Lousy Sleep Compounds Genetic Risk for Asthma in Adults

Poor sleep patterns and high genetic susceptibility together doubled the risk of asthma development in adults, a prospective study using U.K. Biobank data found.

Individuals in the study who had the highest polygenic risk score (PRS) or were poor sleepers had a 47-55% higher risk for asthma over a median 8 years of follow-up compared with their lower-risk counterparts (low PRS or healthy sleep, respectively), according to Fuzhong Xue, MD, PhD, of the Cheeloo College of Medicine at Shandong University in Jinan, China, and colleagues.

But individuals with both of these risk factors together saw their risk more than double (HR 2.22, 95% CI 1.97-2.49, P<0.001) when compared to the lowest risk group, individuals with a low PRS and a healthy sleep pattern, they stated in BMJ Open Respiratory Research.

While the data do not show causality between sleep and asthma, Xue and colleagues wrote that “sleep patterns could be recommended as an effective lifestyle intervention to prevent future asthma, especially for individuals with high-risk genetics.”

Across genetic risk groups, those with a healthy sleep pattern had a 37-44% lower risk of asthma development over study follow-up:

• Low-risk: HR 0.56 (95% CI 0.50-0.64)
• Intermediate-risk: HR 0.59 (95% CI 0.53-0.67)
• High-risk: HR 0.63 (95% CI 0.57-0.70)

“It has been estimated that 19% of asthma cases in the population could be prevented when the five sleep traits (chronotype, sleep duration, insomnia, snoring and excessive daytime sleepiness) were improved under a causal assumption,” Xue and colleagues said.

The researchers suggested that the inflammatory nature of asthma could be a reason for its relationship with sleep.

“Mechanistically, several possible pathways could explain the role of sleep in the development of asthma. First, the negative impact of sleep disorders on asthma, which is generally considered a chronic inflammatory disease, might be mediated by sleep-induced chronic inflammation,” the group wrote.

“Chronotype, snoring, and sleepiness were all shown to be associated with specific inflammatory reactions,” they added. “Overall, the role of all five sleep traits in the risk of asthma could be partly explained by the mechanism of inflammatory response.”

Data for their study were taken from 455,405 participants enrolled in the U.K. Biobank from 2006 to 2010, including 17,836 who received an asthma diagnosis over a follow-up period of 8.10 years.

Participants were questioned regarding their sleep habits and patterns. Healthy sleep patterns and behaviors in patients included sleeping for 7-9 hours per day, no snoring present, no frequent sleepiness during the daytime, either rare or nonexistent insomnia, and an early chronotype.

Overall, patients had a mean age of 56 years, 54% were women, and 85% were white. Patients with asthma were less likely to sleep 7-9 hours compared with those without asthma (68% vs 74%) and were less likely to never or rarely have insomnia (65% vs 73%), to never report snoring (55% vs 59%), and to have no frequent daytime sleepiness (72% vs 77%; P<0.001 for all).

For genetic risk, the authors calculated PRS using data from non-Biobank participants, and included 17 of 18 single nucleotide polymorphisms significantly associated with asthma in a multi-ancestry meta-analysis. In the study, low PRS was more common in those without asthma (34% vs 28% in those with asthma) while high PRS was less common (33% vs 40%, respectively).

Limitations of the study include that the U.K. Biobank only has data on people ages 38-73, and they are largely of European decent. Also, there may have been errors in self-reported sleep in the observational study, and the authors could not adjust for residual confounders, such as chronic diseases.