Sleep deprivation as a neurobiologic and physiologic stressor: allostasis and allostatic load
Introduction
From the personal experience of sleep deprivation and then subsequently “getting a good night's sleep,” there can be little doubt that sleep plays a role in maintaining a good mood and cognitive acuity, as well as in promoting physiologic balance and resilience. These impressions are supported by studies of endocrine function and metabolism, as well as from investigations of sleep deprivation effects on cognitive and neural function. This includes research on the brain that shows a variety of substantial changes resulting from sleep restriction, with reversal after recovery sleep. This article reviews selected aspects of the current state of knowledge in this area and then evaluates what is known using the model of allostasis and allostatic load, which emphasizes the “wear and tear” on the brain and body from coping with stress.
Section snippets
Allostasis and allostatic overload
The maintenance of homeostasis is an active process that requires the output of mediators such as those of the autonomic nervous system, and the neuroendocrine and immune systems.
This process is called “allostasis,” or “maintaining homeostasis through change” [1], [2], [3]. The mediators of allostasis work as a nonlinear network (Fig. 1), meaning that too much or too little of each mediator can have harmful consequences by perturbing the entire network. This is because the mediators
Metabolic and hormonal responses to sleep deprivation
Sleep deprivation produces an allostatic overload that can have deleterious consequences. Sleep restriction to 4 hours of sleep per night increases blood pressure, decreases parasympathetic tone, increases evening cortisol and insulin levels, and promotes increased appetite, possibly through the elevation of ghrelin, a pro-appetitive hormone, and decrease in levels of leptin [15], [16], [17]. Proinflammatory cytokine levels are increased, along with performance in tests of psychomotor
Neural responses to sleep deprivation
The brain is the master regulator of the neuroendocrine, autonomic, and immune systems, along with behaviors that contribute to unhealthy or healthy lifestyles, which, in turn, influence the physiologic processes of allostasis [1]. Alterations in brain function by chronic stress can therefore have direct and indirect effects on the cumulative allostatic overload. Allostatic overload resulting from chronic stress in animal models causes atrophy of neurons in the hippocampus and prefrontal
Interpretation
Sleep deprivation studies in animals have involved radically different methods ranging from the flower pot or treadmill to the use of novelty or gentle stimulation for shorter time intervals. In spite of these different methods, which differ in the amount of physical stress, locomotor activity, and other variables, there is a consistent pattern of results for cognitive function, namely, impairment of learning and retention. For the brain, measures of proinflammatory cytokines have shown an
Conclusions
Sleep is believed to be a neural state during which consolidation of declarative memories are taking place [40]. Sleep deprivation, even for the course of the active period of the day, increases the homeostatic drive to sleep, with resulting changes in proinflammatory cytokines and glycogen levels. Moreover, relatively brief deprivation of sleep promotes an exacerbation of these processes with progressively more severe physiologic, neurobiologic, and behavioral consequences as the sleep
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