Age-related Changes In Sleep Research Articles

Age-related changes in slow wave sleep and REM sleep and relationship with growth hormone and cortisol levels in healthy men.

In young adults, sleep affects the regulation of growth hormone (GH) and cortisol. The relationship between decreased sleep quality in older adults and age-related changes in the regulation of GH and cortisol is unknown. To determine the chronology of age-related changes in sleep duration and quality (sleep stages) in healthy men and whether concomitant alterations occur in GH and cortisol levels. Data combined from a series of studies conducted between 1985 and 1999 at 4 laboratories. A total of 149 healthy men, aged 16 to 83 years, with a mean (SD) body mass index of 24.1 (2.3) kg/m( 2), without sleep complaints or histories of endocrine, psychiatric, or sleep disorders. Twenty-four-hour profiles of plasma GH and cortisol levels and polygraphic sleep recordings. The mean (SEM) percentage of deep slow wave sleep decreased from 18.9% (1.3%) during early adulthood (age 16-25 years) to 3.4% (1.0%) during midlife (age 36-50 years) and was replaced by lighter sleep (stages 1 and 2) without significant increases in sleep fragmentation or decreases in rapid eye movement (REM) sleep. The transition from midlife to late life (age 71-83 years) involved no further significant decrease in slow wave sleep but an increase in time awake of 28 minutes per decade at the expense of decreases in both light non-REM sleep (-24 minutes per decade; P<.001) and REM sleep (-10 minutes per decade; P<.001). The decline in slow wave sleep from early adulthood to midlife was paralleled by a major decline in GH secretion (-372 microg per decade; P<.001). From midlife to late life, GH secretion further declined at a slower rate (-43 microg per decade; P<.02). Independently of age, the amount of GH secretion was significantly associated with slow wave sleep (P<.001). Increasing age was associated with an elevation of evening cortisol levels (+19. 3 nmol/L per decade; P<.001) that became significant only after age 50 years, when sleep became more fragmented and REM sleep declined. A trend for an association between lower amounts of REM sleep and higher evening cortisol concentrations independent of age was detected (P<.10). In men, age-related changes in slow wave sleep and REM sleep occur with markedly different chronologies and are each associated with specific hormonal alterations. Future studies should evaluate whether strategies to enhance sleep quality may have beneficial hormonal effects. JAMA. 2000;284:861-868

Approach to sleep disorders in the nursing home setting. REVIEW ARTICLE.

Evidence suggests that sleep disorders and sleep fragmentation are very common in nursing home residents. A variety of factors contribute to these sleeping difficulties, including age-related changes in sleep; the high prevalence of dementia, depression, medical illness and medications that affect sleep; and sleep disorders such as respiratory disturbance of sleep. Other important factors include common lifestyle characteristics in nursing home residents (such as inactivity, large amounts of time spent in bed, lack of bright light exposure, and poor sleep hygiene) and the disruptive night-time nursing home environment. Recent interventional studies suggest that improvement in the nursing home environment may be an important aspect of the management of sleeping difficulties. Assessment and management of sleeping problems in nursing home residents should involve comprehensive assessment and treatment of the multiple factors that can interfere with sleep. Residents who fail these interventions can be considered for treatment with sleeping medications. Unfortunately, there is little data on the effectiveness of sleeping medications and the specific management of sleep disorders in this setting. Future research should focus on clarifying the contribution of various environmental factors to sleep impairment, and the testing of these various interventions on sleep.

