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Aging-Related Sleep Changes

Article  in  Clinics in Geriatric Medicine · March 2008

DOI: 10.1016/j.cger.2007.08.007 · Source: PubMed

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 Clin Geriatr Med 24 (2008) 1–14

Aging-Related Sleep Changes

Joseph Roland D. Espiritu, MD, FCCP, FAASM
Division of Pulmonary, Critical Care, and Sleep Medicine, Saint Louis University School
of Medicine, 3635 Vista Avenue at Grand Boulevard, PO Box 15250, Saint Louis,
MO 63110-0250, USA

Normal aging results in changes in the function of all organ systems and
impacts the neurophysiology of sleep. Most physicians who care for the el-
derly may have the general impression that aging results in the deterioration
in the quality of sleep and an increase in the prevalence of sleep disorders.
This impression was validated by a large epidemiological study of over
9,000 elderly subjects in three United States communities in 1995, which de-
scribed that the vast majority (more than 80%) of them had one or more
sleep complaints, such as trouble falling asleep, waking up, awaking too
early, needing to nap, and not feeling rested [1]. On the other hand, in
a study of another, much older, population, good quality sleep was surpris-
ingly reported by the majority of this cohort. An analysis of the presence of
sleep disorders, their related pathologies, and pharmacologic treatments in
180 Roman centenarians revealed that more than half (57.4%) had good
quality sleep [2]. In general, predictors of good quality sleep in the elderly
include physical and psychologic health, daytime activity, and naturalistic
light (3000þ lux) [3]. On the other hand, moderate impairment in sleep qual-
ity in these Roman centenarians was found in about one third (35.2%) and
was associated with cardiopulmonary comorbidities (angina pectoris and
chronic obstructive pulmonary disease). A small minority (7.4%) manifested
severe impairments in sleep quality significantly associated with cognitive
dysfunction and increased mortality [2]. Thus, an increase in the number
of sleep complaints may be a marker of poor physical and mental health [4].
This article describes the normal changes in sleep physiology in the el-
derly. Distinguishing ‘‘normal’’ or physiologic age-related changes in sleep
from ‘‘abnormal’’ or pathologic sleep can be problematic, given the close as-
sociation between sleep disorders and a higher prevalence of comorbid con-
ditions in the elderly. In an attempt to ensure that the age-related changes

E-mail address: [email protected]

0749-0690/08/$ - see front matter Ó 2008 Elsevier Inc. All rights reserved.
doi:10.1016/j.cger.2007.08.007 geriatric.theclinics.com
2 ESPIRITU

described herein are indeed physiologic and not associated with adverse
health effects, this article focuses mainly on studies that incorporate healthy
elderly subjects and compares them to younger adults as controls. Specific
sleep disorders that increase in prevalence with aging (sleep breathing disor-
ders, insomnia, restless legs syndrome, rapid eye movement behavior disor-
der, and so on) are discussed elsewhere in this issue.

Sleep initiation and maintenance

Several reports suggest that the ability to initiate and maintain sleep de-
clines with aging. Sleep in older adults tend to become shorter (decreased
total sleep time), more shallow (increased stages 1 and 2 and decreased
slow-wave sleep), and more disrupted (decreased sleep efficiency, increased
arousal index, and prolonged wake after sleep onset) [4–7]. Mathematical
modeling reveals that the rate of increase in initial sleep latency over the
ages is not linear but triphasic, increasing until age 30, plateauing between
ages 30 and 50, and then resuming its upward climb after age 50 [8]. Sleep
efficiency continues to deteriorate in the old elderly (over 70 years old),
with an additional increase in the wake time (plus 28 minutes per decade
of life), at the expense of stages 1 and 2 (minus 24 minutes per decade)
and stage rapid eye movement (REM) sleep (minus 10 minutes per de-
cade) [6]. A meta-analysis published by Floyd and colleagues [9] on age-re-
lated changes in the initiation and maintenance of sleep confirmed that
waking frequency (arousal index) and duration (wake after sleep onset) in-
creased with aging. However, older subjects appear to be somewhat less cog-
nizant of this impaired ability to initiate and maintain sleep. They tend to
underestimate the severity of sleep impairment (ie, longer sleep latency, less to-
tal sleep time, lower sleep time) when their self-report is tested against poly-
somnography [3,10]. Meanwhile, although healthy older people have
a greater number of arousals during their nocturnal sleep period, their ability
to reinitiate sleep remains surprisingly intact and comparable to those of youn-
ger individuals [11].
The decreased ability to initiate and maintain sleep is unfortunately as-
sociated with increased morbidity and mortality in the elderly. A pro-
longed sleep latency at or above the 95th percentile (greater than or
equal to 80 minutes) in a cohort of older Parisians (over 60 years old)
was associated with anxiety, poor health, insomnia, and obstructive sleep
apnea [12]. In a prospective study by Dew and colleagues [13] of 185
healthy older adults 60 to 89 years old, and with no history of neurocog-
nitive deficits, predictors of all-cause mortality (controlled for age, sex,
gender, and baseline medical burden) include a prolonged initial sleep la-
tency (more than 30 minutes), poor sleep efficiency (less than 80%), and
increased (over 25.7%) or decreased (less than 16.1%) proportion of
REM sleep.
 AGING-RELATED SLEEP CHANGES 3

