Sleep Predictors and Sleep Patterns - Carskadon

Journal of Adolescent Health 46 (2010) 124132

Original article

Sleep Patterns and Predictors of Disturbed Sleep in a Large Population

of College Students
Hannah G. Lund, B.A.a, Brian D. Reider, B.A.b, Annie B. Whiting, R.N.c,
and J. Roxanne Prichard, Ph.D.b,*
a
Department of Psychology, Virginia Commonwealth University, Richmond, Virginia

b
Department of Psychology, University of St. Thomas, St. Paul, Minnesota
c
Massachusetts General Hospital, Boston, Massachusetts
Manuscript received March 26, 2009; manuscript accepted June 16, 2009
See Editorial p. 97
Abstract
Purpose: To characterize sleep patterns and predictors of poor sleep quality in a large population of
college students. This study extends the 2006 National Sleep Foundation examination of sleep in early
adolescence by examining sleep in older adolescents.
Method: One thousand one hundred twenty-five students aged 17 to 24 years from an urban
Midwestern university completed a cross-sectional online survey about sleep habits that included
the Pittsburgh Sleep Quality Index (PSQI), the Epworth Sleepiness Scale, the Horne-Ostberg MorningnessEveningness Scale, the Profile of Mood States, the Subjective Units of Distress Scale, and
questions about academic performance, physical health, and psychoactive drug use.
Results: Students reported disturbed sleep; over 60% were categorized as poor-quality sleepers by
the PSQI, bedtimes and risetimes were delayed during weekends, and students reported frequently
taking prescription, over the counter, and recreational psychoactive drugs to alter sleep/wakefulness.
Students classified as poor-quality sleepers reported significantly more problems with physical and
psychological health than did good-quality sleepers. Students overwhelmingly stated that emotional
and academic stress negatively impacted sleep. Multiple regression analyses revealed that tension
and stress accounted for 24% of the variance in the PSQI score, whereas exercise, alcohol and caffeine
consumption, and consistency of sleep schedule were not significant predictors of sleep quality.
Conclusions: These results demonstrate that insufficient sleep and irregular sleepwake patterns,
which have been extensively documented in younger adolescents, are also present at alarming levels
in the college student population. Given the close relationships between sleep quality and physical and
mental health, intervention programs for sleep disturbance in this population should be considered.
! 2010 Society for Adolescent Medicine. All rights reserved.
Keywords:
Sleep quality; Sleep disturbance; Adolescence; Stress; Mood; College students
Little doubt exists among health professionals about the

fundamental importance of sufficient, restorative sleep in maintaining ones physical and mental health. Troubled sleep is
considered both a predictive sign and symptom of many
illnesses, and is associated with substantial decrements in the
quality of life. Briefly, chronic sleep disturbances are associated
*Address correspondence to: J. Roxanne Prichard, Ph.D., University of
St. Thomas, 2115 Summit Avenue, JRC LL56, St. Paul, MN 55105.
E-mail address: [email protected]
with an increased risk of work absenteeism and accidents [1], as

well as significant decrements in vitality, social functioning,
physical and mental health, and general quality of life [14].
Sleep in younger adolescents (ages 1217) has been extensively documented. Because of a multitude of intrinsic and
environmental factors, younger adolescents are particularly
vulnerable to disturbed sleep, and are one of the most sleep
deprived age groups in the country [5]. First, pubertal adolescents experience a biologically based phase change in their
circadian rhythm that delays sleep and wake onset, making
1054-139X/10/$ see front matter ! 2010 Society for Adolescent Medicine. All rights reserved.
doi:10.1016/j.jadohealth.2009.06.016
H.G. Lund et al. / Journal of Adolescent Health 46 (2010) 124132
it physically harder to maintain earlier bedtimes [6,7].

Second, external factors like increasing caffeine consumption
and late night use of electronics further delay sleep onset
[5,8,9]. Third, early start times for middle schools and high
schools demand earlier weekday risetimes [1012]. Finally,
even with sufficient sleep times, adolescents have increased
daytime sleepiness and a greater physiological need for sleep
compared to prepubertal children, which may result from
maturational changes in neuronal connectivity [13,14].
The consequences of this sleep deprivation are severe,
impacting adolescents physical and mental health, as well
as daytime functioning. Population and clinic-based studies
in younger adolescents (ages 1117) have shown strong associations between chronic sleep restriction and anxiety,
depression, and somatic pain [9,1517]. Younger adolescents who report shorter sleep also show decrements in
academic performance [5,18], and increased risk-taking
behaviors including drug use and drowsy driving [9,19]. A
12-month prospective study by Roberts et al. [20] demonstrated that insomnia in younger adolescents significantly
increased the risk for subsequent declines in social, psychological, physical, and mental health.
By comparison, fewer studies have examined how sleep
patterns change when older adolescents enter college, a time
of minimal adult supervision, erratic schedules, and easy
access to over-the-counter (OTC), prescription, and recreational drugs. Of these publications, most have focused on
sleep patterns, fatigue, and academic performance
[17,21,22]. Little is known about what factors contribute to
or exacerbate sleep difficulties in this population. The current
study measures the extent of sleep deprivation and poorquality sleep in a large population of college students (ages
1724), and extends the current literature on adolescent sleep
by examining factors that are both precipitating and perpetuating of poor sleep in this age group. Using a multibehavioral
analysis in a nonclinical population, we focused on three main
questions: (a) What are the sleep habits of college students?
(b) What behavioral outcomes are associated with poor sleep
quality? (c) What physical, emotional, and psychosocial
factors predict poor-quality sleep in college students?
Method
Participants
Participants were students between the ages of 17 and 24
(N 1,125; 420 male, 705 female) at a large private university in the Midwest. Of these participants, 27% were freshmen
(N 305), 27% were sophomores (N 312), 24% were
juniors (N 271), and 20% were seniors (N 232). The
mean age was 20 (SD 1.3 years). Survey respondents
were representative of the age and ethnic diversity of the
school; 86% of participants were Caucasian (N 978), 5%
were Asian or Pacific Islander (N 58), 2% were African
American (N 23), 2% were biracial (N 24), 1% were
American Indian or Alaskan Native, 0.4% were Hispanic,
125
and the remaining 3% identified as other or elected not to

