In dreams, responsibility begins...


Music In Dreams Blogs

Music Libraries



About Us

Contact Us


Asthma Update

Asthma Pathogenesis

Speaking of asthma and environment and dehydration, anyone who lives or works in dry environments or when drastic climate change promotes the development of inflammation in our bodies through the mechanism triggered by chronic water deficiency.  Insensible water loss is enhanced when an individual lives in dry, cold and hot environment through skin (sweat) and breathing (respiration).  The insensible water loss through breathing can be observed especially during cold or winter season, i.e., a person walking inside a big freezer or outside in a snowy winter blowing water mist through the nostrils.

Sick homes and buildings with poor ventilation that causes excessive dryness of skin and mucus membranes, less air moisture, etc. promote inflammation due to uncompensated insensible water loss in the body which is also seen in chronic water deficiency.  Exacerbation by allowing complex mixtures of organic substances, i.e., cleaning products, fragrance, pollens, etc., may trigger more signs and symptoms of wheezing due to chronic water deficiency. 

On high altitude, where the air is extremely dry usually around 10 o 20 percent humidity, high altitude air does not have much moisture, so your eyes, throat, skin, and nasal passages can start to feel dry which may cause nosebleeds.  This may also cause the air pipes to bronchoconstrict or tighten.  Since the lung(s) is 80% water, what the lung does to maintain hydration of the respiratory system is to conserve further water loss.

The proposed involved mechanism of asthma is attributable to the bronchoconstriction of the tracheobronchial tree (tightening of the air pipes) to decrease further water loss through breathing in hyperosmolar state as seen in chronic water deficiency.

It has been known that the tracheobronchial vasculature (blood supply to the air pipe) consists of a subepithelial capillary network and a deeper system of blood sinuses or capacitance vessels.  There seem to be no arteriovenous anastomoses.  Sympathetic nerves constrict the vasculature by the neurotransmitters noradrenaline and neuropeptide-Y, and parasympathetic nerves.  It is dilated by acetylcholine and VIP (vasoactive intestinal polypeptides), as well as neuropeptides including substance P released by sensory nerves.  In addition, inflammatory mediators (histamine, etc.) are also involved as vasodilator.

In asthma, mucosal vasodilatation may be due to the direct action of inflammatory mediators on vascular smooth muscle, neuropeptides released by axon reflexes in sensory nerve receptors, and possibly reflex vasodilation due to stimulation of sensory nerves.  The vasodilation increases the thickness of the mucosa, both by vascular engorgement and by increased interstitial fluid volume.  This mucosal thickening will narrow the airways and increase the rigidity of the tracheobronchial wall.  Nevertheless, the vascular bed is vasodilated by hyperosmolality and other factors, i.e., cold, exercise, etc. which could also cause hyperosmolality due to dehydration.

Hyperosmolar effect in atopic bronchial asthma and preclinical stage of bronchial asthma was also linked to the adrenergic and histaminergic systems.  In exercise-induced asthma, the pathophysiology is unknown.  However, studies have shown that measurement of plasma osmolality is elevated.  It is known that during exercise or exertional physical activities, increased sweat loss, as well as increased insensible water losses contributeto plasma hyperosmolality or dehydration.

Moreover, airway dehydration and subsequent hyperosmolality of periciliary fluid are considered critical events in exercise-induced bronchoconstrition.  In addition, it has been shown that an in-vitro hyperosmolar stimulation of bsaophils and mast cells with mannitol and saline solution can induce the release of histamine and leukotrienes.  Osmoregulators and inflammators, i.e., histamine, that cause vasodilation and opening of the tight junctions allow leakage of fluids into the interstitial space.  In terms of pathophysiology, hyperosmolality causes vascular engorgement and increased interstitial fluid volume, which increases the thickness of the bronchial mucosa.  This bronchial mucosal thickening narrows the airways and increases the rigidity of the bronchial walls.

Simply, in asthma attacks, it causes the blood vessels to dilate and to leak fluids around the breathing pipes because of osmoregulators and inflammators released during hyperosmolar state as in chronic water deficiency.  In so doing, it causes edema or swelling of the breathing pipes, and the lumen or the inside of the breathing pipes becomes narrow.  Narrowing of the breathing pipes cause increase airway resistance, forcing the air to pass through a tight lumen or air passages, and this causes a wheezing sound during exhalation.

Proper hydration is important in asthmatics in general, as well as in exercise-induced asthma to prevent the release of osmoregulators and inflammators of dehydration.  Hydration before and after activity may prevent the attack.  Of course, avoidance of allergen and other substances that may trigger inflammation are also necessary in preventing bronchial asthma.

How do you approach in treating asthmatics now since it is mostly a dehydration-related condition?  First, do not stop the asthma medications.  In addition, institute the RDA for water to the patient, and he or she may take extra water in special circumstances as mentioned in the book (Diseases of Unknown Origin)  as well as proper diet and sea salt intake (AHA).  Frequent follow-up is important in assessing asthma severity and in tailoring asthma medications.  With proper hydration, asthma symptoms usually improve in less than a month or two.  Then, asthma medications may only be necessary as a stand-by meds.

Ref:  "Diseases of Unknown Origin, The Abandoned Theory" by Eliasar A. Simon, M.D.