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Five Theories Explaining Nocturnal Asthma

Nocturnal asthma is an asthma subgroup. It affects up to 75% of asthmatics.1 It’s definitely not a new subgroup, as even ancient physicians recognized it. Despite it being around over 800 years, what causes it remains poorly understood. Still, modern researchers have developed some neat theories. So, here’s 5 theories attempting to explain nocturnal asthma.

Theory #1: Melatonin

This hormone is secreted by the pineal gland in the brain. It’s secreted at nighttime. Levels start increasing in the evening and peak around midnight. It helps induce sleep. Melatonin levels at night are higher in children and decrease with age. So, to help induce sleep, many people take melatonin supplements at bedtime.2-3

There is scanty evidence linking melatonin to nocturnal asthma. Still, there are at least two studies linking the two.

Findings from first melatonin study

The first was published in 2003. It was conducted by National Jewish Health researchers. Their study linked higher levels of melatonin with increased airway inflammation while sleeping.3

The study did not necessarily link this with asthma. However, the researchers concluded that “all patients with asthma should avoid using melatonin supplements until more is known about their safety.”3

Findings from second melatonin study

Another study was published in 2012. It showed similar results to the 2003 study. Like the previous study, there was no specific link to asthma. But, still, there is the potential that melatonin may act as an asthma trigger. Further studies are needed.4

Theory #2: Nitric oxide (NO)

Various studies show that exhaled NO levels drop when bronchospasm is present. Some studies did show that patients experiencing nocturnal asthma had lower NO levels. It’s possible that NO is a natural bronchodilator. When it drops, bronchoconstriction occurs.

There is another idea on nitric oxide that I like a little better. This one is that NO is indirectly the cause of bronchoconstriction. NO breaks down by combining with oxygen. The resulting molecule is peroxynitrite. This molecule is thought to cause oxidative stress. This is thought to cause the release of proinflammatory chemicals (like IL5 and IL13). These, in turn, cause airway inflammation. This inflammation in turn makes airways hypersensitive. This makes airways more sensitive to asthma triggers, which causes bronchoconstriction.1,5-6

Theory #3: B2 and glucocorticosteroid receptors

B2 receptors are beta 2 adrenergic receptors. They line bronchial smooth muscles. Beta 2 adrenergic medicine is attracted to them. These include medicines like albuterol and levalbuterol. They attach to B2 receptors. This tells bronchial smooth muscles to relax. This causes airways to open up. This makes breathing easier.

Glucocorticoid receptors are what corticosteroids attach to. Inhaled corticosteroids (ICS) are commonly used to treat and control asthma. They reduce the immune response that causes airway inflammation. And this makes airways less sensitive to asthma triggers.

B2 Adrenergics and ICS are front line asthma medicines. Studies show these medicines work less well in people experiencing nocturnal asthma. So, a theory arose that these receptors decline in number during sleep. This limits the ability of natural anti-inflammatory and bronchodilator chemicals, resulting in asthma symptoms. This also limits the effect of front line asthma medicines.1

Theory #4: Less cortisol production

Corticosteroids are synthetic cortisol (hydrocortisone). Cortisol is a naturally occurring hormone. It’s produced by the adrenal glands. These are tiny organs above each kidney. Cortisol attaches to corticosteroid receptors in our lungs. It naturally reduces airway inflammation. They do this by suppressing eosinophils. Cortisol also stimulates the release of another hormone called adrenaline. Adrenaline attaches to B2 receptors. It’s a natural bronchodilator.7,8

Some studies show cortisol levels are diminished in nocturnal asthmatics. So, eosinophils remain high and cause persistent airway inflammation. If this theory holds true, it may explain the loss of lung function at night.1

ACTH and cortisol secretion

This theory blames the pituitary and adrenal glands. The pituitary gland is a pea-sized organ. It’s in your brain behind the base of your nose. It secretes a hormone called adrenocorticotropic hormone (ACTH). Sometimes it’s called corticotropin.

They have other functions throughout the body, but a significant one in our case is traveling to the adrenal glands. In turn, they stimulate the adrenal gland to secrete more cortisol. So, It’s ACTH that tells the adrenal glands how much cortisol to secrete.1, 8

The theory speculates that the ACTH impact on the adrenal gland is blunted. This occurs in people with nocturnal asthma. If true, this may explain lower cortisol levels in nocturnal asthma. In turn, this may explain increased inflammation and lower lung function.1

Theory #5: Other causes

Allergens

There may be allergens such as dust mites or animal dander in your room. When you’re sleeping, you may be inhaling them. If these are in your bed or on your pillow, you may be directly inhaling them.

GERD

Gastrointestinal reflux (GERD) may be a cause. This causes gastric contents to creep up your esophagus when you’re lying down. So, gastric juices may creep into your lungs, thereby triggering asthma.

Obesity

Obesity may contribute to nighttime asthma. The exact cause there is also unknown.

What to make of these theories explaining nocturnal asthma?

Any of the above-mentioned theories explaining nocturnal asthma may make asthmatics more sensitive to these triggers. As you can see, researchers have been thinking hard about nocturnal asthma. They have been studying it. They have created these real theories.

The idea is that further studies will confirm or contradict these theories. The ultimate goal is this research will hopefully lead to better treatment options for nocturnal asthma. This is all an attempt to help all asthmatics obtain ideal asthma control.

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This article represents the opinions, thoughts, and experiences of the author; none of this content has been paid for by any advertiser. The Asthma.net team does not recommend or endorse any products or treatments discussed herein. Learn more about how we maintain editorial integrity here.

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