respond. However, there was a female responder bias;
although males and females were enrolled in equal proportions, females comprised 63% of the survey respondents.
Measures
The online survey included five published scales related to
sleep, mood, and stress: (a) the Pittsburgh Sleep Quality Index
(PSQI), (b) the Epworth Sleepiness Scale (ESS), (c) the HorneOstberg Morningness Eveningness Scale (MES), (d) the
Subjective Units of Distress Scale (SUDS), and (e) the Profile
of Mood States (POMS). The PSQI differentiates between
poor- and good-quality sleepers by measuring seven
areas: subjective sleep quality, sleep latency, sleep duration,
habitual sleep efficiency, sleep disturbances, use of sleep medication, and daytime dysfunction over the past month [23].
Scoring is based on a 03 Likert scale, where a score of 3
reflects the negative extreme. A global score greater than 5 is
indicative of a poor-quality sleeper, whereas a score of 5 or
less is indicative of a good-quality sleeper. For this study,
global PSQI scores were split into three categories: optimal
("5), borderline (67), and poor (#8) sleep quality; these categories were created using the specified cutoff scores for the
purpose of achieving relatively even group sizes. The internal
consistency of the PSQI, estimated by Cronbachs alpha, is .73.
The Epworth Sleepiness Scale is a questionnaire used to
identify excessive sleepiness associated with accumulated
sleep debt or clinical sleep disorders [24]. This eight-item scale
assesses how sleepy one has felt in the past 6 months; participants indicate the likelihood that they would fall asleep while
doing certain activities (e.g., watching TV, sitting and talking
to someone, or stopped at a traffic light), with responses from
(0 would never doze to 3 high chance of dozing. Scores
range from 0 to 24, with scores over 10 indicative of significant
levels of daytime sleepiness. Internal consistency for the ESS,
estimated by Cronbachs alpha, is .75.
The Horne-Ostberg Morningness Eveningness Scale is used
to distinguish between chronotypes (an endogenous characteristic describing ones preference for either morning or evening
patterns of activity) [25]. Scores range from 16 to 86, corresponding to extreme eveningness (lower numbers) to extreme
morningness (higher numbers). Questions target individual
preferences for sleep and wake times, etc., such as: Considering only your own feeling best rhythm, at what time would
you get up if you were entirely free to plan your own day? In
response, participants are directed to select a time between the
hours of 5:00 a.m. and 12:00 p.m. Internal consistency for the
MES, estimated by Cronbachs alpha, is 86.
The Subjective Units of Distress Scale is used to assess
an individuals baseline level of stress [26]. Participants indicate how stressed they feel on a typical day using a scale of 1
to 100, where 1 lowest possible stress and 100 highest
possible stress.
The POMS is used to assess how severely participants
experience depression, tension, fatigue, confusion, vigor,
126
and anger [27]. The shortened version includes a list of 30

adjectives that relate to the six different mood states; participants are asked to rank on a five-point scale from not at
all to extremely how much they experience these mood
descriptors on a typical day. Internal consistency for the
POMS, estimated by Cronbachs alpha, is .79.
In addition to the five published scales and basic demographic information, we also included questions relating to
academic performance, physical health, and psychoactive
drug use. To assess academic performance, we asked participants to provide their grade-point average (on a 4.0 scale)
and information about class attendance. To assess physical
health, we asked students about regularity of exercise and
frequency of missing class because of illness. To assess
psychoactive drug use, we assessed the average week and
weekend frequency and intake of caffeine, alcohol, nicotine,
marijuana, and prescription and OTC stimulants and sleep
aids. Alcohol use was measured by total number of drinks
(glass of wine, bottle/can of beer, shot of liquor, etc.) during
the week (SundayThursday) and during the weekend
(FridaySaturday); caffeine was measured in drinks per
weekday or weekend day (8 oz. serving of coffee, espresso,
tea, soft drinks, hot chocolate, or 1.5 oz. of chocolate); nicotine was measured by the number of cigarettes per day, and
marijuana was measured by the number of uses per week,
as well as the number of inhalations per use. Students were
asked to identify motivations for using particular drugs
(e.g., to increase wakefulness, to increase alertness, to be
social, to complement meals, to promote sleep, etc.).
Procedure
Participants were recruited through an e-mail sent to all
full-time undergraduate students (n 5,401). The first page
of the survey informed participants of the purpose and nature
of the study, assured them of their anonymity, and asked
participants to provide informed consent by clicking a statement before proceeding to the first data collection page of the
survey. As incentives for participation, participants received
either class credit if they were enrolled in select psychology
courses (the type of credit depended on the class), or were
entered into a raffle for a chance to win one of four monetary
prizes ($25$150 gift certificates). After the survey was
completed, students were directed to a separate Web site to
enter into the raffle. The survey was accessible online for
4 weeks in the middle of the semester. The procedure was
approved by the universitys institutional review board.
Approximately 21% of the Universitys undergraduate
students completed the survey. Of these respondents,
students older than 24 were excluded from the study
(<0.5% of respondents), as were students with incomplete
surveys (<10% of respondents).
Analyses
t-Tests were used to test for gender differences and paired
t-tests were used to determine differences between week and
weekend behaviors. Multivariate analysis of variance was

