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Mortality Associated With Sleep Duration and Insomnia
Daniel F. Kripke, MD;
Lawrence Garfinkel, MA;
Deborah L. Wingard, PhD;
Melville R. Klauber, PhD;
Matthew R. Marler, PhD
Arch Gen Psychiatry. 2002;59:131-136.
ABSTRACT
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Background Patients often complain about insufficient sleep or chronic insomnia
in the belief that they need 8 hours of sleep. Treatment strategies may be
guided by what sleep durations predict optimal survival and whether insomnia
might signal mortality risks.
Methods In 1982, the Cancer Prevention Study II of the American Cancer Society
asked participants about their sleep duration and frequency of insomnia. Cox
proportional hazards survival models were computed to determine whether sleep
duration or frequency of insomnia was associated with excess mortality up
to 1988, controlling simultaneously for demographics, habits, health factors,
and use of various medications.
Results Participants were more than 1.1 million men and women from 30 to 102
years of age. The best survival was found among those who slept 7 hours per
night. Participants who reported sleeping 8 hours or more experienced significantly
increased mortality hazard, as did those who slept 6 hours or less. The increased
risk exceeded 15% for those reporting more than 8.5 hours sleep or less than
3.5 or 4.5 hours. In contrast, reports of "insomnia" were not associated with
excess mortality hazard. As previously described, prescription sleeping pill
use was associated with significantly increased mortality after control for
reported sleep durations and insomnia.
Conclusions Patients can be reassured that short sleep and insomnia seem associated
with little risk distinct from comorbidities. Slight risks associated with
8 or more hours of sleep and sleeping pill use need further study. Causality
is unproven.
INTRODUCTION
MANY PATIENTS complain to physicians about insufficient sleep and chronic
insomnia. Often they request medications for sleep year after year. There
has been little evidence-based guidance for the physician indicating when
treatment to increase sleep is advisable.1
A patient who sleeps 6 to 7 hours may be concerned that she or he is
not sleeping long enough, not realizing that 6 to 7 hours is currently the
population average.2-3 Many people
believe that 8 hours of sleep is required for health, but there is little
medical basis to recommend sleeping 8 hours or more. For example, a classic
study found that long sleepers reported less energy and had more psychopathology
than did short sleepers.4
Insomnia is not synonymous with short sleep. Patients commonly complain
of insomnia when their sleep durations are well within the range of those
people without sleep symptoms.5-6
A patient may be concerned by a 20-minute latency to fall asleep, or by awakenings
during the night, or by early awakening, when many people with the same sleep
latencies and awakenings consider their sleep perfectly satisfactory. Sometimes,
such complaints arise from misinformation about what sleep pattern is normal
for a person's age. At other times, sleep complaints may reflect a negative
self-view and the somatic concerns arising from depression. Insomnia complaints
are common symptoms of depression and a large variety of other emotional and
medical comorbidities that may not entail particularly short sleep.1, 7-11
Indeed, in the presence of sleep complaints, physicians make a diagnosis of
depression more often than a diagnosis of insomnia.12
Epidemiology can inform us what sleep patterns are associated with the
lowest mortality risk. In 1959 to 1960, the Cancer Prevention Study I (CPSI)
gave health questionnaires to more than 1 million adult Americans who were
followed up prospectively for 6 years. The lowest mortality was experienced
by women and men who reported sleeping 7 hours.6, 13
More excess mortality was associated with sleep durations of 8 hours or more
than with sleep of less than 7 hours. Excess mortality associated with long
sleep has also been observed in smaller prospective studies.14-23
The CPSI results indicated little if any association of "insomnia" with mortality.
In contrast, reported "sleeping pill" use "often" was associated with statistically
robust increased mortality risk after control for insomnia.6
A more recent study, the Cancer Prevention Study II (CPSII) of the American
Cancer Society, offered an opportunity to consider whether sleep durations,
insomnia, or sleeping pill use predicts mortality after more extensive control
for various sources of comorbidity.
