Chapter 3. Causes of chronic hyperventilation Introduction After finding a prevalence of hyperventilation in the present-day population with compromised health and after reviewing the regulation of breathing in health and disease, let us look at the main causes of chronic hyperventilation. Which environmental, life-style, and other factors intensify breathing, causing the breathing centre to readjust to a lower aCO2 (arterial CO2 pressure) norm? What are their mechanisms and degree of influence? Most causes described in this chapter were systematically investigated and summarized by Professor Buteyko (Buteyko, 1969; Buteyko 1970; p.158, Buteyko, 1992; p.177, Khoroscho, 1982), when he used his unique diagnostic complex in different practical situations. Meanwhile, these publications and his lectures described hyperventilation-producing factors often without detailed information about the mechanisms of their influence. In addition, these papers were in Russian. At the same time, there are relevant Western physiological studies showing such mechanisms and providing measurements of their influence. 3.1 Stress, anxiety and strong emotions The notion of "stress" is used with different meanings. For example, the presence of bacteria and their toxins in blood is an example of stress to a medical doctor. Such stress, as it was described in section 1.8, produces chronic visible hyperventilation. Similarly, tiny amounts of other toxins in blood, as a result of, for example, teeth caries, should also cause mild over-breathing, as we are going to see later. However, let us consider here only influences due to personal perception of threat, challenge, or other psychological stress. There are numerous physiological changes generated by anxiety states, fear, fight-or-flight situations, or other situations accompanied by strong emotions. How do these states and factors influence breathing? An early paper "Some physical phenomena associated with the anxiety states and their relation to hyperventilation" (Kerr et al, 1937) included a chart showing physiological changes caused by these states. Hyperventilation is the main factor causing many other consequences described. According to Professor Lum, "Most authors, with the exception of Rice (1950), have described the clinical presentation of hyperventilation as a manifestation of, and secondary to, an underlying anxiety state" (p.197, Lum 1976). Dr. Magarian wrote one of the large hyperventilation reviews, published in "Medicine" (Magarian, 1982), choosing the following title for his paper "Hyperventilation syndromes: infrequently recognized common expression of anxiety and stress". A more recent study "Fear-relevant images as conditioned stimuli for somatic complaints, respiratory behaviour, and reduced end-tidal pCO2" (Stegen et al., 1999) discusses psychological and physiological effects providing numerous references in this area. Authors of the article "Emotions and respiratory patterns: review and critical analysis" (Boiten et al, 1994) suggested, that "...normo-ventilatory responses (which are identified by stable end-tidal CO2 levels that remain within the normal range) seem to be characteristic for behavioural conditions that may either involve withdrawal from the environment, relaxation or active coping...Thus, hyperventilation appears to signify an unsuccessful outcome of the coping process" (p.121). Therefore, not only negative emotions and states, but also many positive strong emotions produce hyperventilation. Stress, according to TV, radio, newspapers and magazine news about medical studies, contributes to the development of most modern health problems. On the other hand, stress-triggering physiological changes had obvious usefulness in terms of evolutionary survival of our species. For example, the diversion of blood from internal organs and the brain to large skeletal muscles prepared the body for possible vigorous physical activity. Increased nervous excitability

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helped our ancestors to give different psychological interpretation to surrounding stimuli and events. Indeed, during peaceful moments, objective perception of the world, quiet and thoughtful relationships with nature and group members were advantageous. At other times, e.g., during hunting, fight-or-flight situations, group conflicts, or mating, subjective perception, in terms of seeing the world in the light of personal needs, was more useful for species survival. Do we have more stress now? From an objective viewpoint, our ancestors living 1, 2 or more thousands of generations ago, had constant life-threatening situations and challenges. Hence, the level of stress and the likelihood of mortality were much higher in the past. Why then, do modern people chronically hyperventilate and get sick because of stress, while our ancestors mostly died from other, more natural causes? A part of the answer lies in breathing. Chronic hyperventilators already have a much-enhanced excitory response to life events and situations due to an abnormal state of the nervous system. The objective perception of the world is difficult for them due to low aCO2 and that predisposes people to strong emotions, excitement, and tendencies to exaggerate, justify, catastrophize, distort, and misinterpret events. Another part of the answer is in the after-stress activities. Our ancestors hunted, struggled, or ran away under stressful conditions. All these are active coping strategies involving physical exercise. Therefore, our attention should be directed to the following question. What are the effects of exercise on breathing? 3.2 Physical inactivity The natural lives of our ancestors, modem primitive people, or modern human-related species and other mammals include many hours of exercise of light, moderate, and, sometimes, high intensity. Typical moderate intensities (40-65% from maximum O2 consumption) produce the following effects in healthy people. 1.While aCO2 remains close to the initial level (about 40 mm Hg), venous CO2 content rises from resting 46 mm Hg to about 60-65 mm Hg due to the metabolism of carbohydrates and fats (p.201, Brooks et al, 1996). Hence, during moderate exercise, the human organism accumulates large additional amounts of CO2. 2. Blood pH in arteries slightly decreases (acidification) from 7.42 to 7.38 (p.201, Brooks et al, 1996), indicating some adaptation of the breathing centre to a more acidic environment. (Lactic acid is the main cause of additional acidity). Possibly, this adaptation, if exercise is long enough, can influence after-exercise breathing in the following manner. When exercise is over, lactate starts to decrease (its normal half decomposition time is about 12-13 minutes). Since blood pH must be restored, an increase in aCO2 may be expected, as a compensation for diminished lactic acid in blood. 3. Arterial oxygenation is reduced by about 2-5 % and venous O2 partial pressure is decreased from resting 40 mm Hg to 20 mm Hg. Thus moderate exercise takes place in the condition of mild tissue hypoxia. That, again, if exercise is long enough, should cause favourable adaptation of the breathing centre and subsequent easy and natural breathing. How do these positive changes come about? Exercise is normally accompanied by movements of limbs causing neuronal discharges from working muscles to the central nervous system. Such muscular movements, as it was discussed in Chapter 2 (how light physical activity can prolong BHT), suppress the drive of the breathing centre to increase ventilation. Thus, any physical prolonged physical activity has positive effects on respiration of healthy individuals. This results in increased tolerance to higher aCO2 and lower vO2 values. Indeed, several physiological studies revealed "the increased 'tolerance' for high CO2 and low O2 in breath holding, during and immediately after exercise" (p.220, Astrad, 1960). Thus, exercise for healthy people also trains the breathing centre to reset its aCO2 threshold to higher values.

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As a result, if exercise normalises (as a response to stress) or reduces ventilation, then lack of exercise, in the post-stress or post-anxiety situations, or after experiencing strong emotions, should normally cause habitual hyperventilation. That conclusion also follows from the quote in the previous section, where the positive influence of active coping strategies on breathing (normo-ventilation) is considered. Exercise, obviously, is an example of active response. Important notice. The positive effect of exercise on breathing can normally be experienced by healthy people. As we found in chapter 2, the aCO2 of sick people gets lower during exercise with moderate or often light intensities. Thus, in poor health the possible benefits, due to exercise, are limited. 3.3 Overeating, especially of animal proteins Let us look, first, at the dynamics of respiration after a single meal. At the end of the meal, when the stomach is at its fullest volume, hydrochloric acid is secreted by the stomach walls for food digestion. Since most H+ (hydrogen ions) are borrowed from the blood, this acidification of the stomach is accompanied by the alkalisation of the blood. The breathing centre (which also monitors blood pH) senses this change and normalizes blood acidity by additional carbonic acid. That is done by storing CO2 in blood due to reduced ventilation immediately after the meal. High aCO2 normally causes muscular relaxation, some pacification of the nervous system, and increased blood flow to internal organs aiding digestion. Usually, faecal and urinary eliminations, because of increased blood flow to internal organs due to aCO2 raise, are also more frequent soon after meals. The magnitudes of these changes are proportional to the calorific value and type of the meal. Therefore, for larger meals, especially with some fats and proteins, these effects are stronger. Thus, an anxious person can consume large meals in order to get rid of excessive excitability of the nervous system, anxiety, stress, or fears. However, these results are short-lived, since in about 1 hour, some hydrogen ions start to return back from the digestive system to the blood. Now, vice versa, blood pH preservation is achieved through removal of bicarbonates by kidneys, in the short run, and increased ventilation, in the long run. Usually, 2-3 hours after the meal, when the stomach gets almost empty, this process is at its maximum. Hence, breathing becomes heavier at the end of digestion. Again, the amplitude of these reverse processes is proportional to the calorific value and type of the meal. These processes should finally produce the same aCO2 as at the beginning. In this case the breathing after digestion should be the same as before the meal. However, increased ventilation and decreased aCO2 are going to take place due to necessity of food digestion. As Professor Buteyko suggested, when digested substances are in the blood, they are to be used or metabolised by body cells. This cellular consumption means “inner breathing”. Thus, the respiration of cells, especially in case of overeating, is intensified. That causes increased ventilation of the human organism (Buteyko, 1969). Such dynamics of breathing, as a response to meals, helps one to understand how overeating can become a strategy of coping with anxiety and stress. Overeating, first, reduces ventilation (eating till "breathless"), but 2-3 hours later, at the end of digestion, breathing becomes even heavier than at the beginning. Hence, the person becomes more anxious, stressed, excited, fearful, etc. Then the food can be again used as a solution of the problem, repeating the whole cycle with the same or aggravated final results. Professor Buteyko also found that meals rich in concentrated proteins and, in a lesser degree, fats considerably intensify breathing, while the influence of fruits and vegetables produces the least impact on ventilation. One difference is due to different availability of digestive enzymes. Fresh fruits, for example, often have their own enzymes making their digestion easy. Meats and fats are hard to digest. Second, amino acids cause blood acidification.

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Therefore, pH norm can be restored by CO2 removal. Third, some essential amino acids can directly affect the breathing centre and intensify respiration (chapter 8). An old study by Haselbalch (1912) revealed that aCO2 after vegetarian diet decreased to 43.3 mm Hg; while meat diet resulted in 38.9 mm Hg (the reader can note typically high normal aCO2 for old investigations). Such difference means that a MP after meat meal can be about 12 s less, than after the vegetarian one. Explaining this finding in his textbook on respiration, Professor Haldane suggested, that "a meat diet, which causes an increase of sulphuric and phosphoric acids in blood, is acid-forming as compared to a vegetable diet, which contains less protein and relative abundance of salts yielding carbonates"(p.183, Haldane, 1922). Thus, additional acids (amino acids) in the blood are compensated by the breathing centre by reduction in carbonic acid and CO2 stores. Vice versa, presence of additional alkaline salts in blood needs extra acids for blood pH preservation. Among all acids in blood, carbonic acid is the main component and its concentration can be changed by respiration. These ideas clearly explain why alkaline diets are considered to be healthy (fruits and vegetables yield alkaline residues, when they are consumed), while acidic diets (that includes meats, fish, eggs, dairy products, most grains, legumes and nuts) less so. In addition to these immediate effects of meals on respiration, lack of normally occurring food substances in the diet can gradually cause chronic hyperventilation. For example, carbohydrates for their digestion require adequate amounts of B vitamins. These vitamins are naturally present in whole grains and root vegetables and almost absent in sugar, white bread and white rice. Thus, eating these refined products diminishes B vitamins content in nervous cells gradually leading to chronic hyperventilation (Buteyko, 1969). Lack of some minerals (especially Mg, Zn, and Ca) and their biochemical unavailability are other causes of chronic over-breathing. A suboptimal immune system, which can be caused by a faulty diet, can result in infections also worsening normal respiration control (chapter 1). Thus, consequences of the usual western diet and typical diets in many other countries, in terms of breathing, are easy to predict, while overeating, so prevalent nowadays, is one of the major causes of chronic hyperventilation. 3.4 Deep breathing exercises Deep breathing exercises, according to Professor Buteyko, were the main cause of hyperventilation in the general population of the USSR (Buteyko, 1969). Indeed, up to the1980's , physical gymnastics combined with deep breathing was advised and promoted by central radio and TV programs, magazine and newspaper articles. As a result of such propaganda, schools, colleagues, universities, boy-scout and military camps, health retreats, sanatoria, hospitals, some state factories and many other establishments used voluntary deep breathing (hyperventilation), which was synchronised with dynamic movements of body limbs during daily gymnastics. Prolonged performance of such exercises gradually resets the breathing centre to lower aCO2, causing chronic hyperventilation years later (Buteyko, 1969). However, this practice was mainly stopped after the Directive of the Soviet Health Minister "Practical actions for application of the method of voluntary regulation of depth of breathing for treatment of bronchial asthma" (Directive N 591, 30 April 1985, Signed by USSR Health Minister S. Burenkov). Thus, Soviet medical authorities officially accepted the Buteyko method of relative hypoventilation (reduced breathing), as a safe and natural alternative to drugs in relation to asthma and bronchitis. Some time ago, when I started to investigate medical literature on respiration, I found that roughly there is only one study, which suggests the usefulness of hyperventilation (over-breathing), against several hundred studies about the dangers of hyperventilation. Moreover, hyperventilation may be advised by medical authorities only for those rare conditions (discussed in chapter 1), when patients breathe too little. Nevertheless, many people still believe that

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breathing more is healthy. In order to check that I started to question people around me with the question (What is better for human health: to breathe more or less?). After such private polls, I realised that well over 95% of my respondents believed that over-breathing, deep breathing, and hyperventilation were useful and should be practised. So far, all those few people, who told me that hyperventilation and deep breathing were not good ideas, professionally studied physiology and/or medicine. It follows from these facts that ideas about usefulness of hyperventilation and deep breathing are still among the greatest modern health-related misconceptions. The physiological effects of these superstitions are probably limited, since few routinely practice hyperventilation exercises. However, there are many people, who couple deep breathing with some physical exercises, dancing, singing, playing musical instruments, praying and other activities. How it is possible then that people do not notice that hyperventilation produces a negative impact on their health? Why do they not notice, for example, that their brains become affected, while nervous excitement can be so strong that rational abilities, memory and cognitive skills are seriously impaired? The answer can be found in the results of experiments conducted by researchers at the University of Oxford, England. In the abstract they wrote,

"A cognitive explanation of the association between acute hyperventilation and panic attacks has been proposed: the extent to which sensations produced by hyperventilation are interpreted in a negative and catastrophic way is said to be a major determinant of panic. Non-clinical subjects were provided with a negative or a positive interpretation of the sensations produced by equivalent amounts of voluntary hyperventilation. As predicted, there was a significant difference between positive and negative interpretation conditions on ratings of positive and negative affect. Subjects in the positive interpretation condition experienced hyperventilation as pleasant, and subjects in the negative interpretation condition experienced hyperventilation as unpleasant, even though both groups experienced similar bodily sensations and did not differ in their prior expectations of the affective consequences of hyperventilation. When the subjects were given a positive interpretation, the number of their sensations correlated with positive affect; when a negative interpretation was given, the number of bodily sensations correlated with negative affect…" (Salkovskis & Clark, 1990). It follows from these results that, when a person has positive expectations about his activity, which is done with deliberate hyperventilation, his brain, due to created excitement and hypoxia, is inclined to select positive final effects, while ignoring certain rational and critical thoughts. For example, a hyperventilating person can have a tendency to exaggerate his abilities and achievements without paying due attention to own weaknesses and possibilities for improvement. Deep breathing for relatively healthy people usually means increased ventilation. In this case it is similar to extended mild hyperventilation provocation test (see chapter 1). Frequent and prolonged repetition of such practice produces chronic over-breathing due to readjustment of the breathing centre to lower aCO2 (Buteyko, 1969). Even deliberate deep and slow breathing with almost unchanged aCO2 can create problems later due to large amplitude of chest and/or diaphragm movements. Indeed, such amplitude can be still present many hours later after the practice, but with usual individual breathing frequency, indicating development of chronic hyperventilation. The person, due to nervous excitement and impaired rationality, may even periodically remind himself after the practice to continue deep breathing in spite of possible chest tightness, dizziness and nausea, created by excessive ventilation.

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3.5 Overheating Overheating, according to Professor Buteyko, is another factor that intensifies breathing. That especially relates to many children, who suffer from the misconceptions of their loving parents and care-takers, since these adults believe that excessively warm dressing is healthy. Children's metabolism is 2-3 times more than that of adults. Hence, their bodies normally generate much more energy. Accordingly, healthy children need much less clothing (Buteyko, 1969). In order to check their thermoregulation, one can hold their hands and feet that are usually warm, even when children wear minimum clothing. Only when their hands and feet are cold, adding more clothes or other actions are necessary. Similar considerations can be applied to adults. During, for example, summer, most people wear shirts, t-shirts, dresses and other very light clothes, while going anywhere, outdoors and indoors. Here it would be useful to spend less time in hot and warm places. When it gets colder, people start to wear pullovers, sweaters, jumpers, jackets, coats, suits, etc. However, these same people wear these heavy clothes in exactly the same places, which have exactly the same (summer) temperature. It happens in libraries and offices, shops and waiting rooms, cars and public transport. Investigations on influence of heat on breathing found that change in air wet-bulb temperature, from 17 to 40 degrees, caused fall in CO2 pressure from 44 to 33 mmHg (or from 5.8% to 4.3%) for 10 healthy male subjects (Gaudio & Neil, 1968). After some math, it follows, that their CPs fell from 46 to 8 s due to conditions of strong heat. Thus, if the assumption of linear influence of temperature on ventilation is accepted (although that may not be true for the whole range of values), one may conclude that each two degrees of surrounding temperature up produce over 1 mmHg of aCO2 down (or minus about 2s CP). Rapid changes in temperature can increase breathing as well. Sudden cold immersion usually produces severe hyperventilation during first few breaths. This topic will be discussed in more details later. 3.6 Talking with deep inhalations, loud voice, or high pitches During lectures and public speeches, or when just talking, it is important not to take deep in-breaths between phrases (Buteyko, 1969). Often, people start their sentences and phrases after deep inhalations quickly blowing out the air, together with CO2, from their lungs. That is a current feature of modern talking style and it can be routinely observed for many TV reporters and commentators. Such a speaking style makes the speech more appealing or even dramatic for viewers. However, it also increases ventilation causing reduced CO2 stores. A study entitled "Influence of continuous speaking on ventilation" (Hoit & Lohmeier, 2000) revealed the following (abstract).

