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Progress in Cardiovascular NURSING (ISSN 0889-7204) is published Quarterly (March, May, July, Nov.) by CHF, Inc.

, Three Parklands Drive, Darien, CT 06820-3652. Copyright ©2004 by CHF, Inc. All rights reserved. No
part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission
in writing from the publishers. The opinions and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for commercial
purposes, please contact Sarah Howell at showell@lejacq.com or 203.656.1711 x106.

Review Paper

The Impact of Daily Sleep Duration on Health:


A Review of the Literature
Gonzalo G. Alvarez, MD; Najib T. Ayas, MD, MPH

A healthy amount of sleep is paramount to leading


a healthy and productive lifestyle. Although chronic
sleep loss is common in today’s society, many people
A dequate daily sleep is an important part of a
healthful and productive lifestyle; however, chron-
ic sleep restriction in today’s society is very common.
are unaware of the potential adverse health effects of American adults only sleep an average of 6.85 hours
habitual sleep restriction. Under strict experimental con- per night.1 Furthermore, only 37% of Americans report
ditions, short-term restriction of sleep results in a variety obtaining ≥8 hours of sleep each night, and 31% of
of adverse physiologic effects, including hypertension, adults report sleeping <6 hours each night.1
activation of the sympathetic nervous system, impair- There are many potential explanations for the high
ment of glucose control, and increased inflammation. prevalence of sleep restriction. First, the demands of
A variety of epidemiologic studies have also suggested today’s 24-hour society, including long work hours
an association between self-reported sleep duration and rotating night shift work, can lead to sleep restric-
and long-term health. Individuals who report both an tion.2 Second, family needs superimposed on work-
increased (>8 h/d) or reduced (<7 h/d) sleep duration related responsibilities result in sleep restriction. Third,
are at modestly increased risk of all-cause mortality, increased time spent watching television and on the
cardiovascular disease, and developing symptomatic Internet reduces the opportunity for sleep.1 Finally,
diabetes. Although the data are not definitive, these stud- some individuals suffer from insomnia, a condition
ies suggest that sleep should not be considered a luxury, characterized by an inability to fall asleep or stay
but an important component of a healthful lifestyle. asleep.3 Although there are a number of causes of
(Prog Cardiovasc Nurs. 2004;19:56–59) ©2004 CHF, Inc. insomnia, including a learned response, psychiatric/
medical disorders, and poor sleep habits, it is idio-
pathic in some patients.
It has been shown that sleep restriction can result
in excessive daytime sleepiness and reduced neuro-
cognitive function. More recently, it has been demon-
strated that this degree of sleep loss may have long-
term health consequences and may lead to premature
death, cardiovascular disease, and the development
From the University of British Columbia and Vancouver of diabetes.4,5 In this article, we discuss the physiolog-
General Hospital, Vancouver, BC, Canada ic effects of short-term and long-term sleep restriction
Address for correspondence: and examine the relationship between sleep restric-
Najib T. Ayas, MD, MPH, Assistant Professor of
tion or sleep excess and a variety of health outcomes
Medicine, University of British Columbia; and
Respiratory Division, Department of Medicine, such as all-cause mortality, coronary heart disease
Vancouver General Hospital, 2775 Heather Street, (CHD), and diabetes.
Vancouver, BC, Canada V5Z 3J5
Manuscript received August 22, 2003; SHORT-TERM PHYSIOLOGIC STUDIES OF
revised October 17, 2003;
SLEEP RESTRICTION
accepted October 23, 2003
Short-term sleep restriction has many adverse endo-
www.lejacq.com ID: 2422 crine and cardiovascular effects. Kato et al.6 subjected

56 Progress in Cardiovascular NURSING Spring 2004


Progress in Cardiovascular NURSING (ISSN 0889-7204) is published Quarterly (March, May, July, Nov.) by CHF, Inc., Three Parklands Drive, Darien, CT 06820-3652. Copyright ©2004 by CHF, Inc. All rights reserved. No
part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission
in writing from the publishers. The opinions and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for commercial
purposes, please contact Sarah Howell at showell@lejacq.com or 203.656.1711 x106.

