Prevalence and Comorbidity of Insomnia and Effect on
Functioning in Elderly Populations
Sonia Ancoli-Israel, PhD z and Jana R. Cooke, MDw
A good night’s sleep is often more elusive as we age, because
the prevalence of insomnia in older people is high. Insuf-
ficient sleep can have important effects on daytime function
by increasing the need to nap, reducing cognitive ability
including attention and memory, slowing response time,
adversely affecting relationships with friends and family,
and contributing to a general sense of being unwell. How-
ever, rather than aging per se, circadian rhythm shifts,
primary sleep disorders, comorbid medical/psychiatric ill-
nesses, and medication use cause sleep difficulties in older
people, which psychosocial factors may also affect. Clini-
cians should ask elderly patients about satisfaction with
sleep. Any sleep complaints warrant careful evaluation
of contributing factors and appropriate treatment. J Am
Geriatr Soc 53:S264–S271, 2005.
Key words: insomnia; elderly; comorbidity; circadian
rhythm shifts
S leep disorders are common, with about one-third of
people in the general population complaining of sleep
difficulties.1 About three-fourths of those who have trouble
sleeping say that the problem is ‘‘occasional,’’ averaging
about 6 nights per month.1 The other 25% have frequent or
chronic insomnia, averaging about 16 nights per month.1
The risk of sleep disorders increases with age,2 and insom-
nia affects approximately 20% to 40% of older adults at
least a few nights per month.3,4 In a study of more than
9,000 participants aged 65 and older, only 12% reported no
sleep complaints, and more than half reported chronic sleep
difficulties occurring most of the time. Sleep complaints
were reported as difficulty initiating or maintaining sleep
(43%), nocturnal waking (30%), insomnia (29%), daytime
napping (25%), trouble falling asleep (19%), waking too
early (19%), and waking without feeling rested (13%).4
From the Department of Psychiatry and wDepartment of Medicine, Division
of Pulmonary and Critical Care, University of California at San Diego,
San Diego, California; and zVeterans Affairs San Diego Healthcare System,
San Diego, California.
Address correspondence to Sonia Ancoli-Israel, PhD, Department of
Psychiatry, University of California at San Diego, 3350 La Jolla Village Drive,
San Diego, CA 92161. E-mail: sancoliisrael@ucsd.edu
DOI: 10.1111/j.1532-5415.2005.53392.x
JAGS 53:S264–S271, 2005
r 2005 by the American Geriatrics Society
However, the prevalence of insomnia appears to be high
mostly in older people who are in poor health and require
medications, as indicated in a recent review of the topic.5 It
should also be mentioned that many of the epidemiological
studies reporting a high prevalence of insomnia in older
people did not simultaneously assess sleep dissatisfaction.5
Studies that evaluated both aspects did not show that the
prevalence significantly increases with age.5
CONSEQUENCES OF POOR SLEEP
Insomnia is an important concern in elderly patients, not
only because it is common, but also because it can cause
clinically relevant daytime impairments. Falling asleep dur-
ing the day is almost always a sign of insufficient sleep; it is
neither normal nor acceptable for a person of any age to
have trouble staying awake during the day or to fall asleep
during normal activities. Inability to sleep can also lead to
difficulty sustaining attention, a slowed response time, im-
pairments in memory and concentration, and decreased
performance. These symptoms are of particular concern in
older people, because they may be misinterpreted as symp-
toms of dementia/mild cognitive impairment.6,7 Slowed re-
sponse time is particularly important because it can affect
driving ability and increase the risk of falls.8 Perhaps most
startling is that insomnia is also associated with shorter
survival. Mortality due to common causes of death (e.g.,
heart disease, stroke, cancer, suicide) is up to two times
higher in elderly persons with sleep disorders than in those
who sleep well.9–11
Other impairments associated with insomnia include
inability to enjoy family and social relationships, increased
incidence of pain and sense of being in poor health, de-
creased ability to accomplish daily tasks, and increased
consumption of healthcare resources.6
HOW AGE AFFECTS SLEEP
Sleep architecture changes with age. In particular, the deep-
er levels of sleep, Stages 3 and 4, decrease, with older adults
having almost no deep sleep.12,13 This results in more of the
night spent in lighter levels of sleep, which makes it more
likely that the older adult will wake up more often during
the night. Many people believe that older adults sleep less at
night because they need less sleep, but recent surveys sug-
gest that, even though sleep architecture changes, most
0002-8614/05/$15.00
JAGS JULY 2005–VOL. 53, NO. 7
older adults report sleeping about 7 hours a night on week-
days and weekends.14,15 Data now suggest that aging per se
does not cause sleep disruption;4,14 rather it is the ability to
sleep that decreases with age. It is therefore crucial for the
healthcare professional to be able to identify the reasons
that the ability to sleep is decreased. These factors include
circadian rhythm disturbances, primary sleep disorders,
medical/psychiatric illness, side effects of drugs/medica-
tions, and psychosocial factors.