"This study was conducted to explore the influence of speaking on ventilation. Twenty healthy young men were studied during periods of quiet breathing and prolonged speaking using noninvasive methods to measure chest wall surface motions and expired gas composition. Results indicated that all subjects ventilated more during speaking than during quiet breathing, usually by augmenting both tidal volume and breathing frequency. Ventilation did not change across repeated speaking trials. Quiet breathing was altered from its usual behaviour following speaking, often for several minutes. Speaking-related increases in ventilation were found to be strongly correlated with lung volume expenditures per syllable. These findings have clinical implications for the respiratory care practitioner and the speech-language pathologist." The authors found that average ventilation increased from resting 7 l/min to almost 14 l/min during speeches. Average initial end-tidal CO2 pressure of these healthy (by year 2000 standards) young men was almost 38 mm Hg. After 10 minutes of speaking it dropped to about 31 mm Hg. A quick calculation shows that their average initial MP was about 29 s, after 10 min speaking their average MP was correspondent to 14s, if the formula connecting aCO2 and MP is

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applied. For most subjects even many minutes of recovery were not enough to completely restore initial CO2 levels. Actual BHT values after such speeches are going to be larger due to effects created by acute hyperventilation. When current aCO2 is less than the usual set point established by the breathing centre (as it is the case for speaking with hyperventilation), BHT gets larger (chapter 2), while MP measurements require 5-10 min of rest with normal breathing. Talking with deep inhalations, raising one's voice in terms of loudness, elongation of vowels, and high pitch phrases should lead to worse results, since in this study the given texts were emotionally neutral. Should these texts evoke emotions, especially strong ones, higher increases in ventilation could be expected. Since nowadays, there are many people, who daily have hours of speaking, the effects of poor speaking skills on personal health can be large. More detailed suggestions about correct ways of speaking will be given later. 3.7 Mouth breathing While seeing many people on the city streets and in other public places, one may notice that up to 20-40% of them breathe through their mouths when walking or just quietly standing or sitting. This phenomenon seems more frequent among children. Does the breathing route influence aCO2? Scientific literature on respiration often mentions a physiological parameter known as dead space volume. It is about 150-200 ml in an average adult: inside the throat, nose and bronchi. This space preserves additional CO2 for the organism, since inhalations take CO2 rich air of dead space back into the lungs. When the mouth is open, the dead space volume becomes smaller due to continuous exchange of air. In addition, nasal breathing produces more resistance to respiratory muscles during breathing in comparison with mouth breathing (mouth-breathing route is shorter and has larger cross sectional area). Since the human organism has an in-built tendency to optimise physiological processes, it is ready, as during nose-breathing, to breathe less and tolerate higher aCO2, than to exert more demands on constantly working respiratory muscles. In the abstract of a physiological study "An assessment of nasal functions in control of breathing" (Tanaka et al, 1988) the researchers wrote:

"Breathing pattern and steady-state CO2 ventilatory response during mouth breathing were compared with those during nose breathing in nine healthy adults...We found the following. 1) Dead space and airway resistance were significantly greater during nose than during mouth breathing. ...These results fit our observation that end-tidal PCO2 was significantly higher during nose than during mouth breathing. It is suggested that a loss of nasal functions, such as during nasal obstruction, may result in lowering of CO2, fostering apneic spells during sleep." This Japanese article gives average end-tidal CO2 43.7 mm Hg for nasal breathing and 40.6 mm Hg for mouth breathing. Practically, in terms of MP that means 45 s and 37 s at sea level. In case of lower initial aCO2 the difference is, probably, going to be less, since relative hyperventilation can also be less. However, it can still be several or a few seconds. As another observation, one can compare old and modern group photos. They also provide a part of the answer regarding causes of poor health in contemporary society. 3.8 Sleeping too much, sleeping on the back or on the right side Breathing, ventilation and aCO2 during sleep depend on the body position and time parameters. Professor Buteyko found that sleeping too much intensifies breathing causing prolonged periods of hyperventilation later (p.177, Khoroscho, 1982). Largest ventilation and lowest aCO2 correspond to early morning hours (4-6 a.m.).

Among body positions, sleeping on the back (supine position) is worst (some people start snoring in this position). Sleeping on the right side also causes increased ventilation in

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comparison with sleeping on the left side or on the chest. Children's ventilation is minimum when sleeping on their tummies (Buteyko, 1969). There are no physiological studies, known to me, in which breathing in different sleeping body positions, in terms of ventilation and aCO2, is considered. Meanwhile, there are at least 8 studies, devoted to physiological affects of different body positions, which advocate the left position due to the least night-time recumbent reflux (e.g., Khoury et al, 1999). That means that the liquid content of the stomach, for the left position cannot escape or leak due to absence of the physical contact with any of the stomach valves. This position is also the most favourable for general peristaltic waves in the large intestine due to the gravitational effect in the transverse colon. There are, possibly, some other reasons for advantages of the left position. 3.9 Embryonic and foetal development in a woman hyperventilating during her pregnancy Normally, a pregnant woman’s aCO2 is about 7 mm Hg (or 1%) less, than her usual values (chapter 1). But since many women hyperventilate before pregnancies, their aCO2 values during pregnancies are lower, than their physiological norms. Her embryo receives all its nutrients through the umbilical cord via blood. Therefore, the embryo gets exactly the same CO2 concentrations, as his mother. Due to Nature’s design, aCO2 of the embryo is greater than normal human values (chapter 1), but the lowered aCO2 of the mother tends to reduce the CO2 stores of the embryo. Hence, when the mother hyperventilates, her embryo also hyperventilates in relation to its physiological norms. Such a child is already developing and will be born in the conditions of over-breathing. Moreover, studies of pregnant women done by Professor Buteyko revealed that numerous complications during pregnancies and deliveries are possible only when aCO2 is low. That relates, for example, to spasms of ovaries, excessive hypoxia of the embryo, and spontaneous abortions. Babies born with hyperventilation often suffer from skin rashes, pneumonia, asthma, eczema, and other problems. These health problems are absent in babies with normal aCO2 (Buteyko, 1969). 3.10 Exposure to toxic chemicals Toxic chemicals, once in the human organism, can generate different waste products, interfere with hormonal balance, and influence the nervous, digestive, cardiovascular and other systems. These negative changes sooner or later cause hyperventilation. The mere appearance of large amounts of waste products from bacteria in blood would be sufficient to cause heavy over-breathing (chapter 1). Therefore, for example, environmental, professional, and any other exposure to heavy metals, pesticides, herbicides, and chemicals due to pollution are also causes of hyperventilation. Many drugs intensify respiration. For example, antibiotics fight microbes by suppressing their metabolism and breathing, but all living cells breathe. Suppression of human cellular breathing excites the breathing centre increasing ventilation. Thus, excessive use of antibiotics is damaging for health. Main drugs used in medicine, like camphor, codeine, cordiamin, theophedrin, ephedrine, etc. - all result in hyperventilation. Caffeine, which can be found in teas, coffee, chocolate, and cacao, also causes over-breathing (Buteyko, 1969). Nicotine is another substance that increases ventilation. The effect of alcohol was previously considered. Conclusions

The following factors gradually intensify breathing of relatively healthy people: 1) Stress, anxiety and strong emotions 2) Physical inactivity

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3) Overeating, especially of animal proteins 4) Deep breathing exercises 5) Overheating 6) Talking with deep inhalations, loud voice, or high pitches 7) Mouth breathing 8) Sleeping too much, sleeping on the back or on the right side 9) Embryonic and foetal development in a woman hyperventilating during her pregnancy 10) Exposure to toxic chemicals The references of this book provide experimental results in respect to various respiratory parameters of people over a period of about 100 years. By analysing this data and some other sources, following average changes for people, who were considered healthy, took place during the 20-th century: - Minute ventilation increased from 5-6 to 8-9 l/min. - Breathing frequency increased from 9-12 to 12-15 times per minute. - Tidal volume increased from 500-600 to 600-700 ml per breath. - End-tidal CO2 and aCO2 decreased from 40-43 mm Hg to 36-39 mm Hg. - MP (BHT after quiet exhalation) decreased from 40-50 s to 25-35 s. The crucial parameter here is aCO2, while other characteristics only support the idea that modern people, who are considered to be healthy, hyperventilate in relation to previous generations. In addition to that, there are sharp increases (ten times or more) in chronic degenerative health conditions (heart problems, asthma, arthritis, diabetes, cancer, and many more), while most people with these health problems have even worse respiratory parameters. Hence, due to readjustment of the breathing centre to abnormal, from the evolutionary viewpoint, environmental conditions and individual choices, people now breathe much heavier than, for example, 100 years ago.

Q&A section Q: Do all emotions cause hyperventilation? A: According to Professor Buteyko, all strong emotions result on over-breathing. However, some emotional attitudes, in my view, do not have negative impact on breathing. For example, when people experience reasonable shame or grief, their breathing is normal or can be even reduced. Similarly, admiration in respect to art creations, Nature’s phenomena, and human deeds causes natural reduced breathing. These experiences are often described as “breath holding” or “breath taking (away)”. By the way, healthy people, when open their mouth, cease to breathe. Q: What are the effects of music on respiration? A: They are complex and individual. Studies found that breathing rhythm can follow the musical rhythm. As about aCO2, heavy or loud music and music with uneven rhythm cause more muscular tension increasing ventilation. Quiet, soft, and peaceful musical pieces induce relaxation, slower heart rate, and establish easy breathing. Music is another cultural factor, which often adversely influences the breathing of modern people. Q: What is the dynamic of changes in ventilation and aCO2 during sleep? A: Healthy people breathe slower, ventilate less, and have higher aCO2 during night sleep. Their sleep is short and refreshing. Sick people usually also breathe less due to decreased metabolic rate, but their aCO2 gets smaller. Therefore, they hyperventilate. This process is especially pronounced during early morning hours (4-6 a.m.), as it was mentioned above.

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As about effects of different sleep stages, during deep sleep stages (or slow wave sleep), ventilation is reduced and that helps to deeply relax skeletal muscles. REM (rapid eye movement) sleep can result in relative hyperventilation and low aCO2 (Krieger, 1986). Q: What is known about breathing and natural processes, like defecation and urination? Can they produce hyperventilation? A: If a person has a desire to defecate but does not have a chance to do that, the breathing can become heavier. Indeed, from chapter 1 it is known, that raised aCO2 increases blood flow to internal organs, together with the group of muscles, which is responsible for effective elimination (this group includes muscles of the descending colon, sigmoid colon, rectum and sphincter). Vice versa, lowered aCO2 reduces blood flow to these muscles up to the possible spasmodic state. The relief, relaxation, and easy breathing after the defecation indicate reduced ventilation and increasing CO2 stores. The act of urination seems to be less connected with hyperventilation. Meanwhile, distension of the bladder causes more slow and shallow breathing (Schodorf & Polosa, 1980) leading to higher aCO2. Thus, deliberately keeping one's bladder full, somehow, reduces ventilation and, possibly, is not detrimental for health. References for chapter 3 Astrid P, Breath holding during and after muscular exercise, J Appl Physiol 1960, 15 (2): 220-224. Bazett HC, The regulation of body temperatures, in Physiology of heat regulation and the science of clothing, ed by LN Newburgh, 1968, Hafner Publishing Co, NY, 109-192. Biotin FA, Brigade NH, Witnesses CJE, Emotions and respiratory patterns: review and critical analysis, Intern J of Psychophysiol 1994, 17: 107-128. Brooks GA, Fahey TH, White TP, Exercise physiology: human bioenergetics and its applications, 2-nd ed., 1996, Mountain View, California, Mayfield. Buteyko KP, Carbon dioxide theory and a new method of treatment and prevention of diseases of the respiratory system, cardiovascular system, nervous system, and some other diseases [in Russian], Public lecture for Soviet scientists at the Moscow State University, 9 December 1969. Buteyko KP, Method of voluntary elimination of deep breathing [in Russian], in Buteyko method. Its application in medical practice, ed. by K.P. Buteyko, 2-nd ed., 1991, Titul, Odessa, p.148-165. Gaudio R & Neil A, Heat-induced hyperventilation, J Appl Physiol 1968, 25(6): 742-746. Hasselbalch, Biochem Zeitschr, 1912, XLVI, p.416. Hoit JD & Lohmeier HL, Influence of continuous speaking on ventilation, J Speech Lang Hear Res 2000 Oct; 43(5): 1240-1251. Khoroscho AE, Interview with K. P. Buteyko (1982), in Buteyko method. Its application in medical practice, ed. by K.P. Buteyko, 2-nd ed., 1991, Titul, Odessa, 168-180.

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Kerr WJ, Dalton JW, Gliebe P, Some physical phenomena associated with the anxiety states and their relation to hyperventilation, Annals of Intern Med 1937, 11: 961-992. Krieger J, Sleep apnea syndromes in adults, Clin Respir Physiol 1986, 22: 147-189. Lum LC, The syndrome of habitual chronic hyperventilation, in: Modern trends in psychosomatic medicine, ed. by O. W. Hill, 1976, London, Butterworths: p.196-230. Magarian GJ, Hyperventilation syndrome: Infrequently recognized common expressions of anxiety and stress, Medicine 1982; 61: 219-36. Salkovskis PM & Clark DM, Affective responses to hyperventilation: a test of the cognitive model of panic, Behav Res Ther 1990; 28(1): 51-61. Schodorf R & Polosa C, Effects of urinary bladder afferents on respiration, J Appl Physiol: Respir Environ Exercise Physiol 1980, 48: 826-832. Stegen K, De Bruyne K, Rasschaert W, Van de Woestijine KP, Van den Bergh O, Fear-relevant images as conditioned stimuli for somatic complaints, respiratory behavior, and reduced end-tidal pCO2, J of Abnorm Psychol 1999, 108 (1): 143-152. Tanaka Y, Morikawa T, Honda Y, An assessment of nasal functions in control of breathing, J Appl Physiol 1988 Oct; 65(4): 1520-1524.

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Chapter 4. Western methods of breathing retraining Introduction This chapter provides a review of Western methods of breathing retraining with some details about the types of breathing exercises used, their duration and frequency, length of the therapy, other auxiliary activities, and immediate and long-term effects of the treatment. The titles of the sections indicate the places where such breathing retraining methods were employed. The patients for these therapies were usually diagnosed with “hyperventilation syndrome” or "panic attacks", without having any other serious diseases. In some cases, the patients also had some diseases of organic or metabolic origin. Such situations are pointed out. References to publications, which describe these therapies, are given at the beginning of the corresponding sections. The last section of the chapter considers common features and some differences of these Western methods of breathing retraining, their advantages and disadvantages. Special attention is paid to the duration of a single breathing session and corresponding physiological studies that defined the time required for aCO2 to penetrate the blood-brain barrier and produce an impact on the part of the breathing centre located in the brain. 4.1 University of California Medical School, San Francisco, USA Kerr WJ, Dalton JW, Gliebe. Some physical phenomena associated with the anxiety states and their relation to hyperventilation, Ann Int Med 1937, 11: 962-992. It became obvious for a group of doctors that a large number of their patients (from one-fourth to one-third) had "a variety of symptoms referable to many structures of the body; and in whom hyperventilation precipitates and maintains a state of hyperirritability approaching clinical tetany. The symptoms may be so well localized in some cases that local disease is suspected without discovery of universal functional disturbance”(p. 961, Kerr et al, 1937). As a treatment, the inhalation of O2-CO2 gas (70% O2 and 30% CO2) was found to be most effective both in speed and adequacy. In other situations, “a paper sack, inverted over patient’s head and sealed with adhesive tape, is successful” (p.989, Kerr et al, 1937). Additionally, a prescription with ammonium chloride, in order to reduce ventilation, was given, although the authors noted that chloride ions were probably not as effective as carbon dioxide. This demonstrated to the patient “the mechanism of the physiological difficulties which he himself caused [due to hyperventilation], and the results are so dramatic, that he is able to follow the procedure and to appreciate what the results mean to him” (p.989, Kerr et al, 1937). However, future work was projected with the use of several chemical drugs, which could suppress the heart action and the respiratory rate. 4.2 Papworth Hospital, Cambridge, UK Lum LC, Hyperventilation: The tip and the iceberg, J Psychosom Res 1975; 19: 375-383. Lum LC, The syndrome of habitual chronic hyperventilation, in Modern Trends in Psychosomatic Medicine, edited by OW Hill, Butterworth, London, 1976, vol 3: 196-230. Professor Lum insisted that therapy must start with the HVPT (hyperventilation provocation test), which demonstrated the reproduction of the patient's symptoms. That brought relief, but only a small number of patients had rapid success. In general, he found that the duration of symptoms and age were the factors in how soon the patients got well. Usually,

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patients were referred to a physiotherapist in order to learn 3 key components of the therapy: awareness about normal and abnormal breathing patterns, relaxation, and diaphragmatic breathing. Thus, patients were informed about the importance of constant control of their breathing paying attention to such acts as sighing, sniffing, coughing, deep breathing, chest inflation, and other actions and factors, which encourage excessive thoracic breathing. Relaxation physiotherapy included learning how to relax habitual tense posture, especially the thorax, shoulders, head and neck and how to recognise those situations, which aggravate tension. Since the majority of his patients had little, if any, control and use of their diaphragm, the physiotherapist taught them how to control it and to use it almost exclusively at rest. Unnecessary thoracic movements should be consciously suppressed. In order to achieve normal breathing, "an extremely slow respiratory rhythm is encouraged, in order to gradually persuade the respiratory centre to readjust to a higher level of arterial carbon dioxide: a slow process if the disorder has persisted for many years" (p.226, Lum, 1976). Then "the patient is initially instructed to devote two periods of 20 minutes each day to breathing exercises, and to constantly check his breathing throughout the day" (p.226, Lum, 1976). He treated 320 patients (up to 1974) using this therapy. 70% were rendered completely asymptomatic. 25% had improved and 5% failed to respond. 18 patients were diagnosed by a cardiologist to have organic cardiac disease. Out of these, 3 failed to improve. 4.3 Portland Veterans Administration Medical Centre, USA Magarian GJ, Hyperventilation syndrome: infrequently recognized common expressions of anxiety and stress, Medicine 1982; 61: 219-236. Magarian GJ, Middaugh DA, Linz DH, Hyperventilation syndrome: a diagnosis begging for recognition, West J Med 1983; 38: 733-736. As a first practical step, it was "important that the patients be confronted with the cause-and-effect relationship and their symptoms. A hyperventilation trial is crucial for therapeutic success" (p. 736, Magarian et al, 1983). During HVPT the patient breathed deeply at a rate 30 to 40 times per minute. Most patients experienced their symptoms within minutes or seconds. Such recognition was a major factor for successful overall outcome of the therapy. The test should be conducted with caution for patients with ischemic coronary disease, sickle cell disease, cerebrovascular insufficiency and baseline hypoxemia. Meanwhile, "it is of far greater detriment for the patient not to recognise the relationship between over-breathing and their symptoms than the potential risks of performing the test” (p.231, Magarian, 1982). The suggested duration of the test was 4-5 minutes. When HVPT was done, breathing into a bag resulted in resolution of the symptoms. Finally, the patients were suggested to use relaxation therapy and retraining of the breathing pattern, from thoracic to diaphragmatic. Low efficiency of different medications for normalisation of breathing was also reported. 4.4 St. Bartholomew's Hospital, London, UK Bonn JA, Readhead CP, Timmons BH, Enhanced adaptive behavioural response in agoraphobic patients pretreated with breathing retraining, Lancet 1984 Sep 22; 2(8404): 665-669.

