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The Journal of Sleep Research recently published a meta-analysis of human studies related to sleep deprivation and peripheral inflammation. Thirty-five studies and nearly 900 participants (mostly young healthy individuals) were included in this analysis, and inflammatory markers primarily included C-reactive protein (CRP), IL-6, and TNF‐α. Sleep deprivation ranged from one full or partial night to multiple nights of partial deprivation.
Overall, a single night of partial or total sleep deprivation was not associated with a significant increase in inflammatory markers, but deprivation over multiple nights (7-9 nights, with sleep duration limited to approximately 4.3 hours per night) was linked to significant increases in CRP and IL-6. The authors pointed out a number of limitations, such as the lack of diverse age groups, poor randomization in some studies, small study sizes, etc. Yet the takeaway is consistent with a growing body of evidence pointing to a strong link between disease, inflammation, and poor sleep, even after a brief period of limited sleep.
It is difficult to determine causation from short-term studies like those included in this meta-analysis; i.e., is the observed increase in peripheral inflammation driving an increase in disease, especially over longer periods? It may be reassuring that a single night of poor sleep does not appear to trigger an inflammatory response, but many adults have weeks, months, or years of poor sleep, so the potential for a low-level, ongoing source of an altered inflammatory response is quite concerning.
Peripheral inflammation may not even be the only consequence of poor sleep. A recent study (published in the Journal of Neuroinflammation), which used positron emission tomography (PET) among healthy adults (aged 50 to 81), found that while no increase was observed in peripheral inflammation (assessed via plasma CRP), both insufficient and prolonged sleep duration were associated with elevated microglial density across multiple brain regions, marked by translocator protein (TSPO) levels, a biomarker of neuroinflammation. Thus, an impaired inflammatory response in the brain, a hallmark of aging itself, may occur even in the absence of peripheral inflammation. It’s worth noting that excessive sleep duration has been associated with increased mortality and an impaired inflammatory response, but this likely reflects a consequence of an underlying condition rather than a cause. Low sleep duration, in contrast, is quite likely causative.
In addition to many long-term conditions and associated symptoms, sleep duration is also linked to all-cause mortality risk. A meta-analysis of 79 cohort studies, published in Geroscience, found that short sleep duration (defined as less than 7 hours per night) was associated with a 14% increase in mortality risk (compared to 7-8 hours/night). Long sleep duration (9 or more hours per night) was associated with a 34% mortality risk increase, but again, this likely reflects long-term (possibly undiagnosed) illness, for which sleep may be a protective response.
Lastly, small trials suggest that therapies that have a positive impact on the inflammatory response may help prevent the increase in peripheral inflammatory markers following sleep deprivation. Thus, it is possible that the inflammatory effects of poor sleep may be mitigated, at least to some degree, but the long-term outcomes remain to be seen.
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