CONTRIBUTION OF CIRCADIAN PHYSIOLOGY AND SLEEP HOMEOSTASIS TO AGE-RELATED CHANGES IN HUMAN SLEEP

The circadian pacemaker and sleep homeostasis play pivotal roles in vigilance state control. It has been hypothesized that age-related changes in the human circadian pacemaker, as well as sleep homeostatic mechanisms, contribute to the hallmarks of age-related changes in sleep, that is, earlier wake time and reduced sleep consolidation. Assessments of circadian parameters in healthy young (∼20–30 years old) and older people (∼65–75 years old)—in the absence of the confounding effects of sleep, changes in posture, and light exposure—have demonstrated that an earlier wake time in older people is accompanied by about a 1h advance of the rhythms of core body temperature and melatonin. In addition, older people wake up at an earlier circadian phase of the body temperature and plasma melatonin rhythm. The amplitude of the endogenous circadian component of the core body temperature rhythm assessed during constant routine and forced desynchrony protocols is reduced by 20–30% in older people. Recent assessments of the intrinsic period of the human circadian pacemaker in the absence of the confounding effects of light revealed no age-related reduction of this parameter in both sighted and blind individuals. Wake maintenance and sleep initiation are not markedly affected by age except that sleep latencies are longer in older people when sleep initiation is attempted in the early morning. In contrast, major age-related reductions in the consolidation and duration of sleep occur at all circadian phases. Sleep of older people is particularly disrupted when scheduled on the rising limb of the temperature rhythm, indicating that the sleep of older people is more susceptible to arousal signals genernpated by the circadian pacemaker. Sleep-homeostatic mechanisms, as assayed by the sleep-deprivation–induced increase of EEG slow-wave activity (SWA), are operative in older people, although during both baseline sleep and recovery sleep SWA in older people remains at lower levels. The internal circadian phase advance of awakening, as well as the age-related reduction in sleep consolidation, appears related to an age-related reduction in the promotion of sleep by the circadian pacemaker during the biological night in combination with a reduced homeostatic pressure for sleep. Early morning light exposure associated with this advance of awakening in older people could reinforce the advanced circadian phase. Quantification of the interaction between sleep homeostasis and circadian rhythmicity contributes to understanding age-related changes in sleep timing and quality. (Chronobiology International, 17(3), 285–311, 2000)

MORE THAN A MARKER: INTERACTION BETWEEN THE CIRCADIAN REGULATION OF TEMPERATURE AND SLEEP, AGE-RELATED CHANGES, AND TREATMENT POSSIBILITIES

The neurobiological mechanisms of both sleep and circadianregulation have been unraveled partly in the last decades. A network of brainstructures, rather than a single locus, is involved in arousal state regulation,whereas the suprachiasmatic nucleus (SCN) has been recognized as a key structurefor the regulation of circadian rhythms. Although most models of sleep regulationinclude a circadian component, the actual mechanism by which the circadiantiming system promotes—in addition to homeostatic pressure—transitionsbetween sleep and wakefulness remains to be elucidated. Little more can bestated presently than a probable involvement of neuronal projections and neurohumoralfactors originating in the SCN. This paper reviews the relation among bodytemperature, arousal state, and the circadian timing system and proposes thatthe circadian temperature rhythm provides an additional signaling pathwayfor the circadian modulation of sleep and wakefulness. A review of the literatureshows that increased brain temperature is associated with a type of neuronalactivation typical of sleep in some structures (hypothalamus, basal forebrain),but typical of wakefulness in others (midbrain reticular formation, thalamus).Not only local temperature, but also skin temperature are related to the activationtype in these structures. Warming of the skin is associated with an activationtype typical of sleep in the midbrain reticular formation, hypothalamus, andcerebral cortex (CC). The decreasing part of the circadian rhythm in coretemperature is mainly determined by heat loss from the skin of the extremities,which is associated with strongly increased skin temperature. As such, alterationsin core and skin temperature over the day could modulate the neuronal activationstate or “preparedness for sleep” in arousal-related brain structures.Body temperature may thus provide a third signaling pathway, in addition tosynaptic and neurohumoral pathways, for the circadian modulation of sleep.A proposed model for the effects of body temperature on sleep appears to fitthe available data better than previous hypotheses on the relation betweentemperature and sleep. Moreover, when the effects of age-related thermoregulatoryalterations are introduced into the model, it provides an adequate descriptionof age-related changes in sleep, including shallow sleep and awakening closerto the nocturnal core temperature minimum. Finally, the model indicates thatappropriately timed direct (passive heating) or indirect (bright light, melatonin,physical activity) manipulation of the nocturnal profile of skin and coretemperature may be beneficial to disturbed sleep in the elderly. Althoughsuch procedures could be viewed by researchers as merely masking a markerfor the endogenous rhythm, they may in fact be crucial for sleep improvementin elderly subjects. (Chronobiology International,17(3), 313–354, 2000)