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21 patients with agoraphobia (sensations of fear, panic, and terror), first, had HVPT (with breathing frequency 60 times per minute, for 3 min maximum, breathing through both mouth and nose as vigorously as possible). Over 95% patients recognised their symptoms but not as severe as usual. 2/3 of patients could not complete 3-min HVPT due to dizziness and distress. Alternatively, only 4% of normal subjects could not hyperventilate for 3 minutes. The authors emphasised the importance of HVPT and subsequent "shock of recognition".

After positive results (recognition of symptoms) 12 of them had 10-week therapy (1-2 laboratory sessions per week, 2h for each session). The laboratory sessions included instructions about diaphragmatic respiration. The lying patients were told to maintain a breathing pattern of 8-10 breaths per minute.

Techniques for coping with panic attacks were suggested - "the use of a paper bag for rebreathing or, in public places, breathing into hands tightly cupped over nose and mouth...The establishment of a normal breathing pattern requires regular and persistent practice over several months...Any relaxation technique that entails the use of deep breathing is contraindicated, since it will probably exacerbate hypocapnia [low aCO2]" (p.668, Bonn et al, 1984).

The results were recorded at the end of the therapy, and for 1-month and 6-months follow-ups. The improvements were similar for all periods. Breathing rate dropped from 28 to 15-19 breaths per minute. Weekly number of panic attacks was reduced from 4-5 to 0.2. Other somatic characteristics were also significantly better. 4.5 Institute of Stress Research, Netherlands Grossman P, de Swart JCG, Defares PB, A controlled study of a breathing therapy for the treatment of hyperventilation syndrome, J Psychosom Res 1985; 29 (1): 49-58. The researchers employed HVPT for 3 minutes with the goal to reach 2.5% etCO2 (end-tidal CO2). Then experienced physical and psychological symptoms were discussed. The treatment was 10-weeks long and included 7 laboratory sessions (each for about 30 min) and daily home assignments. A ventilatory training device was individually adjusted to generate a periodic pattern for breathing with slightly less frequency than the initial one. That was achieved by the use of auditory stimuli for inspiration, expiration, and the pause. Verbal emphasis on abdominal breathing was provided. Laboratory sessions also included CO2 analysis of the expired air. As a result of the therapy, average breathing rate of the experimental group (25 subjects) decreased from 17 to almost 11 breaths per minute, resting etCO2 increased from 4.2 to 4.7%, scores in all somatic complaints significantly improved. Although the subjects of this study were free from serious physical ailments, the researchers suggested, "In a broader sense, the findings indicate that by means of direct voluntary training of respiration, it may be possible to effect long-term alterations in ventilatory control mechanisms. This may have implications for the behavioural treatment of other respiratory disorders (e.g., asthma, sleep apnea and emphysema). Since alterations in ventilatory parameters are known to induce substantial changes in a range of other physiological systems (e.g., cardiovascular and CNS; see [16]), long-term modification of ventilatory control, via breathing therapy may also be useful in treating specific disorders of these other systems" (p. 58, Grossman et al, 1985).

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4.6 Department of Psychiatry, University of Oxford, Warneford Hospital, UK Clark DM, Salkovskis PM, Chalkley AJ, Respiratory control as a treatment for panic attack, J Behav Ther Exp Psychiatry 1985 Mar; 16(1): 23-30. Salkovskis PM, Jones DR, Clark DM, Respiratory control in the treatment of panic attacks: replication and extension with concurrent measurement of behaviour and pCO2, Br J Psychiatry 1986 May; 148: 526-32. "Eighteen patients who experienced frequent panic attacks were given a treatment derived from the literature on hyperventilation and anxiety. The treatment consisted of (i) brief, voluntary hyperventilation. This was intended to induce a mild panic attack; (ii) explanation of the effects of over-breathing and reattribution of the cause of a patient's attacks to hyperventilation; (iii) training in a respiratory control technique. Substantial reductions in panic attack frequency and in self-reported fear during a behaviour test were obtained after 2 weeks' treatment and these reductions occurred in the absence of exposure to feared situations. Further reductions in panic attack frequency were evident at 6-month and 2-year follow-up though interpretation of these results is complicated by the addition of exposure and other psychological treatments" (abstract, Clark et al, 1985). In this study all patients were successfully treated and "...Large and rapid reductions in panic attack frequency and questionnaire report of fear were observed. Patients' resting pCO2 was significantly lower than controls and rose to normal levels during treatment" (abstract, Salkovskis, 1986). High success rate of this therapy could be partly explained by absence of patients with an organic or metabolic illness and absence of old people among the subjects (the average mean age was about 30 years, from 26 to 44). The patients used a tape set at 12 breaths per minute. This tape was to be practiced at home daily. Laboratory sessions were organised about once per week with continuing respiratory training and homework instructions. Statistical analysis revealed that patients with particularly low resting etCO2 were more likely to recognize the symptoms of over-breathing as similar to their panic attacks. 4.7 Department of Psychiatry, University of Utrecht, Netherlands Ruiter de C, Ryken H, Garssen B, Kraaimaat F, Breathing retraining, exposure and a combination of both, in the treatment of panic disorder with agoraphobia, Behav Res Ther 1989; 27(6): 647-655. The study was completed with 40 patients diagnosed with agoraphobia. All participants were selected on their ability to recognize their symptoms during HVPT. The patients were explained how hyperventilation and catastrophic cognition cause panic attacks. The treatment consisted of 8 individual sessions lasting about 60 min each and instructions to practice relaxation and slow breathing in daily situations. The main goal of the therapy was to gradually reduce respiration rate. For that purpose a pacing tape was used. Each time the breathing frequency was slightly lower than the usual one. Slow diaphragmatic breathing was “encouraged by suggesting patients put one hand on their abdomen, and breathing “against the hand”(p. 649, Ruiter et al, 1989). “Treatments that included breathing retraining techniques seemed to result in a decrease in respiratory rate, but not in an increase in alveolar pCO2” (p. 652, Ruiter et al, 1989), since etCO2 slightly decreased during the treatment. Meanwhile, “the present study found breathing retraining plus cognitive restructuring ineffective in reducing panic”(p. 654, Ruiter et al, 1989).

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Professor Ronald Ley, State University of New York at Albany, wrote comments on this study, concluding “Efforts to reduce ventilation through excusive attention to a reduction in respiratory frequency may not only be unsuccessful in reducing ventilation, but may, as in the study in question, produce a paradoxical increase in ventilation, an effect opposite to the express purpose of the breathing retraining. The results here indicate that pCO2 monitoring should be an integral part of breathing retraining process” (p.304, Ley, 1991). 4.8 Cornell University Medical College, New York, USA Fensterheim H, Wiegand B, Group treatment of the hyperventilation syndrome, Int J Group Psychother 1991 Jul; 41(3): 399-403. "Hyperventilation (hv) is increasingly recognized as being significant in a number of psychological and medical conditions. The core of treatment for hv is breathing retraining, usually on an individual basis. This article describes a group therapy for breathing retraining for patients with hv-induced panic reactions. An analysis of group process suggests that such treatment is helpful in ways impossible for individual retraining and that further exploration of this modality is warranted" (abstract, Fensterheim & Wiegand, 1991) The novelty of this study was the use of the group therapy for breathing retraining. The authors found that their patients had a warm supportive acceptance of each other and of the group itself. That "facilitated cooperative performance of their assignments and taking the risks in life situations that are so necessary for progress in this area" (p.401, Fenshterheim & Wiegand, 1991). Moreover, it was found, that group processes helped to alleviate the disturbed reaction to symptoms and to accelerate learning of correct breathing patterns. In particular, the authors emphasized that group treatment, as an addition to individual sessions, should be especially helpful to those patients who had the most difficulty in learning a normal breathing pattern. 4.9 California School of Professional Psychology, San Diego DeGuire S, Gevirtz R, Kawahara Y, Maguire W, Hyperventilation syndrome and the assessment of treatment for functional cardiac symptoms, Am J Cardiol 1992 Sep 1; 70(6): 673-677. DeGuire S, Gevirtz R, Hawkinson D, Dixon K, Breathing retraining: a three-year follow-up study of treatment for hyperventilation syndrome and associated functional cardiac symptoms, Biofeedback Self Regul 1996 Jun; 21(2): 191-198. "Three methods of breathing retraining (guided breathing retraining, guided breathing retraining with physiologic monitoring of thoracic and abdominal movement plus peripheral temperature, and guided breathing retraining with physiologic monitoring of thoracic and abdominal movement, peripheral temperature and end-tidal carbon dioxide) were compared with a no-treatment control group to determine the effectiveness of breathing retraining on modifying respiratory physiology and reducing functional cardiac symptoms in subjects with signs associated with hyperventilation syndrome. Of 41 subjects studied, 16 were diagnosed with mitral valve prolapse. Results demonstrated that all 3 methods of breathing retraining were equally effective in modifying respiratory physiology and reducing the frequency of functional cardiac symptoms. Results determined that respiratory rate and subject's perception that training had generalized were the best predictors of treatment success. Furthermore, it was found that subjects with mitral valve prolapse responded as well to treatment as did those without prolapse" (abstract, DeGuire et al, 1992).

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Each person had 6 individual breathing retraining sessions over a 3-week period. During the first laboratory session, all of them were informed about respiratory physiology and the relation between hyperventilation and functional cardiac symptoms. The patients were shown diaphragmatic breathing and their practice was corrected by the experimenter. Although many patients reported discomfort with slow diaphragmatic breathing, they were encouraged to tolerate the discomfort and were assured about the disappearance of the symptoms with time. The patients were carefully observed not to increase their tidal volumes. Later sessions were focused on correcting errors in diaphragmatic breathing and setting a slow-paced respiratory rate of less than 14 breaths per min. Average etCO2 in all 3 groups increased from about 35 to 40 mm Hg. It was of special interest of the authors, that some functional cardiac problems could be treated with breathing retraining by normalisation of etCO2. Four years later, the effect of breathing retraining was still present in the tested subjects,

“This study was designed to evaluate the long-term effects of paced diaphragmatic breathing on subjects who reported functional cardiac symptoms and who also demonstrated associated signs of hyperventilation syndrome. Subjects were a representative sample composed of 10 out of the original 41 subjects who had participated three years previously in a study designed to evaluate the short-term effects of breathing retraining on functional cardiac symptoms and respiratory parameters (respiratory rate and end-tidal carbon dioxide). The results of this follow-up study indicate that breathing retraining had lasting effects on both respiratory parameters measured. Subjects evidenced significantly higher end-tidal carbon dioxide levels and lower respiratory rates when compared to pretreatment levels measured three years earlier. Subjects also continued to report a decrease in the frequency of functional cardiac symptoms when compared to pretreatment levels. We conclude that breathing retraining has lasting effects on respiratory physiology and is highly correlated with a reduction in reported functional cardiac symptoms” (abstract, DeGuire et al, 1996). 4.10 Lothian Area Respiratory Function Service, City Hospital, Edinburgh, UK Tweeddale PM, Rowbottom I, McHardy GJ, Breathing retraining: effect on anxiety and depression scores in behavioural breathlessness, J Psychosom Res 1994 Jan; 38(1): 11-21.

22 patients with behavioural breathlessness were selected for breathing retraining. HVPT involved 3 minutes periods of rest, voluntary hyperventilation, and recovery. During an initial assessment special attention was paid to observation of existing breathing patterns of the patients (upper chest or abdominal breathing; nasal or oral breathing; presence of sighing, gulping, or yawning; and inappropriate patterns during speech), identification of hyperventilation-triggering situations and clinical details. During their 7 weekly visits to the laboratory, the patients were taught to develop awareness of their breathing patterns, to practice individual breathing exercises, to implement breathing control during speech, to develop control of hyperventilation-triggering situations, and finally, to achieve an effortless breathing pattern. As a result of such intervention, “both groups [with behavioural breathlessness and chronic fatigue] showed improvements in breathing patterns, end tidal CO2 levels and scores for HV-related symptoms which were sustained”(abstract, Tweeddale, 1994). Moderate increase in BHT was noticed for the patients with lowest initial BHT values. The authors also made an important practical conclusion. “In any patient, if there is either resistance to the idea of breathing being related to symptoms, or lack of commitment to regular performance of breathing exercises or unwillingness to check out breathing patterns and exercise

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control during daily activities, breathing retraining is unlikely to be of benefit” (p. 20, Tweeddale, 1994). 4.11 Service de Psychosomatique, Hopital du Sacre-Caeur de Montreal, Quebec, Canada Monday J, Gautrin D, Cartier A, Chronic hyperventilation syndrome. The role of respiratory re-training [in French], Rev Mal Respir 1995; 12(3): 291-298. "This study compares three non-pharmacological approaches to the chronic hyperventilation syndrome (CHS). Eighteen subjects were evaluated at the start of the study then one and 6 months after having received in a random fashion one of the following treatments: group I (teaching approach of one hour on the respiratory physiology of the CHS and on breathing techniques; n = 5); group II (same approach as in group I with breathing retraining of 8 sessions; n = 8); group III (same as group II with the addition of a modified Jacobson's progressive relaxation; n = 5). Whereas all three groups had a similar symptomatic score at the beginning of the study (although subjects of group III had in general higher scores and were symptomatic for a longer period), our results show that all subjects improved after 4 weeks, those in group II showing the greatest improvement (p < 0.05). This confirms the relevance of applied and repeated pedagogy in approaching subjects with the CHS" (abstract, Monday et al, 1995). 4.12 Laboratory of Pneumology, U. Z. Gasthuisberg, Katholieke Universiteit Leuven, Belgium Han JN, Stegen K, De Valck C, Clement J, Van de Woestijne KP, Influence of breathing therapy on complaints, anxiety and breathing pattern in patients with hyperventilation syndrome and anxiety disorders, J Psychosom Res 1996 Nov; 41(5): 481-493. "The effect of breathing therapy was evaluated in patients with hyperventilation syndrome (HVS). The diagnosis of HVS was based on the presence of several suggestive complaints occurring in the context of stress, and reproduced by voluntary hyperventilation. Organic diseases as a cause of the symptoms were excluded. Most of these patients met the criteria for an anxiety disorder. The therapy was conducted in the following sequence: (1) brief, voluntary hyperventilation to reproduce the complaints in daily life: (2) reattribution of the cause of the symptoms to hyperventilation: (3) explaining the rationale of therapy-reduction of hyperventilation by acquiring an abdominal breathing pattern, with slowing down of expiration: and (4) breathing retraining for 2 to 3 months by a physiotherapist. After breathing therapy, the sum scores of the Nijmegen Questionnaire were markedly reduced. Improvements were registered in 10 of the 16 complaints of the questionnaire. The level of anxiety evaluated by means of the State-Trait Anxiety Inventory (STAI) decreased slightly. The breathing pattern was modified significantly after breathing retraining. Mean values of inspiration and expiration time and tidal volume increased, but end-tidal CO2 concentration (FETCO2) was not significantly modified except in the group of younger women (< or = 28 years). A canonical correlation analysis relating the changes of the various complaints to the modifications of breathing variables showed that the improvement of the complaints was correlated mainly with the slowing down of breathing frequency. The favorable influence of breathing retraining on complaints thus appeared to be a consequence of its influence primarily on breathing frequency, rather than on FETCO2" (abstract, Han et al, 1996).

