Sleep Health xxx (2016) xxx–xxx

Contents lists available at ScienceDirect

Sleep Health
Journal of the National Sleep Foundation

journal homepage: http://www.elsevier.com/locate/sleh

From habitual sleep hours to morbidity and mortality: existing

evidence, potential mechanisms, and future agenda
Muhammad Zakir Hossin, MSc ⁎
Centre for Health Equity Studies, Stockholm University, Sweden

a r t i c l e i n f o a b s t r a c t

Article history: Epidemiological studies consistently show a strong U-shaped association between sleep duration and health
Received 28 August 2015 outcomes. That is, both short and long sleepers are exposed to greater risks of death and diseases than normal
Received in revised form 23 January 2016 length sleepers. Moreover, long sleep is often demonstrated as a stronger predictor of mortality than short
Accepted 26 January 2016
sleep. While there is some experimental evidence in favor of a causal connection between short sleep and
Available online xxxx
health, no such evidence exists to explain why excessive sleep might be associated with poor health. One
Keywords:
possible explanation is that long duration sleep, instead of being a real cause of illness, is merely a marker
Sleep duration of poor sleep quality or some unmeasured risk factor that confounds the association of long habitual sleep
Sleep quality with mortality and other health outcomes. As for short sleep, the effect is said to be mediated via the hormones
U-shaped association that alters glucose metabolism and appetite regulation as well as via an overactivity of the stress systems that
Short sleep causes increased heart rate and blood pressure. The mechanisms, however, are still poorly understood and
Long sleep future investigations should take into account sleep quality, objective and longitudinal sleep measures,
Health more confounding biases, and the broad social context that influences the length and quality of sleep.
© 2016 National Sleep Foundation. Published by Elsevier Inc. All rights reserved.

Introduction systems.16 These effects of sleep insufficiency may gradually accumu-

The amount of time spent in day-to-day sleep represents an
important health behavior that received considerable empirical
attention in the past few decades. Epidemiological studies of
both cross-sectional and longitudinal designs, in general, show a
U-shaped association between sleep duration and adverse health
outcomes including mortality. 1–11 This means that both short sleep
and long sleep are associated with elevated health risks relative to
the optimal mid-range sleep which is usually defined as 7-8 hours
of sleep duration per day, although the definition varies from one
study to another. Interestingly, habitual long-duration sleepers are
found to be at greater risk of mortality than habitual short-duration
sleepers. 6,7 Not much is known, however, about the exact mecha-
nisms linking sleep durations to mortality and health outcomes.
There are a few experimental studies documenting the physiologic
mechanisms between short sleep and negative health effects, 12–15
but no such evidence has emerged to date to demonstrate how long
duration sleep might affect health. Available evidence indicates that
sleep insufficiency may lead to metabolic dysregulation 12,13 and
changes in the fundamental properties of the neuro-endocrine stress
⁎ Kungshamra 11, Lgh 1338, Solna 17070, Stockholm, Sweden. Tel.: +46
762328723 (mobile).
E-mail address: ziku133@gmail.com.
late over time and result in a variety of diseases including type 2
diabetes,8–10 obesity,17–21 hypertension,22–29 cardiovascular diseases
(CVD),11,28–31 and so on. Thus, sleep duration is a crucial public health
issue which, when deviates from the normal range, takes a heavy toll
in terms of morbidity and mortality outcomes. Based on a comprehen-
sive review of existing literature, the present paper aims to revisit the
U-shaped association between sleep duration and adult health,
discuss the potential pathways and mechanisms driving this associa-
tion, and suggest directions for future studies.
Sleep duration and health: epidemiological evidence
Sleep duration and mortality
There is a mounting body of epidemiological studies showing that
sleep duration is independently associated with mortality even after
statistically controlling for a wide array of covariates. 1–5 Most of these
studies provide evidence in support of a robust U-shaped association
where both too little sleep and too much sleep significantly interferes
with mortality. The evidence generally holds true for both women
and men, younger and older adults, and across all geographic
locations. 7 Although a handful of studies are not entirely in agree-
ment with the U-shaped association, 32–34 nearly all of the studies

http://dx.doi.org/10.1016/j.sleh.2016.01.006
2352-7218/© 2016 National Sleep Foundation. Published by Elsevier Inc. All rights reserved.

