Cystic Fibrosis in Lungs Is Reversible
with cystic fibrosis in lungs
destroy their alveoli and airways due to their chronic
hyperventilation. Overbreathing is a norm in cystic fibrosis (see the table
below). There are several mechanisms that are responsible for deleterious
effects of hyperventilation on the lung tissue.
Effects of hyperventilation on lungs
While studying the effects of CO2 (carbon dioxide) on lung
tissue a large group of scientists from the Lung Biology Program, The
Research Institute and Department of Critical Care Medicine and Anesthesia,
(University of Toronto, Ontario, Canada) concluded that "CO2 modulates key
physiologic indices of lung injury, including alveolar-arterial oxygen
gradient and airway pressure, indicating a potential role in the
pathogenesis of ventilator-associated lung injury. These effects are
surfactant independent." (Laffey et al, 2003).
Minute ventilation in cystic fibrosis patients at rest
Effects of whole body hypoxia on lungs
showed that the transport of ions of Na and Cl, and water in the
epithelium layers of the lungs depend on oxygen levels (Clerici &
Matthay, 2000; Karle et al, 2004; Mairbaurl et
al, 1997; Mairbaurl et al, 2002 - these references can be found on other
CF pages). This effect is present in all mammals. What about
cystic fibrosis related research? Several medical studies found that the function of
the CFTR (cystic fibrosis transmembrane conductance regulator) gene is directly influenced
by body-oxygen levels, which define concentrations of hypoxia inducible
factor-1 (Bebk et al, 2001; Guimbellot et al, 2008; Yeger et al, 2001; Zheng et al, 2009
- these references are also provided on other CF pages).
hypoxia is a normal outcome of hyperventilation (see links to hundreds of
studies below). Do people with cystic fibrosis hyperventilate? Consider minute
ventilation (how many liters per minute the person inhales) at rest in cystic
Find more details in this YouTube video - Trailer of the Amazon Kindle Book
Hyperventilation and mouth breathing causes drying and overcooling of airways
What are the effects of habitual mouth breathing and hyperventilation? One
study measured the effects of the breathing route on humidity and surface
temperature in airways of normal and CF subjects. During nose breathing, the
nasal passages can
humidify and warm up the incoming flow of air. Mouth breathing leads to
the drying and cooling of airways. For example, during inspiration, the humidity at
the pharynx for nose breathing was about 95%, while for oral breathing it was only 75% (Primiano et al, 1988).
Hence, mouth breathing requires 5 times more water from bronchi and
bronchioles in order to achieve 100% humidity. These doctors
observed that, “… These data suggest that when the rate of evaporation is
sufficiently high, the rate-limiting step may be water transport through the
mucosal tissue and/or secretions. At least for the upper airways, this rate
limitation is more evident for CF patients than for normal subjects.”
An additional effect of hyperventilation
relates to the overcooling of airways, especially in cases of mouth breathing and
coughing through the mouth.
Even stronger effects are expected due to physical exercise with mouth
breathing. All physical activity in patients with
cystic fibrosis must
be done with nose breathing only (in and out).
While measuring the temperature of airways during pulmonary and hyperventilation
tests, a group of Italian doctors discovered that hyperventilation induced a
significant temperature loss (Vitacca et al, 1994). The aim of their study
was to test the usefulness of hygroscopic humidifiers on the secretion
of mucus and on inspired gas temperature in tracheostomized patients. These Italian
doctors found that hygroscopic condenser humidifiers have positive effects
on the thickness and coloring of mucosal secretions: “Statistically significant
differences were found in thickness and coloring of secretions between the
two groups during the period of 10 days. Group 2 showed a significantly
greater trend in number of bacteria than Group 1. The group with the
hygroscopic condenser humidifier showed respiratory function improvement
over time for forced expiratory volume in one second (FEV1) and tidal volume
(VT), maximal inspiratory pressure (MIP), and maximal voluntary ventilation
(MVV) in comparison to the control group, who did not.” In conclusions, they
wrote that hygroscopic condenser humidifiers can be useful, among other
things, to “heat inspiratory airflow, possibly protecting against
temperature loss during a hyperventilation test”.