Daily Social and Physical Activity Increases Slow-Wave Sleep and Daytime Neuropsychological Performance in the Elderly

Decreased levels of physical and social activity associated with aging can be particularly pronounced in residents of assisted living facilities. Reduced exposure to important behavioral and time-giving cues may contribute to the age-related changes in circadian rhythmicity and sleep. The present study was conducted to test the hypothesis that an enforced schedule of structured social and physical activity (0:900 to 10:30 and 19:00 to 20:30 daily for two weeks) can have beneficial effects on circadian rhythmicity, nocturnal sleep, daytime functioning, mood, and vigor. The subjects were 14 elderly residents of continued-care retirement facilities while a similar group of 9 elderly residents served as controls. The group exposed to structured activities had increased amounts of slow-wave sleep and demonstrated improvement in memory-oriented tasks following the intervention. Conversely, no significant changes were noted in the amplitude and phase of the body temperature rhythm or in subjective measures of vigor and mood. These results indicate that short-term exposure to structured social intervention and light physical activity can significantly improve memory performance and enhance slow-wave sleep in older adults without alterations to the circadian phase or amplitude of body temperature. This is the first report to demonstrate that low intensity activity in an elderly population can increase deep sleep and improve memory functioning. The high degree of interest in these activities paired with the simple nature of the tasks makes this a potentially practical intervention which can be adapted for both community dwelling and assisted-living elders.

Age-related changes in sleep in the rat.

Human sleep in old age is characterized by a number of changes, including reductions in sleep efficiency, amounts of visually scored slow-wave and REM sleep, and amplitude of the diurnal sleep/wake rhythm. In older rats, some, but not all, of these traits have been reported, including a decrease in the mean duration of sleep bouts, an increase in the number of sleep bouts, and a modest reduction of REM sleep. Studies of the diurnal rhythm of total sleep have had varied results. There are, however, virtually no data indicating at what point across the rat's lifetime the changes seen in old age begin to occur. In order to more fully characterize sleep in older rats, and to develop data on when they first appear, we have examined sleep in young adult (3 months), middle-aged (12 months), and older (24 months) rats during 24 hours under constant dim light. Analyses of variance revealed no age-related changes in total sleep, NREM or REM sleep, wake time after sleep onset, or three different measures of the amplitude of the sleep/wake circadian rhythm. There were, however, significant age-related reductions in high-voltage NREM sleep ("HS2"), the mean length of sleep bouts, and REM-onset duration. These were seen in the 1-year-old rats, indicating that the changes seen in the older animals were evident by midlife.

Relationships between sleep and body temperature in middle-aged and older subjects.

Although changes in the circadian timing system are thought to be a major factor in the decline of sleep quality that often accompanies aging, few reports have actually examined this relationship in detail. Because some treatments for age-related insomnia are based on putative circadian changes, it is important to expand the limited database that specifically addresses this issue. This study examined age-related changes in sleep, and relationships between those sleep changes and alterations in the circadian timing system, in a group of middle-aged and older subjects. Sixty healthy men and women between the ages of 40 and 84 were studied. A subset of older subjects (< 65 years) had reported sleep disturbance for at least 1 year before participation. Polysomnography was obtained, and body core temperature was recorded continuously for 24 hours. All recordings took place in the Laboratory of Human Chronobiology, Department of Psychiatry, Cornell University Medical College. There were no differences in sleep quality between middle-aged and non-sleep-disturbed older subjects. However, timing of the minimum body temperature was earlier in the older non-sleep-disturbed subjects than in the middle-aged group. In contrast, sleep-disturbed older people had shorter total sleep times, reduced sleep efficiency, more waking time after sleep onset, and a reduced proportion of REM sleep compared with non-sleep-disturbed older subjects. Yet, there were no differences between the two older groups in the rhythm of body temperature. For the entire group, age was correlated negatively with total sleep time, sleep efficiency, percentage of stage 2 sleep, and the timing of the temperature minimum. The results support the widely held notion that sleep and circadian rhythm changes occur with aging. However, the hypothesis that age-related changes in sleep may be associated with aging of the circadian system was supported only to a limited degree, suggesting that age-related sleep disturbance is likely to have multiple causes. Thus, treatment strategies that incorporate a combination of interventions may be the most effective.