Sleep duration
A number of elderly patients complain about not getting enough sleep.
Although this perception of decreased sleep duration may be attributable
to the circadian phase advancement of the sleep-wake schedule in the elderly
(ie, waking up early in the morning while the rest of the household members
are asleep), or the effect of shortened nocturnal sleep because of daytime
napping, measuring the actual time spent sleeping during the 24-hour pe-
riod, using subjective and objective tools, is key to ascertaining this phenom-
enon. Campbell and Murphy [14], compared spontaneous sleep among
young, middle-age, and older adults, using the disentrainment protocol,
where subjects slept for 72 hours while being shielded from natural and
artificial cues to time of day, with the goal of determining the duration of
spontaneous sleep. Total sleep time over 24 hours was significantly shorter
in the middle-age (9.06 hours) and older age (8.13 hours) adults than that in
the younger ones (10.53 hours).
Sleep duration appears to be a predictor of an older individual’s state of
health and longevity. In the Japanese Collaborative Cohort Study on Eval-
uation of Cancer Risk involving 104,010 subjects aged 40 to 79 years, the
optimal sleep duration associated with the lowest risk mortality was found
to be 7 hours [15]. Longer or shorter sleep times were associated with in-
creased all-cause mortality. In a study of a Mediterranean population that
practiced siesta, men who slept more than 8 hours per day (versus those
who slept less than 8 hours per day) had double the risk of dying from all
causes and almost triple the risk from heart disease [16]. Furthermore, short
and long nocturnal sleep duration may also indicate the presence of comor-
bid conditions in the elderly. Ohayon and Vecchierini [12] studied the rela-
tionship between sleep duration and cognitive function in older adults in
7,010 randomly selected metropolitan Parisian households, and found that
extremes in sleep duration may indicate the presence of health risk factors.
Those older individuals with nocturnal sleep durations at or below the 5th
percentile (4 hours and 30 minutes) had a significantly higher prevalence
of obesity, poor health, insomnia, daytime sleepiness, and cognitive impair-
ment. At the other extreme, those total nocturnal sleep times at or above the
95th percentile (9 hours and 30 minutes) were more likely to be male, anx-
ious, less educated, unhealthy, insomniac, or apneic.

Sleep schedule
The current available literature supports the widely held belief that the
nocturnal sleep phase is shifted earlier in the elderly. In an interesting study
of Japanese office workers divided into four age groups (20s, 30s, 40s, and
50s–60s) using a morningness-eveningness questionnaire, Ishihara and col-
leagues [17] not only reaffirmed that older workers preferred earlier bed
and arising times, but also observed that they had a less variable sleep
4 ESPIRITU

schedule and better mood upon arising, compared with younger workers.
This preference for earlier bedtimes was further supported by another study,
which demonstrated that later bedtimes are associated not only with less
time in bed but also less time asleep. For each 10 minute-delay in bedtime
starting after 19:00 hours, there was a corresponding 7 to 8 minute decre-
ment in time in bed and total sleep time [18]. Extremes in bedtime or
wake-up time may also indicate an older person’s state of health. The Ohay-
on’s study on older Parisians concluded that early (9 PM or earlier) or late
(1 AM or later) bedtime, as well as extremely early (5 AM or earlier) and later
(9 AM or later) wake-up times were associated with obesity and loss of au-
tonomy in the activities of daily living [12].