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This study involved 92 patients diagnosed with hyperventilation syndrome. However, the work of physiotherapists was not targeted to decrease ventilation of the subjects and to raise their CO2 values. The article states, that "the therapy consisted of: (1) a reattribution of the threatening symptoms to faulty breathing habits; and (2) training of slow breathing and learning to use the diaphragm more (abdominal breathing) and less the upper part of the thorax" (p.482, Han et al, 1996). Results of the therapy revealed that the patients acquired a slow deep breathing pattern. Their average tidal volume rose from abnormal 740 ml/breath (the norm is about 500-600 ml/breath) to 880 ml/breath, while etCO2 was almost unchanged (4.76% before and 4.84% after the treatment). Normal etCO2, according to most medical sources, is about 40 mm Hg or 5.25% CO2 at sea level. 32 patients improved markedly, according to their questionnaires, and were feeling well. Meanwhile, several symptoms related to hyperventilation did not improve at all after the treatment. These included "confusion or feeling of losing contact with surroundings, feeling of faster and deeper breathing, bloated abdomen, stiff fingers or arms, tightness around the mouth, and cold hands or feet" (p.485, Han et al, 1996). That should not be a surprise, since the main problem (hyperventilation or low aCO2) was not solved in this study. 4.13 New Zealand Guidelines Group

The New Zealand Guidelines Group is a large group of medical professionals, including numerous Professors and physicians (for more details visit their web-site at http://www.nzgg.org.nz). The Chairman of the group is Norman Sharpe, Head of the School of Medicine in the University of Auckland. In their “Guidelines for Assessing and Treating Anxiety Disorders, Appendix 6: Slow Breathing Exercise”, the Group states, “You will remember that when you get anxious your rate of breathing increases. This over-breathing is often referred to as 'hyperventilation'. When you over-breathe you breathe out too much carbon dioxide which leads to a decrease in the level of carbon dioxide in the blood. The decreased level of carbon dioxide causes or worsens a number of symptoms such as breathlessness or light- headedness. You may experience these symptoms if you have panic attacks. To get rid of these symptoms, the level of carbon dioxide in the blood must be increased and steadied. One way of achieving increased levels of carbon dioxide is to breathe into a paper bag. A large portion of the air you breathe out is carbon dioxide, therefore, by rebreathing your old air you are taking higher amounts of carbon dioxide into your lungs. Although breathing into a paper bag is simple and effective, it may not always be convenient or socially appropriate to pull out a paper bag in public! Additionally, although breathing into a paper bag is effective during a panic attack, this method cannot prevent hyperventilation in the future. An alternative method which is less obvious to other people and more effective in the long run is the slow breathing exercise. This method will help you to control your hyperventilation. Also, by learning slow and regular breathing habits you will help to prevent future episodes of hyperventilation and other symptoms of panic. The following exercise is to be practised four times every day for at least five minutes each time, AND at the first signs of panic or anxiety. Combining slow breathing with relaxation is particularly helpful. SLOW BREATHING EXERCISE (TO BE PRACTISED REGULARLY AND AT THE FIRST SIGNS OF ANXIETY OR PANIC) If you recognise the first symptoms of over-breathing, STOP what you are doing and sit down or lean against something. If you are driving, pull over and park in a safe place.

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1. Hold your breath and count to 5 (do not take a deep breath). 2. When you get to 5, breathe out and say the word 'relax' to yourself in a calm, soothing manner. 3. Breathe in and out slowly through your nose in a six second cycle. Breathe in for three seconds and out for three seconds. This will produce a breathing rate of 10 breaths per minute. Say the word 'relax' to yourself every time you breathe out. 4. At the end of each minute (after 10 breaths) hold your breath again for 5 seconds and then continue breathing using the six second cycle. 5. Continue breathing in this way until all the symptoms of over-breathing have gone. It is important for you to practise this exercise so that it becomes easy to use any time you feel anxious. (Treatment Protocol Project 1997) This is the only Western study known to me that involves breath holding as a method of CO2 accumulation. 4.14 Stanford University, Palo Alto, USA Meuret AE, Wilhelm FH, Roth WT, Respiratory biofeedback-assisted therapy in panic disorder, Behav Modif 2001 Sep; 25(4): 584-605. The value of this small study (only 4 patients) is that after the treatment all patients were “below the clinical threshold for the diagnosis of panic disorder” (p.596, Meuret et al, 2001). The patients performed 5 mild HVPT, each 3 min long. These tests were followed by 8 min quiet sitting period. The therapy had 5 individual sessions, each about 80 min long, over the course of 4 weeks. The major components of the therapy were: a) education about hyperventilation and its central role in the mechanism of the panic attack; b) teaching techniques to control respiration; c) directing attention to dangerous breathing patterns; d) instructing in home breathing exercises. Home assignments were performed twice per day, each about 20 min long.

The abstract of the publication states, “The authors describe a new methodologically improved behavioral treatment for panic

patients using respiratory biofeedback from a handheld capnometry device. The treatment rationale is based on the assumption that sustained hypocapnia resulting from hyperventilation is a key mechanism in the production and maintenance of panic. The brief 4-week biofeedback therapy is aimed at voluntarily increasing self-monitored end-tidal partial pressure of carbon dioxide (PCO2) and reducing respiratory rate and instability through breathing exercises in patients' environment. Preliminary results from 4 patients indicate that the therapy was successful in reducing panic symptoms and other psychological characteristics associated with panic disorder. Physiological data obtained from home training, 24-hour ambulatory monitoring pretherapy and posttherapy, and laboratory assessment at follow-up indicate that patients started out with low resting PCO2 levels, increased those levels during therapy, and maintained those levels at posttherapy and/or follow-up. Partial dissociation between PCO2 and respiratory rate questions whether respiratory rate should be the main focus of breathing training in panic disorder” (abstract, Meuret et al, 2001). 4.15 Common features and some differences of Western methods of breathing retraining Usefulness or necessity of HVPT Most authors used HVPT and indicated its necessity for successful outcome of the therapy. Indeed, since many patients (usually over 90%) could recognize their symptoms during

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HVPT, these patients realised the cause of their problems (excessive breathing). That created better trust-based relationships with the doctors, together with interest and enthusiasm of the patients in order to solve own problems. When this test was not done, many patients could have reasonable doubts about the value of the whole therapy and doctors' ability to help. The crucial difference between these two situations (with and without HVPT) is the different attitude of the patients towards the suggested approach. Awareness about normal and abnormal breathing patterns The patient should learn the features of normal and abnormal breathing patterns in order to recognise them in normal life. First, it was explained to the patient that some actions directly involved hyperventilation causing reduced aCO2. These actions included coughing, sneezing, sighing, sniffing, and chest inflation. In order to get healthy, all of them should be stopped or prevented. Second, it was important for the patient to know the features of thoracic and diaphragmatic breathing. Diaphragmatic breathing could be characterised by following adjectives: smooth, quiet, slow, and regular. Thoracic (chest) breathing, on the other hand, is often uneven, noisy, fast, and irregular. Relaxation Since tension is a normal response to stress and hyperventilation, one can conclude that relaxation, due to a feedback mechanism, reduces minute ventilation, decreases metabolism, and raises aCO2. Thus, relaxation alone is a valuable therapeutic tool in health improvement as numerous other studies of a variety of certain health conditions found. Moreover, relaxation could be useful in eliminating the negative consequences of stress, hyperventilation, and subsequent physiological changes. In particular, an ability to reduce tension in large skeletal muscles, especially of the chest-shoulders-neck-jaws region brings natural relaxation, calmness and easy breathing. Diaphragmatic breathing Many authors suggested to their patients to use the practical help of physiotherapists in order to learn diaphragmatic breathing. Two previous features, awareness about normal and abnormal breathing patterns and relaxation, could be considered as theoretical preparation and basic initial practical lessons in order to acquire the normal diaphragmatic breathing pattern. Durations of daily sessions and the therapy Typical durations of the suggested daily sessions were from 20 min to 1-2 hours, apart from recommended daily control of breathing. Are there any physiological grounds for such values? The breathing centre has two groups of specialized cells (chemoreceptors). One group is located near the main arteries close to the heart, and another is in the medulla of the brain.

Those cells, which are located near the heart (the peripheral chemoreceptors), can detect aCO2 changes in a matter of seconds. Therefore, their adaptation and training starts and finishes almost together with voluntary reduction in ventilation. Thus, they are taught all the time, while the person breathes less. (Probably, the adaptation of these cells to acute aCO2 changes during breath holding causes the “training effect” discussed in chapter 2). The second group of cells located in the brain (the central chemoreceptors) are bathed in CSF (cerebro-spinal fluid). Their trainability depends on CO2 pressure and pH of CSF. Hence, it is important to know how CO2 in arterial blood influences CO2 and pH concentrations in CSF, since these fluids are separated by a blood-brain barrier, which allows only certain substances to

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cross it and only with certain rates. What would be the time required for increased arterial CO2 to penetrate this barrier in order to influence the cells located in the main part of the breathing centre? There were several studies by physiologists and neurologists devoted to this subject. Measurements of CO2 tension on the cerebral cortex in anaesthetized cats revealed that this parameter reaches a plateau in 5-10 min after aCO2 in blood had a 5-10% absolute increase (Seisjo, 1961). In another series of experiments with anaesthetized rats, brain tissue CO2 had an exponential increase, with half-time 6-7 min, as a response to 1 mm Hg CO2 pressure increase in inspired air (Seisjo, 1963). Other physiologists recorded 12 min in maximum specific activity of CO2 isotopes in the brain after their appearance in the blood of rabbits (Coxon & Swanson, 1965). Finally, a more recent investigation found that "changes in pH and pCO2 with hyperventilation and hypoventilation occurred rapidly in both arterial blood and CSF. Steady state values were reached within 15 min for hypoventilation and 30 min for hyperventilation... These results are consistent with previous research" (abstract, Andrew et al, 1994). Therefore, it would be sensible to assume that about 10-15 min is required in order to achieve maximum influence on the central chemoreceptors. The optimum duration of this influence would probably depend on the amplitude of the change and current trainability of the breathing centre or how soon fatigue and pain can be achieved. The suggested length of supervised therapies was from 1 to 3 months, while homework sessions could take more time. Meanwhile, most patients experienced decisive improvement in their health during the supervised part. Respiratory rate Increased initial breathing frequencies of patients participating in these therapies were commonly acknowledged. Most authors suggested to their patients to practice slower breathing patterns assuming benefits of this idea in terms of reduced ventilation and increased aCO2. Meanwhile, the voluntary decrease of respiratory rate in the case of natural breathing regulation, makes tidal volume larger, resulting in a slow deep breathing pattern as we learned in section 2.1. On the other hand, most hyperventilators already have deep breathing. Is there a possibility that some of them can start to breathe even deeper in normal conditions as a result of such breathing practice? Probably, such consideration caused Bonn with colleagues to suggest that "any relaxation technique that entails the use of deep breathing is contraindicated, since it will probably exacerbate hypocapnia [low aCO2]" (p.668, Bonn et al, 1984). Moreover, researchers from Stanford University directly questioned whether respiratory rate should be the main focus of breathing training (Meurel et al, 2001). Similar ideas were expressed by Professor Ley (see above). Indeed, the main goal of all these therapies was to normalize (increase) aCO2 by diminishing ventilation, or in other words, by breathing less. That is, by itself, not an easy task, requiring the patient's concentration and will power. Paying additional attention to breathing frequency may result in deeper breathing causing additional tension and further hyperventilation development. There is also one technical aspect regarding the use of capnometers. Many studies revealed that, in cases of deep breathing or prolonged exhalations, the difference between end-tidal and arterial CO2 gets larger in comparison with normal conditions (Jones et al, 1979; Robbins et al, 1990). Jones and colleagues, for example, found that in different exercise conditions “PETCO2-PaCO2 varied between -2.5 and +9.1 Torr [1 Torr = 1 mm Hg], was inversely related to the frequency of breathing (r = 0.475), and directly related to tidal volume”(abstract, Jones et al, 1979). Hence, the slower the breathing, the larger the difference; and the deeper the breathing, the larger the difference. As a result, the reading of capnometers in cases of slow deep breathing over-estimates arterial CO2 tension. That creates an illusion that aCO2 is increasing, whereas real aCO2 values can remain unchanged or even decrease.

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Drug-free nature of therapies Only the earliest study (Kerr et al, 1937), conducted before World War 2, relied on the use of chemical substances in order to normalize ventilation and aCO2. Other therapies were drug-free and some authors claimed uselessness of drugs in breathing normalization. This feature makes these breathing methods different from traditional approaches practiced and advocated by most medical authorities and doctors. There are many problems with drugs and one of the crucial differences between a traditional drug-based approach and any drug-free therapy is discussed in the next section. Acquisition of control over own health by the patients Let us consider two situations in which patients seek help and receive it: in one case in a form of a drug from a doctor, in another as a natural therapy, which requires some patients' personal habits, priorities, routines to be changed. Modern medicine usually can not give a clear and simple explanation about the causes of patient's problems, and many diseases remain "incurable". Instead, the well-meaning doctor often relies on drugs. Problems with drugs are numerous and well-documented. Few of them survived for several decades and are still used now. A typical situation follows: The patient arrives at the doctor's office with his complaints. The doctor listens, asks, thinks, conducts tests, diagnoses, and prescribes a chemical drug which is foreign to the human body. The patient, due to the approach chosen by his doctor, is innocent and the cause of his disease is in stress, heredity, deteriorating environment and other factors, all of which are usually outside of patient’s control. Natural practical recommendations (diet, exercise, relaxation, etc.) are rarely suggested by the doctor. The key of the treatment is the miracle drug, usually a very new one (it can not be without the drug, since the patient is innocent).

After taking the drug for months or years (if he survives), the patient may realise that it does not work or even makes his health worse. By that time, this "new" drug may be withdrawn (as many are), or banned due to dangerous side-effects. Nevertheless, the well-meaning doctor is still here with a miracle pill in his hands. He may retreat temporarily only to bring another new miracle to feed the imagination and hopes of his excited, hyperventilating patient. Thus, this situation is controlled, if it is controlled at all, by the well-meaning doctor, the magic pill, and naive expectations of the patient. Breathing retraining, in opposition, is a natural therapy, which gives the clear mechanism how low aCO2 affects personal health. If convinced, the patient realises that his breathing was and is the cause of his problems. The control over his own health now belongs exclusively to him. Although not all patients may be ready to accept this truth (some may still dream to remain innocent helpless victims seeking help from saviours), it is the doctor's responsibility to inform the patients about the real situation. Otherwise, success is hard to achieve. Therefore, breathing retraining provides the patient with the mechanism of his disease and with practical coping strategies, which can result in actions of the patient combined with self-discipline, persistence, and determination to recover. Q&A section Q: Why are these therapies used mainly for patients diagnosed with panic attacks and hyperventilation syndrome, whereas most other sick people also over-breathe? A: It happened historically that capnometers became popular among psychologists. In addition, there is an almost immediate relationship between hyperventilation and panic attacks, whereas development of an asthma attack is slightly delayed, while development of cholesterol deposits, tumours and certain other pathological tissues and phenomena are even slower. There were also those "lucky" people who could not be diagnosed with conventional disease titles, and they were

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finally called "hyperventilators" (others could be diagnosed with chronic fatigue syndrome or some organic or metabolic problems). With regards to other patients, it is indeed reasonable to ask medical authorities, "Why not treat modern patients with different chronic degenerative conditions from their hyperventilation and then see what happens with their symptoms and complaints, when their breathing is normalized in accordance with medical standards?" Such questions need answers, since, for example, in Russia many ten of thousands of former asthmatics and thousands of former patients with hypertension and stenocardia for years are totally symptom-free after learning the Buteyko breathing. Q: Is pursed-lip breathing helpful? A: Pursed-lip breathing involves exhalation against partially closed (pursed) lips, as if ready to whistle. This technique is supposed to prevent bronchiolar collapse and includes small inhaled breaths and a long pursed-lip exhalation. It is also advised during exercise and panic. The main problem with this method is increased tension in respiratory muscles, while any tension increases ventilation. As a result, several trials involving this method were not very successful. For example, one study of patients with cystic fibrosis managed to demonstrate improved FEV (forced expiratory flow) and FVC (forced vital capacity) (Delk, 1994) without any improvements in their quality of life. Patients with COPD (chronic obstructive pulmonary disease) after pursed-lip breathing sessions increased their exercise performance, while making their blood gases at maximum speed much worse (Casciari, 1981). Meanwhile, both these trials involved relaxation which, probably, made the main positive impact (if any) in spite of tension generated by pursed-lip breathing. When relaxation is absent, the results are different, as it was reported by Ambrosino and his colleagues (1984) in the article “Failure of resistive breathing training to improve pulmonary function tests in patients with chronic obstructive pulmonary disease”. References for chapter 4 Ambrosino N, Paggiaro PL, Roselli MG, Contini V, Failure of resistive breathing training to improve pulmonary function tests in patients with chronic obstructive pulmonary disease, Respiration 1984; 45(4): 455-459. Andrew RJ, Bringas JR, Alonzo G, Cerebrospinal fluid pH and pCO2 rapidly follow arterial blood pH and pCO2 with changes in ventilation, Neurosurgery 1994 March, 34 (3): 466-470. Bonn JA, Readhead CP, Timmons BH, Enhanced adaptive behavioural response in agoraphobic patients pretreated with breathing retraining, Lancet 1984 Sep 22; 2(8404): 665-669. Casciari RJ, Fairshter RD, Harrison A, Morrison JT, Blackburn C, Wilson AF, Effects of breathing retraining in patients with chronic obstructive pulmonary disease, Chest 1981 Apr; 79(4): 393-398. Clark DM, Salkovskis PM, Chalkley AJ, Respiratory control as a treatment for panic attack, J Behav Ther Exp Psychiatry 1985 Mar; 16(1): 23-30. Coxon RV & Swanson AG, Movement of (14)C bicarbonate from blood to cerebrospinal fluid and brain, J Physiol (London) 1965, 18: 712-727. DeGuire S, Gevirtz R, Kawahara Y, Maguire W, Hyperventilation syndrome and the assessment of treatment for functional cardiac symptoms, Am J Cardiol 1992 Sep 1; 70(6): 673-677.