CIRCADIAN RHYTHM DISTURBANCES
Circadian rhythms are 24-hour physiological rhythms such
as endogenous hormone secretions, core body temperature,
and the sleep-wake cycle controlled by an internal pace-
maker housed in the suprachiasmatic nucleus in the anterior
hypothalamus.16 External zeitgebers (literally time-givers
or cues), such as light, synchronize circadian rhythms to the
24-hour day. Loss of neurons in the suprachiasmatic nu-
cleus with advanced age may account for some of the age-
related circadian phase shift.17
As people age, the sleep/wake circadian rhythm may
become less synchronized (may no longer have the same
response to external cues) and may become weaker (less
robust), resulting in less-consistent periods of sleep/wake
across the 24-hour day. The sleep/wake cycle in the older
adult also shifts or advances, a condition called advanced
sleep phase syndrome (ASPS).18 Changes in the sleep/wake
cycle are likely due to changes in the core body temperature
cycle, decreased light exposure, and environmental factors.
More recent research suggests there may also be a genetic
component.19,20
Older adults with ASPS get sleepy in the early evening
and wake up in the early morning hours, in part because the
core body temperature is dropping earlier in the evening
(perhaps at about 7:00 p.m. or 8:00 p.m.) and rising about 8
hours later (at about 3:00 a.m. to 4:00 a.m. (Figure 1).21
This results in complaints of waking up in the middle of the
night and being unable to return to sleep. Other patients
with ASPS may inadvertently fall asleep watching television
or reading in the early evening and then experience insom-
nia when they get into bed later in the evening, yet because
of their circadian clock, they will still wake up in the early
morning hours. This can result in complaints of difficulty
falling asleep and difficulty staying asleep.22,23
Patients who seek treatment might present with symp-
toms that are similar to symptoms of sleep-maintenance
insomnia. The clinician should obtain an extensive sleep
Sleepy,
Go to Bed
Standard
Phase
6:00 7:00 8:00 9:00 10:00 11:00 12:00 1:00 2:00 3:00 4:00 5:00 6:00 7:00 8:00 9:00 10:00 11:00
Midnight
Sleepy Go to Bed
Figure 1. Standard versus advanced phase sleep. Reprinted from All I Want Is a Good Night’s Sleep, Ancoli-Israel S., 1996, with
permission from Elsevier.21
PREVALENCE AND COMORBIDITY IN THE ELDERLY S265
history and at least 1 to 2 weeks of sleep diaries. If possible,
the patient should also wear a wrist actigraph for several
days to 1 week, allowing for the objective examination of
the shifting of the sleep/wake cycle. If these assessments
suggest early evening sleepiness and early evening bedtimes
along with early morning awakenings, the clinician should
suspect ASPS.
