Lack of Sleep May Increase Genetic Risk for Asthma

According to a sizable UK Biobank study that was recently published in BMJ Open Respiratory Research, poor sleep may increase a person’s genetic susceptibility to asthma, possibly doubling their chance of being diagnosed with the condition.
The researchers hypothesized that, regardless of genetic predisposition, identifying and treating sleep disorders early on might reduce the risks because a healthy sleep pattern appears to be associated with a reduced risk of asthma.
Asthma sufferers frequently complain of interrupted or brief slumber as well as insomnia. However, the researchers note that it is unclear whether sleep quality in and of itself may affect asthma risk or whether sound sleep hygiene may reduce this risk. They drew on 455 405 UK Biobank individuals aged 38 to 73 in order to answer this question.

Five distinct characteristics were used to categorize participants’ sleep habits: early or late chronotype (also known as “morning lark” or “night owl”), sleep duration, insomnia, snoring, and excessive daytime sleepiness. Early chronotype, 7-9 hours of sleep each night, no or infrequent insomnia, no snoring, and infrequent midday sleepiness were all considered indicators of a healthy sleep pattern.

73,223 people had a healthy sleep pattern, 284,267 had an intermediate sleep pattern, and 97,915 had a poor sleep pattern based on their answers.

All UK Biobank participants have their genetic makeup routinely mapped, and for each of the 455,405 participants in this research, a genetic asthma risk score was calculated based on the number of genetic variants associated with asthma in their genome.

A third of the subjects (151,970) and about one-third of them (150,429) were deemed to have “intermediate” genetic risk. The remaining people were deemed to be at “low” danger. Up until the time of an asthma diagnosis, until death, or until March 31, 2017, whichever happened first, participants’ respiratory health was monitored.

17,836 people were given an asthma diagnosis over a monitoring span of just under 9 years. Compared to those who were not diagnosed with the disease, they were more likely to have risk factors that could have a significant impact. These included lower levels of schooling, a higher probability of unhealthful sleep habits, obesity, higher genetic asthma risk scores, higher levels of smoking and alcohol use, high blood pressure, diabetes, depression, acid reflux, and more exposure to air pollution.

During the observation time, diagnoses of asthma were made in 7,105 individuals with a high genetic risk and 5,748 individuals with an intermediate genetic risk. Those at the greatest genetic risk had a 47% higher chance of developing asthma than those at the lowest risk, while those with poor sleep habits had a 55% higher chance.

However, those with both a healthy sleep pattern and a low genetic risk were 122% more likely to be identified with asthma than those with both a healthy sleep pattern and a high genetic risk, or more than twice as likely.

A healthy sleep schedule may help offset asthma risk regardless of genetic susceptibility, the researchers claim. Further in-depth analysis on a smaller group of individuals revealed that a healthy sleep schedule may reduce the chance of asthma in those at high genetic risk by 37%.

The researchers hypothesize that low genetic risk and a healthy sleep pattern may result in 19% fewer instances of asthma at the population level. They give a few potential explanations for their findings and speculate that there may be a two-way relationship between sleep and asthma.

The negative impact of sleep disorders on asthma, which is generally considered a chronic inflammatory disease, might be mediated by sleep-induced chronic inflammation. Previous studies have demonstrated that sleep disorders, such as unfavorable sleep duration and insomnia, are associated with chronic inflammation.

“In theory, the immune response to inflammation could generate pro-inflammatory cytokines that result in cellular infiltration and airway inflammation, further increasing the risk of asthma,” they write.

Since this is an observational study, it cannot determine a reason, and the researchers are aware that their results have several limitations. The impact on children and younger adults is still unknown because the UK Biobank only collected data on people aged 38 to 73. Additionally, the results only apply to people with European ancestry. And finally, there’s a chance that the UK Biobank will only choose “healthy volunteers.”

Nevertheless, the researchers conclude, “Considering that poor sleep combined with high genetic susceptibility yielded a greater than twofold asthma risk, sleep patterns could be recommended as an effective lifestyle intervention to prevent future asthma, especially for individuals with high-risk genetics.”

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