Cystic Fibrosis in Lungs Is Reversible

People with cystic fibrosis destroy their lungs 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.

Hypocapnic effects on lungs

While studying 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).

Effects of whole body hypoxia on lungs

Studies 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 present in all mammals. What about cystic fibrosis related research? Several medical studies found that function of the CFTR (cystic fibrosis transmembrane conductance regulator) gene is directly influenced by body oxygen levels that relates to concentrations of hypoxia inducible factor-1 (Bebök et al, 2001; Guimbellot  et al, 2008; Yeger et al, 2001; Zheng et al, 2009 - these references are also provided on other CF pages).

Tissue 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 fibrosis patients.

Find more details in this YouTube video - Trailer of the Amazon Kindle Book Cystic Fibrosis Can Be Defeated with Higher Body Oxygenation

Hyperventilation and mouth breathing causes drying and overcooling of airways

Mouth breathing causes drying of airways

What are the effects of habitual mouth breathing and hyperventilation? One study measured 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 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.”

Hyperventilation and mouth breathing causes overcooling of airways

An additional effect of hyperventilation relates to 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 cystic fibrosis must be done with nose breathing only.

While measuring 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 secretion of mucus and on inspired gas temperature in tracheostomized patients. These Italian doctors found that hygroscopic condenser humidifiers have positive effects of 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.

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 repair of lung tissue.

Since chronic overbreathing creates cell hypoxia and, hence, suppresses the immune system due to 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 all typical symptoms and features of chronic alveolar hyperventilation that is also present in cystic fibrosis, 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 infertility.

Cystic fibrosis in lungs and clinical experience of Russian MDs

Over 170 Soviet and Russian medical doctors found that cystic fibrosis in 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 doctors do not teach silly forceful coughing techniques for removal of mucus since it worsens health of the patients. (These techniques are still used by many medical professionals.)

Kindle Book "Cystic Fibrosis: Defeated
With Natural Self-Oxygenation Methods"

You probably know that thick mucus is the main culprit in cystic fibrosis. It is caused by abnormal transport of ions (e.g., Na and Cl) and water across the mucosal layers. This thick mucus starts to harbor pathological bacteria and cause GI and respiratory infections. However, you probably do not know that transport of ions and active transport of water is controlled by O2 levels in cells. If O2 is low, then transport of chemicals is going to be defective. This effect was found in all people. CFTR gene just makes the whole picture worse. Therefore, cystic fibrosis develops when tiny pumps that transport chemicals to form mucus have too little oxygen. If you have normal O2 in cells, you will not develop CF symptoms and problems even if you have CFTR gene. It makes total common sense that oxygen is the key factor in active transport of ions and water across epithelial layers. Apart from this, low body O2 suppresses the immune system making respiratory and GI infections much worse. Therefore, the solution to cystic fibrosis is to restore normal body O2 content 24/7.  You can click on the book image to visit the Amazon Kindle store and get this book now.

The main features of this book: - over 160 relevant medical studies - cutting-edge research articles about the cellular causes of cystic fibrosis (low O2 pressure in cells of the body leading to malfunction of ionic pumps that transport ions and water across epithelial layers) - causes of low body oxygenation (ineffective breathing patterns) confirmed by numerous studies - crucial lifestyle factors that lead to ineffective breathing - the outline of the program to restore normal breathing and normal body oxygenation

YouTube video: Trailer of the Amazon Kindle Book "Cystic Fibrosis: Defeated with Higher Body O2"

Cystic Fibrosis Web Pages:
- CFTR Mutation Gene Is Triggered by Cell Hypoxia - Review of medical studies that discovered something that makes common sense: tiny pumps that transport ions across mucosal layers in the respiratory and GI tract require oxygen for their normal work
- Cystic Fibrosis Cause: Each and every study that measured breathing in people with CF found that they have ineffective breathing that reduces body O2
- Cystic Fibrosis in Lungs develops according to laws of physiology and due to effects of hyperventilation
- Cystic Fibrosis Symptoms nicely correlate with their parameters of automatic breathing: those who have faster and deeper breathing have less oxygen and worse symptoms
- Cystic Fibrosis Prognosis depends on one key factor: how they breathe 24/7
- Cystic Fibrosis Life Expectancy and Lung CO2 & Body Oxygenation
- Therapy For Cystic Fibrosis: Treatment with Breathing Retraining
- Cystic Fibrosis Treatment is currently missing its most important part: techniques that lead to breathing normalization and improved O2 concentrations in body cells