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DeGuire S, Gevirtz R, Hawkinson D, Dixon K, Breathing retraining: a three-year follow-up study of treatment for hyperventilation syndrome and associated functional cardiac symptoms, Biofeedback Self Regul 1996 Jun; 21(2): 191-198. Delk KK, Gevirtz R, Hicks DA, Carden F, Rucker R, The effects of biofeedback assisted breathing retraining on lung functions in patients with cystic fibrosis, Chest 1994 Jan; 105(1): 23-28. Fensterheim H, Wiegand B, Group treatment of the hyperventilation syndrome, Int J Group Psychother 1991 Jul; 41(3): 399-403. Grossman P, de Swart JCG, Defares PB, A controlled study of a breathing therapy for the treatment of hyperventilation syndrome, J Psychosom Res 1985; 29 (1): 49-58. Han JN, Stegen K, De Valck C, Clement J, Van de Woestijne KP, Influence of breathing therapy on complaints, anxiety and breathing pattern in patients with hyperventilation syndrome and anxiety disorders, J Psychosom Res 1996 Nov; 41(5): 481-493. Jones NL, Robertson DG, Kane JW, Difference between end-tidal and arterial PCO2 in exercise, J Appl Physiol 1979 Nov; 47(5): 954-960. Kerr WJ, Dalton JW, Gliebe PA, Some physical phenomena associated with the anxiety states and their relation to hyperventilation, Ann. Int. Med 1937, 11: 962-992. Ley P, The efficacy of breathing retraining and the centrality of hyperventilation in panic disorder: a reinterpretation of experimental findings, Behav Res Ther 1991; 29(3): 301-304. Meuret AE, Wilhelm FH, Roth WT, Respiratory biofeedback-assisted therapy in panic disorder, Behav Modif 2001 Sep; 25(4): 584-605. Lum LC, Hyperventilation: The tip and the iceberg, J Psychosom Res 1975; 19: 375-83. Lum LC, The syndrome of habitual chronic hyperventilation, in Modern Trends in Psychosomatic Medicine, edited by OW Hill, Butterworth, London, 1976, vol 3: 196-230. Magarian GJ, Hyperventilation syndrome: infrequently recognized common expressions of anxiety and stress, Medicine 1982; 61: 219-36. Magarian GJ, Middaugh DA, Linz DH, Hyperventilation Syndrome: a diagnosis begging for recognition, West J Med 1983; 38: 733-736. Monday J, Gautrin D, Cartier A, Chronic hyperventilation syndrome. The role of respiratory re-training [in French], Rev Mal Respir. 1995; 12(3): 291-298. Robbins PA, Conway J, Cunningham DA, Khamnei S, Paterson DJ, A comparison of indirect methods for continuous estimation of arterial PCO2 in men, J Appl Physiol 1990 Apr; 68(4): 1727-1731.

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Ruiter de C, Ryken H, Garssen B, Kraaimaat F, Breathing retraining, exposure and a combination of both, in the treatment of panic disorder with agoraphobia, Behav Res Ther 1989; 27(6): 647-655. Seisjo BK, A method for continuous measurement of the carbon dioxide tension on the cerebral cortex, Acta Physiol Scand 1961, 51: 297-313. Seisjo BK, The equilibration of (14)CO2 with the acid labile CO2 of brain tissue, J Physiol (London) 1963, 168: 59-60P. Tweeddale PM, Rowbottom I, McHardy GJ, Breathing retraining: effect on anxiety and depression scores in behavioural breathlessness, J Psychosom Res 1994 Jan; 38(1): 11-21.

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Chapter 5. Discoveries and work of Professor Buteyko and trials of his breathing method

Introduction

This chapter, first, gives a short history and information about the theoretical findings and practical work of Professor Buteyko. Later, some basic features and trials of the Buteyko breathing method are considered. 5.1 Some historical facts

Professor Buteyko received his medical degree from the First Moscow Medical Institute, where he studied from 1946 to 1952. During this period he had a practice as a medical doctor attending and treating severely sick and critically ill patients. A series of events helped him to realize the connection between the respiration and health of patients with hypertension, stenocardia, asthma, and some other serious diseases. He noticed that with approaching death, patients’ respiration got heavier. By visual observation of patients’ breathing, he could predict how many days or hours of life were left. After that, he discovered that deliberate acute hyperventilation quickly worsened the health of patients, while breathing less caused elimination of their symptoms. Buteyko also confirmed these findings in his own problem, hypertension. He then decided to devote his life to studying respiration, in general; and CO2 properties, in particular. More details about the early years of his life can be found in the article “The man and his discovery” available on many Internet sites.

After graduation with Honours, in 1952, he joined the Department of Clinical Therapy of the same institute, working as the manager of Laboratory of Functional Diagnostics. However, lack of qualified personnel, equipment, and financial problems caused him to move from Moscow to Novosibirsk, where he headed another Laboratory of Functional Diagnostics organised in 1960 at the Institute of Experimental Biology and Medicine. Buteyko managed to create in his laboratory a unique diagnostic complex, which included 30-40 physiological devices to measure certain important health parameters in real time (or with each breath). These parameters included pulse, EKG, blood pressure, tidal volume, respiratory rate, minute ventilation, aCO2, aO2, and etCO2. The complex produced many thousands of measurements per hour, analysed by a computer. The unique features of this complex were described in the Soviet magazine “Inventor and Efficiency Expert” (Inventor and Efficiency Expert, 1961; Buteyko 1961; Buteyko, 1962). Some characteristics and abilities of this machine were also reported in more than 20 scientific articles written by Buteyko with his colleagues and published in medical, physiological and diagnostic magazines and conference proceedings. Research with the use of this complex was done from 1960 to 1968. That allowed Buteyko to receive information about physiology and respiration of the human organism in health and disease and relationships between respiration and different factors, including those described in chapters 2 and 3. Analysing the scope of more than 50 scientific publications written by Professor Buteyko (many of them in cooperation with his colleagues), one can conclude that most of them are devoted to CO2 effects on the cardiovascular system (e.g., tone of arteries, capillaries and veins as a function of aCO2). Over 15 publications are about different technical improvements in measurements of physiological parameters, their analysis and use for his diagnostic complex. There are also several articles on asthma and its treatment. Al least 5 Ph.D. dissertations in medicine and physiology were written on respiration and hyperventilation under Professor Buteyko’s leadership. Many medical professionals contributed to the development of the Buteyko breathing method, its theoretical foundation, and practical applications. In particular, articles on the

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Buteyko method and its theoretical foundations were written by the following Buteyko colleagues: 1. Djomin D.V., medical doctor, Ph. D. (Novosibirsk), author of numerous research publications on the relationship between: a) aCO2 and tone of arterial vessels in hypertension and stenocardia; b) aCO2 and blood cholesterol. 2. Genina V.A., medical doctor, Ph. D. (Novosibirsk), author of several theoretical and practical articles about the treatment of bronchial asthma using the Buteyko method. 3. Lapa N.A., medical doctor (Children’s Clinical Hospital No. 8, Novosibirsk), author of publications on the Buteyko method for children. 4. Odintsova M.P., medical doctor, Ph. D. (Novosibirsk), author a of Ph. D. thesis on the aCO2 connection with the tone of arterial vessels in patients with coronary insufficiency and hypertension, and articles on: a) aCO2 and its influence on the cardiovascular system in patients with hypertension and stenocardia; b) hyperventilation in bronchoconstriction of asthmatics. 5. Paschenko S.H., research scientist and medical surgeon, Ph. D. (Zaporozshski Medical Institute, Ukraine), author of research articles on: a) CO2 influence on bone regeneration; b) tissue oxidation processes due to free radicals in CO2-deficient asthmatics. 6. Samotesova A.H., medical doctor, main endocrinologist of Krasnojarsk region (Krasnojarsk), author of publications and research on the Buteyko therapy for diabetics. 7. Souliagin S.S., medical doctor (Obskoi Central Hospital, Novosibirsk), author of several practical articles on Buteyko method (including the influence of focal infections, correct use of physical exercise and other auxiliary methods for health restoration). 5.2 Theoretical discoveries

Let us now consider and analyse the main theoretical statements (in bold) done by Professor Buteyko in scientific publications and magazine articles, during interviews and public lectures.

Most modern patients (up to 90%) with a variety of health problems hyperventilate and have chronically low aCO2.

This statement is, indeed, in agreement with numerous investigations presented in chapter 1. All studies, known to me, indicate prevalence of hyperventilation in patients with hypertension, diabetes, chronic fatigue syndrome, the initial stage of asthma, and many other health problems.

Further increase in ventilation worsens their health state, while reduced breathing improves it.

This statement is also consistent with known physiological laws and reviewed practical results and tests done by Western medical doctors, while applying HVPT (hyperventilation provocation test) and breathing retraining therapies. Hyperventilation is the cause of most prevalent modern health conditions, like asthma, hypertension, stenocardia, diabetes, different forms of cancer, ulcers, gastritis, epilepsy, psoriasis, rheumatism, osteoporosis, etc., comprising over 90% of the sick people.

Development of these diseases is usually proportional to the degree of hyperventilation. The lower the aCO2 and MP, the worse the health of the patients.

Restoration of normal breathing is equal to elimination of the disease and its symptoms. Let us look at the suggested mechanisms of developments and possible treatment of particular health conditions. Asthma Since 1952, as it is claimed by Professor Buteyko, he knew that patients with asthma over-breathe, especially during asthma attacks. These were his clinical observations. Normally, during later years it was merely a technical matter for him to establish the causes of asthma. Low

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aCO2, due to chronic hyperventilation, resulted in bronchoconstriction (Buteyko, 1964; Buteyko & Odintsova, 1968; Buteyko, 1969).

Meanwhile, Herxheimer independently suggested that low aCO2 was the cause of bronchial asthma earlier in 1946 and 1952 (Herxheimer, 1946; 1952). Hypertension and stenocardia Due to his own health concerns, Buteyko had keen interest in cardiovascular problems. According to his public lecture, “In 1952 I had blood pressure of 220-120, headaches, insomnia, and heartaches. Since my professional occupation was the general form of malignant hypertension, I predicted my remaining life span to be about 1.5 years” (Buteyko, 1970). During the 1960’s, while testing patients at his diagnostic complex, Professor Buteyko, together with his colleagues, found relationships between aCO2 and parameters of the cardiovascular system. In particular, they found that low aCO2 causes low tone and spasmodic conditions in small arterial blood vessels and capillaries (Buteyko et al, 1964a; Buteyko et al, 1964b; Buteyko et al, 1965; Buteyko, 1968) and the relationship between aCO2 and blood cholesterol level (Buteyko et al, 1965). Other defensive reactions All these problems (asthma, hypertension, and stenocardia), according to Buteyko, are not abnormal pathological states, but defensive mechanisms of the organism against excessive CO2 losses (Buteyko, 1969). Indeed, narrowing of air passages (as in asthma) or narrowing of arterial blood vessels (as in hypertension and stenocardia) causes delays in CO2 removal. Similar defensive mechanisms are observed in many other situations: blocked nose, polyps, excessive mucus production, varicose veins, spasmodic states of different organs leading to migraine, gastritis, ulcers, Raynoud’s disease etc. Gastrointestinal diseases

GI (gastrointestinal) diseases are usually caused by spasmodic states of small blood vessels leading to hypoxia and problems with an inadequate blood supply. Elimination of hyperventilation was found to be an effective method to deal with gastritis, gastric and intestinal ulcers, and other GI problems. Diseases connected with bone metabolism

Since low aCO2 causes abnormal changes in ionic composition of blood, as well as abnormal redistribution of ions in extra-cellular and intra-cellular fluids, that affects regeneration and destruction of bone tissues. Hence, osteoporosis, osteochondrosis, abnormal growth of bone tissues, brittle teeth, and other related conditions are directly influenced by hyperventilation. Indeed, since redistribution and altered availability of Ca are well-documented effects of low aCO2, it is reasonable to expect that chronic over breathing can lead to such problems. Allergies and inadequate immune reactions

Low aCO2, by interfering with activities of vitamins, catalysts, hormones, and other body chemicals, alters normal human immune reactions. In some cases, pathogenic objects do not cause a normal response of the immune system leading to colds, infections, tonsillitis, while in other cases the reaction of the immune system is excessive, as in hypersensitivity, allergies, and autoimmune disorders. Practical work on breathing normalization revealed efficiency of the Buteyko breathing therapy for colds, respiratory viral diseases, allergies, allergic rhinitis, multiple sclerosis, rheumatism, arthritis, lupus, nephrosis and other related disorders.

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Endocrine diseases By affecting production and concentrations of different hormones, chronic

hyperventilation can cause problems with thyroxin, insulin, estrogen, epinephrine and norepinephrine, calcitonin, pancreatic endocrine hormone and other hormones. That leads to hypo- and hyperthyroidism, diabetes, hyperparathyroidism, diseases of the adrenal cortex, and other health concerns.

For example, Professor Buteyko suggested the following mechanism for diabetes development (Buteyko, 1962): During times of stress, it is physiologically normal for the organism to have certain hormonal changes in order to prepare the organism for rigorous physical activity. While increased production of adrenalin and nor-adrenalin (the main stress hormones) are well-known effects, decreased insulin level and higher blood glucagon concentrations increase blood sugar level. Such adaptations are obviously useful from the evolutionary viewpoint in order for this physical activity to be efficient. However, chronic stress without physical activity results in chronically high glucagon and low insulin values. These and some other biochemical changes (due to the changed direction of the Krebs cycle) cause hyperglycaemia.

Practical studies done by professor Buteyko revealed that diabetics usually have 32-34 mm Hg aCO2 and 5-10 s MP. Therefore, diabetes can be also viewed as a normal effect of hyperventilation in people with certain genetic predisposition.

More information on diabetes can be found on Christopher Drake’s web-site at www.buteyko.com.au/Chris.html. Malignant and benign tumours Finally, due to the same abnormal influence on body metabolism, low aCO2 interferes with normal life and metabolism of cells creating conditions for tumours and cancers. In particular, normalization of breathing is an effective method to treat mastopathy, and some other problems. Disappearance of malignant tumours (as a side effect of the Buteyko therapy) has frequently been reported by Buteyko patients and students. Apart from discovering the connection between hyperventilation and various diseases, Professor Buteyko found a way to deal with many of them using his breathing therapy. Such work became possible due to a simple test by which a patient can evaluate his/her own aCO2 using the MP (maximum pause), or breath holding time after normal expiration. Formula for alveolar CO2 tension

The maximum pause reflects aCO2, according to the formula aCO2% = 3.5% + .05*MP (here, aCO2% is the alveolar CO2 concentration in %, aCO2min%=3.5% is minimum CO2 content, K=.05 is a coefficient of proportionality, the MP is breath holding time after quiet expiration, for as long as possible, while sitting, after 10 minutes of rest). Due to the previously discussed “training effect”, those, who often perform breath holding, should substitute their CPs (control pauses), or breath holding time till the first desire to breathe, into this formula. Since this formula was patented during Soviet times, it was probably considered by Soviet bureaucrats, as a significant achievement of Soviet science. Available Western studies indicate that both, aCO2 and BHT, usually get lower with worsening of health. At the same time, there are many physiological studies, which investigated the relationship between aCO2 and BHT, when aCO2 is changed before the test (for example, effect of hyperventilation on BHT). Normally, such investigations found that lower aCO2 extended BHT. There were few systematic attempts to find the connection between usual aCO2 and BHT or to define the meaning of personal BHT in terms of blood gases.

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5.3 Practical discoveries and their application and verification Reduction in ventilation and increase in aCO2 are equivalent to health

improvement, while normalization of breathing parameters is equal to health restoration. From a practical viewpoint this Buteyko finding literally saved thousands of human lives and can save millions more. So far, available Russian and Western studies support this idea.

Health improvement can be measured by increase in the MP (or the CP) up to the norm of 60 s, which corresponds, according to Professor Buteyko, to ideal health and absence of medical pathologies. Buteyko found that some health problems (like asthma, hypertension, and stenocardia) and their symptoms could be solved, when aCO2 reaches the official norm of 40 mm Hg (or about 5.25% CO2 partial pressure in lungs and arterial blood at sea level). That corresponds to about 35 s MP (or CP). Meanwhile, treatment of GI problems, many infertility conditions, psoriasis, certain endocrine disorders, and different forms of cancer required larger aCO2 and MPs. As a result of these tests, he found that 60 s MP (or 6.5% CO2) was the level correspondent to ideal health, when known medical pathologies were absent. According to official statistics, up to 1967, Buteyko laboratory, using his breathing method, successfully treated more than 1,000 severely sick in-patients with asthma, hypertension, and stenocardia. By that time more than 200 medical doctors completed qualification courses in the laboratory, while learning how to apply this method in practice. Closure of the Buteyko laboratory in 1968, silence about a very successful experimental 1968 trial done in Leningrad on 50 severely sick patients, who had years of disease and heavy medication, followed attempts to discredit the method. All these actions resulted in public outcry. Former patients, many of whom were on steroids and with disabilities, literally flooded the Soviet Health Ministry with letters describing their medical histories and success achieved due to the Buteyko method. That resulted in several practical steps indicating official recognition and approval of the Buteyko method.

1. In 1983 USSR Committee on Inventions and Discoveries issued a patent with the title "The method of treatment of hypocapnia [low aCO2]" (Author's certificate No. 1067640 registered on 15 September 1983). What is unusual about this document is that it has the priority date of the discovery 29 January 1962. Thus, the discovery was officially accepted more than 20 years later. The patent describes the treatment of bronchial asthma and 40 patients with hypertension and stenocardia (with over 80 % success rate).