Please cite this article as: Hossin MZ, From habitual sleep hours to morbidity and mortality: existing evidence, potential mechanisms, and
future agenda, Sleep Health (2016), http://dx.doi.org/10.1016/j.sleh.2016.01.006
2 M.Z. Hossin / Sleep Health xxx (2016) xxx–xxx
demonstrate long sleep as a stronger predictor of mortality than
short sleep.
The relationship between sleep duration and mortality, however,
varies depending on age and sex and such variations are rather incon-
sistent and complex. The Older Finish Twin Cohort Study, a large
population-based prospective study of participants older than
18 years, shows that compared to a sleep duration of 7 hours, short
sleep duration (b7 h) significantly increased the risk of all-cause
mortality by 26% in men and 21% in women, whereas long
sleep (N 8 h) increased the risk by 31% and 39% in men and women
respectively. This was after adjustment had been made for the
sociodemographic and lifestyle factors known to affect mortality. 2
While the association between sleep duration and mortality is more
consistent for all-cause mortality, studies focusing on cause-specific
mortality yield somewhat divergent results. Ikehara and colleagues,5
for example, investigated sex specific associations of sleep duration
with cause specific mortality in approximately 98,000 Japanese
men and women 40-79 years old. The study findings reveal that
relative to the average sleep duration of 7 hours, sleeping 4 hours
or less is associated with a 2.32 times increased risk of mortality
from coronary heart diseases in women and an approximately
1.5-fold increased risk of mortality from non-CVDs in both men and
women. As for long sleep, sleep duration of ≥10 hours was associated
with 1.5 to 2 times increased mortality from total stroke, ischemic
stroke, total CVD, non-CVD, and all causes in both women and men.
Mortality from cancer showed no significant association with sleep
duration in either sex. Heslop and colleagues,35 however, associated
sleep duration with mortality from CVDs in men only. Prospectively
examining sleep duration, the British Whitehall II cohort study3
found that a decrease in sleep duration from the regular sleep of 6, 7,
or 8 hours increased the risk of mortality from CVD (hazard ratio
[HR] 2.4, 95% confidence interval [CI] 1.4-4.1) while an increase in
sleep duration from the regular sleep duration of 7 or 8 hours increased
the risk of mortality from non-CVD causes (HR 2.1, 95% CI 1.4-3.1).
Although older adults are more likely to report both short and
long sleep durations than younger adults,36,37 relatively few studies
on sleep and mortality specifically focused on the older age popula-
tions and yielded less definite conclusions. A population-based
cohort study conducted among the 65-85 years old in Japan
shows that long sleep is strongly associated with all-cause and CVD
mortality but no significant association was observed between
short sleep and mortality. 38 A recently published population-based
study in China shows higher risk of mortality in both short and long
sleepers, with longer sleep being associated with a higher risk of
cause-specific CVD mortality than shorter sleep among the elderly.39
The age-stratified analyses carried out in an earlier study in a large
sample in the USA revealed that the U-shaped association between
sleep duration and mortality is reserved for the elderly only, with
no significant relationship found in the middle-aged subjects (HR
0.67, 95% CI 0.43-1.05). 4 This is in contrast with some other studies
which demonstrate that the effect of sleep on mortality is more
strongly pronounced in young adults.2,40
The U-shaped association of habitual sleep duration with mortality
was further confirmed by two independent systematic reviews
and meta-analyses covering men and women of both general adult
and older ages across various geographic regions. 6,7 The first meta-
analysis, conducted in 2009, was based on 23 prospective cohort
studies that investigated the self-reported sleep durations with both
all-cause and cause-specific mortality. The pooled relative risk (RR)
estimates revealed that long sleep duration carried 23% additional
risk of all-cause mortality relative to the average sleep duration
while the corresponding excess risk for short sleep duration was
10%. The pooled effects for specific types of mortality, however, were
less conclusive. Long sleepers were at greater risk of mortality from
both cancer and CVD than medium sleepers whereas short sleepers
Please cite this article as: Hossin MZ, From habitual sleep hours to morbidity and mortality: existing evidence, potential mechanisms, and
future agenda, Sleep Health (2016), http://dx.doi.org/10.1016/j.sleh.2016.01.006
showed an increased, albeit nonsignificant, risk of mortality from
CVD only (RR 1.06, 95% CI 0.94, 1.18).6 One year later, another meta-
analysis covering more than 1.3 million participants came up with
roughly similar patterns of associations between sleep duration and
all-cause mortality. In the pooled analyses, a 30% increased risk of
death was detected in long sleepers while the increased risk of death
in short sleepers was 12% which, if causally linked, would be equiva-
lent to 25 million deaths of people aged over 20 in the US alone.7
Sleep duration and adverse health outcomes
In common with mortality, a heightened risk of obesity, type 2
diabetes, CVDs including hypertension, coronary heart disease and
stroke are also frequently shown on either end of sleep duration
indicating the presence of a U-shaped association, 29,41 although the
evidence of a positive association of long sleep with these health