SUBJECTS AND METHODS
PARTICIPANTS AND PROCEDURES
Data collection methods of CPSII have been described previously by the
American Cancer Society,24 and many results
of CPSII have been published.25-29
The current analyses were approved by the institutional review board of the
University of California, San Diego. Briefly, data were examined from more
than 1.1 million participants, mainly friends and relatives of American Cancer
Society volunteers, who were a diverse selection of American adults ranging
from 30 to 102 years of age. Participants completed health questionnaires
in the fall of 1982. The survival or date of death (from death certificates)
was ascertained 6 years later for more than 98% of the sample. Because recruitment
avoided the institutionalized as well as the most mobile individuals, sample
mortality was about 20% lower than for the US population of the same age,
but major causes of death resembled the distribution for the population. Data
tapes were kindly lent by the American Cancer Society.
Responses to the question, "On the average, how many hours do you sleep
each night?" were coded in categories from 2 to 9 hours. Fractional-hour responses
were coded as rounded integers, ie, 8 hours represented responses from 7.5
to 8.4 hours. All responses from 9.5 to 16.5 hours were combined in a final
category. There were too few responses of 2 hours for analysis. Reports of
sleeping less than 2 hours or more than 16 hours each night were considered
invalid (<0.1% of responses and coded missing). Responses were missing
or invalid for 1.4% of men and 1.7% of women. Responses to the question, "On
the average, how many times a month do you have insomnia?" were compressed
into categories of 0, 1, 2, 3, 4 to 9, and 10 or more times per month. Participants
reported past-month use of "prescription sleeping pills,"30
which probably included a mixture of different classes of medications.
STATISTICAL ANALYSES
To explore whether sleep durations predicted mortality, Cox proportional
hazards survival models31-32 (Cox
models) were computed for 636 095 women and 480 841 men, considering
the sexes as separate replicates. A total of 32 covariates were entered simultaneously
into the models, including sleep duration, insomnia frequency, and variables
reflecting demographic risk factors, habits, health, and medication use, selected
by preliminary identification of variables substantially predictive of mortality
risk (Table 1). The Cox models
estimated hazard ratios for each covariate, which indicated the extent to
which a covariate was associated with increased mortality as compared with
a reference. Hazard ratios for each reported sleep duration were referenced
to a hazard ratio of 1.0, which was assigned to the duration of 7 hours. This
arbitrary reference duration had been selected on the basis of CPSI results
and pilot analyses of CPSII data, suggesting that it would be the minimum.
For example, a hazard ratio of 1.12 for a group sleeping 8 hours would indicate
that those sleeping 8 hours were 12% more likely to die within the 6-year
follow-up than those sleeping 7 hours, other factors being equal. Similarly,
hazard ratios for each reported frequency of insomnia were compared with a
hazard ratio of 1.0 arbitrarily assigned to the reference of never having
insomnia. The 95% confidence intervals for the hazard ratios associated with
each reported sleep duration and each reported frequency of insomnia were
then estimated from the multivariate model. As a P<.05
significance criterion was selected, hazard ratios were considered significant
when a ratio of 1.0 was not included within these 95% confidence intervals.
Unlike the analyses of prescription sleeping pill hazards reported previously,30 all ages were considered together in these models.
Orthogonal linear, quadratic, and cubic terms were included for age and also
for estimated dietary fat and fiber. Categorical variables were entered as
several distinct levels. Model selection by backward elimination was used
to exclude from the models covariates with P>.10,
but almost all variables were retained. Inspection of cumulative hazard functions
based on Kaplan-Meier survival curves indicated that the proportional hazards
assumptions were acceptable.
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Covariate-Adjusted* Mortality Hazard Ratios From the Cancer Prevention
Study II (1982-1988)
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Similar Cox models were computed for 9 specific causes of death and
for all other causes. In addition, to examine interactions among sleep variables,
simplified Cox models were computed with SPSS10.0 (SPSS Inc, Chicago, Ill),
first including sleep duration, insomnia, sleeping pill use, and age in the
models, and then recomputing the models, removing either sleep duration, insomnia,
or sleeping pill use, one at a time.