Sleep problems.

Sleep complaints are common in the elderly, and are often related to physiological changes with ageing, or secondary to illness and drug therapy. Primary sleep disorders, such as sleep apnoea and movement disorders, are also common. Management should be specific to the problem. Attention to underlying factors and sleep hygiene, as well as reassurance and education about age-related sleep changes, will often be sufficient. Hypnotics, which usually offer only temporary symptomatic relief, may be counterproductive, and should be prescribed only in the short term, except in limited specific cases. Short-acting benzodiazepines (e.g., temazepam or oxazepam), or possibly zopiclone, are currently the drugs of choice.

Patterns of Sleep Episodes in Young and Elderly Adults During a 36-Hour Constant Routine

The deterioration of nocturnal sleep and increase in daytime napping that accompany aging may represent changes in homeostatic or circadian aspects of sleep regulation. We addressed these possibilities by examining patterns of unintended sleep episodes, subjective sleepiness and mood during 36 hours of constant wakeful bed rest in 17 healthy 20-30-year-olds (n = 9 men, n = 8 women) and 18 healthy 80-year-olds (n = 11 men, n = 7 women). Subjects had continuous electroencephalographic (EEG) monitoring and core body temperature measurements and completed visual analog scale ratings of sleepiness and mood each hour. Young and elderly groups both showed significant linear and circadian trends in sleep episodes across the interval. Group x time interaction effects revealed a stronger linear trend in the young vs. elderly group, but no difference in circadian trends. Analysis of age groups by sex demonstrated more complex interactions, with elderly men showing weaker rhythmic (circadian) trends than elderly women. Subjective ratings of sleepiness and mood showed no difference in temporal trends between young and elderly groups. These data support the hypothesis that age-related sleep changes result primarily from decreases in homeostatic, rather than circadian, sleep propensity. They also confirm the presence of sex differences in sleep patterns among the elderly and support the distinction between objective and subjective measures of sleepiness.

Sleep and Aging in Animals: Relationships with Circadian Rhythms and Memory

In an earlier review, Ingram et al concluded that research on sleep and aging in animals was sparse and essentially in a formative stage. In the past several years, systematic research on age-related changes in sleep in animals has increased, along with a greater tendency to publish full-length reports with complete methodological details. Consequently, the status of research in the area may be upgraded to an intermediate level. Generally, recent findings confirm and extend earlier ones that a wide variety of age-related changes in sleep occur in several mammalian species. Inconsistencies still exist in regard to how selected parameters change in a particular species (for example, nonparadoxical sleep in aged cats). However, in contrast to the findings of Ingram et al, a larger number of age-related changes in sleep have been recently replicated in separate laboratories. Another area of congruence between earlier and more recent reports involves age-related alterations in circadian rhythms. Multiple changes in circadian function have been reported in many species, suggesting a widespread pattern of temporal disorganization in senescence. Among other changes, both the amplitude and the period of individual rhythms may be altered, often resulting in desynchronization both between rhythms and from environmental cycles. At present, no single animal model demonstrates the age-related changes that occur in human sleep. However, many of the age-related changes that humans exhibit in sleep and in circadian rhythms appear similar to those in other species. For example, rats show several changes in absolute levels of sleep, continuity of sleep, and circadian organization of sleep that approximate those in aged humans, while aged male cats show analogous changes in deep nonparadoxical sleep and in delta waves. These findings suggest that different species may be useful in modelling different aspects of sleep in aged humans. Relationships between sleep and memory in aged rats may also exhibit analogies to human aging. Deficits in paradoxical sleep, and more generally, in the continuity of sleep, have been related to cognitive deficits in aged humans. These similarities between rats and humans further enhance the potential usefulness of rats to model aspects of human aging. Many areas still require further study. The generality of age-related changes in sleep in animals cannot be determined until additional strains and species are evaluated. In addition, many sleep-related phenomena such as phasic events during paradoxical sleep have not yet been examined in old animals.(ABSTRACT TRUNCATED AT 400 WORDS)

Age-related Changes in Sleep

Within a wide range of individual differences, there are age-associated changes in the characteristics of sleep. There are shifts toward the extremities in sleep amounts, increased difficulties in initiating or maintaining sleep at night, and an emergence of naps. There are also changes in sleep structure. It is within these age-related changes that sleep disorders must be considered.

