Neat Hypotheses About My Own Asthma

If you live with a chronic disease, you tend to make observations. You get to know your disease. This is especially true when you live with one as long as I have. Personally, I’ve been dealing with asthma for 48 years. So, I’ve gotten to know mine quite well. Here are some interesting observations and hypotheses I’ve made about my asthma.

Hypothesis #1: I have allergic asthma

I think allergic asthma is my subgroup. This is a hypothesis because I have never been tested.

However, I have severe allergies to mold spores, dust mites, animal dander, and pollen. These allergens are my main asthma triggers. Avoiding these allergens helps me to maintain my good asthma control. So, I think my hypothesis would be proven if I am ever phenotyped.

Hypothesis #2: My asthma is Th2 dominant

My asthma responds wonderfully to traditional asthma medicines. So, this means I have Th2 dominant asthma. It’s chemicals released by Th2 cells that respond to my triggers when I’m exposed to them. So, these chemicals cause inflammation.1

They also recruit eosinophils to cause more aggressive inflammation. And these eosinophils are depleted by inhaled corticosteroids. They respond well to them. They also respond well to beta 2 adrenergic medicine.1 This would explain why Symbicort works so well for me.

Hypothesis #3: I have a high leukotriene phenotype

I have a high leukotriene phenotype. Leukotrienes are among the chemicals released by Th2 cells when you’re exposed to allergens. Like histamine, they are mediators of inflammation. They cause airway inflammation.2,3

Antihistamines have no effect on me, but leukotriene antagonists work wonders for me. Along with Symbicort, Singulair helps me maintain good asthma control.

So, my hypothesis is that I have a certain asthma gene. This gene makes extra leukotrienes. Or, it doesn’t make the chemical to shut of leukotriene production. One or the other will produce too many leukotrienes. Singulair renders leukotrienes harmless.4

Hypothesis #4: Singulair helps me

Singulair makes colds less severe when they occur. This is the hypothesis I find the neatest. Colds seem to hit me harder than others in my family. Like, they wipe me out. They trigger my asthma big time.

But, since I’ve taken Singulair, I’ve noticed cold symptoms are minimized. I still get asthma symptoms when I get colds, but they are way less severe than they used to be. So, my hypothesis is that respiratory viruses trigger the release of leukotrienes by Th2 cells. Singulair diminishes the harm they do. So, while colds still slow me down. They don’t knock me down as much as they used to.

What to make of this?

I was accepted to participate in the SARP study several years ago. They wanted to do tests on me. They would have had me do PFTs. They would have done a bronchoscopy on me. They would have sampled my lung tissues. And they would have phenotyped me. I didn’t want to go through all that testing. But, it would be neat to be phenotyped.

In the meantime, I’m left to making hypotheses. And, occasionally I run my hypotheses by my doctor. So far he pretty much agrees with me. What about you? Do you ever create your own hypotheses about your asthma? Has your doctor agreed with you or shot you down? Let us know in the comments below.

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