Sleep Disorders

The Immune System and Sleep Deprivation

Sleep disruption in humans is connected to an array of health-related ailments. There seems to be a direct correlation between sleep and the restorative role it plays on the human immune system. Through comparative research, specific physical effects and underlying mechanisms altered by sleep deprivation are being elucidated. Studies of sleep-deprived animals previously have shown a progressive, chronic negative energy balance and gradual deterioration of health on animals deprived of sleep. An accumulation of data has presented an inverse relationship between sleep and immune health.

Sleep is now viewed by a significant body of researchers as being key for the proper working of the body's defense systems. There is a host of research applied yet it is still not fully understood.

According to A. Zager et,alAm J Physiol Regul Integr Comp Physiol pg;293 during a study to asses the effects of paradoxical sleep deprivation (PSD) for 24 hours/ 96 hours and sleep restriction (SR) for 21 days on a rats ability to activate the immune system the following conclusion was documented:

After recovery sleep, lymphocyte count in axillary lymph nodes grew when rats had rebound sleep after PSD for 24 h, neutrophils increased after PSD 96 h and lymphocytes numbers were higher after SR 21 days. Such alterations during sleep deprivation suggest only minor alterations of nonspecific immune parameters during acute PSD, and a significant impairment in cellular response during chronic SR.

Auto-immune deficiency disease has also been investigated in relation to sleep deprivation. Beatriz Duarte Palma et. Al have done an investigational study called Effects of sleep deprivation on the development of autoimmune disease in an experimental model of systemic lupus erythematosus this study investigated the link between sleep deprivation and the auto-immune disease lupus. New Zealand black and white mice develop a disease that strongly resembles the auto immune disease found in humans (systemic lupus erythematosus) (SLE). The research was driven by the anecdotal observation of sleep deprivation reported in cases of SLE by patients. SLE is an inflammatory disease thought to be brought on by auto-immune defense reaction. The multiple platform was used in the study with healthy mice and was accomplished using 96h of SD when the mice were 10 weeks old. The mice were than studied until they were 28 weeks old blood serum was drawn each fortnight the conclusion was as follows:

The results indicated that mice submitted to sleep deprivation exhibited an earlier onset of the disease, as reflected by the increased number of antinuclear antibodies. However, no statistical difference was found in the other parameters analyzed. According to these results, sleep deprivation could be considered as a risk factor for the onset but not for the evolution of the disease.

This study indicates that sleep deprivation did indeed effect the immune system, by disabling the initial response to the disease.

Phagocyte cells are the white blood cells that protect the body by ingesting phagocytosing this integral part of the immune system has also been shown to be effected by sleep deprivation/disruption. Although this area of study has larger gone uninvestigated there is some research available which references this important cellular correlation, the study done by Carol A. Everson et al focused on the content of neutrophils in the liver and lung tissue of sleep deprived rats. Sleep deprivation in rats was produced for 5 and 10 days by the Bergmann-Rechtschaffen disk method, which has been validated for its high selectivity under freely moving conditions and which was tolerated and accompanied by a deep negative energy balance. Comparison groups included basal conditions and 48 h of sleep recovery after 10 days of sleep loss. The author concluded the following:

The results indicate neutrophil migration into extravascular liver and lung tissue concurrent with cell stress and consistent with tissue injury or infection induced by sleep loss. Plasma corticosterone was unchanged. Recovery sleep was marked by increased lung heme oxygenase-1, increased intestinal MPO activity, and abnormally low corticosterone, suggesting ongoing reactive processes as a result of prior sleep deprivation.

The author goes on to concede that there is not enough research or evidence to make any absolute conclusions regarding correalation.

The majority of the research reports in this field conclude there is a relationship between sleep deprivation/disruption and the body's restorative capacities. SD over longer period of time appears to affect the bodies defenses the greatest.

References

B. D. Palma, A. Gabriel Jr., F. A. B. Colugnati, and S. Tufik
Effects of sleep deprivation on the development of autoimmune disease in an experimental model of systemic lupus erythematosus
Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2006; 291(5): R1527 - R1532.

C. A. Everson
Clinical assessment of blood leukocytes, serum cytokines, and serum immunoglobulins as responses to sleep deprivation in laboratory rats
Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2005; 289(4): R1054 - R1063.

C. Hendricks
Genetic Models in Applied Physiology: Invited Review: Sleeping flies don't lie: the use of Drosophila melanogaster to study sleep and circadian rhythms
J Appl Physiol, April 1, 2003; 94(4): 1660 - 1672.