MacArthur SES & Health Network
MacArthur SES & Health Network


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Sleep Quality and Endocrine Markers of Sleep Quality

Summary prepared by Eve Van Cauter in collaboration with the Allostatic Load Working Group. Last revised September, 1997.

Chapter Contents

  1. Definition
  2. Measurements
  3. Relationship to SES
  4. Relationship to Health
  5. Sleep Quality as a Marker of Allostatic Load
  6. References

Definition

CSleep quality refers both the subjective assessment given by the subject of how restorative and undisturbed his/her sleep has been (via a standardized questionnaire) and to a series of objective measures which may be derived from polygraphic recordings (in the laboratory or at home) or from recordings of wrist activity movements (wrist actigraphy monitoring), and/or head movements and eyelid movements ("Nightcap" monitoring). Subjective and objective measures of sleep quality are not necessarily concordant. The most commonly used objective measure of sleep quality is an index of sleep fragmentation which may be derived from all three types of recordings. However, the amount and depth of nonREM sleep, the amount of REM sleep and the temporal organization of nonREM and REM stages are clearly major components of the complex concept of sleep quality.

Sleep exerts major modulatory effects on endocrine function (1). For some hormones (e.g. GH), 50-75% of the total daily secretion is dependent on sleep and is eliminated by total sleep deprivation. There is good evidence to indicate that sleep disorders are associated with decreased levels of IGF-1, presumable because of reduced GH secretion. For other hormonal axes (i.e. the corticotropic and thyroid axes), sleep exerts inhibitory influences, resulting in lower nocturnal concentrations when the subject is asleep than if the subject remains awake throughout the night. Finally, sleep also affects endocrine function on the following day. Following a night of partial or total sleep loss or several nights of sleep curtailment, the quiescent period of cortisol secretion is abridged and evening cortisol levels are elevated.

Measurements

A well validated instrument for the measurement of subjective sleep quality is the Pittsburgh Sleep Quality Index questionnaire which provides a global score of sleep quality on a scale of 1-21 (2,3).

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The most commonly used measure of objective sleep quality is "sleep efficiency," defined as the percentage of time in bed spent asleep. Thus, if a subject wishes to have an 8-hour sleep period, takes 30 min to fall asleep, wakes up 30 min before the scheduled end of the sleep period and experienced a number of awakenings interrupting sleep for a total of 60 min, the sleep efficiency is 6 hrs/8 hrs = 75%.

Since there is good evidence to indicate that reduced sleep duration and/or quality is associated with decreased activity of the somatotropic axis and increased activity of the corticotropic axis, measurements of IGF-1 concentrations and of evening cortisol levels may be considered as endocrine markers of sleep quality. Limitations on the use and interpretation of IGF-1 include the need to draw blood and the fact that the hormone is affected by multiple factors besides sleep quality. In contrast, accurate measurements of biologically active cortisol levels may be obtained on saliva samples and multiple saliva samples collected between early evening (e.g. 18:00) and bedtime provide an excellent estimation of the "quiescent period of cortisol secretion."

Relationship to SES

To the best of my knowledge, there is no published information on the possible relationship between sleep quality and SES. It is likely that individuals with high SES may have more control on their sleep duration and sleep conditions and also more opportunities to recover sleep following sleep loss. In an ongoing study, we have shown that metabolic and endocrine disturbances associated with a sleep debt accumulated over several consecutive days may be entirely reversed by extending the rest period for a few days. The opportunity to recover sleep loss is therefore likely to be an important component of health status across adulthood.

High SES is rarely found in shift workers, who have a chronic sleep debt and are at high risk for a number of pathologies, including cardiovascular, digestive, and psychiatric disease. The relative contribution of the accumulated sleep loss versus the misalignment of the imposed sleep-wake cycle and the endogenous circadian rhythms in the development of these pathologies remain to be demonstrated.

Finally, another area where sleep quality and SES may interact is urban violence. In inner city slums, the night is a time of increased danger and violence which is not conducive to good sleep quality. Interestingly, a number of studies have shown that sleep loss increases irritability and depresses mood. The possible contribution of sleep loss to violent behavior has never been considered, let alone investigated.

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Relationship to Health

The importance of good sleep for good mental and physical health may seem obvious but is still a matter of controversy in the field. Well-controlled studies have shown that total sleep deprivation kills a rat in approximately two weeks. Less drastic studies in humans have indicated that sleep deprivation impairs immune function. Sleep apnea is associated with a variety of neuroendocrine disorders. Our own studies have indicated that sleep loss is associated with an alteration in hypothalamo-pituitary-adrenal (HPA) function on the following day, consisting of an elevation of evening cortisol concentrations (4). The normal day long decline in cortisol levels which follows the early morning elevation appears to occur at a slower rate in sleep-deprived subjects or in subjects running a "sleep debt."

