Age-Related Changes in Slow Wave Sleep and REM Sleep and Relationship With Growth Hormone and Cortisol Levels in Healthy Men

Cauter, Eve Van; Leproult, Rachel; Plat, Laurence

doi:10.1001/jama.284.7.861

Cited by 648 publications

(398 citation statements)

References 59 publications

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“…In order to fully understand the effect of the endocrine challenge on delta sleep in PTSD and controls, and address any issues regarding bioavailability of metyrapone, it will be necessary to confirm comparable cortisol suppression across groups by repeated sampling of nocturnal hormone activity during the sleep recordings. In addition, given the known inhibitory effect of CRF on the somatotropic axis (Holsboer et al, 1988;Steiger et al, 1992) and the known relation between delta sleep and growth hormone release (Van Cauter et al, 2000), it will be necessary to measure growth hormone responses in order to understand fully the effect of metyrapone on delta sleep.…”

Section: Discussionmentioning

confidence: 99%

“…Hyperarousal during sleep, a well-established finding in mood and psychotic disorders, is demonstrable on polysomnography by increased awakenings and decreased sleep depth as measured by the levels of slow wave or delta sleep. In healthy subjects, delta sleep activity is maximal in the first half of the night and is temporally associated with peak growth hormone release and the nadir of cortisol output (Van Cauter et al, 2000). Many studies in subjects with major depression have documented reduced delta sleep, increased cortisol release, and reduced growth hormone output as reviewed by Riemann et al (2001).…”

Section: Introductionmentioning

confidence: 99%

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Delta Sleep Response to Metyrapone in Post-Traumatic Stress Disorder

Neylan

Lenoci

Maglione

et al. 2003

Neuropsychopharmacol

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Metyrapone blocks cortisol synthesis, which results in the stimulation of hypothalamic cortiocotropin-releasing factor (CRF) and a reduction in delta sleep. We examined the effect of metyrapone administration on endocrine and sleep measures in male subjects with and without chronic PTSD. We hypothesized that metyrapone would result in a decrease in delta sleep and that the magnitude of this decrease would be correlated with the endocrine response. Finally, we utilized the delta sleep response to metyrapone as an indirect measure of hypothalamic CRF activity and hypothesized that PTSD subjects would have decreased delta sleep at baseline and a greater decrease in delta sleep induced by metyrapone. Three nights of polysomnography were obtained in 24 male subjects with combatrelated PTSD and 18 male combat-exposed normal controls. On day 3, metyrapone was administered during normal waking hours until habitual sleep onset preceding night 3. Endocrine responses to metyrapone were measured in plasma obtained the morning following sleep recordings, the day before and after administration. Repeated measures ANOVAs were conducted to compare the endocrine and sleep response to metyrapone in PTSD and controls. PTSD subjects had significantly less delta sleep as indexed by stages 3 and 4, and total delta integrated amplitude prior to metyrapone administration. There were no differences in premetyrapone cortisol or ACTH levels in PTSD vs controls. PTSD subjects had a significantly decreased ACTH response to metyrapone compared to controls. Metyrapone caused an increase in awakenings and a marked decrease in quantitative measures of delta sleep that was significantly greater in controls compared to PTSD. The decline in delta sleep was significantly associated with the magnitude of increase in both 11-deoxycortisol and ACTH. The results suggest that the delta sleep response to metyrapone is a measure of the brain response to increases in hypothalamic CRF. These data also suggest that the ACTH and sleep EEG response to hypothalamic CRF is decreased in PTSD.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Delta Sleep Response to Metyrapone in Post-Traumatic Stress Disorder

Neylan

Lenoci

Maglione

et al. 2003

Neuropsychopharmacol

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“…Both concentration and timing of many hormones are age-dependent. 41 In young people (16-25 years of age), the time-ofday-dependent secretion of growth hormone reaches its maximum (and cortisol its minimum) at around 1:00 a.m.-approximately 1 h later than in the elderly (470 years). The structure of sleep changes along with these endocrine changes.…”