used to explore differences among optimal-, borderline-,
and poor-quality sleepers on a number of variables, including
mood (POMS), stress (SUDS), and caffeine and alcohol use.
Chi-squared analyses were used to assess differences
between optimal-, borderline-, and poor-quality sleepers in
ordinal and nominal variables. Multiple stepwise regression
analyses were employed to determine predictors of sleep
quality. Variables that have been shown in previous
studies to correlate with sleep quality (including individual
components of the POMS, stress [SUDS], morningness/
eveningness [MES], caffeine and alcohol use, frequency of
exercise, and regularity of sleep scheduling [weekend oversleep and bedtime delay]), but that are not themselves
components of the PSQI score (e.g., total sleep time, sleep
latency, pain during sleep), or direct measures of sleepiness
(e.g., Epworth Sleepiness Score or the fatigue component
of the POMS), were used as independent variables in the
regression.
Results
Sleeping behavior: quantity and quality
Overall, college students reported chronically restricted
sleep. Mean total sleep time (time spent actually sleeping,
as opposed to being awake in bed) was 7.02 hours
(SD 1.15). Twenty-five percent of students reported getting
less than 6.5 hours of sleep a night, and only 29.4% of
students reported getting 8 or more hours of total sleep time
per night, the average amount required for young adults
[28]. Sleep was particularly restricted on weeknights;
mean weekday bedtime was 12:17 a.m. (SD 71 minutes)
and weekday rise time was 8:02 a.m. (SD 76 minutes).
Sleep schedules were erratic. Mean bedtimes (1:44 a.m.,
SD 79 minutes) were delayed and mean rise times (10:08
a.m., SD 88 minutes) were extended on weekends. Additionally, 20% of students reported staying up all night at least
once in the last month, and 35% reported staying up until
3 a.m. at least once a week.
Figure 1 outlines the differences in bedtimes and risetimes
by year, beginning in ninth grade and extending through the
end of college (high school data are from the 2006 National
Sleep Foundation Sleep in America Poll) [9]. Both weekday
bedtimes and risetimes appear to be 75 minutes later in our
cohort of first year college students when compared to a cohort
of seniors in high school. Sleep schedule differed significantly
by year in school. First-year students had significantly later
bedtimes and rise times than juniors and seniors during the
weekends, F(3,994) 5.92, 7.06; h2 .018, .021, respectively, p < .001, but not during the weekdays, leading to
a more pronounced delay in weekend bedtime and weekend
oversleep among first year students and sophomores,
compared to juniors and seniors, F(3,994) 4.57, 5.41;
h2 .014, .026, respectively, p < .001. Sleep schedule also
differed significantly by sex. Males had significantly later

1:58
1:44
1:44
1:27
Bed Time
12:45
12:22
12:14
12:20
12:11
12:25
11:53
12:03
11:02
10:32
Sleep quality, mood, and health
10:15
HS 10
HS 11
HS 12
College
Fresh.
College
Soph.
College Jr. College Sr.
Year in School
10:26
10:09
10:06
9:49
8:08
6:28
HS 9
6:23
HS 10
10:08
9:51
9:52
Rise Time
9:54
a week. Over one-third of students cited other reasons

for sleep disturbances at least once a week; of these responses,
the most common reasons provided for these disturbances
were stress (35%), excess noise (33%), and cosleeping
(sharing the bed with a partner; 7%).
Students also reported significant sleepiness-related
decrements in daytime performance (Table 2). Mean scores
on the Epworth Sleepiness Scale were 6.8 for weekdays
and 6.7 for weekends; 25% of students scored 10 or above
on the scale, indicating significant levels of daytime sleepiness. Seventy-five percent of students reported feeling
dragged out, tired, or sleepy once a week or more, and
15% reported falling asleep in class once a week or more.
week
weekend
10:51
HS 9
127
6:23
HS 11
7:59
7:59
week
weekend
6:31
HS 12
8:03
College
Fresh.
College
Soph.
College Jr. College Sr.
Year in School
Figure 1. Bedtimes and rise times by year in school. Data from the high
school bins are taken from the 2006 Sleep in America Poll (n 1,602) [9].
bedtimes and risetimes during the week than did females,

t(998) 5.34, 2.18, respectively, p < .001, but not during
the weekends.
In addition to low sleep quantity, students also exhibited
poor sleep quality. Table 1 shows responses to individual
questions on the PSQI. Only 34.1% of students scored in
the good range of the PSQI ("5), and 38% had PSQI scores
over 7, indicating poor-quality sleep. The primary contributors to these high PSQI scores were restricted total sleep
time, low enthusiasm, long sleep latencies, and other
factors regularly interfering with sleep (Question 5j). Specifically, 52% of students reported lacking enthusiasm to get
things done at least once a week, and 32% reported an
inability to fall asleep within 30 minutes at least once
Poor sleep quality was associated with significantly higher

self-reported negative moods. Participants categorized as
having poor-quality sleep (PSQI scores #8) had significantly
greater negative mood subscale scores (anger, confusion,
depression, fatigue, and tension), compared to those with
good-quality sleep; for all cases, F(2,897) > 25, p <.001
(Table 3). Poor-quality sleepers also reported higher levels
of stress during the week and weekends, compared to
optimal-quality sleepers, F(2,916) 72.4; 37.7, respectively,
p < .001 (Table 3).
Poor-quality sleepers also reported significantly more
physical illness than optimal- and borderline-quality sleepers,
c2(12, n 947) 39.9, p < .05. Twelve percent of poorquality sleepers reported missing class three times or more
in the last month because of illness, compared to less than
4% of borderline- or good-quality sleepers. Higher scores
on the PSQI were also associated with significantly increased
instances of falling asleep in class and skipping class for
reasons other than illness (Table 3).
Sleep quality was also related to the use of prescription,
OTC, and recreational drugs to help regulate sleep and wakefulness (Table 3). Specifically, those with poor sleep quality
were more than twice as likely to report using OTC or
prescription stimulant medications at least once a month to
help keep them awake, compared to those with good sleep
quality. However, the number of caffeinated drinks per day
did not significantly differ between PSQI groups. Likewise,
more than 33% of students who scored equal to or greater
than 8 on the PSQI used prescription or OTC sleep aids at
least once a month, compared to less than 5% of optimalquality sleepers. Finally, poor-quality sleepers reported
drinking more alcohol per day than optimal-quality sleepers,
and were twice as likely to report using alcohol to induce
sleep compared to those with PSQI scores less than 8 (Table
3). Furthermore, of poor-quality sleepers, those who said
they used alcohol to induce sleep drank significantly more
alcoholic beverages per week, compared to those drinkers
who did not use alcohol to sleep: 12 versus 21,
t(282) $2.43, p .02.
128
Table 1
Prevalence of sleep disturbances as measured by the PSQI
Pittsburgh Sleep Quality Index
Bedtime
Sleep latency
Risetime
Total sleep time
Mean, SD
How often have you had trouble sleeping
because.
Cannot get to sleep within 30 minutes
Wake up in middle of night or early morning
Wake up to use the bathroom
Cough or snore loudly
Cannot breathe comfortably
Feel too cold
Feel too hot
Have bad dreams
Have pain
Other reasons
How often have you.
Taken medicine to aid in sleep?
Had trouble staying awake during social
activities?
Had a problem getting the enthusiasm to get
things done?
Rate overall sleep.
12:21 a.m. 74 min