Naps
A polysomnographic study, incorporating young adults (20–30 years old)
as controls, found a greater number of naps in older adults (over 78 years
old) [19]. An uncontrolled, observational study employing an activity diary
and wrist actigraphy found that healthy elderly individuals spent approxi-
mately one hour napping during the day [20]. In the general population,
daytime napping may have salutary effects on health outcomes. In the Greek
European Prospective Investigation Into Cancer and Nutrition study of
23,681 healthy individuals, siesta was associated with a 37% lower coronary
mortality, especially in working men [21].
There are a few studies published investigating the effect of naps on poly-
somnographic parameters and neurocognitive function in the healthy
elderly population. Monk and colleagues [22] performed a 17-day, 90-min-
ute nap versus no nap interventional study on nine healthy elderly subjects
aged 74 to 87 years, and found a significant increment in total sleep time
(38 minutes) and improvement in sleep latency (15.6 minutes versus
11.5 minutes, respectively) in a single-trial evening mutiple sleep latency
test. Although nocturnal sleep efficiency dropped by a small proportion
(2.4%) mainly because of earlier wake times, there were no reliable effects
on wake after sleep onset or measures of non-REM (NREM) (stages 1, 2,
and delta) sleep. On the other hand, Campbell and colleagues [23] per-
formed polysomnography, body core temperature measurements, and neu-
rocognitive testing on 32 healthy individuals aged 55 to 85 years and found
that napping had little effect on subsequent nighttime sleep quality or dura-
tion, thereby significantly increasing their total 24-hour sleep time. These
increased sleep times were associated with enhanced cognitive and psycho-
motor performance measured the following day.

Sleep architecture
The meta-analysis on age-related sleep changes, published by Ohayon
and colleagues, [24] described the evolution of sleep architecture in healthy
 AGING-RELATED SLEEP CHANGES 5

individuals from childhood to old age. Table 1 summarizes the age-related

changes in sleep architecture based on current literature. The proportion
of time spent in the shallower NREM sleep stages 1 and 2 increases with
aging, mainly as a consequence of the decrease in proportion the more
restorative slow-wave (stages 3 and 4, or N3) sleep. The mean percentage of
slow-wave sleep decreases from 18.9% during early adulthood (16–25 years
old) to 3.4% during midlife (36–50 years old) [25]. The largest decrease in
delta sleep appears to occur during the first 100 minutes of sleep (NREM
period 1) and during early adulthood (between 20 and 40 years old) [7]. There
appears to be no further decrease in slow-wave sleep after age 70 years. Pos-
sible mechanisms for the decrease in slow-wave sleep in older individuals in-
clude the parallel decline in the growth hormone secretion [5] and the
predominant loss of parasympathetic activity, as suggested by the decreased
heart rate variability found in the elderly [26].
The same meta-analysis by Ohayon’s group concluded that the propor-
tion of REM sleep declined with aging [24]. The major decrement in
REM sleep occurs between young and middle adulthood, after which no
further change is noted. Meanwhile, the investigators also found a decrease
in REM latency with age, a finding that may easily be confounded by con-
comitant psychiatric disorders, drugs, alcohol, and sleep disorders. In addi-
tion, the distribution of REM sleep throughout the night appears to shift the
occurrence of REM sleep toward the earlier part on the night. REM sleep
was increased in the first quarter of the sleep episode and the increment
of REM sleep during the course of nocturnal sleep was diminished in the
older age group [27]. Wauquier and colleagues [28] monitored the sleep-
wake activity in 14 elderly individuals over the age of 88 using ambulatory
polysomnography, and also found a shift of REM sleep toward the first part
of the sleep period. Meanwhile, the stage from which sleep termination oc-
curs appears to shift with aging. Murphy and colleagues [29] examined sleep
termination in young adults (19–28 years old) and older adults (60–82 years
old) and found that while younger ones arose preferentially from stage
REM, older subjects were most likely to arise from a NREM sleep stage.
In addition, older subjects with higher sleep efficiencies were more likely
to also arise from stage REM.

Table 1
Age-related changes in polysomnographic characteristics
Increase Decrease
Sleep latency Total sleep time
Stage 1 sleep % Sleep Efficiency
Stage 2 sleep % Slow wave sleep %
Wake after sleep onset REM sleep %
REM latency
6 ESPIRITU

Sleep electrophysiology
Spectral analysis
Aging is associated with a reduction of power in the sleep EEG, as well as
frequency-specific changes in the brain topography. Landolt and Borbely [5]
performed spectral analysis of sleep EEG records comparing middle aged
healthy men (mean age of 62 years) and young men (mean age of 22.3
years), and found that the age-related reduction of EEG power in NREM
sleep (0.25 Hz–14 Hz) and REM sleep (0.75 Hz) is most pronounced in
the anterior derivation (frontocentral) toward the middle (central-parietal)
EEG derivation.