These results suggest that chronic hyperventilation in cystic
fibrosis also leads to overcooling of airways. In addition, even a
slight drop in temperatures of airways can lead to immune dysfunction and
possible respiratory infections. Overcooling may also contribute to thickness and
coloring of sputum, as the above study suggested. All these effects worsen
cystic fibrosis in lungs.
Other effects of overbreathing on development
of cystic fibrosis and problems in lungs
As we discovered before, CO2 dilates airways
(see links below). Furthermore, reduced CO2 in airways and reduced oxygenation
of the cells will suppress the immune system. Medical studies have found that
low CO2 in airways prevents the repair of lung tissue.
Chronic overbreathing creates cell hypoxia and, hence, suppresses
the immune system due to the production of free radicals and cellular damage, as
well as abnormalities in the metabolism of proteins. It is logical then that
heavy and fast breathing in cystic fibrosis patients leads to the typical
symptoms and features of chronic alveolar hyperventilation, including frequent infections of airways,
coughing, pneumothorax, bouts of bronchitis, sinusitis, and pneumonia,
diarrhea, foul-smelling, greasy stools, severe constipation, rectal
prolapse, liver disease, pancreatitis, diabetes, gallstones, and
Cystic fibrosis in lungs and clinical experience of Russian MDs
Over 170 Soviet
and Russian medical doctors found that cystic fibrosis in the lungs is reversible with breathing
normalization. Meanwhile, people with cystic fibrosis can retrain their breathing and learn how to
breathe differently 24/7 or they are able to change their breathing pattern
using direct means (e.g., diaphragmatic breathing exercises and strictly
nasal breathing during physical exercise) and indirect techniques (like
taping one's mouth at night, prevention of sleeping on one's back, correct
posture 24/7, normal thermo-exchange, etc.). To achieve over 20 seconds for the
morning body-oxygen test is the crucial first step to prevent and reverse
main problems with cystic fibrosis in lungs. By the way, these Russian doctors do not
teach silly forceful coughing techniques for the removal of mucus since it
worsens cystic fibrosis in lungs. (Such coughing techniques are still used by many medical
References: CO2 and cystic fibrosis in lungs
Crit Care Med. 2003 Nov;31(11):2634-40.
Carbon dioxide attenuates pulmonary impairment resulting from
Laffey JG, Engelberts D, Duggan M, Veldhuizen R, Lewis JF, Kavanagh BP.
Am J Respir Crit Care Med. 2000 Aug;162(2 Pt 1):399-405.
Injurious effects of hypocapnic alkalosis in the isolated lung.
Laffey JG, Engelberts D, Kavanagh BP.
Am J Clin Nutr 1999;69:913–9.
Energy expenditure and substrate utilization in adults with cystic
fibrosis and diabetes mellitus
Ward SA, Tomezsko JL, Holsclaw DS, Paolone AM
Respiratory Physiology & Neurobiology 153 (2006) 217–225
Mechanical limitation during CO2 rebreathing in young patients with
Brigitte Fauroux, FrŽedŽeric Nicot, Pierre-Yves Boelle,
Mich`ele BoulŽe, Annick ClŽement, FrŽedŽeric
Lofaso, Monique Bonora
Respiratory Physiology & Neurobiology 152 (2006) 176–185
Respiratory factors do not limit maximal symptom-limited exercise in
patients with mild cystic fibrosis lung disease
Jonathan D. Dodd, Sinead C. Barry, Charles G. Gallaghe
Chest. 1990 Jun;97(6):1317-21.
Importance of respiratory rate as an indicator of respiratory
dysfunction in patients with cystic fibrosis.
Browning IB, D'Alonzo GE, Tobin MJ
For complete abstracts of these studies, click here: Abstracts for cystic fibrosis in lungs.
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