth of tumours when the condition of hypoxia is present that a large group of Californian researchers recently wrote a paper Hypoxia - inducible factor-1 is a positive factor in solid tumor growth (Ryan et al, 2000). Echoing their paper, a British oncologist Dr. Harris from the Weatherhill Institute of Molecular Medicine (Oxford) went further with the manuscriipt Hypoxia - a key regulatory factor in tumour growth (Harris, 2002).
When the solid tumour is large enough and the disease progresses, cancer starts to invade other tissues. This process is called metastasis. Does poor oxygenation influence it? “...Therefore, tissue hypoxia has been regarded as a central factor for tumor aggressiveness and metastasis” (Kunz & Ibrahim, 2003). That was the conclusion of a group of German researchers from the University of Rostock and the University of Leipzig.
Since dozens of medical and physiological studies yield the same result, what about the following title? Tumor oxygenation predicts for the likelihood of distant metastases in human soft tissue sarcoma (Brizel et al, 1996). This title claims that tumour oxygenation predicts chances of cancer invasion.
The reader can probably guess about the effect of cancer treatment and the chances of survival for those who suffer from severe chronic hyperventilation. Indeed, “... tumour hypoxia is associated with poor prognosis and resistance to radiation therapy” (Chaplin et al, 1986).
American scientists from Harvard Medical School noted “... Hypoxia may thus produce both treatment resistance and a growth advantage” (Schmaltz et al, 1998).
“Low tissue oxygen concentration has been shown to be important in the response of human tumors to radiation therapy, chemotherapy and other treatment modalities. Hypoxia is also known to be a prognostic indicator, as hypoxic human tumors are more biologically aggressive and are more likely to recur locally and metastasize” (Evans & Koch, 2003).
“Clinical evidence shows that tumor hypoxia is an independent prognostic indicator of poor patient outcome. Hypoxic tumors have altered physiologic processes, including increased regions of angiogenesis, increased local invasion, increased distant metastasis and altered apoptotic programs” (Denko et al, 2003).
The authors of one of the studies cited above mused about the origins of all these problems, “Surprisingly little is known, however, about the natural history of such hypoxic cells” (Chaplin et al, 1986). Why do they appear? What is the source of tissue hypoxia?
Conclusion. Appearance, development and metastasis of tumours are based on tissue hypoxia. Tumours are cries of the human organism for more oxygen.
Brizel DM, Scully SP, Harrelson JM, Layfield LJ, Bean JM, Prosnitz LR, Dewhirst MW, Tumor oxygenation predicts for the likelihood of distant metastases in human soft tissue sarcoma, Cancer Reserach 1996, 56: p. 941-943.
Chaplin DJ, Durand RE, Olive PL, Acute hypoxia in tumors: implications for modifiers of radiation effects, International Journal of Radiation, Oncololgy, Biolpgy, Physics 1986 August; 12(8): p. 1279-1282.
Denko NC, Fontana LA, Hudson KM, Sutphin PD, Raychaudhuri S, Altman R, Giaccia AJ, Investigating hypoxic tumor physiology through gene expression patterns, Oncogene 2003 September 1; 22(37): p. 5907-5914.
Evans SM & Koch CJ, Prognostic significance of tumor oxygenation in humans, Cancer Letters 2003 May 30; 195(1): p. 1-16.
Harris AL, Hypoxia: a key regulatory factor in tumour growth, National Review in Cancer 2002 January; 2(1): p. 38-47.
Kunz M & Ibrahim SM, Molecular responses to hypoxia in tumor cells, Molecular Cancer 2003; 2: p. 23-31.
Rockwell S, Oxygen delivery: implications for the biology and therapy of solid tumors, Oncology Research 1997; 9(6-7): p. 383-390.
Ryan H, Lo J, Johnson RS, The hypoxia inducible factor-1 gene is required for embryogenesis and solid tumor formation, EMBO Journal 1998, 17: p. 3005-3015.
Ryan HE, Poloni M, McNulty W, Elson D, Gassmann M, Arbeit JM, Johnson RS, Hypoxia-inducible factor-1 is a positive factor in solid tumor growth, Cancer Res, August 1, 2000; 60(15): p. 4010 - 4015.