RESULTS
The mean (SD) age for women was 57 (11) years, and for men, 58 (10)
years at the time when initial questionnaires were completed. Of the more
than 98% for whom follow-up was available, 9.4% of the men and 5.1% of the
women had died within the 6 years of follow-up. For women and men, respectively,
the causes of death were ischemic heart disease in 24% and 33%, other heart
disease in 9% and 9%, cerebrovascular accidents in 10% and 7%, breast cancer
in 10% and 0%, colon cancer in 4% and 3%, other cancers in 22% and 26%, accidents
in 2% and 2%, suicide in 1% and 1%, homicide in 0.2% and 0.2%, and other causes
in 18% and 18%.
The modal reported sleep duration was 8 hours among both women and men.
Almost half the sample reported a sleep duration of 7.5 hours or more. Almost
half of the women and more than 70% of men reported that they never had insomnia
(Table 1). Only 4.3% of women
and 2.6% of men reported insomnia 10 or more times per month. As might be
expected, more frequent insomnia and more frequent sleeping pill use were
reported among those sleeping less than 7 hours, but there was also a slightly
greater frequency of reported insomnia and sleeping pill use among those reporting
more than 8 hours sleep (Figure 1
and Figure 2). Partly because of
this U-shaped distribution, the product-moment correlations of reported hours
of sleep and frequency of insomnia were only -0.22 (P<.001) for women and -0.18 (P<.001)
for men, reflecting that reported insomnia had little linear association with
short reported sleep durations. Among women, the body mass index likewise
had a U-shaped relationship to sleep duration (Figure 1), but among men, there was a virtually monotonic trend
toward lower body mass indexes among those with longer sleep durations (Figure 2). Note that the mean body mass index
for men reporting 3 hours sleep had sufficiently wide confidence intervals
to be consistent with this trend.
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Figure 1. For 636 095 women, the average
reported frequency of insomnia, the average number of sleeping pills used
per month, and the mean body mass index (BMI) according to reported hours
of sleep. The 95% confidence intervals of the BMI are shown. Also shown are
the hazard ratios from the 32-covariate Cox models and the percentage of women
reporting each sleep duration. The reference duration of 7 hours is represented
by the lighter bars.
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Figure 2. For 480 841 men, data comparable
to those shown in Figure 1. BMI indicates body mass index.
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The hazard ratios for various sleep durations adjusted for 32 covariates
are given in Table 1. Figure 1 and Figure 2 illustrate that, among both women and men, the best survival
was experienced by those reporting a usual sleep duration of 7 hours, which
was 1 hour less than the modal sleep duration. Participants who reported sleeping
8 hours or more had distinctly and significantly increased mortality hazard:
the longer the reported sleep, the higher the mortality hazard. When reported
sleep exceeded 8.5 hours (as occurred among 7.5% of women and 7.7% of men),
the added risk associated with long sleep exceeded 15%. Reported sleep had
to be less than 3.5 hours among women (as occurred among only 0.1%) or less
than 4.5 hours among men (0.7% of men) for the added risk associated with
short sleep to exceed 15%.
Women reporting insomnia 1, 2, 3, 4 to 9, or 10 or more times per month
had covariate-adjusted hazard ratios between 0.81 and 0.87, all of which were
significantly less than the reference hazard of those reporting no insomnia
(Table 1). Men reporting insomnia
1, 2, 3, 4 to 9, or 10 or more times per month had hazard ratios of 0.87 to
0.94, all of which were likewise significantly less than the reference. Women
and men whose answer was missing also had ratios significantly less than the
reference, which would be expected if some with missing responses had insomnia.
As previously reported,30 participants
who reported prescription sleeping pill use had significantly elevated mortality
hazards, with control for sleep duration, insomnia, and other covariates (Table 1). The sleeping pill x insomnia
interaction terms, when tested, were not significant additions to the models.