Because shifting of the circadian rhythm is a common
and expected development in older age, patients should
be educated that ASPS is not a medical disorder and does
not necessarily need to be treated. Treatment is dependent
on the extent of the discomfort the ASPS has on the patient’s
day-to-day life. Patients often complain that their waking
hours are no longer consistent with societal norms, caus-
ing them to be awake (or asleep) when those around them
are not.
Previous reports have used 1,000 lux or 2,000 lux as
their cutoff for amount of bright light exposure. Healthy
older adults, on average, are exposed to only 60 minutes of
light of more than 1,000 lux a day,24 and elderly demented
patients living in the community are exposed to about
30 minutes of light of more than 2,000 lux a day.25 How-
ever, demented nursing home patients receive, on average,
no light exposure of more than 2,000 lux and only 10 min-
utes of light of more than 1,000 lux per day.26,27
By increasing light exposure later in the day, it is pos-
sible to delay the sleep/wake circadian rhythm. Specifically,
exposure to bright light in the late afternoon or early
evening will delay the rhythm (patient will become sleepier
later in the day, allowing them to stay alert longer). Expo-
sure to bright light will not only delay the sleep/wake cir-
cadian rhythm but will also delay related rhythms, such as
core body temperature and endogenous melatonin. To de-
lay the advanced sleep/wake rhythm, patients with ASPS
should be exposed to very bright light during the late af-
ternoon to early evening. The best source of bright light is
sunlight; therefore, patients should attempt to spend time
outdoors in the late afternoon. Because the mechanism of
the light is primarily through the eyes, sunglasses should not
be worn, although sunglasses should be worn in the morn-
ing to avoid having rhythms advance even more. Normal
room light is not generally bright enough to shift rhythms.
Therefore, if the patient is unable to spend sufficient time
outdoors, another option is a special commercially avail-
able ‘‘light box.’’ Sitting in front of a light box of 10,000 lux
each evening for 30 minutes will help shift the rhythms.28
Light boxes have also been used successfully to improve
sleep in patients with dementia living in nursing homes.29,30
Wake
Up
Advanced
Phase
Wake Up
S266 ANCOLI-ISRAEL AND COOKE
The second potential treatment is the administration of
exogenous melatonin. Melatonin is an endogenous hor-
mone secreted by the pineal gland primarily at night. The
secretion of melatonin is synchronized with the sleep/wake
circadian rhythm because it is stimulated by darkness and
inhibited by light. Melatonin secretion decreases gradually
with age, which may be an important element in the devel-
opment of disturbed sleep and shifted rhythms in this pop-
ulation. Melatonin has been shown to be effective in
synchronizing the sleep/wake circadian rhythms and pro-
moting good-quality sleep in several populations suffering
from inappropriately synchronized rhythms, such as blind
persons and persons suffering from jet lag.31,32 Melatonin
replacement therapy is currently being explored as a treat-
ment for ASPS. Clinicians should be cautious when recom-
mending melatonin for regular use. Although there are no
reports of any significant long-term side effects of me-
latonin, longitudinal studies are still needed. Moreover, in
the United States, melatonin is considered an herbal sup-
plement and is not regulated by the Food and Drug Ad-
ministration. Therefore, there are no clear guidelines for
correct timing and dosage of melatonin and no manage-
ment of the exact composition, purity, or dosage of mel-
atonin sold over the counter.
PRIMARY SLEEP DISORDERS
There are several primary sleep disorders that are common
in older adults, including periodic limb movements in sleep
(PLMS) and the related disorder, restless legs syndrome
(RLS), sleep-disordered breathing, and rapid eye movement
(REM) sleep behavior disorder (RBD).
Clusters of repeated leg jerks characterize PLMS, which
occur approximately every 20 to 40 seconds over the course
of the night, with each jerk causing a brief awakening.