outcomes appears to be less compelling compared to mortality. The
quantitative pooled estimates of a meta-analysis conducted by
Cappuccio et al8 indicate that the RR of developing type 2 diabetes is
1.28 for people who reported a short habitual sleep of ⩽5-6 h/night
and 1.48 for those with a long habitual sleep of ⩾8-9 h/night. These
findings were also confirmed by a recently published meta-analysis
that found a U-shaped dose-response relationship between sleep
duration and risk of type 2 diabetes. 9 Similarly, a meta-analysis of
longitudinal population studies examining the associations between
sleep durations and CVDs linked both extremes of sleep duration
with developing coronary heart disease and stroke but not total
CVD. 11 Data on CVDs from the Jichi Medical School Cohort Study in
Japan, however, demonstrated that sleeping less than 6 hours was
significantly associated with an elevated risk of the incidence of
CVDs in men only (HR 2.14, 95% CI 1.11-4.13) while sleeping more
than 9 hours showed no statistical significance (HR 1.33, 95% CI
0.93-1.92).31
Research also associates short sleep and to a lesser degree long
sleep with hypertension22–29 and obesity.17–21 Much of this evidence,
however, came from cross-sectional studies which do not allow one
to claim causal connections. On the other hand, the pooled analyses
of the longitudinal studies examining the association between sleep
duration and hypertension indicates that only short sleep increases
the risk of developing hypertension (RR 1.23, 95% CI 1.06-1.42)
among the adult populations. 28 For obesity too, only short sleep is
found to consistently show statistical association in prospective
cohort studies.18,19 Emerging evidence, however, is suggestive of an
attenuating effect of sleep duration on hypertension and obesity
with age. 28,42 A prospective analysis from the English Longitudinal
Study of Ageing shows that short sleep predicts incident hyperten-
sion among men and women aged ⩽60 years but not in older
adults. 28 Examining data from the National Health and Nutrition
Examination Survey, a recently published study in the USA 42 also
reported significant interactions between age and sleep duration,
used both as continuous and categorical variables, with regard to
the body mass index (BMI). The study found a negative linear rela-
tionship in young adulthood, with more sleep being linked to lower
BMI; a U-shaped relationship in middle adulthood, with relatively
high BMI in both short and long sleepers; and an attenuated relation-
ship in older adulthood, with only very short sleepers having
minimally higher BMI.
Beyond sleep duration
In addition to sleep duration, sleep quality (ie, trouble falling
asleep, trouble staying asleep, early awakening, etc.) is also found to
be an important risk factor for mortality and other health outcomes.
For instance, a French GAZEL cohort study with a total of 16,989
male and female participants examined the effects of sleep
 M.Z. Hossin / Sleep Health xxx (2016) xxx–xxx
disturbances on mortality as well as on the potent risk factors for
mortality such as BMI, hypertension, and diabetes. It was found that
sleep disturbances were associated with greater risk of overall
mortality among the men only, with the strongest effect on the
younger men who were b45 years of age. Sleep disturbances also
showed significant associations with diabetes and hypertension and
a non-significant association with BMI in both sexes. 40 Given the
role of sleep quality in predicting mortality, a recent trend is to
analyze simultaneously the effects of both sleep duration and sleep
quality in relation to mortality. A British Whitehall II cohort study,
for example, identified both disturbed sleep and sleep duration as
independent risk factors for CVD mortality among women, though
no such link was found among men. However, the combined effect
of both disturbed sleep and sleep duration was greater among
men. 43 A recent study also reveals that the other sleep measures,
that is, night-to-night sleep variability, sleep timing, and daytime
napping were independently linked to obesity in both men and
women even after controlling for the mean sleep duration and
many other potentially confounding factors.44 These study findings
merit particular attention as they suggest that the observed effects
of sleep duration on health are likely to be the consequences of
the sleep characteristics beyond the average sleep duration in a
24-hour cycle. A few studies, moreover, emphasize the waking activi-
ties as important candidates for confounding the associations of
reduced and prolonged sleeping with morbidity and mortality. Basner
et al,45 for instance, examined the sleep duration and its exchange with
waking activities based on the American Time Use Survey database
involving 47,731 participants aged over 14 years. The study results
revealed that both short and long habitual sleeping were reciprocated
with greater and lesser amounts of work time, travel time, and time
spent in socializing, relaxing, and leisure activities. The authors
suggest that the greater risk of adverse health consequences asso-
ciated with short and long habitual sleep durations might not emanate
from the durations of sleep per se but from the associated changes in
waking activities. This suggestion is also in consistent with an earlier
study by John et al 46 who demonstrated considerably higher odds
for nicotine, alcohol dependence, depression, and anxiety disorder
among very short sleepers relative to the average sleepers.
Social-environmental determinants of sleep
Like other lifestyle factors (eg, diet, physical activity), sleep duration
and sleep quality tend to be socially patterned too, with the racial/
