
Asthmatics have increased inflammation of the airways. But why does this lead to asthma?
An article in the journal, Mucosal Immunology, sums up the established thinking.
Airway inflammation is thought to contribute to asthma pathogenesis, but the direct relationship between inflammation and airway hyperresponsiveness (AHR) remains unclear.
In other words, the reason inflammation causes asthma is not known. So let’s try to solve this mystery.
When an unmedicated asthmatic person does vigorous aerobic exercise for half an hour, three or four times a week, the symptoms of asthma can rapidly diminish. The tendency for the airways to constrict can be almost eliminated, and startlingly, the sensitivity to allergy triggers such as dust mites also decreases.
So what’s going on? My hypothesis – that toxic mucous triggers the constriction of the airways – fits this scenario. The aerobic exercise removes the mucous, and the toxins, from the lungs, causing a rapid improvement in asthma symptoms.
The interesting point here is that although the asthma symptoms make a vast improvement, the underlying level of inflammation in the airways remains unchanged. Inflammation levels can be measured with a breath test known as the inhaled nitric oxide (eNO) test. When an eNO test is conducted before and after the asthmatic person begins and extended course of aerobic exercise over a period of months or years, it shows that the inflammation of the airways stays the same.

This indicates that inflammation is not directly causing asthma. The pathway from inflammation to asthma must be a multi-stage process. If you block any one of those stages – like taking steroid medication to control the inflammation, or removing the mucous, or eliminating the fungi and bacteria that cause the toxins – you will reduce or eliminate the symptoms of asthma.
And why do the allergic symptoms also decrease with prolonged aerobic exercise? Even chronic sinusitis (a blocked nose) that becomes inflamed by pollen and other allergens improves.
Let’s think about what’s happening. We are reducing the level of microbes and their toxins, and that in turn reduces allergic sensitivity. Could it be that the microbes are causing allergic sensitivity in asthmatics?
My guess is that any chronic inflammation of the airways will cause an increased level of mucous, which becomes toxic and causes asthma symptoms such as bronchospasm. There are likely to be multiple causes of that inflammation, mostly due to microbial infection of the lungs, but also environmental toxins and chemicals. It’s probable that severe and extreme exercise – such as that done by elite athletes – also causes inflammation of the lining of the lungs, resulting in increased mucous production and asthma.
But sometimes, I think the asthma establishment gets the role of inflammation wrong. According to Asthma UK, increasing inflammation is why asthma gets worse at night:
Asthma symptoms, especially coughing, are often worse at night, especially if the condition is not diagnosed or well managed. This is because the natural process your body uses to control inflammation (including inflammation in your airways) tends to switch off while you’re asleep.
I feel my theory about toxic mucous fits the situation better than Asthma UK’s proclamation about inflammation. You see, when we go to sleep, we move from a vertical to a horizontal position. The toxic mucous migrates to new tissue, triggering constriction and an asthma attack. Many asthmatics have died at night as a result of this.
I believe this is also the reason why a symptom in the early phases of asthma is a ticklish cough. It’s that toxic mucous reaching new tissue again. Interestingly, the ticklish cough can also reappear when asthma symptoms and mucous levels are subsiding, as the edges of the mucous pool alternate between touching and then not touching the surrounding tissue.
The very basic principles of asthma, and the link between inflammation, allergy, microbes and mucous need to be rethought. We need more research about the lung microbiome, and the toxins that develop in the lungs of asthmatic sufferers. Hopefully the ideas expressed in this article can trigger that change in direction.