eight healthy subjects, six of whom were men and two determine if short sleep, per se, was independently
of whom were women aged 40±5 years, to one night of associated with mortality.
normal sleep and one night of total sleep deprivation.
Subjects who were completely deprived of sleep had a LONG-TERM SLEEP RESTRICTION AND THE
significantly higher systolic blood pressure following a DEVELOPMENT OF CHD AND DIABETES
night of sleep deprivation compared with normal sleep Recently published data from the Nurses’ Health
(129±8 mm Hg vs. 123±8 mm Hg). A similar study con- Study (NHS) cohort sheds more light on the relation-
cerning acute partial sleep deprivation was performed ship between sleep restriction and the development of
by Tochikubo et al.7 in 18 male technical workers aged CHD.4 The NHS cohort was established in 1976 when
23–48 years who slept only 3.6 hours had a signifi- 121,700 female, married registered nurses, aged 30–
cantly increased blood pressure. 55 years and residing in 11 large US states, completed
In a landmark study, Spiegel et al.8 studied 11 a mailed questionnaire on their medical history and
healthy men aged 18–27 years and subjected them to lifestyle. Follow-up questionnaires are sent to update
six nights of 4 hours of sleep per night followed by six information every 2 years on potential risk factors and
nights of 10 hours of sleep per night (recovery sleep). to identify newly diagnosed cases of coronary and
During the sleep-deprived portion compared with the other diseases.
recovery portion, patients demonstrated impaired glu- On the 1986 questionnaire, subjects were asked
cose tolerance, increased sympathetic nervous system the following question: “Indicate total hours of actual
activity, higher evening cortisol levels, and reduced sleep in a 24-hour period.” Between 1986 and 1996
leptin levels (an appetite-suppressing hormone). In a the incidence rates of CHD events were assessed in
recent study by Meier-Ewert et al.,9 partial sleep restric- more than 71,617 women 40–65 years of age who
tion (4.2 hours of sleep per night) of 13 healthy subjects, answered this question and did not have a diagnosis
10 of whom were men and three of whom were women of cardiovascular disease in 1986. The primary end
with an age range of 21–35 years, increased levels of point for this study was incident CHD events defined
C-reactive protein, a marker of systemic inflammation as nonfatal myocardial infarction or fatal CHD.4
and a risk factor for coronary artery disease. A total of 934 cases of CHD were recorded
Short-term sleep restriction results in myriad abnor- during the 10-year prospective study. Women who
mal physiologic changes, including reduced glucose self-reported sleeping ≤5 hours per night had a sig-
tolerance, increased blood pressure, activation of the nificantly increased risk of CHD. The age-adjusted RR
sympathetic nervous system, reduced leptin levels, was 1.82 (95% confidence interval [CI], 1.34–2.41).
and increased inflammatory markers. Although the Despite adjustment for smoking status, body mass
magnitude of the physiologic changes found in these index (BMI), alcohol consumption, physical activity,
short-term studies was modest, they provide a poten- shift work, menopausal status, depressed mood, aspi-
tial mechanism whereby long-term sleep restriction rin use, family history of myocardial infarction, snoring,
may affect long-term health. However, the experiments hypercholesterolemia, hypertension, and diabetes, the
described above predominantly studied young, healthy association between sleeping less and CHD prevailed.
subjects and it is not known if similar changes would After adjustment for all of the aforementioned vari-
be found in older subjects. ables, the RR, although blunted, remained significant
at 1.39 (95% CI, 1.05–1.84).4
LONG-TERM SLEEP RESTRICTION AND MORTALITY The same cohort was used to assess the relation-
The adverse effects of long-term sleep restriction ship between diabetes and sleep habits. A total of
have not been as well studied. Kripke et al.10 studied 1969 cases of diabetes were recorded over a 10-year
more than 1.1 million men and women aged 30–102 period (1986–1996).5 The age-adjusted RR of develop-
years and found that individuals reporting <4.5 hours ing diabetes was 1.57 (95% CI, 1.28–1.92) for persons
per night in men and <3.5 hours in women were asso- who slept ≤5 hours a night; however, after adjusting
ciated with a 15% 6-year all-cause mortality rate.10 for shift work, hypercholesterolemia, hypertension,
In addition, Wingard et al.11 in a study that included smoking, snoring, exercise, alcohol use, depression,
men and women between ages 30 and 69 years found postmenopausal hormone use, family history of dia-
that subjects who reported short (≤6 hours per night) betes, and BMI, the result was no longer significant
or long (≥9 hours) had an increased 9-year mortal- for persons who slept <5 hours a night. Much of the
ity rate when compared with persons who slept 7–8 reduction in RR was due to the confounding effect
hours per night when followed prospectively.11 The of BMI. A possible explanation for the findings is
relative risk (RR) was 1.7, and remained significant that a hormone that suppresses appetite, leptin, is
even after adjustment for various covariates (RR=1.3 decreased in subjects who undergo short-term sleep
after adjustment). The study was not large enough to deprivation.12 Therefore if persons who are sleep

Spring 2004 Progress in Cardiovascular NURSING 57


Progress in Cardiovascular NURSING (ISSN 0889-7204) is published Quarterly (March, May, July, Nov.) by CHF, Inc., Three Parklands Drive, Darien, CT 06820-3652. Copyright ©2004 by CHF, Inc. All rights reserved. No
part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission
in writing from the publishers. The opinions and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for commercial
purposes, please contact Sarah Howell at showell@lejacq.com or 203.656.1711 x106.