ethnic minorities and socially disadvantaged groups having less or
poorer sleep. 47–53 A growing body of literature documents that the
social groups who identified themselves as non-Whites (ie, Black,
Asians, and Hispanics), unmarried or females are typically more likely
to report being short sleepers than their White, married or male coun-
terparts respectively.47–51 Hale and Do49 showed that those who self-
reported their race/ethnicity as Black are at greater risk of both short
and long sleeping than the self-rated White. The study further pointed
out that the elevated risk of short sleeping among the Blacks might be
partially attributed to their higher prevalence of living in an inner city
which was associated with an increased risk of reduced sleeping.
Using 2007-2008 National Health and Nutrition Examination Survey
data, Whinnery et al 53 in 2013 investigated multiple dimensions of
race/ethnicity and socioeconomic status in relation to sleep duration.
They found that minority status and certain socioeconomic factors
including low income, low education, and very low food security
were significantly associated with short sleep independent of overall
health status. In contrast to some previous studies, however, Whinnery
et al found that the study participants identifying themselves as never
married and the women had an increased risk of oversleeping
compared to the self-identified married individuals and the men
respectively. Interestingly, those with public insurance were more
Please cite this article as: Hossin MZ, From habitual sleep hours to morbidity and mortality: existing evidence, potential mechanisms, and
future agenda, Sleep Health (2016), http://dx.doi.org/10.1016/j.sleh.2016.01.006
3
likely to report both short and long sleep durations than the uninsured,
although no significant association was observed between private
insurance and sleep duration. Past research also showed disparities
in sleep duration and quality as well as the associated health out-
comes by immigration status, although little is known about the
role of acculturation in the relationship among socioeconomic status,
race/ethnicity, and sleep duration.54,55
Similar to the uneven distribution of the social inequalities in sleep,
the consequences of high risk sleep durations may be differentially
experienced by the ethnic or racial minority and socially disadvan-
taged groups. In a recent publication, Jean-Louis and colleagues,56 for
example, have demonstrated that the risk of overweight and obesity
associated with inadequate sleep was higher among Black Americans
compared to the White Americans. In 2012, Zizi et al57 also observed
significant interactions of sleep duration with Black and White race,
with the short and long sleepers of Black race reporting greater risk
for diabetes independent of their sociodemographic profile or the
presence of comorbid conditions.
Sleep duration and mortality: pathways and mechanisms
Short sleep and mortality
From the epidemiological evidence accumulated over the past
several decades, it is evident that short and long sleepers constitute
two heterogeneous groups. Epidemiological evidence also indicates
that long sleep is likely to increase mortality risk mostly via the
effects on non-CVD deaths whereas short sleep tends to exert its
effects through CVD deaths.3 Several pathways have been implicated
in the relationship between short sleep and mortality.58 While short
sleep may exert its effect on mortality through direct or indirect
pathways, it can also plausibly play a mediating role in the
well-established socioeconomic gradient in health and mortality.
Counter-intuitively, short sleep might also be argued as an outcome
rather than a cause of poor health. The next section provides a detailed
discussion of the proposed mechanisms, as illustrated in Fig. 1.
Short sleep directly causes mortality
Short sleep may directly cause mortality as laboratory studies
in rodents indicate that sleep deprivation leads to deaths within
2-3 weeks from the onset of sleep deprivation.14 Besides, numerous
epidemiological studies report a net effect of short sleep on mortality
after adjusting for a wide variety of potential confounders, indicating
a direct causal relation. 1–5The study conducted by Kripke and
colleagues 1 in approximately 1.1 million American men and women
aged 32-102 years stands out as a good example. The study shows
that the shorter or longer the sleep duration than a 7-hour sleep
duration, the greater the mortality risk, with 33% heightened risk of
mortality found in 3-hour sleep duration even when controlling for
multiple sources of confounding biases. These include the demo-
graphic risk factors (eg, age, race, education, occupation, marital
status), behavioral factors (eg, smoking at intake, smoking in years,
churchgoing, intake of fat, intake of fiber), prior health status
(eg, BMI, leg pain, and the history of heart disease, cancer, diabetes,
stroke, bronchitis, emphysema, kidney diseases), use of medications
(eg, sleeping pills, blood pressure pills), and the frequency of insomnia.
Short sleep indirectly causes mortality
Short sleep may indirectly cause mortality by increasing the risk of
obesity, diabetes, hypertension, CVD, and other medical conditions.
Experimental evidence suggests that sleep loss modulates the
metabolic and endocrine hormones involved in the process of appetite
regulation and glucose control 12,15—insulin, cortisol, leptin and
ghrelin—the hormones which mediate the effects of sleep loss on
BMI and diabetes. As demonstrated in Fig. 2, short sleep might
4 M.Z. Hossin / Sleep Health xxx (2016) xxx–xxx