These awakenings result in complaints of difficulty falling
asleep and difficulty staying asleep, with subsequent day-
time sleepiness. The number of limb movements followed
by arousals per hour of sleep is called the periodic limb
movement index (PLMI). A clinical diagnosis of PLMS is
made when a patient has a PLMI greater than 5. The prev-
alence of PLMS increases significantly with age. The prev-
alence of PLMS in older adults is estimated at 45%,
compared with 5% to 6% in younger adults.33,34 There is
no sex difference.33
Another disorder, often comorbid with PLMS, is RLS.
Dysesthesia in the legs, usually described by patients as ‘‘a
creeping crawling sensation’’ or ‘‘pins and needles,’’ which
can only be relieved with movement, characterizes RLS.35
These sensations often occur whenever the patient is in a
restful, relaxed state. About 80% of patients with RLS have
PLMS, but only about 30% of patients with PLMS have
RLS. Debate continues regarding the exact nature of rela-
tionship between these two entities and whether PLMS is a
diagnosable condition separate from RLS.
The most common complaints of patients with PLMS
are sleep initiation insomnia, sleep maintenance insomnia,
and excessive daytime sleepiness. Patients may or may not
be aware of leg kicks or jerks. Some may complain simply of
having difficulty falling asleep or staying asleep, with no
knowledge that they kick. Often, bed partners may be aware
of the leg movements and may move into a separate bed.
JULY 2005–VOL. 53, NO. 7 JAGS
Table 1. Dopaminergic Agents for Treatment of Periodic
Limb Movements in Sleep and Restless Legs Syndrome
Dose Other Dosing
Drug mg/d Instructions
Levodopa/carbidopa 25/100
Pergolide 0.05–1.00 Divided doses
(dinner/bedtime)
Pramipexole 0.125–0.500
Ropinirole 0.5–4.0
Gabapentin 600–2,400 1/3 dose at noon;
2/3 dose at 9 p.m.
Those with PLMS and RLS may also complain of uncom-
fortable sensations in their legs during the day. Clinicians
should assess patients with symptoms of RLS for anemia,
uremia, and peripheral neuropathy before treatment.
Fortunately, treatment for PLMS and RLS is improv-
ing. Although sedative hypnotics used to be favored, do-
paminergic agents (Table 1) are now preferred for their
greater efficacy.36,37
Levodopa/carbidopa appears to reduce PLMS symp-
toms during the first few hours of sleep but less so during the
morning hours.38 More-effective treatments of choice are
pergolide, pramipexole, and ropinirole.38 Dramatic results
were reported in a double-blind, randomized, crossover
study of 10 patients with RLS, in which pramipexole nor-
malized sensory and motor functions,39 and there was no
evidence of a decrease in therapeutic effect over a mean 7.8
months of follow-up.40 In placebo-controlled, randomized
studies of patients with RLS, pergolide significantly reduced
symptoms of RLS and PLMS and increased total sleep time
and sleep efficiency41,42 and in a comparative study was
found to be superior to levodopa.43 Similarly, ropinirole has
also been shown to be more effective than placebo in im-
proving symptoms of RLS,44,45 with complete resolution of
symptoms in eight of 22 patients (36%) in one study.44
Gabapentin also was found effective in reducing PLMS
symptoms and improving sleep architecture in patients with
RLS in a randomized, placebo-controlled, crossover
study.46 In another randomized study, gabapentin and
ropinirole were found to be similarly tolerated and effective
in treating PLMS and sensorimotor symptoms in patients
with idiopathic RLS.47 The underlying pathophysiology of
PLMS is poorly understood, but the efficacy of do-
paminergic agents in treating this condition suggests that
the dopaminergic system plays a role in the disorder.
Sleep disordered breathing (SDB) is another disorder
common in the older adult, contributing to a decreased
ability to sleep at night. Hypopneas (partial respiration) and
apneas (complete cessation of respiration) during sleep
characterize SDB. Each respiratory event lasts a minimum
of 10 seconds, and the events occur repeatedly over the
course of the night. The cessations in breathing in SDB lead
to repeated arousals from sleep, as well as reductions in
blood oxygen levels over the course of the night, which
result in nighttime hypoxemia.
