Lifestyle disease is defined as those health problems that react to changes
Lifestyle risk factors have one common property: they make breathing heavier
and body O2 low. Cell hypoxia is the driving force of lifestyle diseases.
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.
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:
- coronary artery spasms (Nakao et al, 1997) 206 patients, 100% specific;
- bronchial asthma (Mojsoski N & Pavicic F, 1990) 90 patients, 100% specific;
- panic attacks (Bonn et al, 1984; Holt PE & Andrews, 1989; Nardi et al, 2000),
- epileptic absence seizures (Esquivel et al, 1991; Wirrel et al, 1996).
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.
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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