Metabolic & Obesity,

endocrine diabetes,
alterations hypertension,
CVD

Mortality
Short sleep

Socioeconomic
status

Fig. 1. Schematic of the different pathways in the association between short duration sleep and mortality.

contribute to the development of obesity and diabetes in at least three
distinct pathways which include: (i) reduced energy expenditure,
(ii) up-regulation of appetite, and (iii) altered glucose metabolism. 59
First, insufficient sleep is associated with feelings of fatigue60 which
results in low energy expenditure through reduced physical activity.
Second, being awake for longer time gives a higher chance of consuming
more calories. At the same time, after sleep restriction, the level of
ghrelin—the hunger hormone that increases appetite—goes up and the
level of leptin—the hunger hormone responsible for decreasing
appetite—goes down.15This leads to increased appetite and calorie
intake which eventually results in obesity which itself is a forerunner
for a wide variety of diseases including type 2 diabetes, hypertension,
CVD, cancer, and increased mortality rates. 61,62 Third, after a re-
stricted sleep, the level of cortisols gets lower in the evening and
so does the level of growth hormones leading to increased insulin
resistance and reduced glucose tolerance which, in turn, leads to type
2 diabetes. Spiegel and colleagues, 12 for example, observed a 30%
decrease in insulin response to glucose within six nights of partial
sleep restrictions in healthy subjects, resulting in impaired glucose
tolerance. A recently conducted randomized, crossover clinical study
also found that 4 nights of sleep restrictions resulted in approximately
30% reduced cellular insulin sensitivity in subcutaneous fat, a

Short sleep

Leptin Evening cortisol Sympathetic

Fatigue Time to eat Ghrelin Nighttime GH activation

Energy Appetite Insulin resistance

expenditure Food intake Glucose tolerance

Obesity Diabetes

Fig. 2. Schematic of the pathways leading from short sleep to obesity and diabetes. Source: Modified Annals of the New York Academy of Sciences. 2008;1129(1):287-304.

