By Dr. Geoffrey Modest
There have been several articles finding an association between short sleep duration and various infectious diseases. The current study was a better-documented clinical trial supporting this (see SLEEP 2015;38(9):1353–1359). Details:
- 164 healthy adults (94 men and 70 women, mean age 30) volunteered for the study
- These volunteers were monitored for 7 consecutive days for their sleep duration and continuity, both by subjective questionnaires and by wrist actigraphy (which correlates well with polysomnography, the gold standard)
- Then they were given nasal drops containing rhinovirus 39 and subsequently monitored for 5 days in a quarantined hotel. A “clinical cold” was defined if they were both infected and met the illness criteria (objective measures of mucous production and nasal congestion)
Results:
- 124 of 164 participants (75.6%) were infected with rhinovirus (antibody measurements before and 28d after viral exposure, and daily nas
al rhinovirus cultures) - 48 (29.3% of them) developed a clinical cold
- Objective sleep duration (by actigraphy) was associated with an increased likelihood of developing a clinical cold, with odds ratios of developing a cold, as compared to those sleeping >7hrs per night:
- <5 hrs/night had OR=4.50 (1.08-18.69)
- <5-6 hrs/night had OR=4.24 (1.08-16.71)
- 6-7 hrs/night had a nonsignificant OR=1.66 (0.40-6.95)
- These results were independent of prechallenge antibody levels, demographics (e.g. SES, education), season of the year, BMI, various psychological variables (e.g. perceived stress), and health practices (e.g. smoking, physical activity, alcohol)
- Sleep continuity was not associated with developing a cold
- Sleep duration was not related to getting the infection, just in getting sick
I bring up this study for a few reasons:
- This study fits in with the very large literature on stress and diseaseover the past many decades, showing that both acute and chronic stressors, both physical and mental, can create huge changes in both hormones (essentially all hormones are affected), and in immunologic function (esp T cell and natural killer NK cell function), perhaps largely through the effects of the cortisol increases from the stressors. Of note, at least in several studies which directly looked at this: the issue is not so much the intensity of the stressor, but how the stressor is perceived by the person; and the physiologic effect of the stressor (including cortisol levels) is moderated by the degree of social support that the person has (not surprising that there are mediators to the effect of stress on individuals, since people exposed to the same physical or mental stressor often have different physiological reactions to it).
- It brings up the limitations of the “germ theory”. Perhaps the main conclusion (to me) of this study is that infectious diseases (at least the vast majority of them) reflect a complex interplay between the characteristics of the bug and the host response to that bug. It is not just the presence of an external stimulus, but its interaction with the human organism. Not everyone exposed to an organism gets infected (in this study 75.6% actually got infected, though this was not related to decreased sleep) and not everyone who gets infected develops disease (in this study 29.3% got a cold, which was related). In addition, not assessed in this study, there is great variability in the disease severity in those who get the disease, perhaps related to the individual’s immunologic response that is partly determined by the social environment. One summary article noted that even relatively acute sleep deprivation (less than one week) is associated with increases in cortisol, decreases in TSH, increases in prolactin, increases in growth hormone, and increases in ghrelin/decreases in leptin, which might cause the munchies found with sleep deprivation (see http://www.medscape.org/viewarticle/502825, as well as the whole issue of the journal Brain, Behavior, and Immunity, volume 18, 2004 devoted to the hormonal/immunological effects of sleep deprivation). Other studies have found sleep deprivation related to increases in inflammatory markers (e.g. C-reactive protein), down regulation of T cell production of interleukin-2, overall decreased proliferative capacity of T cells in vitro, and decreases in NK cells. Of interest, there seems to be a bidirectional association between sleep deficiency and inflammation, with studies finding that cognitive behavioral therapy for older adults with insomnia leads to decreased levels of systemic inflammation (Sleep. 2014; 37: 1543-52).
- And, as the graph below showed, overall we are getting less sleep over the past 50 years.
- The presumed association between disease and social conditions, by the way, has been articulated for a long time. For example, Virchow in 1879 wrote: “Don’t crowd diseases (epidemics) point everywhere to deficiencies of society?”
(Visited 2 times, 1 visits today)