Section: Chronotype and Agementioning

confidence: 99%

Epidemiology of the human circadian clock

Roenneberg

Kuehnle

Juda

et al. 2007

Sleep Medicine Reviews

1,230

1,057

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Summary Humans show large inter-individual differences in organising their behaviour within the 24-h day-this is most obvious in their preferred timing of sleep and wakefulness. Sleep and wake times show a near-Gaussian distribution in a given population, with extreme early types waking up when extreme late types fall asleep. This distribution is predominantly based on differences in an individuals' circadian clock. The relationship between the circadian system and different ''chronotypes'' is formally and genetically well established in experimental studies in organisms ranging from unicells to mammals. To investigate the epidemiology of the human circadian clock, we developed a simple questionnaire (Munich ChronoType Questionnaire, MCTQ) to assess chronotype. So far, more than 55,000 people have completed the MCTQ, which has been validated with respect to the Horne-Østberg morningness-eveningness questionnaire (MEQ), objective measures of activity and rest (sleep-logs and actimetry), and physiological parameters. As a result of this large survey, we established an algorithm which optimises chronotype assessment by incorporating the information on timing of sleep and wakefulness for both work and free days. The timing and duration of sleep are generally independent. However, when the two are analysed separately for work and free days, sleep duration strongly depends on chronotype. In addition, chronotype is both age-and sex-dependent.

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“…Thus, some (Czeisler et al, 1992;Münch et al, 2005;Van Coevorden et al, 1991;Weitzman et al, 1982), but not all, studies report a decline in the amplitude of CBT, melatonin, and cortisol (Monk, 2005;Niggemyer et al, 2004;Zeitzer et al, 1999). The disparity of these findings points to rather large interindividual differences in sleep and circadian rhythmicity with age and leaves the question open as to what is driving these individual differences (Van Cauter et al, 2000). Progress in understanding the genetic and molecular basis of sleep and circadian rhythmicity has led to the identification of genes contributing to interindividual differences in sleep architecture, timing, and duration in humans and mice (Franken and Dijk, 2009;Landolt, 2008;Rétey et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Interindividual differences in circadian rhythmicity and sleep homeostasis in older people: effect of a PER3 polymorphism

Viola

Chellappa

Archer

et al. 2012

Neurobiology of Aging

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Aging is associated with marked changes in the timing, consolidation and structure of sleep. Older people wake up frequently, get up earlier and have less slow wave sleep than young people, although the extent of these age-related changes differs considerably between individuals. Interindividual differences in homeostatic sleep regulation in young volunteers are associated with the variable-number, tandem-repeat (VNTR) polymorphism (rs57875989) in the coding region of the circadian clock gene PERIOD3 (PER3). However, predictors of these interindividual differences have yet to be identified in older people. Sleep electroencephalographic (EEG) characteristics and circadian rhythms were assessed in 26 healthy older volunteers (55-75 years) selected on the basis of homozygosity for either the long or short allele of the PER3 polymorphism. Homozygosity for the longer allele (PER3 5/5 ) associated with a phase-advance in the circadian melatonin profile and an earlier occurrence of the melatonin peak within the sleep episode. Furthermore, older PER3 5/5 participants accumulated more nocturnal wakefulness, had increased EEG frontal delta activity (0.75-1.50 Hz), and decreased EEG frontal sigma activity (11-13 Hz) during non-rapid eye movement (REM) sleep compared with PER3 4/4 participants. Our results indicate that the polymorphism in the clock gene PER3 may contribute to interindividual differences in sleep and circadian physiology in older people.

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Age-Related Changes in Slow Wave Sleep and REM Sleep and Relationship With Growth Hormone and Cortisol Levels in Healthy Men

Cited by 648 publications

References 59 publications

Delta Sleep Response to Metyrapone in Post-Traumatic Stress Disorder

Delta Sleep Response to Metyrapone in Post-Traumatic Stress Disorder

Epidemiology of the human circadian clock

Interindividual differences in circadian rhythmicity and sleep homeostasis in older people: effect of a PER3 polymorphism

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