Cystic Fibrosis Symptoms/Stages Correlate with Cell O2
it was considered on other web pages, dysregulation in the work of the CFTR
mutation gene are caused by low levels of oxygen in body cells by overbreathing in patients with CF. This conclusion
was independently tested and confirmed by three teams of scientists from the USA
and Germany (see the links to these studies in a side menu). These teams also found that the
degree of CFTR mutation gene abnormalities is proportional to the level of
tissue hypoxia and these abnormalities are expressed in cystic fibrosis symptoms and stages of CF gradually leading to the end stage.
Over 200 Russian doctors tested hundreds of people with CF and found that
their body O2 content accurately reflects their health. Let us consider
details of this dysregulation, or effects of cell
hypoxia on symptoms and stages of cystic fibrosis.
Initial symptoms of cystic fibrosis
Clinical evidence of
more than 150 Russian medical doctors teaching breathing retraining
(the Buteyko method and Frolov respiration device) have found that the
initial or very mild symptoms of CF and abnormalities in the work of the CFTR
protein are triggered when the body oxygen level is below
30 s. (We assume here that the person with cystic fibrosis previously had normal
body-oxygen levels and, as a result, he or she did not experience any negative
symptoms.) This stage is accompanied by the appearance and dominance of pathogens in the GI
tract with light symptoms in pulmonary and hormonal areas.
Mild or moderate symptoms (stage 2) of cystic fibrosis
pages of this website refer to 20 s threshold for the body-oxygen test as a very significant
number. It corresponds to appearance of numerous physiological and
biochemical abnormalities in the human body, including cell hypoxia,
suppression of the immune system, problems with protein metabolism and
synthesis of various fundamental substances, including hormones and
neurotransmitters and many others.
In relation to airways, overbreathing causes chronic inflammation,
mucociliary dysfunction, generation of extra mucus (as in asthma and
bronchitis), appearance of allergic reactions and bronchoconstriction. The
effects are mostly triggered by hypocapnia (or CO2 deficiency).
It is suggested here that abnormal breathing parameters affect
the mutated CFTR protein, which is responsible for synthesis of a
protein that functions as a channel for chloride ions and is controlled by
cyclic adenosine monophosphate. Mutations in the transmembrane conductance
regulator gene causes abnormalities of chloride transport across mucosal
surfaces. Defective CFTR gene causes diminished
secretion of chloride ions and increased reabsorption of Na and water across the
epithelial cells. This causes mucus that is thicker and stickier.
More severe symptoms (stage 3) of cystic fibrosis
inflammation and pathological load on the human organism due to
infections further intensify breathing in people with cystic fibrosis. Later
stages are characterized by less than 10 s CP during early morning hours
(the patient has less than 10 s of oxygen in the body; that means they
breathe about 4 times more than the tiny medical norm) or transition to the
pre-final stage in the Buteyko Table of Health Zones.
With less than 10 s CP, even human blood does not resist the spread of
various infections and the whole clinical picture quickly deteriorates.
Involvement in the respiratory system becomes progressive: bronchitis and bronchiolitis
transform into bronchiectasis. Possible complications include hemoptysis and pneumothorax.
Severe dyspnea, strong chest pain and difficulty breathing are frequent
complaints. The clinical picture is worsened by severe abnormalities in CFTR
Severe hyperventilation also promotes development of complication due to
The last stage (stage 4)
less than 5 s CP, as the Buteyko Table of Health
Zones suggests, patients with cystic fibrosis enter into the zone where
they fight with death. Severe alveolar hyperventilation leads to critically
low CO2 levels in airways with frequent development of cor pulmonale (high
blood pressure in the pulmonary arteries and right heart overload). Such
a 0 clinical picture is typical for the end-stage lung disease, which is the
principal cause of death in most patients with CF.
Which CF stages (end stage too) and symptoms are reversible?
Experience of Russian medical doctors with hundreds of people with cystic
fibrosis suggests that it is generally (for most people with CF) possible to slow down their heavy breathing and
move in the opposite direction. Does it work for all stages? Is it easy or possible to reverse the end stages of cystic fibrosis? Find out answers in the bonus content right below here.
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