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 Studies
of insomnia have been conducted most often using comparative descriptive
designs where the correlates of insomnia are measured in people
reporting insomnia (or poor sleep) and compared to those reporting
good sleep (control subjects). Differentiation of correlates that
are antecedents to versus those that are consequences of poor
sleep is elusive. This means the conceptual or theoretical perspectives
about insomnia are obscure. However, much of the science related
to insomnia can be seen as fitting a stress framework: the interface
of mind and body.
Negative changes in
sleep quality in people not previously experiencing insomnia consistently
accompany circumstances of profound physical and emotional/mental
distress and environmental duress (e.g. divorce or bereavement
and major catastrophes). Furthermore, sleep difficulties have
been long recognized in the face of emotional disorders such as
depression and anxiety disorders (Lustberg
and Reynolds, 2000; Thase,
2000) as well as with somatoform, personality, obsessive-compulsive,
and posttraumatic stress disorders (Pillar
et al., 2000; Mellman,
1997).
As previously mentioned,
insomnia is also highly associated with major physical illness.
While the pathologies involved in major disease processes might
affect physiologic sleep regulation mechanisms, it is difficult
to separate such hypothetical mechanisms from the similarly plausible--and
intimately related--physical effects brought on by the psychological
distress of "being sick."
Stress is an ill-defined
scientific term but is a concept that represents the interface
of mind and body. Viewpoints in this field include that stressors
are those environmental elements that provoke emotional arousal
and physiological activation adjustments to defend against or
be protected from harm or adapt to novel circumstances within
one's environment. While minor stressors occur daily, the more
intense ones generally represent perceived or real threats to
one's integrity or status within one's environment, e.g. impending
injury or job loss. The dominant physiological activation pattern
associated with exposure to stressful circumstances, whether social
or physical, largely involves up-regulation of the hypothalamic-pituitary-adrenal
axis and sympathetic nervous system (SNS). The neuroendocrine
components most often assessed include corticotropin-releasing
hormone (CRH), adrenocorticotropic hormone (ACTH), vasopressin,
and cortisol (humans) or corticosterone (rats). Metabolic or neurotransmitter-related
correlates of norepinephrine and epinephrine system activity are
also used.
SNS activation drives
a catabolic enhancement of metabolic state. Adjustments to stressors
are seen to be adaptive when they occur only episodically with
a short timeline of dissipation. Intense or continuous exposure
to stressors and/or a biological propensity towards chronic up-regulation
of the stress state is seen as negative for health.
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