Not during the past month
23.8 min, 19.2 min

Less than once a week
8:05 a.m.,76 min

Once or twice a week
7.02 hours, 1.15 hours

3 or more times a week
26.2%
44.2%
56.1%
87.5%
80.6%
71.0%
33.5%
70.2%
73.1%
49.4%
41.4%
34.2%
32.7%
9.6%
13.3%
23.4%
42.8%
21.7%
19.2%
17.3%
21.5%
16.0%
7.4%
2.1%
4.7%
4.5%
19.3%
6.5%
5.4%
22.0%
10.9%
5.6%
3.8%
0.7%
1.4%
1.1%
4.5%
1.6%
2.3%
11.0%
82.1%
75.7%
11.0%
20.8%
4.0%
3.3%
2.9%
20.0%
19.8%
30.1%
33.0%
17.2%
Very good
11.0%
Global PSQI
Fairly good
55.0%
Optimal(15)
34.1%
Fairly bad
30.0%
Borderline(67)
27.7%
Very bad
3.9%
Poor(#8)
38.2%
PSQI Pittsburgh Sleep Quality Index.
Predictors of sleep quality

Several lines of evidence point to stress as a major contributor to poor sleep quality in college students. First, 20.1% of
students reported stress interfering with sleep at least once
a week. Women were significantly more likely to report
stress-related sleep troubles than men; t(927) 5.49, p <.001.
Second, when asked to provide a written answer to PSQI question 5j, How often have you had trouble sleeping because of
other reason(s); please describe reasons, the most common
answers were related to stress. Answers such stress about
school, racing thoughts, or worry about the future, accounted for 35% of the responses, followed by excess noise
(33%), cosleeping (7%), and talking with friends (6%). Third,
when asked If your sleep is at all compromised, to what one
factor do you most strongly attribute this? in forced-choice
question, the majority of students responded that academic
(39%) or emotional (25%) stress most interfered with their
sleep. By comparison, light or noise accounted for 17% of the
responses, illness or pain accounted for 8%, and cosleeping
accounted for an additional 4% of responses. Moreover, when
asked what factor most interferes with initiating sleep, 68% of
students responded with stress, compared to 10% citing temperature, and 8% responding with light or noise.
To evaluate what factors predict sleep quality, we performed a multiple stepwise regression using factors previously shown to be related to sleep quality (e.g., mood,
caffeine and alcohol use, regularity of sleep schedule, and
electronics exposure). The tension component of the Profile
of Mood States predicted 21% of the variance in sleep quality
(PSQI score), with stress (SUDS) accounting for an addi-
tional 3%, and morningness/eveningness (MES) accounting

for another 2% of the variance (Table 4). Alcohol per day,
caffeine per day, exercise frequency, and daily hours of television and video game exposure were not significant predictors of the PSQI score.
Discussion
Overall, the results demonstrate that the epidemic of insufficient sleep documented in high school students extends past
early and midadolescence to college students. Total sleep
time is similar between high school and college students,
but bedtimes and risetimes are shifted later by about
90 minutes on both week and weekend days. The tendency
to delay bedtimes and extend risetimes during weekends
also continues into young adulthood. In addition to short
sleep and irregular schedules, college students also experience low sleep quality, when assessed by standard measures.
Surprisingly, perceived stress (rather than sleep schedule
regularity, alcohol or drug use, exercise frequency, or electronics usage) provided the most explanatory power for
poor sleep in this population.
Limitations
The results of this study must be interpreted in light of the
limitations inherent in its design. First, this sample consisted
of college students from one geographic area who were
generally healthy and well-educated, and thus our findings
are not necessarily generalizable to the United States young
adult population. However, basic sleep schedules (week
129
Table 2
Sample characteristics by class and gender
N
ESS week
Class
Post hoc
1>4
*Gender
ESS weekend
Class
*Gender
Total PSQI
Class
Gender
SUDS week
*Class
1 < 2,3,4
*Gender
SUDS weekend
*Class
1<3
*Gender
Mean
SD
1
2
3
4
262
270
244
205
7.3
7.1
6.7
6.2
3.6
3.9
3.7
3.7
M
F
359
625
6.2
7.2
3.6
3.8
1
2
3
4
M
F
262
270
244
205
359
625
6.7
6.8
6.6
6.4
6.0
7.0
3.5
3.7
3.8
3.5
3.6
3.6
1
2
3
4
M
F
254
254
236
202
349
600
6.7
6.9
7.3
7.1
6.7
7.2
3.0
3.1
3.3
3.1
3.1
3.2
1
2
3
4
M
F
248
244
234
196
345
580
55.1
62.3
63.0
62.2
53.6
64.7
25.1
22.3
21.7
24.5
26.0
21.1
1
2
3
4
M
F
248
243
234
195
345
578
34.9
40.2
40.9
39.1
31.8
43.0
23.0
23.1
22.7
24.1
23.4
22.3
Morningness/eveningness
Class
Gender
Caffeinated drinks/weekday
*Class
1 < 3,4 2 < 4

Gender
Caffeinated drinks/weekend day
Class
1<3
Gender
Alcoholic drinks/weekday
*Class
1,2 < 3,4