Schmaltz C, Hardenbergh PH, Wells A, Fisher DE, Regulation of proliferation-survival decisions during tumor cell hypoxia, Molecular and Cellular Biology 1998 May, 18(5): p. 2845-2854.
Part 2. Tissue pollution and hypoxia: how they affect our breathing
There are two processes of respiration: respiration of living cells and our outer respiration or breathing. During their life, our cells consume oxygen for energy generation and produce carbon dioxide. This process is called inner or cellular respiration. Our cells breathe. They live in a certain gaseous environment. “But the cells of animals and humans need about 7 % CO2 and only 2% O2 in the surrounding environment. This is the way our cells live: cells of the heart, brain, and kidneys” noted a famous Soviet respiratory physiologist Dr. Buteyko KP (Buteyko, 1977.) The process of outer respiration, that is taking oxygen from the air and expelling some CO2 with each exhalation, constitutes our breathing.
How does our cellular respiration relate to our breathing? Imagine a healthy person with normal breathing parameters. Oxygenation of their body can be easily measured using the stress-free breath holding time test done after usual exhalation. (Exhale normally, pinch the nose, and see how long you can hold your breath but only until first signs of stress or discomfort. As soon as stress appears and starts to grow, release the nose and resume breathing. Your breathing rhythm should be the same both before and after the test.) The stress-free breath holding time (or index of oxygenation) of a healthy person is about 40-60 s indicating normal body oxygenation (Flack, 1920; Buteyko, 1977; McArdle et al, 2000). Hence, in health, our breathing defines breathing of our cells (or cellular respiration) providing them with sufficient oxygen for maintenance of normal homeostasis.
Now let us assume now that some tissues or cells of the body accumulate toxic or carcinogenic substances (e.g., tobacco smoke in the lungs, indigested toxins in the gastrointestinal tract, free radicals in the skin due to excessive sun radiation, etc.). This micro-pollution generates free radicals, alters the normal micro-environment, behaviour, and functions of normal cells, hampers blood supply, and creates local hypoxia. The degree of these effects depends on the dosage and toxicity of the carcinogens.
Apart from local effects, the toxins gradually diffusing into neighbouring tissues, can reach the blood and travel to other tissues and organs. It is a known physiological and toxicological fact that the presence of toxic substances intensify respiration (our outer breathing) due to stress on the immune system and organs of elimination (the kidneys, liver, skin, etc.). Hence, a person’s breathing will be deeper (increased tidal volume) and heavier (greater minute ventilation).
Similar effects are produced by most medical drugs. “Antibiotics (penicillin, streptomycin etc.) intensify breathing… Camfora, codein, cordiamin, adrenalin, theoephedrine, and ephedrine – also intensify breathing” (Buteyko, ibid.). The degree of intensification depends on toxicity, dosage, possible allergies, and individual abilities to eliminate them from the system.
Western research also demonstrated increased ventilation in humans due to endotoxin (Preas et al, 2001), flumazenil and midazolam (Kawauchi et al, 2000), testosterone (Ahuja et al, 2007), theophylline (Pesek et al, 1999), adenosine (Smits et al, 1987; Reid et al, 1987), and bronchodilators: pirbuterol and ipratropium (Ashutosh et al, 1995) and aminophylline (Montserrat et al, 1995). Generally, any drug with known toxicity for the liver or kidneys produces increased ventilation.
Even those drugs or substances which are classified as respiratory depressants (diacetylmorphine or heroin, morphine, alcohol, etc.) first suppress respiration for several hours, but later produce significant increase in minute volume above the initial values due to stress on organs of elimination.
Conclusion: Local pollution causes systemic stress and increased ventilation (outer respiration). We breathe heavier.
The next question is: what is the effect of deeper breathing (increased minute ventilation) on cellular oxygenation?
Ahuja D, Mateika JH, Diamond MP, Badr MS, Ventilatory sensitivity to carbon dioxide before and after episodic hypoxia in women treated with testosterone, J Appl Physiol. 2007 May;102(5): 1832-1838.
Ashutosh K, Dev G, Steele D, Nonbronchodilator effects of pirbuterol and ipratropium in chronic obstructive pulmonary disease, Chest. 1995 Jan; 107(1): 173-178.