Please cite this article as: Hossin MZ, From habitual sleep hours to morbidity and mortality: existing evidence, potential mechanisms, and
future agenda, Sleep Health (2016), http://dx.doi.org/10.1016/j.sleh.2016.01.006
 M.Z. Hossin / Sleep Health xxx (2016) xxx–xxx
peripheral human tissue that plays a pivotal role in energy
metabolism. 13 Further, the sympathetic nervous activation also
mediates the pathway between sleep loss and insulin sensitivity.
Sleep deprivation is also known as a stressor that overactivates the
two classical stress systems ie, the autonomic sympatho-adrenal
system and the hypothalamic-pituitary-adrenal axis and elevates the
plasma levels of stress hormones such as adrenaline and cortisol. 16
Experimental evidence further suggests that sleep deprivation is asso-
ciated with a decreased para-sympathetic activity and increased sym-
pathetic activity causing increased heart rate and blood pressure. 63–65
Habitual short sleep duration and the consequent prolonged exposure
to increased heart rate and blood pressure might, in the long run,
contribute to the development of hypertension and CVDs.22–31,66
Short sleep is a mediator
Short sleep duration may potentially play an intermediary role
along the causal pathway between socioeconomic determinants
and health. 67 While both socioeconomic status and insufficient
sleep affect health, low status groups are more likely to be sleep
deprived since they experience higher levels of stress and have
lower levels of resources and social support to combat the unsafe
living and working conditions. On the other hand, high status groups
have reduced risks of stress, better knowledge about the health risks
associated with sleep loss as well as the greater means and resources
to avoid it, eg, safer working conditions, better housing, etc. Thus, the
differences in morbidity and mortality among different categories of
sleepers tend to originate from their socioeconomic backgrounds,
although empirical evidence supporting this claim is scarce.
While the researchers have examined the role of other health
behaviors such as smoking, alcohol consumption, diet, and physical
activity in the social gradient in health, 68,69 a health behavior which
is yet to be sufficiently examined in this context is the role of sleep.
Only two studies have so far addressed the issue. Moore and
colleagues 70 investigated the role of sleep in the socioeconomic
gradient of health in a community of 1139 adults. Findings of their
study indicate that the association between income and health was
mediated by sleep quality, but not sleep quantity. The finding that
sleep quantity did not mediate the main association in the study is
not unexpected given the strong correlation between sleep quantity
and quality which, when adjusted simultaneously, may not indi-
vidually mediate the association of interest. The other study conducted
among 3684 Japanese civil servants revealed that the various aspects of
sleep quantity and quality accounted for approximately 20% of the
social inequalities in physical health and 40% of the inequalities in
mental health among the men, but not among the women.71 Taken
together, the findings of these two studies indicate that role of sleep
as a mediator between socioeconomic status and health is likely to
vary between men and women, between the length and quality of
sleep, and between physical and psychological health.
Poor health causes short sleep and/or vice versa
There is a possibility of reverse causation with health affecting
sleep durations or bidirectional causal associations with reduced
sleep duration and health being reinforced by each other. Thus, the
less healthy people are less likely to have an optimal amount of
sleep than those with good health. For instance, in the Zurich Cohort
Study that repeatedly measured sleep duration and BMI on four
different occasions, weight emerged as a better predictor of sleep
duration than the other way round.72
The association between short sleep and mortality is spurious
The possibility of a spurious correlation between short sleep and
health cannot be ruled out either. The correlation may result from a
third omitted factor that is associated with both short sleep and
Please cite this article as: Hossin MZ, From habitual sleep hours to morbidity and mortality: existing evidence, potential mechanisms, and
future agenda, Sleep Health (2016), http://dx.doi.org/10.1016/j.sleh.2016.01.006
5
health where short sleep is just a bystander or a surrogate marker
of other underlying conditions.
Long sleep and mortality
Unlike the short sleep-mortality association, the association
between long duration sleep and mortality is still a public health
conundrum since the underlying mechanisms through which over-
sleeping might affect health and mortality is yet to be understood.
It, therefore, remains an open question whether long sleep is a real
cause of mortality or simply a marker of illness. Given the etiological
uncertainty, it can be argued that the individuals with poor sleep
quality are also the ones staying longer time in bed to compensate
their lost or disturbed sleep and hence report long duration sleep.