Reference Web Pages: Breathing norms, Medical Graphs and Tables about Breathing Rates (Minute Ventilation) and Body Oxygen in Healthy, Normal and Sick People
Breathing norms Parameters, graph, and description of the normal breathing pattern
6 breathing myths 6 myths about breathing and body oxygenation (prevalence: over 90%)
Hyperventilation Definitions of hyperventilation: their advantages and weak points
Hyperventilation Syndrome in the Sick. Table 1. Western scientific evidence about prevalence of CHV (chronic hyperventilation) in patients with various chronic conditions (34 medical studies)
Normal Minute Ventilation in Healthy Subjects: Easy and Light Breathing (14 Studies)
Hyperventilation Prevalence Present in Over 90% of Normal People (24 medical publications)
HV and hypoxia How and why deep breathing reduces oxygenation of cells and tissues of all vital organs
Body oxygen test How to measure your own breathing and body oxygenation (a simple DIY test)
Body oxygen in healthy Table 4. CP (body oxygen level) in healthy people (27 medical studies)
Body oxygen in sick Table 5. CP (body oxygen level) in sick people (14 medical studies)
Buteyko Table of Health Zones with clinical description of most common zones
Morning HV Morning hyperventilation effect or how and why critically ill people are most likely to die during early morning hours

References: CO2 Effects Web Pages
Vasodilation: CO2 expands arteries and arterioles facilitating perfusion (or blood supply) to all vital organs
The Bohr effect How and why oxygen is released by red blood cells in tissues
Cell Oxygen Levels and oxygen transport are controlled by alveolar CO2 and breathing
Oxygen Transport depends on breathing and these two effects (Vasoconstriction-Vasodilation and the Bohr effect) are parts of two diagrams that summarize influences of hypocapnia (low CO2 content in the blood and cells) on circulation and O2 delivery
Free Radical Generation takes place due to anaerobic cell respiration caused by cell hypoxia. Hence, antioxidant defenses of the human body are also regulated by CO2 and breathing
Inflammatory Response is controlled by breathing since hypoxia leads to or intensifies chronic inflammation through over-expression of the hypoxia-inducible factor 1, while normal breathing reduces these processes
Nerve stabilization takes place due to calmative or sedative effects of carbon dioxide in neurons or nerve cells
Muscle relaxation or relaxation of muscle cells is normal at high CO2, while hypocapnia causes muscular tension, poor posture and, sometimes, aggression and violence
Brochodilation - dilation of airways (bronchi and bronchioles) by carbon dioxide, and their constriction due to hypocapnia
CO2: Best Natural Cough Suppressant and "home remedy" since it calms urge-to-cough nerve receptors located in the tracheobronchial tree and larynx
Blood pH regulation and regulation of other bodily fluids
CO2: Lung Damage Healer: Elevated carbon dioxide prevents injury and promotes healing of lung tissues
CO2: Skin and Tissue Healer
Synthesis of Glutamine in the Brain, CO2 fixation, and other chemical reactions
CO2 myth "CO2 is a toxic waste gas" myth
Breathing control How is our breathing regulated? Why hypocapnia makes breathing uneven and erratic?

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References (cystic fibrosis in lungs and )

