Abstract
Sleep has important homeostatic functions, and sleep deprivation is a stressor that
has consequences for the brain, as well as many body systems. Whether sleep deprivation
is due to anxiety, depression, or a hectic lifestyle, there are consequences of chronic
sleep deprivation that impair brain functions and contribute to allostatic load throughout
the body. Allostatic load refers to the cumulative wear and tear on body systems caused
by too much stress and/or inefficient management of the systems that promote adaptation
through allostasis. Chronic sleep deprivation in young healthy volunteers has been
reported to increase appetite and energy expenditure, increase levels of proinflammatory
cytokines, decrease parasympathetic and increase sympathetic tone, increase blood
pressure, increase evening cortisol levels, as well as elevate insulin and blood glucose.
Repeated stress in animal models causes brain regions involved in memory and emotions,
such as hippocampus, amygdala, and prefrontal cortex, to undergo structural remodeling
with the result that memory is impaired and anxiety and aggression are increased.
Structural and functional magnetic resonance imaging studies in depression and Cushing's
disease, as well as anxiety disorders, provide evidence that the human brain may be
similarly affected. Moreover, brain regions such as the hippocampus are sensitive
to glucose and insulin, and both type 1 and type 2 diabetes mellitus are associated
with cognitive impairment and (for type 2 diabetes mellitus) increased risk for Alzheimer's
disease. Animal models of chronic sleep deprivation indicate that memory is impaired
along with depletion of glycogen stores and increases in oxidative stress and free
radical production. Taken together, these changes in brain and body are further evidence
that sleep deprivation is a chronic stressor and that the resulting allostatic load
can contribute to cognitive problems, which can, in turn, further exacerbate pathways
that lead to disease.
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© 2006 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