Buteyko KP, Soviet national journal Nauka i zshizn’ [Science and life], Moscow, issue 10, October 1977.)
Flack M, Some simple tests of physical efficiency, Lancet 1920; 196: 210-212.
Kawauchi Y, Oshima T, Saitoh Y, Toyooka H, Flumazenil abolishes midazolam-induced increase in the work of nasal breathing, Can J Anaesth. 2000 Dec; 47(12): 1216-1219.
McArdle WD, Katch FI, Katch VL, Essentials of exercise physiology (2-nd edition); Lippincott, Williams and Wilkins, London 2000, p.252.
Montserrat JM, Barberà JA, Viegas C, Roca J, Rodriguez-Roisin R, Gas exchange response to intravenous aminophylline in patients with a severe exacerbation of asthma, Eur Respir J. 1995 Jan; 8(1): 28-33.
Pesek CA, Cooley R, Narkiewicz K, Dyken M, Weintraub NL, Somers VK, Theophylline therapy for near-fatal Cheyne-Stokes respiration. A case report, Ann Intern Med. 1999 Mar 2; 130(5): 427-430.
Preas HL 2nd, Jubran A, Vandivier RW, Reda D, Godin PJ, Banks SM, Tobin MJ, Suffredini AF, Effect of endotoxin on ventilation and breath variability: role of cyclooxygenase pathway, Am J Respir Crit Care Med. 2001 Aug 15; 164(4): 620-626.
Reid PG, Watt AH, Routledge PA, Smith AP, Intravenous infusion of adenosine but not inosine stimulates respiration in man, Br J Clin Pharmacol. 1987 Mar; 23(3): 331-338.
Smits P, Schouten J, Thien T, Respiratory stimulant effects of adenosine in man after caffeine and enprofylline, Br J Clin Pharmacol. 1987 Dec; 24(6): 816-819.
Part 3. Effects of unnoticed increased breathing on cellular oxygenation (or how our slight over-breathing influences breathing of cells)
Do we notice that our breathing is heavy? Usually, people notice that their breathing is heavy when they breathe more than 25 l/min at rest (or 4-6 times the norm!). Why is this? Air is weightless, and breathing muscles are powerful. During rigorous physical exercise we can breathe up to 100-150 l/min. Some athletes can breathe up to 200 l/min. So it is easy to breathe "only" 10-15 l/min at rest (only 10% of our maximum capacity), throughout the day and night and not be aware of this rate of breathing. However, in health, we should breathe only about 3-4% of our maximum breathing rate.
When a person starts to over-breathe or hyperventilate (breathe more air per minute), blood oxygenation in the lungs has negligible changes. Why? During normal breathing human blood has 98-99% O2 saturation. Hence, big breathing cannot increase the blood oxygenation in any significant degree.
What are the other effects, if a healthy person starts to breathe more or deeper?
Hence, too much CO2 is removed from all cells. When the breathing is big all the time, the CO2 level in all body cells is chronically low. How can CO2 influence oxygenation of the tissues? There are two direct CO2 effects on the oxygenation of tissues.
A. Vasodilation-vasoconstriction effect
Imagine that a person at rest starts to hyperventilate or breathe very heavy and very fast. What would happen? The person would feel dizzy and can faint or pass out. Why? It cannot be due to too much oxygen, since their blood is almost fully saturated with O2 with very shallow (or normal) breathing at rest.
This scan below shows brain oxygenation in two conditions: normal breathing and after 1 minute of hyperventilation. The red color represents the most O2, dark blue the least. Brain oxygenation for overbreathing is reduced by 40%. (Litchfield, 2003).
CO2 is a dilator of blood vessels (arteries and arterioles). Arteries and arterioles have their own tiny smooth muscles that can constrict or dilate depending on CO2 concentrations. When the breathe more, CO2 level becomes smaller, blood vessels constrict and vital organs (like the brain, heart, kidneys, liver, stomach, spleen, colon, etc.) get less blood. As physiological studies found, blood flow to these organs is proportional to blood CO2 concentrations. The less we breathe, the more blood and oxygen can reach the tissues of vital organs.