2. In 1985, the method was officially approved by the Soviet Health Minister (Burenkov, 1985).

3. In 1986 USSR Committee on Inventions and Discoveries issued another patent "Method of defining CO2 content in alveolar air" using breath holding time (Buteyko, 1986). The formula from this patent was described in the previous section.

Up to now, several hundred medical professionals adopted the Buteyko breathing method in their work in Russia, while the total number of treated people is over 100,000. Most of these former patients were asthmatics (about 70%, according to P. Kolb, private communication, 2001). It was found experimentally that asthmatics usually quickly respond to the therapy. This phenomenon can be explained by minimum organic damage typically found in this disease. Most other patients had problems with the cardiovascular, nervous and endocrine systems. A typical success rate was about 90 %. Currently there are more than 20 Buteyko medical centres and clinics functioning in major Russian cities.

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5.4 Experimental trials of the Buteyko breathing method 1968, Institute of Pulmonology, Leningrad, USSR

50 patients with severe bronchial asthma, hypertension and stenocardia, all of them with many years of heavy medication, most with steroid deficiencies and organic complications; success rate 95% (Khoroscho, 1982). 1981, Sechenov's Medical Institute, Moscow, USSR

52 children (34 in-patients and 18 out-patients; 3-15 years old) with regular asthma attacks (once per day or more); 41 of them had pneumonia, 27 rhinitis, 36 chronic tonsillitis. All had problems with breathing through the nose, palpitations, and were bronchodilator users. In 1-5 days the patients were able to stop the attacks, cough, blocked nose, and wheezing, using the method. Observations in 1-3 months showed considerable improvements (cessation of heavy attacks or a total disappearance of the symptoms) in 83%, some improvement (less heavy attacks and considerable reduction in medication) in remaining 17%. Their average CP increased from 4 to 30 s, aCO2 from 25 to 36 mm Hg. Higher blood concentrations of IgA, IgM, IgG, and IgE were found, according to laboratory reports. Blood pressure normalised, forced expiratory volume raised over 5 times. Significant increases in lung volume, expiratory speed, and other parameters were found. 1990, Shevchenko's Central Hospital, Kiev, Ukraine

50 patients with radiation sickness due to Chernobyl's nuclear plant disaster. 82% patients had considerable improvement in blood analysis, cardiovascular parameters (blood pressure, pulse, etc.), work of the digestive system, and reduction in medication. No cases of side effects or complications due to the breathing exercises were reported (p.221, Zimchenko & Romanenko, 1991). 1995, Mater Hospital, Brisbane, Australia

20 patients with long history of asthma and significant medication. In 3 months, they decreased use of bronchodilators by 90%, inhaled steroids by 50%. The symptoms' score was improved by 71% (Bowler et al, 1998).

1999, Alfred Hospital, Prahan, Australia

18 patients with mild to moderate asthma were taught the Buteyko method by a video and compared with 18 control subjects (Opat et al, 2000). The study found a significant improvement in quality of life and significant reduction in inhaled steroid use. Reports from two conferences in Moscow and Krasnojarsk in 1988

In addition to these trials, there were about 30 published reports of Russian medical doctors and health professionals, who met during two conferences in Moscow and Krasnojarsk in 1988 in order to share their practical experience of application of the Buteyko method in over 20 medical hospitals and clinics in Russia. The total reported number of treated people, according to the conference proceedings, was over 3,000. Although most of them had respiratory (asthma, bronchitis, rhinitis, etc.) and cardiovascular (hypertension, stenocardia, ischemia, etc.) problems, hundreds were treated or relieved from arthritis, osteoporosis, epilepsy, ulcers, gastritis, kidney stone problems, hepatitis, different infertility conditions, skin diseases (e.g., dermatitis, psoriasis, eczema), etc. Typical reported results were either some or essential improvement for over 90% patients, while remaining patients were not able to normalise their breathing parameters due to absence of desire or motivation and quitting the method during its initial stages. None of these

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trials or reports revealed any complications or side effects due to the Buteyko breathing method, although there are many important practical rules and possible complications in cases of incorrect application of the method. Appendix 3 (from Novosibirsk Buteyko web site) provides a list of health conditions, which are characterised by hyperventilation and low aCO2 and which favourably respond to correct application of the Buteyko method. Appendix 4 (from Moscow Buteyko web site) gives symptoms of hyperventilation syndrome, which are treated in the Moscow Buteyko Clinic. Q&A section Q: There are many medical studies indicating that acute hyperventilation produces asthma attacks in asthmatics. However, several studies found that acute hyperventilation with CO2 enriched air also results in asthma attacks. Therefore, as some doctors claimed, low aCO2 could not be considered as a single cause of asthma. Is this opinion correct? A: Before being tested with CO2 enriched air in laboratories, typical asthmatics had many hundreds of times the following course of events. On the background of chronic hyperventilation (all known studies reported presence of hyperventilation for initial stages of asthma), asthmatics experienced the influence of some other triggering factors (like exercise, overeating, oversleeping, allergies, etc.), which resulted in additional hyperventilation and further bronchoconstriction or in further inflammation of airways with the same results: feelings of air shortage (due to airway obstruction), chest tightness, laboured breathing, etc. all signs of an asthma attack. (Sometimes, this airway obstruction could be due to, for example, excessive mucus production or inflammation. That could result in anxiety and panic causing acute hyperventilation.) In all cases these asthmatics breathed normal air with about 0.04% CO2 concentration. Thus, before the attacks the following physiological changes were repeated many hundreds times: abnormally hard work of the respiratory muscles, increased air flow through the respiratory tract, increased amplitude of pressure variations in internal organs, etc. All these changes, before the attacks, were sensed many hundred times by the millions of nervous cells of the nervous system. Finally, further lowered aCO2 produced additional bronchoconstriction and the attacks.

Now exactly the same asthmatics arrive in the laboratories, where they perform the same acute hyperventilation, which is accompanied by the all these described additional features (again sensed by the millions of nervous cells) with one difference, the inspired air is CO2-rich. Such air has never been experienced by these asthmatics before, but the whole nervous system learned that such situation causes bronchoconstriction. What would be the result now?

The result due to the changed stimulus would be defined by how much of the previous stimulus is left. Since less than 1% stimulus is absent (low CO2), while the remaining more than 99% left, clearly the reaction would be exactly the same, as for the whole stimulus.

But assuming that the human nervous system is incapable of learning from the previous experiences repeated hundreds of times, and that all these events sensed and recorded by the nervous system did not produce habituation and conditioning, then acute hyperventilation can be ignored, as one of the causes of asthma attacks.

Even in conditions of greatly increased aCO2, the influence of so many areas of the nervous system should be more powerful, than that of the breathing centre. Meanwhile, if such tests with CO2-rich air were repeated many times, the effect of gradual relearning can be observed and acute hyperventilation would not cause bronchoconstriction and the attacks.

Moreover, physiological studies found the confirmations of this psychological effect based on physiology of the nervous cells. It is known that, for example, some breathing maneuvers (chapter 2), e.g., Valsalva and Müller maneuvers, or breathing air with the same composition at the end of the breath hold, as in the lungs, extends BHT. Why? All previous life, movements of respiratory muscles resulted in new oxygenated air coming into the lungs.

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Normally, the nervous system learned millions of times, that such respiratory movements are signs of new (fresh) air flow. When, all of the sudden, the conditions are different, only the breathing centre creates the stimulus to breathe, while the rest of the nervous system is “happy” and does not contribute to the urge to breathe. It is now a clear fact, which has been confirmed by all published studies, that development and first stages of asthma are always accompanied by hyperventilation. The situation with medical respiratory professionals and asthma was accurately reflected by Peter Kolb, “… asthma is a disorder which is investigated by thousands of respiratory specialists with millions of dollars worth of equipment to measure breathing. Yet after more than half a century of work by all these people measuring patients’ breathing, they haven’t picked up that asthmatics are just breathing too much” (Kolb, private communication, 2001). Q: Professor Buteyko claimed that, for example, gastritis is caused by hyperventilation. However, it is known that, poor dietary habits (like eating when not hungry, not chewing food properly, eating spicy and hot meals) can create gastritis without any influence of breathing. How can such facts be explained? A: Practical studies done by Professor Buteyko revealed that it was necessary for the patients with GI (gastrointestinal) problems to have low levels of aCO2 pressure (e.g., less than about 40 mm Hg) in order for gastritis and other GI disorders development to take place. That is probably due to appearance of certain pathological substances generated by affected mucosa of the stomach lining. In practical terms, low CPs (e.g., less than 35 s) are required for the progress of the disease. At the same time, the ideal CP of 60 s makes such pathological processes impossible due to normal repair, adequate oxygenation and blood supply of the stomach. The ideal CP and GI disorders are incompatible.

Thus, if we accept 40 mm Hg (or 5.3 %) aCO2 level as normal (as it is done by official medicine), when GI problems and hyperventilation are independent events. A person can have GI problems with or without hyperventilation.

If our norm is 6.5% aCO2 (60 s CP), then gastritis and other GI problems can not take place, unless this aCO2 level is lowered. Q: What about hyperventilation being the cause of cancer? A: It takes a long time to develop malignant tumours. As in cases of GI problems, such development, according to Professor Buteyko, is possible only when aCO2 is below the official physiological norm (5.3% or 40 mm Hg aCO2 at sea level). Moreover, there is evidence that pathological processes due to focal infections often contribute to the onset of the initial stages of cancer. The effect of these focal infections on breathing will be investigated later. Thus, while for example, many toxic chemicals can cause particular forms of cancer, pathological changes on tissue level are possible only with the background of chronic hyperventilation. Therefore, if higher aCO2 standards are accepted, then hyperventilation can be and should be considered as a cause of cancer. References for chapter 5 Bowler SD, Green A, Mitchell CA, Buteyko breathing techniques in asthma: a blinded randomised controlled trial, Med J of Australia 1998; 169: 575-578. Burenkov S, About practical actions for application of the method of voluntary regulation of depth of breathing for the treatment of bronchial asthma [in Russian], Order No. 591, 30 April 1985, Ministry of Health of the USSR, Moscow.

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Buteyko KP, Pneumotahometer with automatic closure of air jet as a part of a medical combine [in Russian], Inventor and Efficiency Expert 1961, 6: 16-17. Buteyko KP, Oscillographs and hypertension. Is "big" breathing useful? [in Russian], Inventor and Efficiency Expert 1962, 5: 7-9. Buteyko KP, Instruction for treatment of bronchial asthma, stenocardia, hypertension, and obliterating endarteritis using the method of voluntary normalization of breathing [in Russian], Preprint, Novosibirsk, 1964. Buteyko KP, Odintsova MP, Djomin DV, Influence of hyper- and hypocapnia on tone of peripherial blood vessels [in Russian], Proceedings of the 2-nd Siberian scientific conference of family physicians, Irkutsk, 1964a. Buteyko KP, Djomin DV, Odintsova MP, Application of the regressive analysis for differentiation of influence of gas components of arterial blood on functional state of small peripherial blood arteries [in Russian], Proceedings of the 2-nd Siberian scientific conference of family physicians, Irkutsk, 1964b. Buteyko KP, Djomin DV, Odintsova MP, The relationship between lung ventilation and tone of peripherial blood vessels in patients with hypertension and stenocardia [in Ukranian], Physiological magazine 1965, 11 (5). Buteyko KP & Odintsova MP, Hyperventilation as one of the causes of spasms in smooth muscles of bronchi and arterial vessels [in Russian], Proceedings of the 4-th scientfico-practical conference on medical control and therapeutic physical exercises, Sverdlovsk, 1968. Buteyko KP, Carbon dioxide theory and a new method of treatment and prevention of diseases of the respiratory system, cardiovascular system, nervous system, and some other diseases [in Russian], Public lecture for Soviet scientists at the Moscow State University, 9 December 1969. Buteyko KP, Carbon dioxide theory of breathing and a new method of treatment and prevention of diseases of the respiratory system, cardiovascular system, and some other diseases [in Russian], Public lecture for Soviet scientists at the Moscow State University, 1970. Buteyko KP, The method of treatment of hypocapnia [in Russian], USSR Committee on Inventions and Discoveries, Author's certificate No. 1067640, 15 September 1983. Buteyko KP, Method of defining CO2 content in alveolar air [in Russian], Soviet patent N. 1593627, 17 October 1986. Herxheimer H, Hyperventilation asthma, Lancet 1946, 6385: 83-87. Herxheimer H, The late bronchial reaction in induced asthma, Int Arch Allergy Appl Immunol 1952; 3: 323-328. Inventor and Efficiency Expert (editorial), A combine against hypertension in the Institute of Experimental Biology and Medicine [in Russian], 1961, 6.

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Khoroscho A, Interview with Buteyko [in Russian] 1982, in Buteyko method. Its application in medical practice, ed. by K.P. Buteyko, 2-nd ed., 1991, Titul, Odessa, p.168-180. Opat AJ, Cohen MM, Bailey MJ, Abramson MJ, A clinical trial of the Buteyko Breathing Technique in asthma as taught by a Video, J Asthma 2000; 37(7): 557-64. Souliagin SS, Treatment of patients with focal infections using VEDB method [in Russian], in Buteyko method. Its application in medical practice, ed. by K.P. Buteyko, 2-nd ed., 1991, Titul, Odessa, p.56-63. Zimchenko VN & Romanenko NF, Conclusions on practical trial of Buteyko method, conducted in Department of Radiation Pathology of Central Republican Hospital of Shevchenko region (Ukraine) during 06.03.1990-07.04.1990 [in Russian], in Buteyko method. Its application in medical practice, ed. by K.P. Buteyko, 2-nd ed., 1991, Titul, Odessa, p.222-227.

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Chapter 6. Background and basics of the Buteyko method Introduction This chapter provides the foundation for the Buteyko breathing method, advantages and disadvantages of MPs (maximum pauses) and CPs (control pauses), their connection with physiological systems of the human organism, goals of the Buteyko therapy, its main typical features, and initial practical steps (use of the Emergency Procedure and treatment of possible focal infections). 6.1 Potential dangers of MPs (maximum pauses) There are many health conditions, when MP measurements must not be done. Let us look at the causes of possible problems with MPs. Breath holding causes a fast rate of accumulation of CO2 in the lungs. Although CO2 has numerous useful properties, sharp and large increases in aCO2 can cause sudden dilation of arteries and capillaries in internal organs and increase blood flow to these organs, intensifying or adversely interfering with their natural work. In cases of some serious health conditions, many complications are possible or even likely. 1. In a diabetic, the sudden increase in blood flow to the pancreas can cause a quick release of large amounts of insulin into the blood, a rapid drop in blood sugar, and hypoglycaemic coma. 2. In a person with hypertension, the MP can result in largely increased blood pressure. Such a practical result was received in many hypertensives. Moreover, some of them had a systolic blood pressure increase from about 200 to 260 mm Hg during MPs, making the whole procedure dangerous (Ayman & Goldshine, 1939). Indeed, in rare, but possible cases of undetected serious organic defect in the heart muscle, the MP may cause severe complications, including mechanical damage to the heart muscle. 3. Many gastro-intestinal problems (gastritis, gastric ulcers, Crohn's disease, inflammatory bowel disease, irritable bowel syndrome, intestinal ulcers, etc.) can dramatically worsen due to the suddenly incoming blood intensifying peristalsis. Flare-ups, gases, cramps, opening of healed lesions, intensive wear of mucosal surfaces, all are possible complications. 4. Patients with extensive damage to kidneys' nephrons can experience so sudden an increase in blood flow to kidneys, that remaining working nephrons may be overburdened with the extra work to clean large amounts of blood. Their possible congestion could result in kidneys' failure. Therefore, existing organic damage, lesion, or inflammation in any internal organ may create serious complications, as a direct result of long breath holds. 6.2 CP, as a safe MP alternative Practical work with patients, done by Professor Buteyko and his colleagues, resulted in the conclusion that measurement of MPs are not as safe as measurements of, for example, CPs. For example, the Buteyko manual (Buteyko, 1991) has a warning that MPs should be measured only in the presence of practitioners in order to check if the training session is done correctly. Many patients reported a discomfort, while doing MPs, and the subsequent heavy breathing. That often resulted in the negative attitude of the patients. Thus, CP became a more popular measuring tool.

