The 11-year Nord-Trøndelag Health Study (or HUNT) was published in the European Respiratory Journal in February 2017 with interesting results: The ongoing study of 17,927 adults aged 20-65 suggests a clear association between asthma and insomnia.
The HUNT study is a longitudinal population survey quite similar to the survey conducted in the United States known as the NHANES (National Health Assessment Nutrition and Education Survey). Both studies use extensive surveys to collect data from subjects. The data sets are then used by researchers looking for correlations between behaviors and health outcomes.
In the HUNT study, conducted at the Norwegian University of Science and Technology, researchers found that adults with chronic symptoms of insomnia were more than three times likely to develop asthma. This higher risk was independent of factors such as anxiety, depression and other chronic symptoms which might be found concurrently in people struggling with insomnia.
What is not clear from HUNT is whether there is a simple and direct association between the two conditions, or whether co-morbid conditions in each are contributing to the link. Because there are different subtypes among patients with asthma, could there be a stronger correlation between insomnia and specific groups of asthmatics, known as "endotypes?" These asthma endotyptes have distinct pathophysiological mechanisms driving the asthma process. Further exploration of this theory would carry implications with regard to identifying measures that would prevent or lower the risk of asthma, in the presence of ongoing insomnia.
At the start of the HUNT study, none of the participants had asthma. About five percent of the subjects developed asthma during the study follow-up.
The researchers looked at possible theories that would explain why some of the subjects developed asthma. One possible mechanism linking both insomnia and asthma was ongoing inflammation. Though clinically we focus on inflammation of the airways in asthma, we also know that the inflammatory process is systemic and may be initiated by the consequences of insomnia in some select individuals. What else may be at play here?
Studies done on individuals suffering with sleep loss show that there are specific EEG activity patterns, steroid (hormone) secretions, and inflammatory markers that suggest a state of hyper-arousal. This state persists during the night and also persists during the following day, despite the fact that most patients complain about feeling fatigued. Several psychological and physiological factors perpetuate the state of insomnia in these individuals. These factors include negative thoughts associated with the sleep loss that cause a vicious cycle perpetuating the inability to sleep. They know they are not sleeping well, they know it impacts energy and performance, and they worry it will continue — and that worry further interferes with sleep.
This state of hyper-arousal can be construed as the brain “running on empty” after brain fuel and energy are exhausted. This hyper-arousal state interferes with the ability to get sleep, even during the daytime, with the person unable to "shut down" to take a nap. It's also important to note that the brain cannot function optimally while this state of (chronic) fatigue persists. This affects performance, concentration, alertness and memory. There is also reduced attention span.
The best evidence supporting the finding that insomnia instigates inflammation is the observation of increased activation of the adrenal gland as a by-product of insomnia. This gland secretes corticosteroids in response to stress. On the other hand, when someone experiences regular, restorative sleep, especially deep sleep, there is an inhibitory effect on the stress system. How do we connect these findings to an increased risk of asthma?
Asthma is an inflammatory process that results in thickening of the inner layer of the bronchial airways. This inflammatory process can be instigated by irritants that are inhaled, but in the case of asthmatics, there is an exaggerated response. In the presence of chronic insomnia, there are increased levels of pro-inflammatory substances called “cytokines." They include substances called interleukins (Il6, Il7) and tumor necrosis factor (TNF) also found in other inflammatory conditions. Their elevated levels in insomnia are the results of all the processes just explained. Some research postulates that some people develop asthma from inflammation that is not provoked by inhaling air particles but rather from intrinsic factor — possibly due to insomnia, for example. In fact, in the past, people with asthma were grouped into those with “intrinsic” and those with “extrinsic” asthma.
This theory may help to explain why asthmatics called “endotypes” are especially sensitive to insomnia and poor quality sleep. This may also help to give clinicians clues when considering preventive measures (in insomnia) once these individuals are identified as "at higher risk of developing asthma."
In conclusion, the concept of systemic inflammation is being considered in a growing number of disease processes. This may bring about common preventive measures that help to limit some of the triggers to diseases, including asthma.
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