Since hyperventilation is an important part of our “fight-or-flight” response, during hyperventilation the blood is generally diverted from the vital organs to the large skeletal muscles. Indeed, studies found decreased perfusion of the heart (Okazaki et al, 1991), brain (discussed above), liver (Hughes et al, 1979; Okazaki, 1989), kidneys (Okazaki, 1989), and colon (Gilmour et al, 1980).
Why did Nature provide us with this physiological reaction: vasoconstriction due to hyperventilation? Breathing is closely connected with blood flow to all vital organs, sensitivity of the immune system, permeability of cellular membranes, and many other functions. As soon as vital organs (the brain, heart, stomach, kidneys, liver, etc.) are under stress (chemical, viral, bacteriological, etc.), or inflammation, or injury, the breathing gets heavier.
That helps to prevent:
All these preventive effects can save the life of the organism in the short run. At the same time, it is not normal to be in a state of stress (or fight-flight mode) all the time. Our breathing, if there is no emergency, should be normal. In order to normalize breathing (or to retrain the breathing centre), all organs and tissues should be gradually repaired, restored and rebuilt.
B. The Bohr effect
The descriiption of the Bohr law (discovered over a century ago) can be found in standard physiological textbooks since it was confirmed by dozens of professional studies.
What is the Bohr effect? As we know, oxygen is transported in the blood by hemoglobin cells. How do these red blood cells know where to release more oxygen and where less is needed? Or why do they unload more oxygen in those places where more is required? For example, at rest the heart muscle requires more oxygen, but blood travels everywhere.
The hemoglobin cells sense higher concentrations of CO2 (end product of energy production) and release oxygen in such places. The effect strongly depends on the absolute CO2 values in the blood and the lungs.
If the CO2 concentration is low, O2 cells are stuck to the red blood cells. Hence, CO2 deficiency leads to hypoxia or low oxygenation of the body cells (the suppressed Bohr effect). The more we breathe at rest, the less the oxygenation of our cells in the vital organs, like brain, heart, liver, kidneys, etc.
The Bohr effect is crucial for our survival. Why? At each moment of our lives, some organs and tissues work harder and produce more CO2. These additional CO2 concentrations are sensed by the hemoglobin cells and cause them to release more O2 in those places where it is most required. This is a smart self-regulating mechanism for efficient O2 transport.
For example, without the Bohr effect, you could not walk or run even for 3-5 minutes. Why? In normal conditions, due to the Bohr effect, more O2 is released by red blood cells in those muscles, which generate more CO2. Hence, these muscles will get more O2 and can continue to work with the same high rate.
Western studies confirmed that hyperventilation compromises oxygenation of vital organs, like liver and kidneys (Hughes et al, 1979; Okazaki et al, 1989), and heart (Okazaki et al, 1991) (e.g., Hughes et al, 1979; Hashimoto et al, 1989; Okazaki et al, 1991).
Conclusions: Even slight unnoticed over-breathing or increased ventilation decreases blood and oxygen supply for all vital organs causing tissue hypoxia and poor perfusion.
Gilmour DG, Douglas IH, Aitkenhead AR, Hothersall AP, Horton PW, Ledingham IM, Colon blood flow in the dog: effects of changes in arterial carbon dioxide tension, Cardiovasc Res 1980 Jan; 14(1): 11-20.
Hashimoto K, Okazaki K, Okutsu Y, The effects of hypocapnia and hypercapnia on tissue surface PO2 in hemorrhaged dogs [Article in Japanese], Masui 1989 Oct; 38(10): 1271-1274.
Hughes RL, Mathie RT, Fitch W, Campbell D, Liver blood flow and oxygen consumption during hypocapnia and IPPV in the greyhound, J Appl Physiol. 1979 Aug; 47(2): 290-295.
Litchfield PM, A brief overview of the chemistry of respiration and the breathing heart wave, California Biofeedback, 2003 Spring, 19(1).
McArdle WD, Katch FI, Katch VL, Essentials of exercise physiology (2-nd edition); Lippincott, Williams and Wilkins, London 2000.
Okazaki K, Hashimoto K, Okutsu Y, Okumura F, Effect of arterial carbon dioxide tension on regional myocardial tissue oxygen tension in the dog [Article in Japanese], Masui 1991 Nov; 40(11): 1620-1624.
