Sleep, Don't Sneeze: Longer Sleep Reduces the Risk of Catching a Cold

Catching a common cold can temporarily turn everyday life into an annoying, unpleasant condition. People spend substantial efforts to avoid this state, and many of us are probably aware of the link between a running nose and a preceding period of insufficient sleep. Indeed, conventional wisdom tells us that those who are well rested are better equipped to avoid an infection. It is all the more surprising that only now, in the current issue of SLEEP, Prather and colleagues present the first solid scientific evidence that sleep makes us more resistant to the common cold.¹ They measured sleep via wrist actigraphy in 164 women and men over 7 consecutive days. Afterwards, participants received nasal drops containing a cold-inducing rhinovirus and were isolated and kept in quarantine in a local hotel. The development of a clinical cold, conceptualized as an infection in the presence of objective signs of illness, was monitored over 5 days. Infection was defined as persistence of the challenge virus or elevated virus-specific antibody titers, and signs of illness were determined each day by measuring nasal mucus production and nasal clearance time. The authors found that participants who slept 6 hours or less during the pre-infection 7-day interval had a 4-fold higher risk of developing a cold than subjects who had slept more than 7 hours per night. Of note, sleep fragmentation was unrelated to developing the cold.

So far only a handful of human studies have addressed the question whether lack of sleep increases the organism's susceptibility to infectious illness. None of these studies objectively measured sleep behavior, and only one of them by the same group² excluded possible interfering infections by quarantining the participants after experimental infection, which was what was done in the current study. Another study conducted in healthy women found self-reported short sleep was associated with an elevated pneumonia risk assessed over 4 years.³ Likewise, healthy men and women reporting less than 7 hours of sleep in the weeks before exposure to a rhinovirus had a nearly 3-fold higher cold risk compared to those reporting 8 hours or more.² Although substantially contributing to our knowledge about the importance of sleep with regard to infectious risk, these studies were based on self-reported sleep, which can substantially differ from objective sleep measures, even in healthy young adults.⁴

Unlike other studies analyzing the effect of sleep on single immune parameters such as cytokine production or natural killer cell activity in vitro, the assessment of nasal clearance and mucus production by Prather¹ aimed at examining the full-blown acute immune response to the viral challenge in vivo, thus ensuring high external validity. Due to the prospective-correlational design of the study, which did not actively manipulate sleep duration, causal inferences in a strict sense need to be made with caution. However, the results nicely complement and corroborate experimental data indicating that sleep manipulation strongly affects distinct immune parameters, including leukocyte numbers, cytokine production, and cytotoxic activity of immune cells.^5–7 Whereas short-term total sleep deprivation of only a single night seems to primarily compromise adaptive immune functions, as has been revealed in several human studies relying on vaccination as an experimental model of acute infection,^8–10 prolonged sleep restriction induces an immunological condition mainly characterized by small but distinct increases in inflammatory markers.¹¹ This is often referred to as “low-grade inflammation,” and it is of major clinical relevance because it has been associated with an increased risk of developing severe afflictions like diabetes mellitus and cardiovascular diseases.^12,13 Increases in inflammatory markers have also been observed in habitual short sleepers and patients with primary insomnia,^14–17 and might represent a mechanism that mediates also increased susceptibility to clinical signs of common cold infections.

Interestingly, when Prather¹ separately analyzed the two components of a clinical cold (i.e., [1] infection indicated by the persistence of the challenge virus or elevated virus-specific antibody titers, and [2] signs of illness defined by mucus production and nasal clearance), sleep duration was not associated with the rate of infection, but seemed to be more related to illness expression. Although ceiling effects cannot be excluded—75% of the participants were infected after administration of the rhinovirus—the lack of a relationship between infection rate and sleep duration suggests that sleep does not primarily affect the very first lines of defense, such as the mucosal barriers. Instead, in subjects with less sleep the local inflammatory processes responsible for illness expression might be overreacting, which fits with the above-mentioned evidence that prolonged sleep curtailment induces signs of low-grade inflammation. Thus, habitual sleep loss might disturb the delicate balance between pro- and anti-inflammatory processes, which is essential for conferring an effective immune response to infectious agents that is appropriately limited in time and space. Disruptions of this homeostatic process might not only lead to an overshooting acute immune response but, on the long run, also increase the risk of developing inflammation-related disorders. It is worth noting that elderly people not only often present reduced sleep, but typically also show impaired immune responses,¹⁸ which tempts to speculate that aging-related changes in sleep behavior causally contribute to the development of low-grade inflammation and associated morbidity and mortality. Of course, this hypothesis requires further elaboration in experiments that are based on the study by Prather¹ and that directly examine the effects of prolonged sleep restriction on inflammatory markers and possible hormonal mediators of inflammatory processes following an acute infection.

In the central nervous system, sleep has a twofold function for information processing: on the one hand, sleep, particularly slow wave sleep, fosters the consolidation of memories encoded during preceding wake phases.^19,20 On the other hand, sleep enhances the encoding and immediate processing of novel information during subsequent wakefulness.²¹ This beneficial janiform effect of sleep might well pertain also to the immune system. There is now compelling evidence that sleep after an infection supports the development of an adaptive immune response that ultimately forms effective antigenic long-term memories.⁶ On the other side, there are early hints that sleep supports the encoding and immediate containment of an antigenic challenge.^22,23 Indicating a reduced risk of full-blown illness in well-rested people, the findings of Prather¹ add to this latter function of sleep. Seen from a broader perspective, their findings further the notion that sleep not only benefits the brain, but basically all those organismic systems that serve the processing of environmental information.²⁴

CITATION

Besedovsky L, Born J. Sleep, don't sneeze: longer sleep reduces the risk of catching a cold. SLEEP 2015;38(9):1341–1342.

DISCLOSURE STATEMENT

The authors have indicated no financial conflicts of interest.