Crit Care Med. 2003 Nov;31(11):2634-40.
Carbon dioxide attenuates pulmonary impairment resulting from hyperventilation.
Laffey JG, Engelberts D, Duggan M, Veldhuizen R, Lewis JF, Kavanagh BP.
Lung Biology Program, The Research Institute and Department of Critical Care Medicine and Anesthesia, Hospital for Sick Children, Interdepartmental Division of Critical Care, University of Toronto, Ontario, Canada.
OBJECTIVE: Deliberate elevation of PaCO2 (therapeutic hypercapnia) protects against lung injury induced by lung reperfusion and severe lung stretch. Conversely, hypocapnic alkalosis causes lung injury and worsens lung reperfusion injury. Alterations in lung surfactant may contribute to ventilator-associated lung injury. The potential for CO2 to contribute to the pathogenesis of ventilator-associated lung injury at clinically relevant tidal volumes is unknown. We hypothesized that: 1) hypocapnia would worsen ventilator-associated lung injury, 2) therapeutic hypercapnia would attenuate ventilator-associated lung injury; and 3) the mechanisms of impaired compliance would be via alteration of surfactant biochemistry. DESIGN: Randomized, prospective animal study. SETTING: Research laboratory of university-affiliated hospital. SUBJECTS: Anesthetized, male New Zealand Rabbits. INTERVENTIONS: All animals received the same ventilation strategy (tidal volume, 12 mL/kg; positive end-expiratory pressure, 0 cm H2O; rate, 42 breaths/min) and were randomized to receive FiCO2 of 0.00, 0.05, or 0.12 to produce hypocapnia, normocapnia, and hypercapnia, respectively. MEASUREMENTS AND MAIN RESULTS: Alveolar-arterial oxygen gradient was significantly lower with therapeutic hypercapnia, and peak airway pressure was significantly higher with hypocapnic alkalosis. However, neither static lung compliance nor surfactant chemistry (total surfactant, aggregates, or composition) differed among the groups. CONCLUSIONS: At clinically relevant tidal volume, 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.

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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.
Department of Critical Care Medicine and The Lung Biology Program, The Research Institute, The Hospital for Sick Children, University of Toronto, Ontario, Canada.
Mechanical ventilation can worsen morbidity and mortality by causing ventilator-associated lung injury, especially where adverse ventilatory strategies are employed. Adverse strategies commonly involve hyperventilation, which frequently results in hypocapnia. Although hypocapnia is associated with significant lung alterations (e.g., bronchospasm, airway edema), the effects on alveolar-capillary permeability are unknown. We investigated whether hypocapnia could cause lung injury independent of altering ventilatory strategy. We hypothesized that hypocapnia would cause lung injury during prolonged ventilation, and would worsen injury following ischemia-reperfusion. We utilized the isolated buffer-perfused rabbit lung model. Pilot studies assessed a range of levels of hypocapnic alkalosis. Experimental preparations were randomized to control groups (FI(CO(2)) = 0.06) or groups with hypocapnia (FI(CO(2)) = 0.01). Following prolonged ventilation, pulmonary artery pressure, airway pressure, and lung weight were unchanged in the control group but were elevated in the group with hypocapnia; elevation in microvascular permeability was greater in the hypocapnia versus control groups. Injury following ischemia-reperfusion was significantly worse in the hypocapnia versus control groups. In a preliminary series, degree of lung injury was proportional to the degree of hypocapnic alkalosis. We conclude that in the current model (1) hypocapnic alkalosis is directly injurious to the lung and (2) hypocapnic alkalosis potentiates ischemia-reperfusion-induced acute lung injury.

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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
Pediatric Pulmonary and Cystic Fibrosis Centers, Hahnemann
University Hospital, Philadelphia; the Department of Physical Education, Temple University, Philadelphia; and the Department of Physical Education and Exercise Science, Norfolk State University, Norfolk, VA.
Background: The onset of cystic fibrosis–related diabetes mellitus (CFDM) is often associated with a decline in clinical and nutritional status.
Objective: The purpose of this study was to characterize energy expenditure (EE) and substrate utilization during rest, exercise, and recovery from exercise in patients with CF diagnosed with diabetes mellitus.
Design: EE, substrate utilization, minute ventilation, tidal volume, and respiratory rate were calculated by indirect calorimetry during rest; a 30-min, low-to-medium-intensity exercise bout on a treadmill; and a 45-min postexercise recovery period (in reclining position) in 10 CF, 7 CFDM, and 10 control subjects between 18 and 45 y of age.
Results: In all 3 periods, minute ventilation was higher in the CF and CFDM groups than in the control subjects (P < 0.01). During rest and exercise, the CF and CFDM groups maintained EE values at the high end of the normal range of the control subjects. However, during recovery, EE was higher in the CF and CFDM groups than in the control group (P < 0.01).
Conclusions: EE may be higher than usual for the patients with CF and CFDM during periods of recovery from mild exercise or activity because of increased work of breathing consistent with higher ventilatory requirements. This information may be useful for patients receiving nutritional counseling who may choose to exercise regularly, but are concerned about possible weight loss.

