Lifestyle Disease and Low Body Oxygen
Lifestyle disease is defined as those health problems that react to changes in lifestyle.
Lifestyle risk factors have one common property: they make breathing heavier and body O2 low. Cell hypoxia is the driving force of lifestyle diseases.
For example, when we are stressed, do not exercise, have poor posture or nutritional deficiencies, or eat too much, our breathing at rest become more intensive.
Here are medical facts related to final outcomes of abnormal lifestyle changes.
Minute ventilation rates (chronic diseases)
| All references or
click below for abstracts
|Normal breathing||6 L/min||-||Medical textbooks|
|Healthy Subjects||6-7 L/min||>400||Results of 14 studies|
|Heart disease||15 (~+mn~4) L/min||22||Dimopoulou et al, 2001|
|Heart disease||16 (~+mn~2) L/min||11||Johnson et al, 2000|
|Heart disease||12 (~+mn~3) L/min||132||Fanfulla et al, 1998|
|Heart disease||15 (~+mn~4) L/min||55||Clark et al, 1997|
|Heart disease||13 (~+mn~4) L/min||15||Banning et al, 1995|
|Heart disease||15 (~+mn~4) L/min||88||Clark et al, 1995|
|Heart disease||14 (~+mn~2) L/min||30||Buller et al, 1990|
|Heart disease||16 (~+mn~6) L/min||20||Elborn et al, 1990|
|Pulm hypertension||12 (~+mn~2) L/min||11||D'Alonzo et al, 1987|
|Cancer||12 (~+mn~2) L/min||40||Travers et al, 2008|
|Diabetes||12-17 L/min||26||Bottini et al, 2003|
|Diabetes||15 (~+mn~2) L/min||45||Tantucci et al, 2001|
|Diabetes||12 (~+mn~2) L/min||8||Mancini et al, 1999|
|Diabetes||10-20 L/min||28||Tantucci et al, 1997|
|Diabetes||13 (~+mn~2) L/min||20||Tantucci et al, 1996|
|Asthma||13 (~+mn~2) L/min||16||Chalupa et al, 2004|
|Asthma||15 L/min||8||Johnson et al, 1995|
|Asthma||14 (~+mn~6) L/min||39||Bowler et al, 1998|
|Asthma||13 (~+mn~4) L/min||17||Kassabian et al, 1982|
|Asthma||12 L/min||101||McFadden, Lyons, 1968|
|COPD||14 (~+mn~2) L/min||12||Palange et al, 2001|
|COPD||12 (~+mn~2) L/min||10||Sinderby et al, 2001|
|COPD||14 L/min||3||Stulbarg et al, 2001|
|Sleep apnea||15 (~+mn~3) L/min||20||Radwan et al, 2001|
|Liver cirrhosis||11-18 L/min||24||Epstein et al, 1998|
|Hyperthyroidism||15 (~+mn~1) L/min||42||Kahaly, 1998|
|Cystic fibrosis||15 L/min||15||Fauroux et al, 2006|
|Cystic fibrosis||10 L/min||11||Browning et al, 1990|
|Cystic fibrosis*||10 L/min||10||Ward et al, 1999|
|CF and diabetes*||10 L/min||7||Ward et al, 1999|
|Cystic fibrosis||16 L/min||7||Dodd et al, 2006|
|Cystic fibrosis||18 L/min||9||McKone et al, 2005|
|Cystic fibrosis*||13 (~+mn~2) L/min||10||Bell et al, 1996|
|Cystic fibrosis||11-14 L/min||6||Tepper et al, 1983|
|Epilepsy||13 L/min||12||Esquivel et al, 1991|
|CHV||13 (~+mn~2) L/min||134||Han et al, 1997|
|Panic disorder||12 (~+mn~5) L/min||12||Pain et al, 1991|
|Bipolar disorder||11 (~+mn~2) L/min||16||MacKinnon et al, 2007|
|Dystrophia myotonica||16 (~+mn~4) L/min||12||Clague et al, 1994|
Note that advanced stages of asthma can lead to lung destruction, ventilation-perfusion mismatch,
and arterial hypercapnia causing further reduction in body oxygen levels.