In line with this argument, Grandner and Drummond73 suggest that
some uncontrolled factors eg, sleep fragmentation, depression,
fatigue, sleep apnea, failing health, heart disease, etc. might confound
the observed associations of excessive sleep with morbidity and
mortality. Still, this argument does not seem to be strongly con-
vincing especially when numerous studies indicate that long
duration sleep predicts mortality after the adjustment for
depression, 4,5,74 sleep fragmentation, 1,4 and the risk factors for
mortality including heart diseases. 1,75 The only exception is the 45
and Up Study in Australia 76 which failed to show any association
between sleep duration and mortality in the healthy subjects. There-
fore, despite a large volume of epidemiological literature showing
long sleep as a stronger predictor of mortality, no valid judgement
can be made about the links between long sleep, health and mor-
tality. Further scientific investigation is required for a clear under-
standing of the physiologically plausible pathways through which
long duration sleep might explicitly cause poor health or mortality.77
Agenda for future research
The burden of sleep problems is rapidly emerging as a global public
health epidemic in the 21st century.78,79 Of particular concern is the
progressive decline in the mean sleep duration and continuously
rising prevalence of short sleepers. In the USA alone, the absolute
size of the adult population experiencing short sleep, arbitrarily
defined as ≤6 hours of sleep in a 24-hour cycle, has increased from
38.6 million in 1985 to 70.1 million in 2012—an almost 45% increase
over a 27-year period.80 The rising trend in short sleep duration led
to the inclusion of adequate sleep as one of the key goals of the
whitepaper by Zee et al 81 released by the American Academy of
Sleep Medicine (AASM) and Sleep Research Society (SRS). The appre-
ciation of the importance of “sufficient sleep” also prompted the US
Department of Health and Human Services to recognize it as a national
health priority in the Healthy People 2020 program. The objective is to
“increase the proportion of adults who get sufficient sleep”. 77 Until
recently, however, there was a lack of clear recommendations as to
what constitutes “sufficient sleep”. An important development is
the recent guidelines published by the AASM/SRS that recommend
7-9 hours of sleep per night to promote optimal health and func-
tioning in the adults. 77,82,83 The scientific community in the fields
of sleep research and sleep medicine, however, still have a long
way to go to ascertain if sleeping more than 9 hours per night is
physiologically harmful for adult health.
Given the rapidly exacerbating sleep problems in the modern
society and the accompanying health problems, any evidence
suggesting the causal mechanisms about the health effects of over-
sleeping and undersleeping will carry substantial importance from
a population health standpoint. However, there are some crucial
issues which have to be taken into consideration in future research
to provide a more comprehensive and clearer understanding of the
underlying mechanisms.
6 M.Z. Hossin / Sleep Health xxx (2016) xxx–xxx
Improve sleep measures and study designs
The scientific measures of sleep such as actigraphy and
polysomnography, as opposed to the current trend towards self-
reported sleep measures, is highly warranted. This is because the
objectively measured sleep duration and self-reported sleep duration
have been found to be not strongly correlated 84–86 and a self-
reported measure of sleep can potentially lead to an underestimation
or overestimation of the associations studied. Also, the previous
studies, with a few exceptions, 3,35 measured sleep duration in one
occasion only. This is a genuine cause for concern since sleep duration
is not a stable trait and it is short or long sleep over a prolonged
period that accelerates the risk of morbidity and mortality. Future
epidemiological investigations should place due emphasis on mea-
suring sleep variables over time and across the life-course. Findings
obtained from such epidemiological studies, in turn, need to
be complemented by laboratory studies aimed at systematically
examining the metabolic, cardiovascular, and neuro-cognitive corre-
lates of sleep duration. 27 In particular, future experimental studies
carefully designed specifically to assess the physiological impact
of sleep extension can make a giant step forward. As the potential
pathways through which short sleep and long sleep affect health
are likely to be fundamentally different, such studies should
turn the spotlight on the biological, psychological, and behavioral
differences among the short, mid-range, and long sleepers. In addi-
tion, intervention studies, as emphasized by the Joint Consensus
Statement of AASM/SRS, 27 can also help to determine if modified
sleep durations are associated with improved health outcomes and
to further clarify if long duration sleep plays a causal role or serve
as an underlying marker of other sleep disorders.
Investigate sleep duration and sleep quality simultaneously