*Gender
Alcoholic drinks/weekend day
Class
*Gender
Mean
SD
1
2
3
4
273
279
255
213
49.3
50.4
49.4
50.3
9.0
9.3
9.9
10.1
M
F
378
645
49.6
50.0
10.0
9.4
1
2
3
4
M
F
305
312
271
232
420
705
0.7
0.7
0.9
1.0
0.8
0.8
1.0
1.1
1.1
1.2
1.2
1.0
1
2
3
4
M
F
305
312
271
232
420
705
0.9
1.0
1.2
1.1
1.0
1.1
1.0
1.3
1.6
1.6
1.3
1.5
1
2
3
4
M
F
305
312
271
232
420
705
0.2
0.2
0.5
0.5
0.5
0.3
0.6
0.6
0.9
0.8
1.0
0.5
1
2
3
4
M
F
305
312
271
232
420
705
2.8
2.5
3.0
3.2
3.9
2.2
4.2
3.7
4.0
4.0
5.1
3.0
Difference from total N reflects omissions in survey reporting. Asterisks indicate significant differences between class or gender. Bonferroni tested significant
differences (a .01) between classes are provided in the left side of the columns.
SUDS Subjective Units of Distress Scale; PSQI Pittsburgh Sleep Quality Index; ESS Epworth Sleepiness Scale.
and weekend bedtimes and risetimes) in this report were

similar to ones at a Chinese university and a small liberal
arts college in New England [22,29]. Also, with respect to
differences between student and nonstudent sleep patterns,
Oginska and Pokorski [17] documented similar relationships
between shortened sleep and excessive drowsiness, poor
mood, and tension in both university students and working
young adults in a European population.
Second, as this study consisted of a one-time survey, it is
impossible to determine directionality in the relationships
between poor sleep quality, mood, and stress, or to what
extent poor sleep is secondary to or predictive of stress
and anxiety. However, much evidence suggests that this is a
complex, bidirectional relationship. In a large populationbased study (N 14,915), mood disorder diagnoses were
more often preceded by, rather than concurrent with, periods
of poor sleep [30]. Furthermore, in longitudinal studies,
periods of disturbed sleep are significant predictors of devel-
oping depressive mood disorder [31,32]. Also, as in any

survey data, there is the potential for a recall bias.
Sleep and stress
In this age group, tension and stress seemed to be the most
important factors in predicting sleep quality, accounting for
24% of the variance in PSQI score. Similarly, in a study of
Chinese younger adolescents (N 1,629), perceived stress
was the most significant risk factor for poor sleep quality,
accounting for 13.5% of the variance in sleep quality score
[18]. Perceived stress can serve as predisposing, precipitating, and perpetuating factors for sleep difficulties in this
population. First, the college lifestyle creates precipitating
factors that enhance stress-related sleeping difficulties (e.g.,
erratic schedules, high-stress periods like final exams).
Second, students may be more susceptible to hyperarousalrelated sleep difficulties because of maturational changes in
130
Table 3
Differences in behavior by PSQI group
Sleep schedule
Total sleep time (h)
Bedtime, weekday
Risetime, weekday
Bedtime, weekend
Risetime, weekend
Bedtime Delay (h)
Weekend Oversleep (h)
Morningness/Eveningness
(df)
2,952
2,948
2,948
2,946
2,947
2,946
2,947
2,949
(df),N
Stayed up to 3 a.m. >13/week

All-nighter >13/month
Stress and mood
Anger
Confusion
Depression
Fatigue
Tension
Vigor
Weekday distress (SUDS)
Weekend distress (SUDS)
Psychoactive drug use
Caffeinated drinks/day
Alcoholic drinks/day
6,948
6,947
(df)
2,897
2,897
2,897
2,897
2,897
2,897
2,916
2,916
(df)
Sleepiness and performance

Epworth SS weekday
Epworth SS weekend
Fall asleep in class #13/week
Skip class >2/mo, due to illness
Skip class >2/months, other reasons
!2
h
Post hoc
Optimal
Borderline
Poor
102.8
9.5
2.8
5.5
3.0
0.8
4.0
33.1
<.001
<.001
0.062
0.004
0.060
0.448
0.019
<.001
.01
.02
<.01
.01
<.01
<.01
<.01
.07
O > B>P
O,B < P
7.61
12:07 a.m.
8:06 a.m.
1:34 a.m.
10:03 a.m.
1.46
1.95
53
7.08
12:13 a.m.
7:54 a.m.
1:42 a.m.
10:03 a.m.
1.48
2.7
50
6.47
12:28 a.m.
8:06 a.m.
1:52 a.m.
10:16 a.m.
1.38
2.2
47
c2
Optimal
Borderline
Poor
<.001
<.001
25%
12%
32%
16%
46%
28%
Post hoc
Optimal
Borderline
Poor
O < B<P
O < B<P
O < B<P
O < B<P
O < B<P
O > B>P
O < B<P
O < B<P
7.48
8.6
7.01
9.44
8.29
14.29
49.9
30.8
9
9.56
8.76
12.09
9.96
13.38
59.9
38
10.61
10.31
10.66
14.92
11.82
12.09
70.7
46.6
Post hoc
Optimal
Borderline
Poor
46.4
30.8
!2
h
66.8
32.2
71.2
146.2
81.1
28.4
72.4
37.7
<.001
<.001
<.001
<.001
<.001
<.001
<.001
<.001
!2
h
0.59
0.03
<.01
<.01
2,952
2,952
0.53
3.42
.13
.07
.14
.25
.16
.06
.14
.08
O<P
O > B>P
1.0
1.07
0.990
1.24
1.08
1.35
c2
Optimal
Borderline
Poor
23.3
118
14.0
0.003
<.001
<.001
12%
4%
5%
22%
13%
2%
26%
33%
10%
(df)
Post hoc
Optimal
Borderline
Poor
2,917
2,915
(df),N
6,951
12,948
10,950
42.2
16.7
c2
39.2
39
29.3
<.001
<.001
p
<.001
<.001
<.001
O < B<P
O < B<P
5.32
5.58
Optimal
9%
4%
16%
6.95
6.83
Borderline
12%
3%
18%
8.08
7.34
Poor
21%
12%
22%
(df),N
Use OTC/Rx meds to wake >13/month
Use OTC/Rx meds to sleep >13/month
Use alcohol to get to sleep
6,871
6,949
2,681
h
!2
.04
.10
O optimal (PSQI >6), B borderline (PSQI 67), P poor (PSQI >7). a .01.
PSQI [ Pittsburgh Sleep Quality Index; OTC over the counter.
the neuroendocrine system. Developmental changes in the