Okazaki K, Okutsu Y, Fukunaga A, Effect of carbon dioxide (hypocapnia and hypercapnia) on tissue blood flow and oxygenation of liver, kidneys and skeletal muscle in the dog, Masui 1989 Apr, 38 (4): 457-464.
Santiago TV & Edelman NH, Brain blood flow and control of breathing, in Handbook of Physiology, Section 3: The respiratory system, vol. II, ed. by AP Fishman. American Physiological Society, Betheda, Maryland, 1986, p. 163-179.
Part 4. Lifestyle factors and their interactions with breathing
The way we breathe and our breathing patterns are tightly connected with the surrounding environment and numerous factors that influence or interact with the human organism. Virtually any significant change causes changes in breathing. Hence, some factors can make breathing lighter, others heavier reducing body oxygenation. The particular effects of these factors can be checked using the stress-free breath holding time test that reflects tissue oxygenation. Compare the CP (Control Pause or stress free-breath holding time discussed in Part 2) before and after any activity to measure the effects of these factors on oxygenation and tumours.
Among common factors which make breathing stronger and intensify tumour hypoxia are:
The detailed analysis of these factors and the methods for their correction are crucial elements of the Buteyko breathing re-training method targeted to restore body oxygenation using natural means.
Conclusion: Presence of various abnormal lifestyle factors makes breathing bigger and deeper and creates chronic hypoxia of vital organs.
Part 5. A dynamic model for development of cancer (theoretical and practical ideas)
Theory
Since CO2 is a dilator of small blood vessels, low CO2 concentrations lead to the constriction of the arteries and arterioles causing problems with blood and oxygen delivery. In addition, low CO2 values cause the inability of red blood cells to efficiently release whatever little oxygen they bring (the suppressed Bohr effect). The final outcome is hypoxia in the tissues, including vital organs.
Since all vital organs are going to suffer from hypoxia, malignant cells can thrive in tissues and parts of the body which are most compromised in relation to their oxygenation (the genetic component of cancer). Toxic overload due to smoking, dietary toxins and poisons, radiation, and other causes can intensify local hypoxic effects in certain parts or organs of the organism (the environmental component of cancer). Further growth of the tumour and its metastasis are also controlled by the same factors, where tissue hypoxia plays the central role.
Development of cancer or growth of tumours is a dynamic process which is sensitive to changes in our breathing. For example, for modern man early morning hours are the times of severe hypoxia. Hence, usually tumours grow during early morning hours and stagnate or even regress during the remaining part of the day.
This model does not explain the basis for all cancers since more research is required to establish the exact chain of events for various conditions.
Practice
The Buteyko method was tested by various western and Soviet trials on patients with asthma, heart disease, chronic fatigue syndrome, sleep apnea, radiation disease (after Chernobyl disaster), liver cirrhosis, and HIV/AIDS. During the large western trials on asthmatics, the disappearance of malignant tumours was the side effect of the therapy. Many Soviet patients who learned the Buteyko breathing method also had cancer. What were the observations of Russian and Soviet doctors in relation to cancer?
Large CPs (over 60 s 24/7) are incompatible with malignant and benign tumours. Normal breathing parameters indicate good perfusion (blood supply) of all vital organs and tissues and the enhanced Bohr effect. Vital tissues get sufficient O2 supply and this eradicates the foundation for cancer (tissue hypoxia). Hence, normal breathing of the person creates conditions for normal breathing of all cells.
Normal breathing parameters were accepted about a century ago. However, very few people have them now. We, in health, breathe about 50% more air every minute (about 9 instead of 6 l/min). Thus, relatively healthy modern day people have about 25-30 s CP during day time and about 15-20 s CP or less in the early morning hours. Sick people (asthma, heart disease, diabetes, cancer) chronically breathe about 2-3 times more air than the medical norm. They have shorter CPs (e.g., 12-15 s for people with mild asthma and heart disease; and less than 10 s for the severely sick and terminally ill).