MPs and CPs of novices are physiologically different from MPs and CPs of experienced Buteyko students due to the “training effect” (chapter 2). Therefore, with the same subjective perception of air hunger, experienced students have greater accumulation of aCO2, in comparison with those students who are at the initial stages of the breathing exercises. Hence, those people, who have never manipulated their breathing (in terms of relative hypoventilation and breath holding), should substitute their MPs in the formula for defining their aCO2. (If MPs, due to certain health conditions, are not safe, check Appendix 3 how to get your

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MP from the CP). Other people, who performed breath holding many times, should substitute their CPs in the formula in order to define their aCO2. There is one other aspect, which is not mentioned in the Russian Buteyko literature regarding the difference between the MP and the CP. That relates to those practical situations, when people naturally hold their breath. For example, gradual cold water immersion, bare foot walking, and certain static yoga postures are such examples. Normally, in these cases breath holding is done until the first desire to breathe, as during CP measurements. Therefore, apart from situations, when people are involved in daily diving, the CP was and can be a part of natural life, while the MP was and is a very rare natural experience. Meanwhile, many patients and Buteyko practitioners continue to use the MP in measurements and exercises. They believe in its effectiveness and stronger overall impact on the organism. 6.3 CP measurements Generally, for healthy and relatively healthy people, the duration of BHT (breath holding time) is defined by how soon current aCO2 level reaches the aCO2 threshold established by the breathing centre. Thus, BHT mainly depends on three parameters: 1) initial aCO2, currently existing in arterial blood or in the alveoli of the lungs; 2) final aCO2, the level preset by the breathing centre as a threshold of tolerance; 3) the rate of CO2 accumulation. As we examined in chapter 2, for diseased states hypoxia can be an essential factor in the CP threshold. Due to importance of the CP, let me review the main factors and conditions for its correct measurement, together with possible effects of these factors on BHT duration. 1. Sufficient preliminary rest (10 min is suggested, according to Buteyko). For example, if measurements are done after physical activity, BHT is going to be smaller due to elevated initial CO2 concentration in venous blood, working muscles and their surrounding tissues. 2. In a sitting position. Different postures have different metabolism and, therefore, a different CO2 production rate. The standing position results in shorter BHT, while lying increases BHT in comparison with the sitting position. 3. With normal breathing before the test. Acute hyperventilation, due to reduction in aCO2, increases BHT, while reduced breathing initially decreases it. However, for people with severe breathlessness and very low aCO2 acute hyperventilation does not extend BHT, but can even reduce it (chapter 2). 4. At the end of the normal expiration. BHT is linearly proportional to the amount of air in the lungs, since the rate of CO2 accumulation is also proportional to this volume. 5. While inhaling air of normal composition. Normal air has about 20% O2, 0.04% CO2, and 80%N2. Normal barometric pressure (about 760 mm Hg) and air temperature (about 20 degrees C) are other important factors. 6. Without influence of medicines, street drugs, steroids, other respiration-affecting chemicals. Certain substances can influence BHT 2-4 times in both directions. 7. Preferably on empty stomach. Meals, first, slightly increase aCO2 and BHT, and then reduce them, when food substances enter the blood stream. For example, MPs that are performed soon after meals can significantly intensify peristalsis and may cause vomiting in some people. 8. Till the first desire to breathe for experienced people (and as long as possible for others, who do not have serious health problems). 9. Without any muscular movements. Physical movements distract the nervous system and suppress the signals from the breathing centre. That increases BHT.

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6.4 CP, as an integrative indicator of human health, and its connections with the functioning of different physiological systems of the human organism The CP, according to Professor Buteyko, is a simple and effective indicator of individual health. Analyzing available data in relation to former Buteyko patients and case histories described by Russian medical doctors, the following approximate results regarding CP durations were obtained: 1-5 s - severely sick and critically ill patients, usually hospitalised. 5-10 s - very sick patients, often hospitalised. 10-20 s - sick patients with numerous complaints and, often, on daily medication. 20-30 s - people with poor health, but often without serious organic problems. 30-40 s - people with normal health, according to official medical standards, while some serious, often undetected health problems are possible (gastrointestinal, hormonal, and skin problems, caries, intestinal parasites, etc.). 40-60 s - good health. Over 60 s - ideal health, when any organic or other pathological health conditions are virtually impossible. However, it is possible that a person may have no complaints and no serious organic or metabolic health problems with a low or very low CP. It follows from chapter 1 that the effects of hyperventilation are individual, and these above-given relationships (between CPs and corresponding health states) reflect measurements in patients with asthma, hypertension, stenocardia, emphysema, cancer, diabetes and other health conditions. While measuring and analyzing your CP and its dynamics, it is important to understand that the CP is an integrative characteristic of your individual health. The CP approximately reflects the general state of all systems of the human organism. CP restrictions are usually due to the influence of the weakest system or the most vulnerable part or organ of the body. Let us consider in more details the connections between the CP and different parameters and systems of the organism keeping in mind that the effects of hyperventilation are individual. 1. CP and aCO2. They are linearly proportional to each other. 2. CP and tissue oxygenation. Poor oxygenation normally results in an excited state of O2 chemoreceptors causing small CPs. On the other hand, good tissue oxygenation is impossible without sufficient aCO2 values and correspondingly long CPs. Vice versa, when the CP is short, aCO2 is low and, hence, tissue oxygenation is impaired. 3. CP and blood pollution. From chapter 1, it is known that bacteraemia (presence of bacteria in blood) or sepsis (presence of pathogens or toxic products in the blood) produces chronic hyperventilation, causing critically low aCO2 and, correspondingly very low MPs and CPs of probably not more than 5-10 s. Thus, long CPs are impossible, when blood is polluted. Short CPs do not indicate bacteraemia or sepsis, but a poor state of the eliminative organs and the immune system (due to low aCO2) can favour infections and appearance of pathogens in blood. For example, according to physiological studies, the blood flow to kidneys and liver (main blood-cleansing organs) is proportional to aCO2 (Okazaki et al, 1989). 4. CP and the immune system. The experience of patients practicing Buteyko breathing revealed that an increased CP decreases the number of viral and bacterial infections. Blood laboratory results found significant increases in white blood cell count (Zimchenko and Romanenko, 1990) and in several types of immunoglobulins, including IgA, IgM, IgG, and IgE (Genina et al, 1982). 5. CP and the nervous system. Section 1.2 described the main effects of hyperventilation on the nervous system. Short CP and small aCO2 indicate a low threshold of excitability of many brain areas, quick changes in mood, possible sleeping problems, anxiety, panics, fearfulness, exaggerations, and other perceptual problems. A large CP and a high aCO2 reflect calmness; concentration; objectivity; and short, deep, and refreshing sleep.

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6. CP and the digestive system. Stress and hyperventilation divert blood flow from internal organs to skeletal muscles. Thus, chronic hyperventilation and correspondingly small CPs mean chronic problems with perfusion and oxygenation of the digestive system. This CO2 effect was known to Professor Yandell Henderson, who found that low aCO2 resulted in loss of tone in the blood vessels of the abdominal viscera of dogs, producing extreme congestion. Saturation of blood with CO2 rapidly eliminated the congestion (Henderson, 1907).

A more recent investigation entitled “Hyperventilation, central autonomic control, and colonic tone in humans” had the following abstract.

“Symptoms attributable to hyperventilation are common among patients with the irritable bowel syndrome (IBS); indeed, some have suggested that hyperventilation may exacerbate the alimentary symptoms of IBS. Hyperventilation changes haemodynamic function through central and peripheral mechanisms; its effects on colonic motor function, however, are unknown. The aim of this study, therefore, was to assess the effects of hyperventilation on colonic tone and motility and on cardiovascular autonomic activity, and to discover if hypocapnia was critical to elicit the response. Phasic and tonic motility of the transverse and sigmoid colon, end tidal PCO2, pulse rate, and beat to beat pulse variability were assessed before, during, and after a five minute period of hypocapnic hyperventilation in 15 healthy volunteers; in seven other subjects, effects of both eucapnic and hypocapnic hyperventilation were evaluated. Hypocapnic but not eucapnic hyperventilation produced an increase in colonic tone and phasic contractility in the transverse and sigmoid regions and an increase in pulse rate and pulse interval variability. The findings are consistent with inhibition of sympathetic innervation to the colon or direct effects of hypocapnia on colonic smooth muscle, or both. These physiological gut responses suggest that some of the changes in colonic function are caused by altered brain or autonomic control mechanisms” (abstract, Ford et al, 1995). It follows from this study that low aCO2 (hypocapnia) is directly responsible for an irregular peristalsis and an abnormal tone of the GI tract. 7. CP and the cardiovascular system. Numerous studies and Ph.D. dissertations about CO2 relationships with blood vessels and cholesterol deposits were written in Russia. Western studies (section 1.2) also confirmed a local vasodilating CO2 effect. Investigating hypertension it was found that, when the organism reacts to hyperventilation by increasing blood vessel cholesterol deposits, every 0.1% in aCO2 decrease is equal to about 10 mg % of extra cholesterol deposits. This is how hypertension develops. Vice versa, every 0.1% CO2 increase (or 2 s CP increase) is equivalent to 10 mg % reduction in blood cholesterol level. Therefore, normalization of breathing is equivalent to normalization of cholesterol level and blood pressure. Relationships between aCO2 and various heart problems were considered in section 1.3. Thus, the CP is connected with both specific and general parameters of the cardiovascular system. 8. CP and the respiratory system. Two main general parameters of the respiratory system, in terms of their profound influence on the whole organism, aCO2 and aO2, were considered here at the very beginning (points 1 and 2 above). Concerning specific respiratory CO2 effects, the main problem of asthmatics, bronchoconstriction due to low aCO2, was described in section 1.2. As explained in chapter 2, the mechanism of breathing control is different in good health and disease. Hence, the CP reflects the efficiency of this control. Small CPs usually correspond to laboured thoracic breathing, whereas large CPs and ideal health are characterised by regular, smooth, quiet, invisible, noiseless, and easy diaphragmatic breathing with relatively longer exhalations and automatic pauses after exhalations. In some health conditions (e.g., asthma and emphysema), the lungs have uneven distribution of incoming air. Some lungs get more air than others. How can normal breathing, compared to hyperventilation, help with this problem? The cause of the problem is low aCO2 leading to bronchoconstriction and excessive mucus formation. Both effects are defensive mechanisms of the organism from chronic CO2 losses. As a result,

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those people who breathe within the physiological norm (about 6 l/min), have even distribution of in-coming air due to less obstruction to air flow (Buteyko, 1969). 9. CP and the endocrine system. Low CPs can result in abnormal blood glucose regulation (Buteyko, 1969; Lavrent'ev, 1993). That causes delayed, or excessive, or inadequate response of the pancreas to blood sugar variations. Practical work with patients diagnosed with hyper- and hypo-thyroidism revealed that normalization of blood thyroid hormone is proportional to CP growth. Studies on physiological effects of yoga also revealed that blood thyroxin level, which is usually low in people, significantly increases, together with BHT, after yoga practice (p.74 and 206, Funderburk, 1977). Normalization of menstrual cycles with the large CP (over 40 s) is another practical finding. Significant improvements in other areas (weight, appetite, and sleep) are other typical effects of increasing CP values. When previous health problems are eliminated and all systems of the organism are in good shape, achievement of large CP values (up to 60 s or more) is possible. Vice versa, practice indicates, that large CPs (over 60 s) correspond to absence of medical pathologies. Thus, the goal of the Buteyko method, in medical terms, is to normalise blood gases disturbed by hyperventilation. In practical terms, the goal is to have the stable CP of over 60 s. This goal is achieved by gradual normalization of breathing and training of the breathing centre in order to increase aCO2 values up to the Buteyko norm (6.5% aCO2). 6.5 Some general features of the Buteyko breathing method Although the Buteyko method was developed mainly during 1960's, it has many features similar to those, discussed for Western breathing therapies (chapter 4), which were created later. Let us look, at these common features, important practical findings of Russian doctors, and some new characteristics of the Buteyko therapy in comparison with the Western methods. HVPT (hyperventilation provocation test) could be done repeatedly by Russian Buteyko doctors until the patient realized the simple connection between his health state and his breathing, which he can regulate. Due to possible complications, this test was performed with constant monitoring of the patient's pulse (e.g., every 10-15 s). If the pulse during the HVPT increases by more than 30% the test should be stopped to prevent possible heart problems. The test, according to Buteyko, helps to define the most damaged system or organ of the organism (Buteyko, 1991). In some cases, it helped to diagnose a patient with another, more serious or life-threatening condition. "For example, if an asthmatic gets, during the HVPT, not an asthma attack, but dizziness and other symptoms of brain vessel spasms or spasms of pain near the heart (stenocardia), then not the lungs' damage, but stroke is the main threat to his life" (Buteyko, 1991). Cases, when deep frequent breathing improved the health state, while decreased breathing made it worse, during over 30 years of clinical practice have never been observed (Buteyko, 1991). Immediately after the test, it was suggested to the patient to eliminate the symptoms of the HVPT and his disease using the Emergency Procedure described in the next section. (Repeated use of the HVPT by Russians was possible due to the following and immediate application of this Emergency Procedure). Awareness about normal and abnormal breathing was not just a recommendation or some information to consider. The patient, according to Buteyko, should constantly, days and nights, pay attention to his breathing and use different methods, measures, and actions to normalize his respiration and prevent CO2 losses. These methods will be described later. Relaxation should be experienced not only in relation to the skeletal muscles and muscles responsible for thoracic breathing, but also in relation to the diaphragm. Most Western methods, as we found, used low frequency breathing, which often resulted in relatively large diaphragmatic movements and large tidal volume (slow, but deep breathing) since breathing

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frequency was one of the factors which should be controlled by the patient. Therefore, low frequency breathing can cause tension in the diaphragm. The Buteyko breathing, as it will be clear from the next section, consists of a shallow, low-volume voluntary breathing pattern, which is later automatically (unconsciously) corrected by the breathing centre to a slow and shallow pattern (with decreased tidal volume) corresponding to larger aCO2 values.

Courtney-Belford also suggested that “The Buteyko method of breathing teaches people to utilize posture, focus attention on the breath and control breath-holding to raise the level of C02. It is also probably one of the only forms of breathing retraining that teaches people to reduce the volume of air while maintaining a relaxed diaphragm” ( Courtney-Belford, 1997). Diaphragmatic breathing, because of proper relaxation, should be more natural during the Buteyko breathing causing greater general relaxation and greater accumulation of CO2. 6.6 The Emergency Procedure Patients with mild to moderate asthma, hypertension, epilepsy, and many other health problems usually have chronically low average aCO2. In addition, as with all people, they have many factors (stress, meals, exercise, hormonal changes, overheating, etc., all discussed in chapter 3) causing daily fluctuations in aCO2 from preset aCO2 average values. As a result, these hyperventilators are on the brink of having asthma, heart, epilepsy and other attacks or acute deterioration of their health problems due to these triggering factors, when their aCO2 is critically low. The Emergency Procedure was developed by Professor Buteyko in order to prevent such attacks and/or eliminate undesirable problems and symptoms by aCO2 increase. Here are the steps to take, when one's health is threatened. 1. Relax all your muscles in any comfortable position (sitting, lying, etc.), which is favourable for complete relaxation. Such relaxation normally produces quiet spontaneous exhalation. 2. At the end of this exhalation, pinch your nose with two fingers and hold your breath as long as you comfortably can (or, in case of above-mentioned problems, till the first desire to breathe). 3. Since the feeling of air hunger at the end of this breath holding is not strong, take in as little air as possible, while keeping all, especially chest-shoulders-neck-jaws and diaphragm, muscles completely relaxed. 4. After a short pause completely relax again. That again results in a slow, light, exhalation. 5. Continue to breathe in such a shallow relaxed manner, with constant air hunger for 2-3 minutes. 6. If your symptoms persist, repeat the procedure from steps 1 to 5. Russian medical doctors and practitioners found that usually patients could eliminate their symptoms in 1-5 minutes (Buteyko, 1969). In some cases, especially when patients were severely sick, the Emergency Procedure could not solve the onset of the attack and traditional medication, in a reduced dose, was used. This procedure, unlike discussed Western approaches, uses breath holding, as a natural method of CO2 accumulation. According to individual conditions and preferences, different pauses can be applied. Apart from known breath holds, the CP, the MP, and the EP (expended pause) can be used. The later pause (EP) is between the CP and the MP in duration. The EP is done till some distinctive, not slight and not strong, desire to breathe. In addition to that, some practitioners and patients found the AMP (absolute maximum pause) helpful and effective. The AMP is accompanied by muscular movements (e.g., swallowing/breathing imitations, or stomping, or arms rotations, or fists clenching, etc.) at the end of breath holding in order to prolong BHT. The SP (short pause) is another possible variation. It is shorter, than the CP (e.g.,

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half of your usual CP), and can be the optimum choice for people with some mechanical damage or inflammation in interior organs. The main differences among different pauses are that the longer pauses (the MP and the AMP), on the one hand, accumulate CO2 quicker, but, on the other hand, exert more pressure on internal organs (in terms of suddenly increased blood flow) and make relaxation and the following control of breathing more difficult. Thus, longer pauses are powerful tools, but should be exercised, if one wants to, with caution. When the Emergency Procedure is used in order to increase critically low aCO2 level (as during asthma and heart attacks), the MP and AMP are usually safe. Indeed, first, the pauses are not going to be very long and, second, the initial blood flow to internal organs is dangerously low due to the existing stress state. Therefore, the final intensity of blood perfusion (at the end of the Emergency Procedure) is not going to be hazardous. The effects of these pauses can be different when initial aCO2 is higher since larger final blood flow parameters to internal organs are expected. There are additional practical recommendations in order to have better relaxation. 1. When you are not sure about chest-shoulders-neck-jaws muscles, tense them maximally or almost maximally for 1-2 s and, then, relax. That can be done with the whole area of muscles or, if difficult, with separate muscular groups, one by one. 2. During such tensing-relaxing, clearly and vividly visualise your body or body parts, first, during tensing, as a steel spring, which is hard and strong, and seconds later, during relaxation, as a large soft piece of dough or jelly fish floating in the ocean. Other images, of course, can be used, e.g., first, as an over-inflated water-filled balloon, resilient and firm, which suddenly loses pressure and becomes soft and shapeless and filled with air. 3. You can massage this area (chest-shoulders-neck-jaws muscles) with your hands or, if you have a relative around, ask him/her to do that. During the Emergency Procedure, the relaxation of the diaphragm and skeletal muscles is possible, only if the amount of air in the lungs is near the physiological volume (such a lung state is achieved, when people suddenly lose their consciousness or are properly relaxed). Having more air in the lungs is undesirable, due to the appearance of tightness in respiratory muscles. 6.7 Other possible applications of the Emergency Procedure Apart from preventing attacks, the Emergency Procedure can be used in many other situations, when CO2-deficiency causes problems with different systems and organs of the organism. For example, numerous spasmodic conditions, due to local constrictions of arteries, can be effectively eliminated by means of aCO2 increase. That relates, to cold feet and hands, blocked nose, constipation, etc. Since clear understanding of the mechanisms of CO2 influence is important for final results let us consider constipation as an example. Here is a part of my revised old note, which describes how breathing can be used against constipation. CONSTIPATION Causes Normally, during elimination, the descending colon and all subsequent muscles function together, as a well-trained team. Constipation usually happens as a result of local spasms due to strained muscles and poor oxygenation. Suggested practical actions Relax all muscles (too much strain can lead to diverticuli). Such relaxation will produce spontaneous exhalation. At the end of this exhalation hold your breath as long as you comfortably can. Inhale a small amount of air and breathe during next 1-2 min in a slow, shallow, relaxed manner with constant air hunger. If no progress (rare, but possible), repeat the procedure.