Sleep spindle and K-complex

The hallmarks of stage 2 sleep (sleep spindles and K complexes, [Fig. 1]) are
also altered with aging. Crowley and colleagues [30] analyzed the properties of
sleep spindles and K-complexes in 20 neurologically and medically healthy,
older adults (mean age of 75.5 years) not taking psychoactive medications,
and found a decrease in spindle number, density, and duration, as well as de-
crease in the number and density of K-complexes from young adult control
values. They also found a subtle yet significant increase (plus 0.5 Hz) in the
EEG frequency of spindles in the elderly. Nicolas and colleagues [31] corrob-
orated the progressive decrease in sleep spindle number, density, and dura-
tion, as well as the progressive increase in intraspindle frequency with age.
There also appears to be an altered circadian modulation of spindle frequency
in older adults. In young adults, spindle density and amplitude are higher,
while spindle frequency and its variability are lower during the biologic night
(when melatonin secretion is high) than during the day. In contrast,

Fig. 1. Hallmarks of Stage N2 sleep: K complexes and spindles.

 AGING-RELATED SLEEP CHANGES 7

Knoblauch and colleagues [32], using a 40-hour multiple-nap design under

constant-routine condition, detected a weaker circadian modulation (ie, de-
creased night-day difference and variability) of spindle frequency in older
adults (57–74 years old). These changes in the generation of spindles and
K-complexes may signify certain age-related changes in the thalamocortical
regulatory mechanisms involving NREM sleep.

Delta activity
Aging not only decreases the time spent in slow-wave (stages 3 and 4 or
stage N3) sleep, but also alters delta activity (Fig. 2). Smith and colleagues
[33] analyzed all slow waves (greater than 5 muV in magnitude between 0.5
Hz and 3.0 Hz) during the first 6 hours of nocturnal sleep in 25 healthy sub-
jects between 3 and 79 years old, and found that increasing age was associ-
ated with a decrement in the average peak amplitude of the delta waves,
slowing of delta frequencies, and a decrease in the incidence of waves greater
than 20 muV, particularly in the frontal areas. Meanwhile, Ehlers and
Kupfer [7] evaluated sleep EEG’s in 24 men without medical and psychiatric
illness, classified them into three age groups (21–30, 31–40, and 51–70 years
old) and performed computer-assisted delta and REM quantification, and
power spectral analysis. While Ehlers group corroborated Smith’s findings
on the expected age-related decrease in delta activity, the former group
found a shift in the spectral distribution of delta power toward the higher
rather than lower frequencies.

Rapid eye movements

Aside from the decrease in REM sleep proportion and distribution during
nocturnal sleep, REM density may be affected by aging. Darchia and col-
leagues [34] compared the eye movement density between elderly subjects
and young adults who underwent EEG and extraoculography for four

Fig. 2. Hallmark of Stage N3 (slow-wave sleep or Stages 3 and 4 sleep: delta waves).
8 ESPIRITU

nonconsecutive baseline nights, and found that the former had a significantly
lower incidence of rapid eye movements. Further studies are needed to
determine the neurocognitive implications of this decrease in REM activity
in the elderly. In summary, aging is associated with changes in the
electroencephalographic hallmarks of both NREM and REM sleep stages
(Table 2).

Body movements during sleep

In a study comparing 12 elderly with 7 young healthy subjects, Gori and
colleagues [35] found a significant general decrease in the number of body
movements during sleep, from infancy to adulthood and even into the later
ages. While body movements occurred predominantly during stage REM
(ie, phasic twitching of the skeletal muscles) in the young adult, they were
not specifically associated with any sleep state or stage in the elderly. The
investigators attributed the loss of preferential occurrence of body move-
ments during stage REM to the age-related change in the control of the sub-
cortical circuits by the motor cortex. Moreover, body movements in the
elderly appear to be significantly more disruptive of sleep than in the young
adults, as they are more often followed by either a shift in the sleep state or
a behavioral awakening.

Circadian rhythm
There is growing evidence that alteration of circadian rhythm (biologic
sleep-wake clock) may partly be responsible for age-related sleep changes.