SDB is more common in older adults than younger
adults. The prevalence of SDB is approximately 4% to 9%
in middle-aged men and women (30–60), compared with
JAGS JULY 2005–VOL. 53, NO. 7 PREVALENCE AND COMORBIDITY IN THE ELDERLY S267

45% to 62% in older adults (
60).48,49 In addition, in the Examples of chronic illness or conditions that are known to
older population, SDB is more common in men than women disrupt sleep include arthritis or other musculoskeletal pain,
and in patients with hypertension.49 Some research has malignancy, menopause, dementia/Alzheimer’s disease, Par-
suggested that SDB is more severe in older African Amer- kinson’s disease, angina pectoris, congestive heart failure,
icans than in older Caucasians.50,51 asthma, stroke, chronic obstructive pulmonary disease, and
The main symptoms of SDB are snoring and excessive gastroesophageal reflux disease. A survey conducted by the
daytime sleepiness. It is often these symptoms that bring the National Sleep Foundation helped to elucidate the extent to
patient into the clinic to seek help. The snoring, which is which medical illnesses affect sleep in older adults. Results
often extremely loud, is reflective of the airway collapse. suggested that there was a greater prevalence of insomnia in
The loud snoring sometimes forces bed partners to move those with a variety of chronic illnesses, particularly heart
into separate bedrooms. disease, lung disease, arthritis, and stroke (Table 2).14,15
The excessive daytime sleepiness in SDB has been as- In addition, those with four or more medical conditions
sociated with repeated nighttime awakenings, which fre- had significantly more complaints of difficulty sleeping
quently follow the apneic events, and with intermittent and increased dissatisfaction with their sleep.14,15 Treating
nighttime hypoxemia. Daytime sleepiness can be a debili- comorbid medical problems may reduce their effect on sleep
tating symptom, causing social and occupational difficul- but is not likely to cure insomnia entirely. It is important to
ties, reduced vigilance, and cognitive deficits, including keep in mind that, in patients with insomnia and comorbid
decreased concentration, slowed response time, and mem- illnesses that contribute to poor sleep, both conditions must
ory and attention difficulties. These symptoms may be par- be addressed.
ticularly relevant to older adults, who are at an increased Psychiatric disorders, particularly depression, are also
risk of developing such symptoms with aging. SDB may associated with an increased risk of insomnia. In a recent
unnecessarily exacerbate these cognitive deficits. survey conducted by the National Sleep Foundation, older
SDB is a risk factor for other health problems, includ- adults with depression were more likely than those with no
ing hypertension and cardiac and pulmonary problems,52,53 depression to complain of sleeping less than 6 hours per
which can then lead to increased risk of mortality.54–56 Al- night, any insomnia, and excessive daytime sleepiness
though cause and effect have not been determined, treating (Table 2).39,40 In fact, insomnia is one of the diagnostic
the SDB reduces the severity of the hypertension and heart criterion for a major depressive episode.62 In older people,
disease as well as reducing the risk of shorter survival. the presence of depressed mood may also be a predictor
Treatments for SDB include continuous positive airway of insomnia.63 Insomnia is also more common in a variety
pressure (CPAP) (a device that pushes positive pressure into of other psychiatric disorders such as anxiety.64–66
the airway through a nose mask that acts as a splint to keep Nevertheless, the relationship between insomnia and
the airway open during sleep), weight loss, use of dental/ depression is complex. Depression is not only known
mechanical devices, and surgery. to contribute to sleeplessness, but the reverse is also true;
