Sleep and Endocrinology

• Sleep–wake regulators and neuroendocrine controllers are colocated in the hypothalamus and are responsible for functional integration to accomplish and protect homeostasis; this likely underlies the overlap of sleep maladies and endocrine disorders.

• The endocrine diseases associated with abnormal sleep include: type 2 diabetes mellitus, obesity, acromegaly, hyperthyroidism, hypothyroidism, and polycystic ovarian syndrome.

• Normal sleep preserves normal 24-hour hypothalamic–pituitary hormone axis cycling for several hormone systems. Sleep deprivation and obstructive sleep apnea (OSA) can impair hormone cycling.

• Mechanisms responsible for 24-hour hypothalamic–pituitary hormone cycling are circadian, sleep–wake homeostatic, or both. These mechanisms are complex, distinct, and superimposed on classic hormonal feed-back loop mechanisms.

• The master circadian clock is located in the suprachiasmatic nucleus of the hypothalamus, which relays an intrinsic rhythm to peripheral organ systems using genetic clockwork: two positive loop genes are CLOCK and BMAL1 , and two negative loop components are PER and CRY .

• Current evidence links the circadian system to diabetes pathophysiology and treatment.

• States of sleep and wake are best conceived as flip-flop switches. Transitioning from sleep to wakefulness is accomplished by the reticular activating system and is composed of a series of cortical activating nuclei with multiple neurotransmitters. The transition from wake to sleep is accomplished by primarily one neurotransmitter, gamma-aminobutyric acid.

• Sleep architecture changes with aging to consist of less total sleep time and less slow-wave sleep (SWS).

• OSA requires polysomnography for diagnosis.

• Acute sleep loss eliminates the normal nocturnal suppression of thyroid-stimulating hormone secretion.

• Sleep deprivation disrupts SWS, resulting in a decrease in levels of the hormones that are entrained to SWS (growth hormone and prolactin).

• Short-term sleep deprivation increases serum cortisol levels, suppresses insulin secretion, and diminishes glucose tolerance. It also decreases serum leptin and increases ghrelin levels such that sleep-deprived subjects gain weight compared with non–sleep-deprived subjects.

• OSA results in less predictable hormone changes depending on the extent of sleep fragmentation, elevation of adrenergic tone, and hypoxia. It is associated with decreased insulin sensitivity and worsened glucose tolerance proportional to the severity of OSA, and inversely proportional to the time amount of continuous positive airway pressure use.

• Effective treatment of OSA improves sleep architecture, normalizes hormone release, and improves abnormal glucose metabolism.


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