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Respiratory Physiology & Neurobiology 153 (2006) 217–225
Mechanical limitation during CO2 rebreathing in young patients with cystic fibrosis
Brigitte Fauroux, Fr´ed´eric Nicot, Pierre-Yves Boelle, Mich`ele Boul´e, Annick Cl´ement, Fr´ed´eric Lofaso, Monique Bonora
Armand Trousseau Hospital, Assistance Publique-Hˆopitaux de Paris, Paris, France
The aim of the study was to determine whether a decrease in the ventilatory response to carbon dioxide (CO2) in children with cystic fibrosis (CF) is related to a mechanical limitation of the respiratory muscle capacity. The ventilatory response during CO2 rebreathing was performed in 15 patients (mean forced expiratory volume in 1 s (FEV1): 37±21% predicted, mean arterial CO2: 41±5 mmHg). The slope of the minute ventilation normalised for weight per mmHgCO2 increment correlated negatively with respiratory muscle output, assessed by the oesophageal (p = 0.002), the diaphragmatic pressure time product (p = 0.01), and the tension time index (p = 0.005). In addition, this slope was correlated with dynamic lung compliance (p < 0.0001) and FEV1 (p = 0.03) but not with airway resistance and maximal transdiaphragmatic pressure. Therefore, an excessive load imposed on the respiratory muscles explains the blunting of the ventilatory response to CO2 in young patients with CF.

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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. Gallagher
Department of Respiratory Medicine and National Referral Centre for Adult Cystic Fibrosis, St. Vincent’s University Hospital, Dublin 4, Ireland
To evaluate whether respiratory factors limit exercise capacity in patients with mild cystic fibrosis (CF) lung disease (mean FEV1 =76±7.7% predicted) we stressed the respiratory system of seven patients using added dead space (VD). Primary outcomes were exercise duration (Exdur) and maximal oxygen uptake (VO2 max). Dyspnoea/leg-discomfort were assessed at end-exercise. Exdur was identical between control and VD studies (520±152 versus 511±166 s, p = NS) as was ¨VO2 max (1.6±0.5 versus 1.6±0.6 L/min, p = NS). Significant resting, sub-maximal and maximal workload increases in minute ventilation (VE) were detected (70.8±13.7 versus 79.5±16.9 L/min, p < 0.05). Analysis of breathing pattern revealed increases in VE were attributable to increases in tidal volume (2.0±0.5 versus 2.2±0.6 L, p < 0.05) with no change in respiratory frequency. There was no difference in dyspnoea/leg discomfort between tests. The increase in VE in response to VD, with no change in Exdur/VO2 max suggests maximal symptom-limited exercise limitation is not primarily limited by respiratory factors in mild CF lung disease. Focused investigation and treatment of non-respiratory factors contributing to exercise limitation may improve exercise rehabilitation in this patient group.

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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.
Department of Medicine, University of Texas Health Science Center, Houston.
Abstract
Bedside measurement of respiratory frequency is commonly performed in a cursory manner and judged to be of little clinical importance. However, in a recent study of patients being weaned from mechanical ventilation, we found that tachypnea was quite accurate in predicting an unsuccessful weaning outcome. The present study was undertaken to examine the relationship between nonobtrusive measurements of respiratory frequency, using a calibrated inductive plethysmograph, and detailed measurements of pulmonary function in 11 adult patients with cystic fibrosis of varying severity. Respiratory frequency was increased in the patients with cystic fibrosis compared with a group of healthy control subjects, as was minute ventilation and mean inspiratory flow. Respiratory frequency was a sensitive predictor of respiratory dysfunction, being significantly (p less than 0.05) correlated with airway obstruction (r = 0.76), hyperinflation (r = 0.52), arterial oxygenation (r = -0.59), rib cage-abdominal discoordination (r = 0.54), and maximum ventilation during exercise (r = 0.66). Despite the presence of tachypnea, the patients did not display shallow breathing; indeed, tidal volume was not correlated with any of the above abnormalities. In conclusion, respiratory rate was a useful indicator of respiratory dysfunction in this group of patients with cystic fibrosis.

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