Age-Related Sleep Disturbances
Age-Related Sleep Disturbances
ABSTRACT & COMMENTARY
Source: Cauter EV, et al. Age-related changes in slow wave sleep and REM sleep and relationship with growth hormone and cortisol levels in healthy men. JAMA 2000;284(7): 861-868.
Older adults often complain of decreased subjective sleep quality. The most common sleep disturbances detected in aging individuals are decreased deep (stages 3 and 4 or delta) slow wave (SW) sleep, and increased number and duration of nocturnal awakenings. REM sleep appears to be relatively preserved during aging. Normal aging also is associated with a variety of changes in endocrine-metabolic functions. The association of the chronology of age-related changes in sleep patterns and their possible temporal relationships with changes in neuroendocrine function has yet to be elucidated.
Sleep is a major modulator of endocrine function, particularly of pituitary-dependent hormonal release. In men, 60-70% of daily growth hormone (GH) secretion occurs during early sleep in association with SW sleep. Whether decrements in SW sleep contribute to the known decreases in GH secretion in normal aging men, is not known. As well as activation of the GH axis during sleep, the hypothalamic-pituitary-adrenal (HPA) axis is acutely inhibited during early SW sleep. Therefore, even partial sleep deprivation results in an elevation of cortisol levels the following evening. An elevation of evening cortisol levels is a hallmark of aging that is thought to reflect an impairment in the HPA axis, and could underlie a constellation of metabolic and cognitive alterations.
In the present study, Cauter and colleagues define the chronology of age-related changes in sleep duration and quality, GH secretion, and cortisol levels in healthy men, and examine whether decrements in sleep quality are associated with alterations of GH and cortisol levels. The study reviews data collected from 149 healthy, normal weight men, aged 16-83 years. Subjects spent 1-3 habituation nights in the sleep laboratory. Blood samples for hormonal measures were collected at 15-30 minute intervals for 24-25 hours. All night polygraphic sleep recordings were also obtained. Sleep, cortisol, and GH profiles were obtained in 132; 124 and 114 subjects, respectively. Concomitant sleep, cortisol, and GH profiles were obtained in 94 subjects.
Total sleep time decreases markedly with aging, but significant reductions in total sleep time did not occur until after midlife. From midlife until the eighth decade, total sleep time decreased, on average, by 27 minutes per decade. SW sleep decreased from 18.9% to 3.4%, and this decrease in deep non-REM sleep was compensated by an increase in light non-REM sleep (51.2-67.3%) without significant time spent awake. Increases in wake time and decreases in REM sleep became significant starting in midlife. GH secretion during the 24-hour cycle show significant GH secretion decreases from young adulthood to midlife. GH secretion decreased by 75%. Age was associated with an elevation of the evening nadir of cortisol, but morning maximum values remained stable across all age ranges.
Next, Cauter et al investigated if the concomitant sleep alterations and its interaction with age contributed to the hormonal changes seen with aging. Analysis of variance of GH secretion during sleep in relation to age, SW sleep, and their interaction, indicated that in young to middle aged subjects, but not in older men, increased amounts of SW sleep were associated with higher levels of GH secretion. The analysis of the variance of evening cortisol levels in relation to age, REM sleep, wake time, and their interaction, showed no significant interactions.
COMMENT BY CLAUDIA A. ORENGO, MD, PhD
Cauter et al demonstrate in a cross-sectional survey of healthy men, that the amount of deep SW sleep decreases by about 80% from early to midlife, and also, a similar reduction (75%) in spontaneous GH secretion occurs. Cauter et al also report that SW sleep, independent of age, is a major determinant of 24-hour nocturnal GH release. In contrast, the effect of age on REM sleep, sleep fragmentation, and HPA function does not become apparent until later in life. The study further suggests that age-related changes in the somatotropic and corticotropic axes may partially reflect decreased sleep quality.
The present data suggest that an alteration in sleep-wake homeostasis is an early biological marker of aging in adult men. The study is limited by being a cross-sectional study, and confirmation of these findings in a longitudinal study should be pursued. Also, the androgen status of the men was not specified. As men age, total and free testosterone levels decrease and the interrelationships between androgens, GH axis, and sleep quality was not addressed. The study group consisted of only healthy, nonobese men, so the generalizability of this study to other populations is limited.
In conclusion, the changes in sleep quality that are characterized by aging are associated with specific alterations in hormonal systems that are essential for metabolic regulation. These age-related alterations in sleep quality may contribute to the changes in body composition (i.e., fat distribution) and function (i.e., decrease sexual function) via their influence on neuroendocrine parameters. It may be that interventions that augment SW sleep may potentially serve as useful GH secretagogues. Further investigations are needed to determine if hormonal therapies may be helpful in preventing or limiting decrements in sleep quality, and in turn, also provide beneficial health consequences.
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