RBD is a parasomnia, characterized by loss of normal insomnia is an independent risk factor for depression.67
muscle skeletal atonia during REM sleep associated with Insomnia is more strongly associated with major depress-
vivid, usually frightening or disturbing dreams. With this ion than with any other medical disorder.68 As part of a
condition, patients typically ‘‘act out’’ their dreams, result-
ing in violent or injurious behavior in some. About 90% of
RBD patients are male, with a typical age of onset in the
sixth or seventh decade of life.57,58 Table 2. National Sleep Foundation: 2003 Sleep in Amer-
Evolving literature suggests that RBD may reflect a ica Poll15
dysfunction of REM sleep control that has significant im- Prevalence of Prevalence
plications for understanding certain neurodegenerative dis- Any Symptom of Daytime
orders, particularly Parkinson’s disease (PD) and dementia of Insomnia Sleepiness
with Lewy bodies (DLB). Some of the initial work on RBD Comorbid
was incidentally studied in several patients who also had Condition %
PD.59 Further studies have elucidated the fact that RBD
Hypertension
tends to herald the onset of parkinsonism or dementia in
Yes 51 17
patients with PD, DLB, and multiple system atrophy by No 45 13
years to decades.58 In several series, RBD has preceded de- Heart
mentia and parkinsonism in more than 60% of pa- Yes 57 22
tients.60,61 Some speculate that, if RBD represents the No 46 13
earliest clinical manifestation of an evolving neurodegener- Arthritis
ative disorder, intervening at this stage with agents that Yes 56 18
affect the underlying neurodegenerative process may delay No 41 12
or prevent its development.58 Lung disease
Yes 64 24
No 46 13
MEDICAL/PSYCHIATRIC ILLNESSES THAT Depression
CONTRIBUTE TO INSOMNIA Yes 70 32
Most elderly persons suffer from one or more chronic med- No 44 11
ical illnesses, many of which can cause difficulty sleeping.
S268 ANCOLI-ISRAEL AND COOKE
Figure 2. Three-day actigraphy recording in a nursing home patient with severe dementia. The actigraphy device measures wrist
movement, with greater movements producing spikes of greater amplitude on the recordings and quiet periods suggesting sleep. Note
that in this patient, no extended period of sleep occurs, as is common in many nursing home patients with dementia. Reprinted with
permission.72
National Institute of Mental Health Epidemiologic Catch-
ment Area study, 7,954 persons were questioned about their
sleep and any psychiatric symptoms at baseline and again a
year later. Psychiatric disorders were identified in 40.0% of
those with insomnia and 46.5% of those with hypersomnia,
compared with only 16.4% of those with no sleep com-
plaints. Those who had insomnia at both interviews were
far more likely to develop new major depression than those
without insomnia (odds ratio (OR) 5 39.8, 95% confidence
interval (CI) 5 19.8–80.0). In contrast, those whose insom-
nia had resolved by the second visit had a much lower risk
of depression (OR 5 1.6, 95% CI 5 0.5–5.3).64
Dementia also contributes to poor sleep. A study of
sleep and circadian rhythm patterns in nursing home pa-
tients with dementia was performed using actigraphy,
which measures wrist movement to distinguish periods of
sleep from periods of wakefulness, and measuring light ex-
posure.69,70 This study showed that nursing home patients
with dementia spent the entire 24-hour day dozing and
waking without ever being completely awake or completely
asleep for a full hour71 (Figure 2).72 Patients with severe
dementia slept more during the day and night but did not
significantly differ from a composite group of patients with
moderate, mild, or no dementia with regard to number of
awakenings or naps, and both groups had extremely frag-
mented sleep.73
Light exposure may be an important contributing factor
to sleep disturbance in nursing home patients. Even common
areas and multipurpose rooms at nursing homes are often
kept too dim, providing insufficient daytime light exposure.