Effects of age on delta and REM sleep parameters

Sleep EEGs were evaluated in 24 men without medical and psychiatric disease segregated into 3 age groups: 21–30, 31–40, and 51–70 years of age. Sleep was evaluated by 3 different methods: traditional sleep stage scoring, computer-assisted delta and rapid eye movement (REM) quantification, and power spectral analysis. Analysis of manually scored sleep variables revealed that age-related changes in sleep were most pronounced in the oldest age group (51–70). Older subjects spent more time awake, had low sleep efficiency and sleep maintenance, displayed a decreased REM latency, and spent less time in delta sleep. Computer quantification further confirmed that the largest drop in delta activity occurred between the 21–30 and the 31–40 year olds. The largest decrease in delta activity occurred to the greatest extent during the first 100 min of sleep (NREM period 1), and was characterized by a shift in the spectral distribution of power towards higher delta frequencies. Total nighttime REM was increased in the 31–40 year-old group as compared to older and younger subjects. This unexpected non-linear trend may reflect a progressive tendency toward ‘lightening’ of sleep with increasing age. These studies further suggest that the effects of aging should be incorporated into models aiming at explaining the physiology of sleep.

The effect of sleep fragmentation on sleep and performance in younger and older subjects

Groups of 12 normal 55-70-year-old and young adult subjects had their sleep experimentally disturbed at a rate of approximately 14 times per hour to determine the residual effects of moderate sleep disturbance and to determine any differential impact as a function of age. Normal age-related changes in sleep were seen on baseline and recovery nights. In the second night of sleep disturbance, the older subjects had a smaller increase in total awakenings than young adults. Older subjects had a slower increase in auditory arousal threshold as sleep disturbance progressed. The older subjects also tended to have less performance deterioration on morning testing than did young adults, and this difference was significant for numbers of correctly completed addition problems. These evidences led to the conclusion that, while both age groups were sensitive to moderate sleep disturbance, the older individuals appeared somewhat less sensitive than the young adults.

Sleep disorders in the later years.

Preview“Poor sleep” is a common complaint of elderly patients experiencing the diminished quality and quantity of sleep associated with aging. The cause may be a true sleep disorder or other medical problems that contribute to sleep disturbance. In this article, Dr Bannerman reviews age-related sleep changes and discusses current dos and don'ts in the treatment of sleep disorders.

Introduction to Sleep and Sleep Disorders

This overview of normal and disordered sleep introduces techniques for recording and classifying sleep stages, physiological and temporal characteristics of sleep, age-related changes in sleep, consequences of sleep deprivation, theories on the function of sleep, and neurophysiological and biochemical mechanisms regulating sleep. Various categories of sleep disorders are briefly surveyed, with special emphasis on differential diagnosis of sleep apnea syndromes and other disorders characterized by symptoms of excessive daytime somnolence.

Age-related changes in sleep in depressed and normal subjects

All-night electroencephalographic (EEG) sleep data were examined as a function of age in normal control subjects and hospitalized, unmedicated depressed patients with primary affective illness. By analysis of variance, Total Sleep time, Delta Sleep, Sleep Efficiency, Rapid Eye Movement (REM) Sleep, and REM Latency decreased as a function of age, whereas Early Morning Awake time and Intermittent Awake time increase. Compared with normal controls, after the effects of age were covaried out, depressed patients had a greater Sleep Latency, Early Morning Awake time, Intermittent Awake time, Duration and REM Density of the first REM period, and average REM Density for the night, as well as less Sleep Efficiency, less Delta Sleep, and shorter REM Latency. Early Morning Awake time increased with age in depressive but not in normals.