Table 2
Age-related changes in properties of sleep stage hallmarks
Sleep stage Change in sleep stage hallmarks
Stage 2 (N2) Decrease in spindle number
Decrease in spindle density
Decrease in spindle duration
Increase in intraspindle frequency
Attenuation in modulation (ie, decrease in
night-day difference and variability) of spindle
frequency by the circadian rhythm
Decrease in the number of K complexes
Decrease in the density of K complexes
Stages 3 and 4 (N3 or slow-wave sleep) Decrease in the peak amplitude
Decrease in the incidence of slow waves
O 20 muV, especially in the frontal areas
Stage REM Decrease in the incidence of rapid eye movements
 AGING-RELATED SLEEP CHANGES 9

Monk and colleagues [36] compared a group of 45 healthy older men and
women (71–91 years old) with 21 young controls (19–28 years old) and
found that despite the older group’s similar social activities, involvement,
and greater regularity in daily lifestyle than the younger group, the older
group still had worse subjective and objective sleep as measured by the Pitts-
burgh Sleep Quality Index and nocturnal polysomnography, respectively.
Because sleep disruption in the elderly cannot be blamed solely upon the
age-related changes in daily social activities, it is, therefore, worthwhile to
explore other possible mechanisms for these sleep changes in the elderly.
Several studies have detected alterations in the circadian modulation of
sleep that may help explain findings, such as excessive daytime sleepiness, im-
paired sleep initiation and maintenance, altered sleep architecture, and phase-
advanced sleep schedule in elderly individuals. Münch and colleagues [37]
studied the circadian rhythms and spectral components of the sleep EEG in
17 young (20–31 year old) and 15 older (57–74 year old) volunteers under con-
stant posture conditions during a 40-hour nap protocol (75-minute sleep and
150-minute wake schedule). The investigators concluded that aging is associ-
ated with a weaker circadian arousal signal, based on the increased occurrence
of sleep episodes during the wake maintenance zone and the higher subjective
sleepiness ratings in the late afternoon and evening in the older group. They
also found a diminished melatonin secretion and a reduced circadian modula-
tion of REM sleep, together with less pronounced day-night differences in the
lower alpha and spindle range of sleep EEG activity in the older group.
Cajochen and colleagues [38] compared the responses of a group of
healthy older volunteers with those of younger adults to sleep deprivation
protocol (high sleep pressure condition) versus a nap protocol (low sleep
pressure condition). They also noted an age-related weakening of the circa-
dian arousal signal based on the higher propensity for sleep during the wake
maintenance zone, higher subjective sleepiness ratings in the late afternoon
and evening, diminished melatonin secretion, and reduced circadian regula-
tion of REM sleep and spindle frequency in the older subjects. Dijk and col-
leagues [27] investigated the circadian and homeostatic regulation of human
sleep during forced desynchrony in 13 older men and women and 11 young
men, and found that older people had reduced sleep duration at all circadian
phases and that sleep consolidation deteriorated more rapidly during the
course of sleep, especially when the second half of the sleep occurred after
the crest of the melatonin rhythm.
Vitiello and colleagues [39] also noted age-related changes in the circa-
dian temperature rhythms. Older men had higher temperatures at the nadir
of the temperature curve and lower peak-to-trough temperature curve am-
plitudes than younger men. Czeisler and colleagues [40] corroborated this
decreased amplitude of the endogenous circadian temperature oscillation,
but also noted that its phase occurred almost 2 hours earlier in the older
age group. Finally, in a study of 44 older subjects under a constant routine
protocol, Duffy and colleagues [41] noted that although the average wake
10 ESPIRITU

time and endogenous circadian phase of the older subjects did occur earlier
than that of 101 young men, the older subjects’ endogenous circadian tem-
perature nadir occurred later than relative to their wake time when com-
pared with the younger subjects. All of these studies demonstrate
alterations in the circadian modulation of sleep that may be partly respon-
sible for age-related changes in sleep quantity, quality, architecture, and
schedule in the elderly.

Sleep deprivation
The deleterious neurocognitive effect of sleep deprivation in healthy older
adults seems to be blunted. Bonnett [42] designed an experiment disrupting
sleep 14 times per hour, using auditory stimulus, in 12 normal 55- to 70-
year-old adults and another 12 normal young adults, and demonstrated that
older subjects had a smaller increase in total awakenings during the second
night of sleep disturbance and a slower increase in auditory arousal threshold
as the sleep disturbance progressed. More interestingly, the older subjects had
less performance deterioration in completing addition problems in the morn-
ing, when compared with the younger ones [18]. Adam and colleagues [43]
compared the psychomotor vigilance task performance of 11 older men
(mean age of 66.4 years) with a dozen healthy young men (mean age of 25.2
years) after 40 hours of prolonged wakefulness, and found that vigilant atten-
tion is less impaired in older men. In terms of age-related changes of the EEG
responses to sleep deprivation, Münch and colleagues [44] subjected healthy
young (20–31 year old) and older (57–74 year old) subjects to a 40-hour sleep
deprivation protocol, and noted that the frontal predominance of delta activ-
ity after sleep loss decreased with aging.