In a study that used a wrist-mounted monitor to measure
light exposure in nursing home residents, median light ex-
posure was only 52 lux (mean 485 lux). As mentioned
above, patients spent a median of only 10.5 minutes (mean
34 minutes) in light stronger than 1,000 lux, and 17% were
JULY 2005–VOL. 53, NO. 7 JAGS
never exposed to light brighter than 1,000 lux. Regardless of
dementia level, greater daytime light exposure was associ-
ated with fewer awakenings at night, although severe de-
mentia was associated with increased daytime sleep.27
Bright light therapy during the day helps consolidate sleep
and makes the circadian rhythm more robust.29,30
Nursing home residents are also commonly exposed to
too much light at night because lights are often left on or
turned on during the night in sleeping rooms to facilitate
nursing care.74
Darkness at night is needed to promote secretion of
melatonin from the pineal gland, which induces sleepiness
and helps control the sleep-wake cycle.75 Nursing homes
also often have noisy nighttime environments, which can
further contribute to difficulty sleeping at night.76,77
DRUGS/MEDICATIONS
In evaluating a patient with insomnia, it is important to
consider not only comorbid illnesses, but associated treat-
ments as well. A number of medications are stimulating and
can cause insomnia, including central nervous system stim-
ulants, beta blockers, bronchodilators, calcium channel
blockers, corticosteroids, decongestants, stimulating anti-
depressants, and thyroid hormones. Use of sedating drugs
(e.g., long-acting hypnotics, antihypertensives, antihista-
mines, tranquilizers, and certain antidepressants) that pro-
mote daytime napping can also result in subsequent night-
time insomnia. It is sometimes possible to improve sleep by
adjusting the dose or timing of administration of these
drugs. If possible, sedating medications should be taken
at night and stimulating medications should be taken early
in the day.
Use of other drugs, such as alcohol, caffeine, and nic-
otine, should also be considered in evaluating insomnia.
JAGS JULY 2005–VOL. 53, NO. 7
Many older adults who are having difficulty sleeping will
indulge in a glass of alcohol at night to help make them
sleepy. Although alcohol does promote sleep initially, it
subsequently promotes insomnia by causing awakening as
its concentration in the bloodstream declines. A patient
who drinks just before bedtime to get to sleep is likely to
wake at around 1:00 a.m. to 2:00 a.m., whereas someone
who drinks at dinnertime is likely to be sleepy after dinner
but then wide awake and unable to fall asleep at bedtime.
Because patient perception is usually that alcohol helps
promote sleep, clinicians should ask patients with sleep
complaints about the extent and timing of their alcohol
consumption and should educate patients that these be-
haviors may be contributing to their sleep problems.
Caffeine is known to decrease total sleep time and in-
crease awakenings.78 It is important to remind older adults
that caffeine is found not just in coffee but also in decaf-
feinated coffee, teas, and sodas. For the older adult with
difficulty sleeping, caffeine, with a half-life of 3 to 5 hours
(but with such variability that in some adults the half-life is
extended to 10 hours) should be avoided after lunch. Sim-
ilarly, because nicotine contributes to sleep difficulties, cli-
nicians should remind patients that this provides yet
another good reason to quit smoking.
PSYCHOSOCIAL FACTORS
Psychosocial factors such as retirement, isolation, loneli-
ness, and bereavement may promote insomnia in older
people. Decreased activity, particularly in those who are
bedridden or sedentary, may also affect sleep patterns,79
although the relationship between exercise and sleep is less
clear. Older adults who are physically fit have better sleep at
night. Subjective sleep quality has been shown to improve in
depressed older people who participate in a supervised
weight-training program three times per week.80 Similarly,
otherwise healthy elderly with subjective complaints of
sleep found improvement in sleep quality with moderately
intense aerobic exercise,81 although recent epidemiological
data on the value of exercise for sleep show only modest
effects of exercise on sleep.82 Others have found that older
adults who exercise earlier in the day had longer exposure
to natural bright light and reported better sleep quality, but
there were no strong associations between physical exercise
and subjective reports of sleep.83 In a recent review of the
association between exercise and sleep, several important
points were discussed, including the tendency of studies to
use small groups of good sleepers as subjects, the differences
in the exercise protocols used, and the potential interactions
between individual characteristics (age, sex, fitness level).84
Meta-analyses have shown that exercise affects several
sleep architecture parameters, including increasing the total
sleep time and slow wave sleep, delaying REM onset, and
reducing REM sleep,84 but the generally accepted belief
that exercise is a nonpharmacological sleep promoter has
yet to be proven scientifically.
