Napping Interleukin-6 Stress Sleep

Napping May Correct Interleukin-6 Changes and the Stress Induction Caused By Sleep Deprivation

Napping – Interleukin-6 – Sleep Deprivation

A study published in the March issue of The Journal of Clinical Endocrinology & Metabolism (JCEM) indicates that short-term napping is able to restore, to a great extent, the neurohormonal and immune changes induced by sleep deprivation.

Insufficient sleep is well-known to be associated with poor attention and performance deficits. It is commonly thought that the most important effect of night-time sleep loss is daytime sleepiness, resulting in cognitive impairment and an increased incidence of errors and transport accidents.

However, sleep deprivation is also increasingly described as inducing an imbalance in metabolic, hormonal, and immune homeostasis, with important public-health relevance. This, in turn, may affect cardiovascular health, and increase the risk of coronary heart disease, impaired glucose tolerance or the development of diabetes (Janet M Mullington et al., 2009). In mice, lack of sufficient sleep resulted in accelerated tumor growth (Fahed Hakim et al., 2014).

The physiological mechanisms linking sleep deprivation and immune and inflammatory changes and leading to the progression of cardiovascular pathogenesis are poorly understood. Under normal physiological conditions, there are low concentrations of cytokines in the blood, except for interleukin (IL)-6, which is a cytokine with hormone-like actions.

Several studies have reported diurnal variations in various cytokines, including IL-6, IL-12 or tumor necrosis factor (TNF)-α, as well as in the leukocyte subset cells that are responsible for their production. The change in inflammatory cytokines, such as IL-6, possibly induced by the enhanced release of the stress mediators, cortisol and catecholamine, is one potential pathway occurring in postsleep deprivation.

Napping – previous research

Napping countermeasures may reduce these deleterious health effects by improving the recovery of the neuroendocrine and immune systems. A population-based study investigated 23 681 individuals and reported that midday napping in healthy working men was inversely associated with coronary mortality after controlling for potential confounders. Previous laboratory studies mainly assessed the countermeasure aspect of napping on vigilance, and to a lesser extent its effects on neuroendocrine stress and immune biomarkers.

Napping (mainly acting on the homeostatic process) is an effective strategy to combat fatigue and sleepiness during long working hours, especially in young people who are more sensitive to sleep loss and show a greater homeostatic pressure postsleep deprivation than do older subject.

However, the effects on neuroendocrine stress and immune responses of a short nap following sleep restriction in healthy subjects are largely unknown.

Napping – the new study

In the JCEM study, Brice Faraut and colleagues from the Paris Descartes University – Sorbonne Paris Cité, Paris, France showed that daytime naps for no more longer than 30 minutes after a night with only 2 h of sleep restores urinary catecholamine and salivary IL-6 levels altered by sleep loss to baseline levels.

This is perhaps the first study in this area as no experimental data have previously reported stress-releasing and immune effects of a multinap protocol in continuously PSG-monitored subjects.

The authors report that a night of sleep restricted to 2h resulted in a 2.5-fold increase in 24h-urinary norepinephrine (noradrenaline) levels, and a reduction of salivary IL-6 levels.

The day after the sleep deprivation, however, two 30 minute morning and afternoon naps were able to reverse the neurohormonal and immune changes induced by a night of poor sleep. These observations substantiate a 2007 study by Vgontzas et al., showing that a short mid-afternoon nap reversed the effects of one night of sleep loss on cortisol and IL-6 changes.

These studies indicate that napping may counterbalance sleep deprivation and its stress-induced effects by restoring the immune and neurohormonal ‘milieu intérieur’ or homeostasis.

Source: J Clin Endocrinol Metab, 2015 Mar;100:E416. doi: 10.1210/jc.2014-2566. Epub 2015 Feb 10.
Read more: JCEM

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