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Physiological foundation Decreased ventilation leads to gradual accumulation of carbon dioxide in the lungs, blood, and all body tissues. Since carbon dioxide is a relaxant of all smooth muscles (see physiol. textbooks), a dilator of the arteries, and a catalyst of chemical release of oxygen from haemoglobin (the Bohr effect), its elevated level naturally produces muscular relaxation and oxygenation removing the spasm and bringing relief. Professor Buteyko suggested to use the Emergency Procedure for many other situations as well: persistent cough, panic attacks, phobias, nocturia, migraine headaches, spasms of the stomach, spasms of the bile duct, edema and eyes' puffiness, and skin itching (Buteyko, 1969). When feeling angry or upset, the Emergency Procedure would help you to calm down excited nerves and become reasonable again. Russian Buteyko practitioner Alexander Stalmatski described the use of the Emergency Procedure for insomnia (Stalmatski, 2001). 6.8 Focal infections Practical application of the breathing exercises in Russia revealed that some existing, relatively minor health problems, if unsolved, could interfere with the ability of patients to increase their CPs or even to recover from relapses of the main disease. Moreover, these problems often caused disappearance of enthusiasm of patients, absence of progress, and therapy quitting. Such situations could take place, when the organism had its own hidden sources of infections, which released pathogens in blood. Typical practical examples of focal infections included degenerated or inflamed tonsils, dental problems (like caries, periodontosis, gingivitis, etc.), intestinal parasites (e.g., worms), and feet mycosis. The detailed mechanism of interaction of these focal infections with the immune system, each other, and the symptoms of the main disease was described by Dr. S. S. Souliagin (1991). Dr. Frank Billings was the most visible Western proponent of the theory of focal infections. He suggested in 1898 that micro-organisms could contribute to numerous diseases. His theory was, first, very popular among medical professionals, but later it was largely forgotten. (For a historical review of his theory one can consult the recent paper “Germs, Dr. Billings, and the theory of focal infection” by R.V. Gibbons published in 1998 in “Clinical Infectious Diseases”). However, numerous recent studies confirmed the connection between local pathological processes and various systemic diseases.

This connection can be better understood in the light of Professor Buteyko’s hyperventilation theory. Normalization of breathing and raised aCO2 increases sensitivity of the immune system, which in the past dealt with the main health problem (e.g., asthma or hypertension). Now, the body defences turn their attention to pathogens released by, for example, degenerated tonsils or teeth bacteria. Thus, previously dormant focal infection becomes the main concern of the more sensitive immune system (Souliagin, 1991). Some readers may recall a statement, which was given above in this chapter, "CP restriction is usually due to the influence of the weakest or most vulnerable part of the body." When the main health problem is eliminated, these focal infectious sources are the main obstacles for health normalization and further aCO2 increase. As Russian doctors found, breathing exercises, although very powerful tools, could not solve problems with existing focal infections. Moreover, their practice revealed, that continuation of breathing exercises and larger CPs and aCO2 values worsen the problem with focal infections. In the case of bad tonsils, for example, high temperature, angina, fever, and throat pain are normal outcomes of increased CPs and an improved immune system. That causes the “rebound effect”: hyperventilation, low CPs and aCO2 undermining determination and discipline of the patients. Moreover, such a reaction of the immune system often makes relapses of the main health problem possible.

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The most successful practical Western methods for treatment, for example, of cancer are typically based on due attention to focal infections. Dr. Josef Issels in his famous book “Cancer: a second opinion” wrote “The emphasis I place on removal of devitalised teeth and chronically-diseased tonsils is one of the better-known aspects of my work, but also one of the most criticised and misunderstood. I do not, for instance, recommend that healthy tonsils and teeth be removed from a healthy person. But I believe if they are diseased, they cause the body’s natural resistance to be lowered, thus acting as an important contributory factor to tumour development. In these cases, I insist on their removal” (p. 117, Issels, 1975). Interestingly, his chart with the title “Hypothesis of pathogenesis of cancer” lists the following causal (or primary) factors for cancer development: foci, teeth, tonsils, fields of natural disturbance, abnormal intestinal flora, faulty diet, chemical factors, physical factors, and psychic factors (p. 53, Issels, 1975). It is possible to see the large overlap between Issels ideas and Buteyko ideas in this area. I separated all these factors in two groups: those described in chapter 3 (these factors can usually be controlled by the person) and the focal infections which need medical attention. Thus, Professor Buteyko not only views the focal infections as factors which contribute, often indirectly, to different pathologies, but he also suggested the mechanism of their influence. The contribution is expressed in increased breathing. If a healthy person, for example, can improve his breathing while, for example, taking a vacation, by exercising, dieting and/or fasting (even without any ideas about importance of normal breathing), the person with any focal infection would not be able to progress beyond about 4.5-5.5% aCO2 or about 20-40 s CP, as the practice of Russian doctors and other practitioners indicate). Later, in times of stress and other negative influences the healthy person may suffer, but he has good chances to recover due to a large safety zone in his breathing, better immunity, and other parameters. The person with already compromised health can quickly deteriorate due to dangerously low aCO2. He is going to affected by those health problems to which he is genetically predisposed. Thus, without preliminary elimination of these local toxic sources, one would not be able to achieve the Buteyko standard of ideal health (6.5% aCO2 or 60 s CP). Focal infections, depending on the type and amount of released toxins and individual sensitivity to them, usually restrict the CP to the region of 20-40 s (Souliagin, 1991). Another finding, described by Dr. Souliagin, is that, since all these focal infections and their symptoms are hidden, often for years, and not manifested due to the symptoms of the main disease, most patients do not have complaints about, for example, their tonsils. When asked about their examination, some patients reacted negatively, while others did not see any necessity to treat them. Ideally, the treatment should be done before starting the Buteyko breathing exercises or, during their initial stages, when aCO2 and the CP are low and the immune system is dealing with the main disease (Souliagin, 1991). Here are some practical steps suggested by Dr. Souliagin and relevant Western studies in these directions. 1. Infectious tonsils can be hypertrophic (enlarged) or atrophic (small), often infiltrated, cyanotic or congested and have accumulation of pus. Most dangerous tonsils are atrophic, hidden behind arches and filled with pus. The tonsils should be examined by a professional. By depressing the root of the tongue with one spatula and pressing on tonsils from down to up with another spatula, the presence of pus in the tonsils can be checked. Normal tonsils are pus-free, of pale-pink colour, of soft-elastic consistency (not hard), and slightly visible behind arches (Souliagin, 1991).

If tonsils are infectious for several years, it was found to be impossible to restore their functional abilities. In this case, tonsillectomy is necessary for breathing normalization. Children who have had infectious tonsils for few years only sometimes can restore them.

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The influence of tonsils on psoriasis was investigated by Japanese dermatologists who found, using a tonsillar provocation test, certain negative biochemical changes in the blood contributing to psoriasis (Mizutani et al, 1997).

Moreover, fever and other complications can be successfully treated by tonsillectomy, as another group of Japanese doctors reported. “Thirty patients (above 18 years) who had complained of low grade fever were diagnosed as having tonsillar focal infection. We performed tonsillectomies on all the patients. A total of 24 were cured and 6 patients improved after the operation. These results indicate that tonsillectomy is often an effective treatment for tonsillar focal infection. However, the provocation test did not always give a good result” (Takeuchi et al, 1996). Thus, all 30 patients in this study benefited from the operation. 2. Dental problems are to be revealed by a dental professional with natural orientation. A recent review by Shay from University of Michigan School of Dentistry suggested that

“Dental caries occurs when acidic metabolites of oral streptococci dissolve enamel and dentin. Dissolution progresses to cavitation and, if untreated, to bacterial invasion of dental pulp, whereby oral bacteria access the bloodstream. Oral organisms have been linked to infections of the endocardium, meninges, mediastinum, vertebrae, hepatobiliary system, and prosthetic joints. Periodontitis is a pathogen-specific, lytic inflammatory reaction to dental plaque that degrades the tooth attachment. Periodontal disease is more severe and less readily controlled in people with diabetes; impaired glycemic control may exacerbate host response. Aspiration of oropharyngeal (including periodontal) pathogens is the dominant cause of nursing home-acquired pneumonia; factors reflecting poor oral health strongly correlate with increased risk of developing aspiration pneumonia. Bloodborne periodontopathic organisms may play a role in atherosclerosis. Daily oral hygiene practice and receipt of regular dental care are cost-effective means for minimizing morbidity of oral infections and their nonoral sequelae”(Shay, 2002).

Use of silver amalgam fillings, which are more than 50% mercury and which are often associated with chronic fatigue syndrome, or use of other metals is not desirable due to possible individual sensitivity to metals (Andrei Novozshilov, Director of Moscow Buteyko Clinic, private communication, 2001).

Serious health complications are expected in case periodontal problems as American authors of the recent article “Periodontal disease and its association with systemic disease” revealed.

“…Currently, there is increasing evidence that the relationship between these entities may be bidirectional. Recent case-control and cross-sectional studies indicate that periodontitis may confer a 7-fold increase in risk for preterm low birth weight infants and a 2-fold increase in risk for cardiovascular disease. These early reports indicate the potential association between systemic and oral health. Additionally, these studies support the central hypothesis that periodontal disease involves both a local and a systemic host inflammatory response. This knowledge of disease interrelationships may prove vital in intervention strategies to reduce patient risks and prevent systemic disease outcomes” (Fowler et al , 2001). Russian publications do not have any suggestions about the impact of root canals on the personal health and breathing. Meanwhile, Christopher Drake, one of the most experienced Western Buteyko practitioners (www.buteyko.com.au/chris.html), while teaching his own patients with multiple sclerosis, noticed that dental caries or presence of dead teeth is their frequent problem. Quick removal of dead teeth, treatment of caries, and robust application of the Buteyko method create favourable conditions for total success at early stages of this disease (Christopher Drake, private communication). Probably, that in cases of individual sensitivity of the immune system to miniscule amounts of toxins released by anaerobic bacteria harboured by kilometres of tiny channels of dead teeth (after root channel operation), no progress (beyond about 40 s CP) in breathing

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normalization is possible, unless the toxic source is eliminated. If such a sensitivity is absent, one may achieve larger CP values. A group of Norwegian dentists checked their 26 patients with asymptomatic apical periodontitis of single-rooted teeth. “…All root canals contained anaerobic bacteria. The frequency of bacteremia varied from 31% to 54%. The microorganisms from the root canal and blood presented identical phenotype and genetic characteristics within the patients examined. These characteristics differed between patients. The present study demonstrated that endodontic treatment can be the cause of anaerobic bacteremia and fungemia. The phenotypic and genetic methods used appeared valuable for tracing microorganisms in the blood back to their origin” (Debelian et al, 1998). 3. Several stool analyses for parasites and their eggs (since many parasites have cycles of eggs laying) are suggested. Note, that more than half of Western people, usually when young, have or had worms. The negative effects of intestinal parasites on host’s immune system are well-documented facts, which can be found in any medical textbook on parasitology. 4. Feet mycosis, if any skin problems on feet are present, should be investigated and treated, according to Souliagin, by traditional methods. “About 15% of the population have fungal infections of the feet (tinea pedis or athlete's foot)” (Bell-Syer et al, 2002), as US researchers report. These infections also seriously affect the immune system.

“…Patients with mycoses of the soles with involvement of the nail plates, as well as those suffering from eczemas combined with mycoses developed a most marked reduction of the activity of the leukocyte migration inhibition factor (LMIF) and of the T lymphocyte mediator activity in the presence of the fungal antigen. The studies have detected the pattern of the leukocyte phagocytic reaction disturbances in the patients with mycoses and eczemas of the soles” (abstract, Iutskovskii, 1989). If somebody can not eliminate these focal infections (e.g., an aged person with severe periodontal disease does not want all his teeth to be pulled out), it is not advisable and even dangerous to increase the CP beyond 30-40 s (Souliagin, 1991). In my view, there are other types of focal infections which are not very prevalent in Russia, but are typical for Western people. These infections, due to pathogens found in blood, should also intensify breathing and restrict the CP in lower ranges (20-40 s). There is no strict medical definition for the term “focal infections”. As a result, the range of infections included varies according to accepted implications of authors. Russian doctors consider infections “focal” if these infections can not be eliminated using the breathing exercises and other auxiliary methods described later.

However, there are certain other infections which can be considered focal. Urinary tract infections are manifested in frequent urination and decreased urine output.

The problem should be addressed with regular and frequent hand washing (to prevent new infections) and chosen methods of treatment.

Candida yeast overgrowth is another “popular” problem which can be dealt with by appropriate diet, fasting, and other measures.

Helicobacter Pylori overgrowth (typically found in patients with gastritis, ulcers, and certain other digestive problems) should also be addressed by diet and other methods.

Some of these infections can become systemic in certain conditions. In addition, there are systemic infection (e.g., Listeria monocytogenes, Streptococcus agalactiae, Mycobacterium, Herpes Simplex, Syphilis, and many more), which also restrict CP and make breathing normalization impossible unless they are treated.

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In all these last cases (not considered by Russian sources) the patients should also seek professional medical advice, while the Buteyko breathing exercises and larger CP values would be very helpful, in order to successfully combat these problems. Q&A section Q: I have a CP of 5 s and I go about normal life fine, and a CP of 60 s seems quite hard to achieve… Am I missing something? A: “Chronic hyperventilation affects everyone differently. Some people get asthma. Some get CFS. Some get chest pains. Some get all of them. It just depends on genetic predisposition.

Even though [there are] people who habitually hyperventilate,[they] may not experience any immediate symptoms. Don’t forget that Alzheimer, motorneurone disease, Parkinson’s etc. have not been understood and nobody knows what causes them. But the hyperventilation theory could [explain them]” (Peter Kolb, private communication, 2002) References for chapter 6 Ayman D & Godshine AD, The breath holding test, a simple standard stimulus of blood pressure, Archiv of Intern Med 1939, 63: 899-906. Bell-Syer SE, Hart R, Crawford F, Torgerson DJ, Tyrrell W, Russell I, Oral treatments for fungal infections of the skin of the foot, Cochrane Database Syst Rev 2002; (2): CD003584. Buteyko KP, Public lecture for Soviet scientists at the Moscow State University, Carbon dioxide theory and a new method of treatment and prevention of diseases of the respiratory system, cardiovascular system, nervous system, and some other diseases [in Russian], 9 December 1969. Courtney-Belford R, Healthy breathing, Australian Wellbeing 1997, 68: 86-93. Debelian GJ, Olsen I, Tronstad L, Anaerobic bacteremia and fungemia in patients undergoing endodontic therapy: an overview, Ann Periodontol. 1998 Jul; 3(1): 281-287. Ford MJ, Camilleri MJ, Hanson RB, Wiste JA, Joyner MJ, Hyperventilation, central autonomic control, and colonic tone in humans, Gut 1995 Oct; 37(4): 499-504. Fowler EB, Breault LG, Cuenin MF, Periodontal disease and its association with systemic disease, Mil Med 2001 Jan; 166(1): 85-89. Funderburk, J, Science Studies Yoga, A Review of Physiological Data, Glenview, IL, Himalayan International Institute of Yoga Science & Philosophy of USA, 1977. Genina BA & Buteyko KP, Treatment of bronchial asthma in children by the method of voluntary normalisation of breathing in Children's Clinic of the 1-st Moscow Medical Institute [in Russian], Pediatria, 1982, 2. Henderson Y, Production of shock by loss of carbon dioxide, and relief by partial asphyxiation, Am J Physiol 1907, 19: XIV-XV. Issels J, Cancer: a second opinion, Hodder and Stoughton: London, 1975.

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Iutskovskii AD, The immune status of patients with foot mycosis and eczema [in Russian], Vestn Dermatol Venerol 1989; (1): 52-57. Lavrent'ev MM, Averko NN, Eganova IA, Hyperventilation as a fundamental stimulator of pathological processes [in Russian], Dokl Akad Nauk 1993 Apr;329(4):512-524. Mizutani H, Ohmoto Y, Mizutani T, Murata M, Shimizu M, Role of increased production of monocytes TNF-alpha, IL-1beta and IL-6 in psoriasis: relation to focal infection, disease activity and responses to treatments, J Dermatol Sci 1997 Feb; 14(2): 145-153. 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. Souliagin SS, Treatment of patients with focal infections using VEDB method [in Russian], in Buteyko method. Its application in medical practice, ed. by K.P. Buteyko, 2-nd ed., 1991, Titul, Odessa, p.56-63. Stalmatski A, Freedom from insomnia, Kyle Cathie Ltd, London, 2001. Takeuchi J, Yagisawa M, Nishimura T, Tonsillar focal infection: clinical observations of low grade fever, Acta Otolaryngol Suppl 1996; 523: 204-205. Zimchenko VN & Romanenko NF, Conclusions on practical trial of Buteyko method, conducted in Department of Radiation Pathology of Central Republican Hospital of Shevchenko region (Ukraine) during 06.03.1990-07.04.1990 [in Russian], in Buteyko method. Its application in medical practice, ed. by K.P. Buteyko, 2-nd ed., 1991, Titul, Odessa, p.222-227.