HPA axis during adolescence result in increased perisleep
onset cortisol secretion [33]. This neuroendocrine hyperactivity could contribute to both the hyperarousal observed in
delayed sleep onset [34] as well as increased feelings of
anxiety and depression. Third, college students may have
not yet developed sufficient coping strategies for handling
stressful events, and subsequently experience more internalizing, rumination, and worry [35]. Thus, biological factors
(e.g., hyperarousal of the autonomic nervous system and
HPA axis overactivation) provide a predisposition for
stress-induced sleep difficulties, stressful events common in
this population (e.g., midterm examinations, relationship
troubles) precipitate bouts of sleep difficulties, and rumination and worry can perpetuate the sleep difficulty.
Of particular concern is the tendency for older adolescents

to self-medicate sleep-wakefulness. Self-administration of
OTC medication in an older adolescent population is associated with psychological distress [36]. In our sample, poorquality sleepers reported higher alcohol consumption and
more frequent use of alcohol and OTC drugs to help regulate
their sleep/wake schedule. A potential consequence of such
behaviors is the stimulantsedation loop (use of caffeine
and other stimulants to counteract daytime sleepiness, and
subsequent use of depressants to counteract the effects of
the stimulants). Students who get caught in this pattern
may be at a higher risk for developing drug dependence
[37]; approximately 90% of adolescents entering drug rehab
programs report self-medicating with psychoactive drugs to
control sleep and combat fatigue [38].
131
Table 4
Stepwise multiple regression predicting PSQI scores
F(5,877) 882, p < .001
Std. Error
(Constant)
Predictors, R2 29%
POMS-Tension
SUDS
MES
POMS-Depression
POMS-Anger
Nonsignificant variables
Age
Sex
Ethnicity
Caffeine/day
Alcohol/day
Bedtime delay
Weekend oversleep
GPA
Hrs Exercise/week
Hrs TV/Video/week
POMS-Confusion
7.449
3.453
.118
.024
$.060
.112
.102
.041
.005
.014
.036
.038
.080
.152
.115
$.103
.105
$.178
.031
$.214
$.065
$.018
$.010
.071
.210
.288
.083
.067
.104
.082
.250
.071
.055
.046
Beta
Sig.
2.158
.031
.143
.182
$.187
.149
.119
2.857
5.278
$4.290
3.088
2.669
.004
<.001
<.001
.002
.008
.034
.024
.012
$.038
.052
$.054
.013
$.027
$.028
$.010
$.009
1.125
.724
.398
$1.247
1.561
$1.707
.377
$.858
$.906
$.323
$.222
.261
.469
.691
.213
.119
.088
.706
.391
.365
.747
.825
GPA grade-point average; PSQI [ Pittsburgh Sleep Quality Index; SUDS Subjective Units of Distress Scale; MES Morningness Eveningness Scale;
POMS Profile of Mood States.
Recommendations
These results highlight a growing need for professionals to
focus on the quality as well as the quantity of sleep when
promoting mental and physical health in adolescents and
young adults. College students who are consistently getting
poor-quality sleep are at risk for problems far more serious
than simply struggling to function in daily activities. As
chronic insomnia is a risk factor for major mood [39] and
substance abuse disorders [40], physicians, college healthcare professionals, and residence life workers should be
more proactive in screening for sleep difficulties and in articulating the importance of sufficient, restorative sleep in
college students well-being.
Disclosure Statement
The authors have indicated no financial conflicts of
interest.
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Sleep Medicine 8 (2007) 602612

www.elsevier.com/locate/sleep
Sleep, circadian rhythms, and delayed phase in adolescence

Stephanie J. Crowley
a,c,*
,
Christine Acebo
b,c
, Mary A. Carskadon
b,c
a
Department of Psychology, Brown University, Providence, RI 02906, USA
Department of Psychiatry and Human Behavior, Brown Medical School, Providence, RI 02906, USA
E.P Bradley Hospital Sleep and Chronobiology Research Laboratory, East Providence, RI 02915, USA
b
c
Received 11 August 2006; received in revised form 14 November 2006; accepted 4 December 2006
Available online 26 March 2007
Abstract
Sleep/wake timing shifts later in young humans during the second decade of life. In this review we describe sleep/wake patterns,
changes in these patterns across adolescence, and evidence for the role of environmental, psychosocial, and biological factors underlying these changes. A two-process model incorporating circadian (Process C) and sleep/wake homeostatic (Process S) components
is outlined. This model may help us to understand how developmental changes translate to shifted sleep/wake patterns. Delayed
sleep phase syndrome (DSPS), which has a typical onset during the second decade of life, may be an extreme manifestation of
homeostatic and circadian changes in adolescence. We describe symptoms, prevalence, and possible etiology of DSPS, as well as
treatment approaches in adolescents.
2006 Elsevier B.V. All rights reserved.
Keywords: Adolescent; Development; Circadian rhythms; Sleep patterns; DSPS; Delayed sleep phase syndrome
1. Introduction
This review describes changes to sleep/wake behavior
during adolescent development and the contribution of
the circadian and sleep/wake homeostatic systems to
this changing behavior. We also review delayed sleep
phase syndrome (DSPS), which may be an extreme manifestation of these changes or may be a distinct clinical
entity. Last, we describe approaches to treat DSPS in
adolescents. For the purpose of this review, we consider
biological adolescence to span the second decade of life.
2. Developmental changes in sleep/wake (light/dark)
patterns
Sleep/wake patterns of developing adolescents are
often described in the context of a school year and have
*
Corresponding author. Tel.: +1 401 421 9440; fax: +1 401 453