In the simplified models without full covariate control for comorbidities,
hazard ratios (95% confidence interval) associated with 3 hours and 10 hours
of sleep reached 2.05 (1.68-2.50) and 2.14 (2.04-2.28) for women and 2.49
(2.05-3.01) and 2.19 (2.09-2.29) for men, respectively. However, removing
insomnia or sleeping pill use from these simplified Cox models had only negligible
effects (well within the confidence intervals) on the hazards ratios associated
with sleep duration. When sleeping pill use was removed from the simplified
models (ie, not controlled), the hazard ratio associated with insomnia increased
slightly; eg, for insomnia 10 or more times per month, the ratio increased
from 0.99 (0.94-1.05) to 1.05 (0.99-1.10) for women and from 1.15 (1.09-1.21)
to 1.24 (1.17-1.30) for men. Removal of sleep duration had even smaller effects
on insomnia hazard ratios. Moreover, there were only negligible effects on
the hazard ratios associated with sleeping pill use when insomnia or sleep
duration were removed from the simplified models.
For 8, 9, and 10 or more hours of sleep, the hazard ratios for cerebrovascular
deaths were elevated over the hazard ratios for death from all causes among
both women and men (P<.05 in 3 of 6 comparisons
in data not shown). Hazard ratios for deaths from accidents, cancers, heart
disease, suicide, and homicide were not consistently higher than the all-cause
hazard ratios associated with short and long sleep.
COMMENT
A physician can reassure a patient that it is no longer average to sleep
8 hours. The lowest mortality hazard was experienced by participants reporting
usual sleep of 7 hours (6.5-7.4 hours) per night. Sleep durations as short
as 4.5 hours were associated with mortality hazards lower than that of almost
half the sample. Comparison of the 32-covariate models with the simplified
CPSII models and the less-controlled CPSI tabulations6
showed that most mortality risk associated with short sleep could be explained
by comorbidities. Also, a recent population sampling found that short sleep
durations were not related to impaired health-related quality of well-being.33
Insomnia was not well defined in CPSII. There was only a weak correlation
of reported insomnia with short sleep and little interaction. Reported insomnia
was associated with no excess mortality hazard whatsoever, once sleeping pill
use and other comorbidities were controlled. The absence of significant insomnia
hazard noted in CPSI and CPSII has likewise been observed in smaller epidemiologic
studies that controlled for comorbidities.9-10,19, 23, 34-38
There is evidence that sleep complaints of various forms (not necessarily
insomnia) predict coronary heart disease, but the odds ratios may be reduced
with control for medications.39 Moreover, some
studies indicate that primary insomnia causes no substantial impairment of
function.1, 11 For example, patients
with insomnia may have no demonstrable loss of daytime alertness.1, 40 Less than 25% of patients referred
for insomnia have primary insomnia as a first diagnosis.41
Although there may be risks in depression, anxiety, heart disease, cancer,
lack of exercise, sleep apnea, and other conditions in which insomnia is often
present, patients with insomnia without underlying comorbidities can be reassured
that there appears to be no survival risk, as long as the patients refrain
from long-term use of sleeping pills. In one study, awakening during the night
predicted decreased mortality,8 similar to
the hazard ratios less than 1.0 shown in Table 1. However, we are not persuaded that insomnia is beneficial,
because we found no dose-response relationship of insomnia frequency to decreasing
hazard ratio, and a protective effect of insomnia was not suggested by the
simplified models before 32-covariate adjustment. By comparison, mortality
increased progressively in both men and women from 7 to 10 hours of sleep
and with increasing sleeping pill use, and these associations were even stronger
before adjustment for 32 covariates.
It is likely that control for additional risk factors or qualitatively
improved control would further reduce apparent sleep-associated risks. However,
there is a possibility that controlling statistically for comorbidities underestimates
the mortality risk associated with short or long sleep. For example, if short
or long sleep causes heart disease,42 then
correcting for a history of heart disease might obscure an underlying effect
of sleep duration.