Respiratory function during sleep

Age-related degenerative changes in respiratory function have been re-
ported and may be partly responsible for the increased cardiovascular mor-
bidity and mortality in the elderly. Naifeh and colleagues [45] compared the
several respiratory variables in 11 healthy elderly subjects (older than 60
years) with 12 younger controls (30–39 years), and reported that the occur-
rence of sleep apneas, hypopneas, and arousals because of respiratory events
were increased in the older subjects. Although there were transient swings in
the pulse oximetry oxygen saturation and end-tidal and transcutaneous car-
bon dioxide tension associated with the respiratory events in the older sub-
jects, their mean values were maintained during sleep at the expense of the
loss of the sleep-related, physiologic drop in minute ventilation and tidal
volume found in the younger subjects [44]. Meanwhile, Hudgel and col-
leagues [46] documented an increased prevalence of periodic breathing in
healthy elderly individuals, which may be related to wide oscillations in
 AGING-RELATED SLEEP CHANGES 11

upper airway resistance producing fluctuating hypoventilation. Degenera-

tive changes in the hypercapnic ventilatory drive cannot be blamed for these
changes in respiratory parameters. Browne and colleagues [47] compared
the change in the hypercapnic ventilatory response from wakefulness to
sleep between 10 elderly and 10 young individuals without sleep apnea,
and found no difference. Further studies are needed to help elucidate the
mechanisms underlying these age-related changes in respiratory function.

Endocrine function during sleep

The widely known age-related changes in neuroendocrine function have
been responsible for the deterioration of health and quality of life in the el-
derly. Alterations in hormonal secretion during sleep may also be related to
the impaired sleep quality in older adults. Sherman and colleagues [48] stud-
ied the effect of age on the circadian rhythm of plasma cortisol in 34 normal
subjects, and demonstrated a negative correlation between age and the max-
imum cortisol secretion, the time of the nadir of the cortisol concentration,
and the acrophase. Kern and colleagues [49] measured the changes in corti-
sol and growth hormone secretion during nocturnal sleep in 30 male volun-
teers, aged 20 to 92 years, and found that growth hormone secretion
decreased while the cortisol nadir increased linearly as a function of age.
Several studies have tried to correlate these age-related changes in cortisol
and growth hormone secretion with sleep impairment in the elderly. Prinz
and colleagues [50] measured the 24 hour urine-free cortisol levels in 88
healthy, older, nonobese men and women (mean age of 70.6 years) and ob-
served that subjects with higher cortisol levels had more impaired sleep
(lower sleep efficiency, fewer minutes of stages 2, 3, and 4 sleep, and more
EEG beta activity during NREM sleep). Van Cauter and colleagues [25]
noted a biphasic decline in growth hormone secretion: early adulthood to
midlife is accompanied by a major decline in growth hormone secretion (mi-
nus 372 micrograms per decade) followed by a slower decline (minus 43 mi-
crograms per decade) from mid- to late-life. This biphasic decline in growth
hormone secretion correlated with a parallel decline in slow-wave sleep.
They also detected an age threshold of 50 years of age, after which evening
cortisol levels rose (plus 19.3 nmol/L per decade) together with worsening
sleep fragmentation and decline in REM sleep. The above reported changes
in nocturnal growth hormone and cortisol levels correlated significantly with
an age-dependent decrease in slow-wave sleep and REM sleep, and may be
partially responsible for the reduced restorative neurocognitive and anabolic
functions of sleep in the aged.

Summary
Normal aging is accompanied by changes in the sleep quality, quantity,
and architecture. Specifically, there appears to be a measurable decrease
12 ESPIRITU

in the ability to initiate and maintain sleep accompanied by a decrease in the

proportion of the deeper, more restorative slow-wave sleep and REM sleep
in the healthy elderly. There is epidemiologic evidence that this impaired
ability to initiate and maintain adequate sleep may be a marker of increased
mortality and neurocognitive dysfunction. On the other hand, napping
appears to have a salutary effect on neurocognitive function in the elderly.
Possible mechanisms related to these age-related changes in sleep include
age-related changes in circadian modulation, homeostatic factors, cardio-
pulmonary function, and endocrine function.

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