3578.
E-mail address: [email protected] (S.J. Crowley).
1389-9457/$ - see front matter 2006 Elsevier B.V. All rights reserved.
doi:10.1016/j.sleep.2006.12.002
been described separately for school (weekday) and nonschool (weekend) days. Sleep timing is often quite dierent during school vacations. Describing sleep patterns
during both school and vacation times provides a more
comprehensive account of developmental sleep/wake
behavior changes, yet few studies have examined vacation sleep patterns.
Table 1 summarizes adolescent self-reported sleep
patterns derived from survey studies that reported weekend and weekday data during the school year. These
data show that adolescents report going to bed later as
they get older. Studies from such countries as Canada
[1], Poland [2], Belgium [3], Australia [4], Finland [5],
and Brazil [6] show similar trends. Investigators associate this age-related change in bedtime on school nights
with a number of environmental factors, including
reduced parental inuence on bedtimes [7,8], increased
homework [9], and extra-curricular activities, such as
sports, musical groups, clubs, and service groups [10],
or part-time work [7,10,11]. Other environmental, usually stimulating activities, that often aect bedtime
S.J. Crowley et al. / Sleep Medicine 8 (2007) 602612
603
Table 1
Mean self-reported school-year weekend and weekday sleep patterns from survey reports in the U.S
Weekday Bedtimea
Weekend Bedtimea
Weekday Rise Timea
Weekend Risetimea
Middle School Years (11-13 years old)

Carskadon, 1990 [7]
11 years
NSF Poll 2006 [8]
Grade 6
Carskadon, 1990 [7]
12 years
NSF Poll 2006 [8]
Grade 7
Manber et al., 1995 [9]
middle school
Carskadon, 1990 [7]
13 year
NSF Poll 2006 [8]
Grade 8
Wolfson & Carskadon, 1998 [13]
13-14 years
2130 (2140)
2124
2145 (2150)
2152
2137
2206 (2228)
2153
2205
2222 (2250)
2231
2255 (2305)
2305
2311
2320 (2342)
2326
2354
0705 (0700)
0642
0655 (0705)
0635
0610
0650 (0700)
0636
0559
0825 (0745)
0853
0835 (0835)
0912
0847
0845 (0845)
0921
0922
High School Years (14-19 years old)

OBrien & Mindell, 2005 [12]
Grade 9
NSF Poll 2006 [8]
Grade 9
Wolfson et al., 2003 [16]
13.8 - 19.9 years
Carskadon, 1990 [7]
14 years
Carskadon, 1990 [7]
15 years
15 years
Grade 10
NSF Poll 2006 [8]
Grade 10
Link & Ancoli-Israel, 1995 [15]
15-18 years
Manber et al., 1995 [9]
high school
Carskadon, 1990 [7]
16 years
16 years
Grade 11
NSF Poll 2006 [8]
Grade 11
Carskadon, 1990 [7]
17 years
17-19 years
Grade 12
NSF Poll 2006 [8]
Grade 12
2238
2215
2246
2210
2224
2220
2307
2232
2244
2238
2252
2237
2313
2251
2258
2251
2324
2302
2359
2353
0017
2357
0011
0006
0042
0003
0041
2356
0028
0030
0115
0025
0039
0049
0124
0045
0628
0620
0556 (0615)
0605 (0627)
0600
0954
0940
0914 (0912)
0924 (0925)
0940
0623
0555
0608
0613 (0638)
0605
0952
0951
0915
0921 (0937)
0946
0623
0626 (0645)
0610
1006
0921 (0927)
0932
0631
0951
Reference
age/school grade
(2216)
(2243)
(2308)
(2314)
(0006)
(0027)
(0044)
(0051)
Values followed by parentheses indicate that authors computed means for boys and girls separately in the original report; the rst value = mean
time reported by girls; parenthetical value = mean time reported by boys.
include watching TV, playing video games, and using

the computer [3,8].
Adolescents consistently report going to bed later on
weekend nights compared to school nights (see Table 1).
The dierence between weekend and school-night bedtimes (weekend bedtime delay) in adolescents averages
between 1 and 2 h [79,1216], usually greater in the
older than the younger adolescents.
Most school systems in the United States are organized so that high school students are required to report
to school earlier than middle school students [8]. Rise
time on school days reects this pattern (see Table 1).
Several reports note that girls rise signicantly earlier
than boys on school mornings [79,13,15]. Early rising
for school is unwelcome and forced for most adolescents. For example, one survey study showed that 61%
of a suburban high school student sample reported commonly being too sleepy to get out of bed in the morning [17]. A longitudinal study completed in Switzerland
reported that about 63% of participants at the average
age of 15 and 17 years reported being tired upon awakening [18]. A more recent telephone poll by the U.S.
National Sleep Foundation reported that approximately
70% of middle school and high school students required
an adult to wake them on school mornings [8].
Another consistent nding is that the reported rise

times on weekend mornings are signicantly later than
those on school mornings, especially for older adolescents (see Table 1). Findings are inconsistent about
whether or not boys and girls have dierent sleep patterns. For example, LaBerge and colleagues found sex
dierence in a group of 1013 year olds, with girls sleeping later on weekends compared to boys [1]; however, in
another study this dierence did not emerge in a group
of 13- to 19-year-old adolescents [13]. With an average
school-day rise time between 0600 and 0700 h, the dierence between weekday and weekend rise time (weekend
rise time delay) averages about 1.53 h in 1013 year
olds and 34 h in high school students. One study marks
this weekend sleep delay at almost 3 h in adolescents,
dened as less than 21 years old [19].
The adolescents social milieu changes from school
months to vacation months. Most adolescents experience less constrained daily schedules during vacation,
yet little research has focused on changes to sleep/wake
patterns under this more unconstrained schedule.
Hansen and colleagues [20] studied sleep patterns of
fourth-year high school students in August (before
school started) and again in September (after school
started). Sleep diary data showed that weekday bedtimes
604
in September averaged about 1.5 h earlier than in