When the CP is less than 20 s, the Krebb cycle (also called citric acid cycle) is reversed. The chemical reactions of this cycle provide mitochondria with oxygen and ability to generate energy aerobically. Abnormalities in the Krebb cycle intensify the anaerobic metabolism, production of lactic acid, generation of free radicals, fatigue, and tissue hypoxia. The practice of Russian doctors, as well as western breathing teachers, show that most people have their shortest breath holding times during the early morning hours (usually 4-7 a.m.). Hence, if a person's CP drops below 20 s, cancer progresses, and the tumour grows.
Moreover, in severely sick cancer patients, the CP can be below 10 s. Such critically low levels of oxygen indicate severe hypoxia, a very weak immune system, and the ability of malignant cells travel via blood, attach themselves in new organs and initiate formation of new tumours (metastasis).
Clinical observations revealed that there are 3 crucial CP numbers involved in understanding the general development and progress of disease, cancer included. They are as follows.
However, our breathing and the CP are not the same throughout the day. Meals, stress, exercise, emotions, and hundreds of other factors influence tissue oxygenation and breathing. The dynamic of these changes in cellular oxygenation is the decisive factor that controls the life of malignant tumours or development of other forms of cancer.
Conclusions: The dynamic nature of cancer can be expressed by the index of oxygenation, or stress-free breath holding time after usual exhalation: 1-10 s – metastasis; 10-20 s – growth of tumours and advance of cancer; 20-40 s – the intermediate state (deadlock); over 40 s – reversal of hypoxia and disappearance of cancer.
Part 6. General approach to the treatment of cancer
The main goal of cancer treatment is to eliminate the foundation of cancer: tissue hypoxia. Cancer treatment, therefore, should be based on the restoration of normal breathing parameters (minute ventilation, blood carbon dioxide content, tissue oxygenation, the CP, etc.). Normalization of breathing can take days or months depending on age, obesity, and general tissue pollution especially due to medication.
The most advanced system of breathing retraining is based on the Buteyko breathing method. The ultimate goal of the Buteyko method is to achieve his standard of ideal health manifested in 60 s CP at any time of the day or night. Such breath holding time ensures thorough oxygenation of all tissues and inability of appearance of any tumor or existence of conditions for tumor elimination.
The Buteyko method includes 2 components: breathing exercises (to be practiced about 1 hour per day or more) and common sense activities based on optimization of lifestyle factors. In relation to the life style, the Buteyko method includes simple and easy to follow rules:
Some ideas or principles of the Buteyko method are adjusted to individual needs of the patient (e.g., exercise, sleep positions, diet, and supplements). Russian practice clearly revealed that very few patients are able to learn the method from the manual or book. The presence of a breathing teacher is crucial for permanent breathing retraining.
An important practical observation of breathing teachers is that restoration of tissues, including elimination of inflammation, malignant and benign tumours, various types of fibroblasts, plaque, cysts, papillomas or polyps, adenomas, lymphomas, keratoacanthomas, and granulomas need at least 30-35 s CP at all times. The duration of restoration depends on many factors related to the current homeostasis and input parameters of the biological system that is monitored through changes in respiratory characteristics, especially the CP (Control Pause). According to observations of Russian doctors, the Buteyko method can reverse earlier stages of cancer (stages 1 and 2), while there is definite improvement in the quality of life for patients who have cancer in stages 3 and 4.
Specifically, cancer treatment also requires appropriate nutritional support, including use of enzymes, raw diet, sprouting, etc. However, it should be noted, that none of these auxiliary factors (or special diet or supplements) or even all of them are not going to work, unless the fundamental cause of cancer (hypoxia) is addressed. The person may adhere to the best diet and eat kilograms of super foods but if, for example, the morning CP is about 15 s or less general progress is unlikely. Indeed, the cancer patient may have about 30-35 s CP during the day but only 15 s in the morning due to morning hyperventilation between 4 and 7 am. The positive effects of light easy breathing and good oxygenation during the day, when the tumour is shrinking is size, will be counteracted by growth of the tumour during the 3 hours of morning hyperventilation.
Hence, it is crucial to better manage the minimum or morning CP for faster recovery. The personal program in relation to morning hyperventilation depends on such factors as breathing through the mouth at night, sleeping on the back, overheating, poor air quality, etc.
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