PUTTING IT INTO PRACTICE: TIPS FOR
IMPROVING SLEEP IN ELDERLY PATIENTS WITH
INSOMNIA
Sleep difficulties are common, particularly in elderly pa-
tients, and can cause significant impairments. Therefore,
PREVALENCE AND COMORBIDITY IN THE ELDERLY S269
elderly patients should be asked whether they are getting
enough sleep and feel well rested during the day. All patients
with complaints of sleep difficulties should undergo a de-
tailed sleep history regarding the nature of the sleep com-
plaint and possible contributing factors, including circadian
rhythm shifts, PLMS/RLS and apneas, comorbid medical/
psychiatric conditions and their treatments, and use of al-
cohol/caffeine/nicotine. In some cases, it may be useful to
have patients keep sleep diaries for at least 2 weeks and to
interview the patient’s sleep partner to find out more about
sleep habits, daytime sleepiness, snoring, or other abnormal
behavior during sleep. Underlying conditions should be
treated, but clinicians should be aware that the insomnia
may need direct treatment as well. Doses and timing of
administration of concomitant medications should be re-
viewed. Exposure to light should be maximized during the
day, particularly in the evening hours, and light should be
avoided during sleep time. Patients should also be advised
to limit naps to no more than 30 minutes in the early af-
ternoon and to avoid all caffeine after lunch. Heavy meals
and alcohol should also be avoided before bedtime, al-
though a light snack before going to sleep may be helpful in
some patients. Reduced fluid intake before sleep can be
helpful for patients awakened by nocturia.
Clinicians who practice in nursing home settings
should consider all possible underlying causes of sleep
problems and should also consider use of bright light boxes
and environmental strategies to promote daytime light ex-
posure and to minimize light exposure and noise at night.
For example, nurses can be instructed to use flashlights
rather than turning on room lights during nighttime assess-
ments and to minimize nighttime noise. Ideally, nursing
home residents should also be matched with appropriate
roommates so that good sleepers are not paired with room-
mates who frequently pace the room or are agitated during
the night.74
Pharmacological management of insomnia in older
people is discussed in detail elsewhere in this supplement. In
addition to pharmacotherapy, direct treatment of insomnia
may also include cognitive-behavioral therapy,85,86 stimu-
lus-control therapy,87 or sleep-restriction therapy.88 In ad-
dition, teaching good sleep hygiene rules should be included
with all other treatments. By addressing sleep complaints
and helping patients to achieve a better night’s sleep, cli-
nicians are also helping patients to function at a more op-
timal level during the day.
ACKNOWLEDGMENT
Financial Disclosure: Dr. Sonia Ancoli-Israel is a member of
the advisory board/speakers bureau and is a consultant for
King Pharmaceuticals, Inc., Neurocrine Biosciences, Se-
pracor Inc., Takeda Pharmaceuticals North America, and
Sanofi-Aventis. She has also received a consulting fee from
Sepracor Inc. Dr. Ancoli-Israel is supported by NIA
AG08415, NCI CA85264, GCRC Grant M01 RR00827,
the Department of Veterans Affairs VISN-22 Mental Illness
Research, Education and Clinical Center, and the Research
Service of the Veterans Affairs San Diego Healthcare Sys-
tem. Dr. Cooke has not specified any significant relation-
ships with industry.
S270 ANCOLI-ISRAEL AND COOKE
Authors’ Contributions: Sonia Ancoli-Israel presented
at the CME symposium and reviewed and edited the sup-
plement manuscript for content. Jana R. Cooke assisted
with the writing of the manuscript.
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