Some patients with lung disease fare worse than others. Could sleep explain it?

Flare-ups in COPD linked to sleeplessness, UCSF-led study shows

Peer-Reviewed Publication

UNIVERSITY OF CALIFORNIA - SAN FRANCISCO

A study led by UC San Francisco researchers shows that insufficient or interrupted sleep may have more of an impact than smoking history in patients with a progressive lung disease. 
 
The researchers found that for patients with COPD (chronic obstructive pulmonary disease), inadequate sleep may boost their risk of a flare-up by up to 95% compared to those with good sleep. Over time, these flare-ups, which manifest with worsening shortness of breath and cough, may cause irreversible lung damage, and accelerate disease progression and mortality.  
 
The findings appear online in the journal SLEEP on June 6, 2022. They may partially explain why African American patients with COPD tend to fare worse than white patients, said first author Aaron Baugh, MD, a clinical fellow at the UCSF Division of Pulmonary, Critical Care, Allergy and Sleep Medicine, and the Cardiovascular Research Institute.  
 
“African Americans are over-represented in low-income neighborhoods, where people are less likely to have good quality sleep. They may live in crowded spaces with multiple roommates, and have less comfortable sleeping conditions, such as a couch, and they may work in a job with a varying schedule that lends itself to sleep disruption,” said Baugh, noting that research shows sleep deprivation is associated with a drop in infection-fighting antibodies and protective cytokines.  
 
The researchers followed 1,647 patients with confirmed COPD, who were enrolled in the national, multi-center SPIROMICS study, designed to monitor the progression of the disease and evaluate effectiveness of treatments. Over a three-year duration, the researchers recorded flare-ups, defined as short-term worsening of symptoms requiring treatment, and compared their incidence with self-reported data on sleep quality. 
 
Poor Sleep Raises Risk of Flare-Ups From 25% to 95% 
 
At the start of the study, the average age of the participants was 65 and the average stage of the disease was moderate. Over half of the participants (57%) were male; 80% were white and 14% were African American. All were current or former smokers, who underwent at least one sleep evaluation at enrollment. The researchers found that compared to participants with optimal sleep, those at the base level of poor sleep had a 25% increased chance of a flare-up within the next year, rising to almost 95% within the next year for those with the worst sleep.  
 
This may amount to a more pronounced effect than the impact of smoking over a 40-year period, versus a 60-year period, said Baugh.  
 
As expected, more African Americans reported poor sleep than did white participants: 63% versus 52%. 
 
 “While factors like health insurance coverage or respiratory hazards may play important roles in severity of the disease, poor sleep may gain even more significance when African Americans’ social status improves,” said Baugh. “This can lead to a kind of paradox; in reducing one risk factor, a new risk factor – poor sleep – may take its place.” 
 
Yet-to-be published data will show that African Americans have worse sleep even when socio-economic factors and severity of COPD are accounted for, Baugh said.  
 
Senior author and pulmonologist Neeta Thakur, MD, of the UCSF School of Medicine said that questions about sleep are often overlooked by physicians evaluating patients with COPD. “Sleep hygiene and sleep aids may significantly improve their health,” she said. “Sleep should be considered both in the clinic and at the wider community/neighborhood level, where the structural factors that contribute to worse sleep can be addressed.”  
 

Co-Authors: Please refer to the paper. 

Funding: SPIROMICS was supported by contracts from the NIH/NHLBI (HHSN268200900013C, HHSN268200900014C, HHSN268200900015C, HHSN268200900016C, HHSN268200900017C, HHSN268200900018C, HHSN268200900019C, HHSN268200900020C), and grants from the NIH/NHLBI (U01 HL137880 and U24 HL141762). Please refer to the paper for full disclosures. 
 

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