Fig. 1

Cortisol Levels

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This delay in the onset of the quiescent period of cortisol secretion, which normally occurs during the evening and early part of the night, suggests that the mechanism of HPA recovery from stimulation is affected by sleep loss. Thus, sleep loss may alter the rate of recovery of the HPA response to endogenous stimulation by circadian factors. These findings raise the possibility that the resiliency of the HPA axis to exogenous stimulation by stressors may also be affected by sleep loss. Because both animal and human studies have indicated that deleterious central as well as metabolic effects of HPA hyperactivity are more pronounced at the time of the usual trough of the rhythm (i.e. in the evening in the human) than at the time of the peak (i.e. in the morning in the human), modest elevations in evening cortisol levels occurring in conditions of chronic sleep loss could facilitate the development of central as well as peripheral disturbances associated with glucorticoid excess, such as memory deficits and insulin resistance (5,6).

Sleep Quality as a Marker of Allostatic Load

Sleep loss resulting from a biological inability to obtain sufficient amount and/or quality of sleep is highly prevalent. In particular, sleep disturbances are one of the major health complaints of older adults and consist primarily of increased amounts of wakefulness and reduced amounts of deep sleep as well as REM sleep.

Fig. 2

Cortisol Levels

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Figure 2 shows the chronology of the age-related alterations in deep sleep (slow wave sleep), GH secretion, REM sleep and evening cortisol levels. Interestingly, the same alteration in HPA regulation demonstrated in normal young subjects after sleep loss is found in normal aging (7), which is also associated with increased evening levels of plasma cortisol and decreased resiliency of the HPA axis (8,9). Age-related sleep disorders could be involved in a feedforward cascade of negative effects because the fragmentation of sleep which typically occurs in the elderly (10) is likely to result in elevated evening cortisol secretion and, since nocturnal exposure to increased HPA activity may promote sleep fragmentation (11,12), further impairing sleep quality. It is also likely that the mechanisms of recovery from sleep loss are impaired in aging, resulting in an ever decreasing ability to reverse the adverse impact of sleep loss on HPA function.

References

Van Cauter E, Turek FW. 1995. Endocrine and other biological rhythms. In: DeGroot LJ (eds). Endocrinology. W.B. Saunders:Philadelphia. 2487-2548.

Buysse DJ, Reynolds III CF, Monk TH, Berman SB, Kupfer DJ. The Pittsburgh Sleep Quality Index: A New Instrument for Psychiatric Practice and Research. Psychiatry Research. 1989. 28:193-213.

Buysse DJ, Reynolds CF III, Monk TH, Hoch CC, Yeager AL, Kupfer DJ. Quantification of subjective sleep quality in healthy elderly men and women using the Pittsburgh sleep quality index (PSQI). Sleep. 1991. 14:331-338.

Leproult R, Buxton O, Van Cauter E. Nocturnal sleep deprivation results in an elevation of cortisol levels the next evening. Sleep. 1997. 20(10):865-870.

McEwen BS, Sapolsky RM. Stress and cognitive function. Current Opinions in Neurobiology. 1995. 5:205-216.

Dallman MF, Strack AL, Akana SF, et al. Feast and famine: Critical role of glucocorticoids with insulin in daily energy flow. Frontiers in Neuroendocrinology. 1993.14:303-347.

Van Cauter E, Leproult R, Kupfer DJ. Effects of gender and age on the levels and circadian rhythmicity of plasma cortisol. J Clin Endocrinol Metab. 1996. 81:2468-2473.

Greenspan SL, Rowe JW, Maitland LA, McAloon-Dyke M, Elahi D. The pituitary-adrenal glucocorticoid response is altered by gender and disease. J. Gerontol. 1993. 48:M72-M77.

Seeman TE, Robbins RJ. Aging and hypothalamo-pituitary-adrenal response to challenge in humans. Endocrine Reviews. 1994. 15:233-260.

Bliwise DL. . Normal aging. In: Kryger MH, Roth T, Dement WC (eds). Principles and Practice of Sleep Medicine. 1994. W.B. Saunders:Philadelphia. 26-39.

Holsboer F, von Bardelein U, Steiger A. Effects of intravenous corticotropin-releasing hormone upon sleep-related growth hormone surge and sleep EEG in man. Neuroendocrinol. 1988. 48:32-38.

Born J, Spoth-Schwalbe E, Schwakenhofer H, Kern W, Fehm HL. Influences of corticotropin-releasing hormone, adrenocorticotropin, and cortisol on sleep in normal man. J Clin Endocrinol Metab. 1989. 68:904-911.

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