Above 7.5 hours, the longer participants reported sleeping, the greater
their mortality hazard. Slightly elevated mortality hazard was noted even
among those with the modal sleep duration (8 hours), suggesting that sleep
duration is not merely a proxy for nonspecific hazardous deviations from modal
health. This result was highly consistent between replications for women and
men. It was also entirely consistent among age groups (unpublished observations
from Cox models described previously, examining 4 age ranges from age 30-50
to >70 years).30 Moreover, CPSII results were
consistent with those of smaller studies14-23
and with the previous results of CPSI.6
Currently, we do not know why sleep exceeding 7.5 hours was associated
with excess mortality. Sleep duration in itself may not be a causal factor.
Our group has suggested that sleep apnea might be a crucial underlying abnormality.43 The elevated hazard for cerebrovascular deaths might
be consistent with an apnea effect. Nevertheless, in a population study, we
more recently found no significant relationship of long sleep to sleep disordered
breathing.44 Furthermore, since obesity is
a key cause of sleep apnea, if sleep apnea were the major explanation, we
would have expected more association of high body mass indexes with long sleep
than is shown in Figure 2. Also,
the hazard ratios were controlled for body mass index. Depression was not
measured effectively in CPSII questionnaires, although depression might be
associated with short and long sleep. However, because most insomnia complaints
are accompanied by depression, we would have expected insomnia to predict
excess mortality if depression explained the mortality hazard associated with
short and long sleep. In addition, suicide deaths were not associated with
short or long sleep out of proportion. Lacking understanding of causality,
we cannot answer the crucial question of whether patients who sleep long could
extend their survival by curtailing their sleep.
Long sleepers composed more than 90% of those whose sleep duration was
associated with 15% or greater excess risk, although even for those sleeping
10 hours or more, the excess risk was modest. We may estimate that the sample
excess fraction of deaths related to sleep duration was 6.3% for women and
5.3% for men.45 If we allow the unproven assumption
that long and short sleep cause the excess hazards with which they are associated,
these would be the attributable risk fractions. In women, 83% of the excess
and 78% of the excess in men were associated with sleep of 8 hours or more.
Although polling and other data suggest a reduction in US population sleep
durations in the latter part of the 20th century since CPSI and CPSII questionnaires
were collected,2, 46-48
the health of the population has been improving. These data do not support
any speculation that the population is sleeping too little on average.
As previously observed30 and reiterated
in Table 1, the CPSII risk associated
with sleeping pill use was greater than any risk associated with insomnia.
Important limitations are that CPSII did not associate this mild mortality
risk with particular hypnotic compounds or prove causality. The most popular
hypnotics at the time CPSII data were collected, temazepam, triazolam, and
flurazepam hydrochloride, have been largely supplanted by new benzodiazepine
agonists with greater receptor specificity. It is unknown whether contemporary
hypnotics are associated with comparable risks.30
A multitude of factors are associated with insomnia, short sleep, and
the use of sleeping pills. No epidemiologic approach could leave us completely
confident that statistical control for comorbidities would be sufficient but
not excessive. To define causality, following the example of large randomizing
trials examining diet, exercise, and critical medications, it might be possible
to ascertain experimentally whether voluntary curtailment of sleep can prolong
life or influence comorbid conditions. Likewise, it should be possible to
determine experimentally whether any long-term treatment of chronic insomnia
is safe and efficacious.
AUTHOR INFORMATION
Accepted for publication June 26, 2001.
The American Cancer Society, New York, NY, supported collection of these
data. Analyses were supported by grants HL55983, HL61280, AG15763, and AG12364
from the National Institutes of Health, Bethesda, Md (Dr Kripke).
Presented in part at the Third International Congress of the World Federation
of Sleep Research Societies, Dresden, Germany, October 7, 1999, and the 14th
Annual Meeting of the Associated Professional Sleep Societies, Las Vegas,
Nev, June 20, 2000.
Corresponding author and reprints: Daniel F. Kripke, MD, Department
of Psychiatry 0667, University of California, San Diego, 9500 Gilman Dr, La
Jolla, CA 92093-0667 (e-mail: DKripke{at}UCSD.edu).
From the Departments of Psychiatry (Drs Kripke and Marler) and Family
and Preventive Medicine (Drs Wingard and Klauber), University of California,
San Diego; and The American Cancer Society, New York, NY (Mr Garfinkel).
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