deprived have increased appetite they may tend to The association between increased long sleep
gain weight, which would in turn contribute to the duration and adverse health is consistent over a num-
development of diabetes. ber of studies. The underlying mechanisms for this
To determine whether severity of diabetes was association are unclear. One possible explanation is
associated with sleep duration, symptomatic cases of that an unrecognized confounder could lead to poor
diabetes were also analyzed. A total of 1187 symptom- health and an increased need for sleep. An example
atic cases of diabetes occurred over this time period.5 of such a confounder might be obstructive sleep
The age-adjusted RR was 1.84 (95% CI, 1.43–2.35) in apnea. Sleep apnea is independently associated with
persons who slept ≤5 hours a night, and this increased decreased glucose tolerance, cardiovascular disease,
risk persisted even after adjustment for BMI and other and is known to cause hypersomnolence.14,15 Second,
variables (RR, 1.34; 95% CI, 1.04–1.72). There are a long sleep duration may be an early symptom of dis-
number of limitations to these two studies.4,5 First, ease, possibly predating its official diagnosis. Third,
the studies only included women, and therefore, the long sleep duration could directly lead to poor health.
results may not apply to men. Second, people may Although this hypothesis is consistent with these stud-
develop sleep disturbance from undiagnosed CHD ies, there is no plausible biologic explanation for such
or diabetes. In other words, abnormal sleep habits a cause-and-effect relationship.
may be a consequence of disease rather than cause
the disease (reverse causation). Third, although an SUMMARY
attempt was made to adjust for potential confound- It is commonly believed that the average person
ers, the presence of residual confounding cannot be requires 7–8 hours of sleep each night. The concept of
excluded. Fourth, sleep duration was based on self- 7–8 hours of sleep is supported by several epidemio-
reports rather than objective measures of sleep dura- logic studies that indicate that this duration of sleep is
tion such as polysomnography. associated with the lowest mortality and morbidity.
Research demonstrates that experimentally induced
LONG SLEEPERS short-term sleep restriction of healthy volunteers
Individuals who report >8 hours of sleep are also at results in a number of adverse physiologic sequelae,
risk of adverse health effects. Qureshi et al.13 studied including reduced glucose tolerance, increased blood
7884 persons older than age 31 years, of whom 8.5% pressure, activation of the sympathetic nervous sys-
self-reported >8 hours of sleep per night. The group tem, reduced leptin levels, and increased inflammatory
that reported >8 hours sleep had an incidence of markers. Consistent with these physiologic studies,
stroke that was 50% greater than that of people sleep- epidemiologic research demonstrate that a short self-
ing 6–8 hours per night. The study also attempted to reported sleep duration is modestly associated with
associate coronary disease with long sleep duration; symptomatic diabetes, CHD, and mortality. Although
however, after adjusting for differences in age, race, these findings are suggestive, further physiologic and
gender, education, cigarette smoking, BMI, serum epidemiologic studies are needed to better define the
cholesterol level, systolic blood pressure, and diabetes relationships between sleep duration and health, and
mellitus, the association was not significant (RR, 1.4; to understand the underlying pathogenic mechanisms.
95% CI, 0.9–2.2). The study was able to demonstrate Nonetheless, these studies suggest that sleep should
that all-cause mortality was increased in long sleepers not be considered a luxury, but instead one of the pil-
(RR, 1.3; 95% CI, 1.1–1.5). Also, Kripke et al.10 showed lars of a healthful lifestyle.
that subjects who reported >8.5 hours of sleep per Long sleep duration is also associated with an
night also had an increased mortality risk. increased risk of long-term health effects. The reasons
Data from the NHS also support a relationship for this association are currently unclear. Potentially,
between long sleep duration and the development future studies that better define these participants
of diabetes and coronary disease. The age-adjusted from a physiologic and biochemical perspective could
RR for developing CHD in persons reporting sleeping lead to a logical explanation for this increased risk.
≤9 hours per day was 1.57 (95% CI, 1.18–2.11). The That is, more in depth physiologic and biochemical
relationship between long sleep duration and CHD assessment of long sleepers using polysomnography
remained significant (RR, 1.37; 95% CI, 1.02–1.85) to measure objective sleep duration and indices of
even after adjustment for a variety of potential con- sleep fragmentation (respiratory disturbance index,
founders. Similarly, the RR of developing diabetes was arousal index), and biochemical markers (C-reactive
1.47 (95% CI, 1.19–1.80) for those who slept ≥9 hours protein, leptin levels) could allow us to understand bet-
and remained significant after adjustment for a variety ter why long sleepers are at increased risk of adverse
of confounders (RR, 1.29; 95% CI, 1.05–1.59). health outcomes.

58 Progress in Cardiovascular NURSING Spring 2004


Progress in Cardiovascular NURSING (ISSN 0889-7204) is published Quarterly (March, May, July, Nov.) by CHF, Inc., Three Parklands Drive, Darien, CT 06820-3652. Copyright ©2004 by CHF, Inc. All rights reserved. No
part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission
in writing from the publishers. The opinions and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for commercial
purposes, please contact Sarah Howell at showell@lejacq.com or 203.656.1711 x106.

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Spring 2004 Progress in Cardiovascular NURSING 59

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