A salient characteristic of the existing sleep-health literature is
that the vast majority of studies exclusively rely on sleep duration
as a measure of sleep. This is problematic because sleep is a multi-
dimensional concept beyond sleep duration, including quality
of sleep. With the increasingly emerging evidence, it can be safely
argued that sleep quality is just as important as sleep duration or
even more powerful to precisely capture the influences that drive
the sleep-health relationships. However, little work has been devoted
to exploring if sleep duration and sleep quality predict health inde-
pendent of each other. Experimental evidence indicates that out of
the several discrete stages of sleep, the restorative Slow Wave Sleep
which is an important marker of sleep quality, has the most serious
repercussions for health. Tasali and colleagues,87 for instance, found
that the selective suppression of Slow Wave Sleep causes reduction
in insulin sensitivity and glucose tolerance independent of the dura-
tion of sleep. Similarly, the increased sympathetic activity, which
causes elevated blood pressure and increased heart rate, is also
found to be more strongly linked to the disruption of sleep than the
amount of sleep lost.64,88 It is, therefore, quite reasonable to question
whether the observed link of sleep duration, especially long duration
sleep, to mortality is due to sleep duration per se or due to the poor
sleep quality or the combined effects of both. The separation
of sleep quality from seep duration, however, might pose some diffi-
culty because of their shared variance, yet they represent two distinct
analytic concepts. Moore and colleagues, 70 for example, found that
although sleep quality and sleep quantity were strongly related
to each other, they were linked quite differently to the outcome
measures, ie, physical and psychological wellbeing. Hence, in order
to better elucidate the sleep-health relationship, future investigations
should aim to go beyond sleep quantity, identify the elements that
constitute sleep quality, and ascertain the magnitude of its indepen-
dence from sleep quantity. Yet, when sleep quantity and quality
Please cite this article as: Hossin MZ, From habitual sleep hours to morbidity and mortality: existing evidence, potential mechanisms, and
future agenda, Sleep Health (2016), http://dx.doi.org/10.1016/j.sleh.2016.01.006
combine to exert their effects on health, investigating their indepen-
dent effects may be a misleading approach. Therefore, a more
meaningful and pragmatic approach is to examine their separate,
combined, and interactive effects simultaneously.
Further control for confounders
There are other aspects of sleep behavior like daytime napping,
variability in sleep duration, and sleep-wake cycle that might con-
found the associations of interest but were not controlled for in
most of the previous studies. Many waking activities and behavioral
factors that are likely to have a reciprocal relationship with short
and long sleep durations, as suggested by Basner et al,27 might also
complicate the frequently observed U-shaped associations between
sleep duration and mortality. Hence, further studies taking these
potential confounders into account are necessary.
Better examine the social determinants
Although sleep is a biological imperative, how long or how well
one sleeps appears to be primarily driven by the social and environ-
mental factors. The evidence addressing the social determinants of
sleep, however, is insufficient and often characterized by a lack
of causality. Therefore, the hypothesis that social disadvantage is
associated with sleep debt and/or poor quality of sleep requires
rigorous scientific testing. Equally important is to examine how social
disadvantages alter the health risks associated with sleep duration
and quality so as to identify the targets for future interventions and
tackle the social disparities in sleep health. The fact that multiple
social dimensions including age, sex, race/ethnicity, socioeconomic
position, and immigration have the potential to alter the effects of
sleep duration on health requires an increased attention to the
ways in which different axes of social stratification intersect with
each other to exacerbate sleep disparities. Today there has been a
growing interest among the public health researchers in the phe-
nomenon of “intersectionality” that allows for a more thorough
investigation of the complex interactions between immigration,
racialization processes, and gender discrimination in producing
health inequalities. 89 Although methodologically challenging, such
an approach is useful for an in-depth examination of the multifarious
sources of social inequalities that negatively impact the duration and
quality of sleep and the associated health outcomes.
Disclosure
The author has no conflicts of interest to disclose.
Acknowledgements
This article has been produced during my scholarship period at
Stockholm University, thanks to a Swedish Institute scholarship. I
also wish to thank the two anonymous reviewers for their expert
comments on the paper.
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