Furthermore, since more than 90% of modern normal people also have abnormal breathing parameters and reduced body-O2 levels (see references below), it is logical that we have got an explosion of lifestyle disorders during the last several decades.
The negative effects of ineffective automatic breathing and resultant low body-oxygen levels are found in all people with hyperventilation. However, the degree of these problems and their personal symptoms (what is felt) are individual. In some people, hyperventilation affects mostly the nervous system, in others the cardiovascular system, or the respiratory, or the digestive, or the hormonal system, or their combinations. There are people who experience a wide range of negative physiological effects, while some individuals can be less affected. The particular problems depend on genetic makeup (or hereditary predisposition), lifestyle factors, and environmental influences. Hence, development of lifestyle diseases requires some abnormalities in O2 transport and breathing.
Now we are going to consider and prove our old ideas using another method: use of conclusions from medical research studies devoted to the hyperventilation provocation test. What is the method to provoke chronic lifestyle diseases? It is very simple and under your nose.
Lifestyle disease: voluntary hyperventilation often triggers symptoms
Yugoslavian doctors from Zagreb asked 90 asthmatics to do voluntary overbreathing (Mojsoski & Pavicic, 1990). All patients (100%) experienced symptoms of asthma attacks (chest tightness, wheezing, feeling of suffocation and lack of air).
In 1997, the American Journal of Cardiology published results of a similar study with the title, Hyperventilation as a specific test for diagnosis of coronary artery spasm (Nakao et. al, 1997). Over 200 heart disease patients were asked to hyperventilate, and as you probably guessed, all of them had coronary artery spasms (or symptoms of impending heart attacks).
Here is a short summary of medical studies regarding different health
conditions, number of patients investigated, and the percentage of patients who
reproduced their specific lifestyle health problem:
Similarly, people with histories of, for example, migraine headaches also experience their specific symptoms. If breathing more can provoke these problems, is it possible that breathing less can prevent them?
Hence, the hyperventilation provocation test can and does reveal "bad" genes in the sick. Lifestyle risk factors produce the same physiological effect: our breathing becomes heavier, either temporarily or chronically, depending on particular parameters.
Furthermore, lifestyle diseases are prominent when a person has less than 20 seconds for the body-oxygen test. The medical norm is about 40-60 seconds, and this level of oxygenation protects from lifestyle diseases.
Hence, style of living disorders are controlled by - and develop or disappear due to - changes in breathing.
Related web page: Human genetics and lifestyle diseases.
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.
Esquivel E, Chaussain M, Plouin P, Ponsot G, Arthuis M, Physical exercise and voluntary hyperventilation in childhood absence epilepsy, Electroencephalogr Clin Neurophysiol 1991 Aug; 79(2): p. 127-132.
Holt PE, Andrews G, Provocation of panic: three elements of the panic reaction in four anxiety disorders, Behav Res Ther 1989; 27(3): p. 253-261.
Mojsoski N, Pavicic F, Study of bronchial reactivity using dry, cold air and eucapnic hyperventilation [in Serbo-Croatian], Plucne Bolesti 1990 Jan-Jun; 42(1-2): p. 38-42.
Nakao K, Ohgushi M, Yoshimura M, Morooka K, Okumura K, Ogawa H, Kugiyama K, Oike Y, Fujimoto K, Yasue H, Hyperventilation as a specific test for diagnosis of coronary artery spasm. Am J Cardiol 1997 Sep 1; 80(5): p. 545-549.
Nardi AE, Valenca AM, Nascimento I, Mezzasalma MA, Lopes FL, Zin WA, Hyperventilation in panic disorder patients and healthy first-degree relatives, Braz J Med Biol Res 2000 Nov; 33(11): p. 1317-1323.
Wirrel CW, Camfield PR, Gordon KE, Camfield CS, Dooley JM, and Hanna BD, Will a critical level of hypocapnia always induce an absence seizure? Epilepsia 1996; 37(5): p. 459-462.
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