Cystic Fibrosis in Lungs is Caused by Ineffective Breathing

While the cause of cystic fibrosis in lungs remains the mystery for the mainstream official medicine, most clinical physician and nurses are well aware that with progression of many chronic diseases, cystic fibrosis included, the patient has more complains about dyspnea, breathlessness and difficulty breathing, especially during physical exercise, and chest pain. All these symptoms are signs of chronic hyperventilation that washes out CO2 (carbon dioxide) from the airways and lungs. When alveolar CO2 tension is below the norm (40 mm Hg or about 5.3%), there are several effects on bronchi, bronchioles, and lung tissue. This effects are present even in people without the CFTR gene that is currently implicated as the cause of cystic fibrosis. However, chronic hyperventilation, as decades of medical research indicate, is the necessary factor for the following abnormal changes.

Known effects of chronic hyperventilation on airways and lungs of normal people

- Alveolar hypocapnia (low CO2) immediately causes bronchoconstriction or constrictions of bronchi and bronchioles due to irritation or an excited state of the cholinergic nerve.

- Alveolar hypocapnia destroys lungs tissue. In their study, Canadian doctors observed that "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" (Laffey et al, 2003). Other published studies also reported healing effects of CO2 or "permissive hypocapnia", in cases of mechanial ventilation, on lung tissue (the same effect is present in other vital organs of the human body).

- Chronic alveolar hyperventilation reduces cell oxygen content in all vital organs due to disturbances in oxygen transport.

- Cell hypoxia leads to anaerobic energy production mechanism, elevated lactic acid level in the blood, generation of reactive oxygen species, suppression of the immune system, and cellular damage.

The cause of CF

There are many other known effects of hyperventilation, but this list is sufficient to claim that presence of the faulty CFTR gene in CF does not guarantee pathological changes that are common for CF (the gene is not the cause of cystic fibrosis). However, if chronic hyperventilation is present, the gene can enhance or strengthen these pathological effects.

Then the central question related to CF pathology is following. Is chronic hyperventilation a common finding in CF? The review of medical literature reveals that according to 7 published studies, all tested CF patients demonstrated abnormal respiratory characteristics, while some doctors indeed claimed that "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" (Browning et al, 1990).

Average minute ventilation in CF patients ranged, according to these 7 publications, from 10 to 18 l/min, while healthy subjects have between 6 and 7 l/min at rest (over 20 medical studies all available at www.NormalBreathing.com).

Hence, if heavy breathing is the problem, there are natural therapies available to address chronic hyperventilation and restore normal breathing parameters 24/7 so that to restore normal CO2 level in the lungs and trigger the healing process.

References

Browning I, D'Alonzo G, Tobin M.
Importance of Rf (respiratory rate) as an indicator of respiratory dysfunction in patients with cystic fibrosis.
Chest, 1990 Jun; 97(6): p. 1317-1321.
Department of Medicine; University of Texas Health Science Center, Houston, USA

Laffey JG, Engelberts D, Duggan M, Veldhuizen R, Lewis JF, Kavanagh BP.
Carbon dioxide attenuates pulmonary impairment resulting from hyperventilation.
Crit Care Med. 2003 Nov;31(11):2634-40.
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.

Laffey JG, Engelberts D, Kavanagh BP.
Injurious effects of hypocapnic alkalosis in the isolated lung.
Am J Respir Crit Care Med. 2000 Aug;162(2 Pt 1):399-405.
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.