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A recent study found that low-dose acetylsalicylic acid, commonly known as aspirin, can reduce inflammatory responses caused by sleep deprivation.
The study will be presented at the SLEEP 2024 Annual Meeting.
The results show that previous treatment with low-dose aspirin during sleep deprivation reduced pro-inflammatory responses compared with placebo. Aspirin specifically decreased interleukin-6 expression, COX-1/COX-2 double-positive cells in lipopolysaccharide-stimulated monocytes, and C-reactive protein serum levels.
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“The novelty of this study is that it examined whether we could pharmacologically reduce the inflammatory consequences of sleep restriction,” said lead author Larissa Engert, who has a doctorate in behavioral physiology and is a postdoctoral fellow in the department of neurology at Beth Israel Deaconess Medical Center and the department of sleep medicine at Harvard Medical School in Boston. “We used a nonsteroidal, anti-inflammatory medication because it has been shown to affect specific inflammatory pathways previously shown to be dysregulated by experimental sleep restriction or sleep disturbance.”
The researchers collected data from 46 healthy adults in a randomized placebo-controlled crossover trial with three protocols – sleep restriction/aspirin, sleep restriction/placebo, and control sleep/placebo – each of which included a 14-day stay-at-home phase followed by an 11-day hospital stay. In the sleep restriction/aspirin condition, participants took low-dose aspirin during the stay-at-home phase and the hospital stay. Each hospital stay began with two nights of an eight-hour sleep opportunity. Then, under sleep restriction conditions, participants were exposed to five nights of a four-hour sleep opportunity, followed by three nights of recovery sleep. The control sleep condition provided an eight-hour sleep opportunity during the hospital stay. Sleep and immunological measures were assessed at baseline and at various points during the study.
The data also showed that aspirin decreased the activity of inflammatory pathways in participants who were sleep restricted, as well as decreased the rate of awakening after sleep onset and increased sleep efficiency during recovery sleep, Engert said.
“These findings suggest that it is possible to blunt the inflammatory pathways activated by sleep restriction through pre-emptive administration of low-dose aspirin. This may spur the development of new treatments that specifically target those pathways, and do not exhibit the undesirable side effects associated with aspirin, such as bleeding and stroke. Such treatments could complement behavioral sleep improvement therapies to better prevent or control inflammation and its consequences in people experiencing sleep deprivation,” Engert said.
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