August. These data suggest that older adolescents report
later bedtimes during school vacation compared to the
school year.
We compared sleep patterns of a group of adolescents
(916 years old) on self-selected sleep schedules during
the summer (n = 59) to other adolescents during the
school year (n = 149) [21]. Data were derived from daily
verbal reports of bedtime and wake-up time via morning
telephone messages over a week. Overall, adolescents
reported later bedtimes in the summer (means = 2256,
standard deviation (SD)=61 min) compared to during
the school year (means = 2200, SD = 49 min); however,
when subdivided into age groups (912 versus 1316
years), the younger participants showed a 64-min dierence between the school and summer vacation bedtimes
while older participants showed a 32-min dierence.
Summer vacation wake-up times were also later
(means = 0819, SD = 76 min) compared to school-year
times (means = 0703, SD = 32 min). In this case, the
average dierence between school and summer vacation
rise times was 91 min for the older participants and
60 min in the younger participants. (We note that the
school year means are weekend and weekday sleep times
combined.)
The less restrained daily schedule during vacation
likely accounts for later sleep schedules, and changes
to parental inuence over sleep schedules may also inuence these dierences. Thus, parents may place less
emphasis on a good nights sleep during the school
vacation because academic performance is not necessarily emphasized. A similar idea has been proposed by
Roenneberg and colleagues [19,22], who argue that an
individuals chronotype, which is controlled in part by
genetic factors, is estimated best using the midphase of
sleep on free days or days without social constraints.
Their data show a progressive delay of midphase of
sleep from age 10 to 20 [22]. When schedules are not
as constrained during the summer or on free days as
during school days, the adolescent may be able to sleep
when his or her body feels it needs to, doing so at a relatively late clock time. On the other hand, the summer
(or free day) pattern does not necessarily reect biological factors alone, since environmental and psychosocial
factors dier in the summertime and may inuence sleep
patterns.
In summary, older adolescents tend to have later
school-year bedtimes on both school and non-school
nights compared to younger adolescents; reported
wake-up times are later primarily on weekends for older
adolescents compared to younger adolescents. Furthermore, sleep/wake patterns are later during the summer
vacation compared to the school year, and the magnitude of the summer delay depends on the youngsters
age. Changes in the circadian timing system and the
homeostatic sleep system during adolescent develop-
ment provide some insight into these sleep/wake behavioral changes. We provide a general background of both
systems and then discuss how these processes appear to
change during adolescent development.
3. The circadian timing system
The circadian timing system provides temporal organization for regulatory mechanisms to facilitate adaptive
behavior, such as feeding, reproduction, and sleep/wake
cycles [23]. These coordinated temporal patterns, or circadian rhythms, are self-sustained and oscillate with a
period of about 24 h. The internal mechanism (pacemaker) that organizes these rhythms in mammals has
been localized to a small paired nucleus in the hypothalamus, the suprachiasmatic nucleus (SCN; [24]). Biological events or markers associated with these rhythms can
be used to estimate circadian time or phase.
Melatonin is a hormone secreted by the human pineal
gland that oscillates with a circadian rhythm. Levels of
the hormone are nearly absent during the daytime, rise
in the evening near ones usual bedtime, stay relatively
constant during the nighttime, and decline near ones
habitual wake-up time. Melatonin is suppressed by light
[25], and recent studies show that even room light levels
(200300 lux) can have a suppressive eect on human
endogenous melatonin production [2628]. The onset
of melatonin secretion, also called the dim light melatonin onset (DLMO) phase, is a marker of the circadian
timing system [29] and can be measured from saliva
samples collected at 30-min intervals in dim light
(<30 lux) [30]. Research laboratories often dene
DLMO phase as the time at which melatonin concentration rises above a designated threshold (e.g., 4 pg/mL
for saliva and 10 pg/mL for plasma melatonin). The
decline of melatonin, also called the dim light melatonin
oset (DLMO) phase, and the midpoint between
DLMO and DLMO are other phase markers of the circadian timing system derived from the melatonin
rhythm. Other rhythms such as core body temperature
have also been used to mark the circadian system; however, DLMO phase is currently thought to be the most
reliable marker of phase [31,32].
The circadian timing system oscillates with an intrinsic period slightly dierent from 24 h but synchronizes
(entrains) to the 24-h day in response to external timegivers, or zeitgebers. The primary synchronizing stimulus for the circadian timing system is the daily variation
of daylight and darkness [33]. The circadian system is
sensitive to light, especially during the nighttime, which
for humans is the usual sleep period. A phase response
curve (PRC) describes how light input is able to shift circadian rhythms earlier or later in time. Fig. 1 shows a
PRC to light for adult humans, constructed by Khalsa
and colleagues (2003) [34]. These researchers measured
circadian phase by way of plasma melatonin before
605
tate entrainment in humans who have an intrinsic period

greater than 24 h, whereas evening light exposure will
entrain individuals with an intrinsic period shorter than
24 h.
The circadian clock is one part of the system that
coordinates sleep/wake behavior. Homeostatic sleep/
wake processes, which are controlled by brain mechanisms that are not entirely understood, also play a role
in the regulation of sleep and wake.
4. The homeostatic sleep system
Fig. 1. Figure and gure legend are reprinted with permission from
Khalsa et al. (2003) [34]. Phase advances (positive values) and delays
(negative values) are plotted against the timing of the centre of the light
exposure relative to the melatonin midpoint on the pre-stimulus
constant routine (dened to be 22 h), with the core body temperature
minimum assumed to occur 2 h later at 0 h. Data points from circadian
phases 68 are double plotted. The lled circles represent data from
plasma melatonin, and the open circle represents data from salivary
melatonin in subject 18K8 from whom blood samples were not
acquired. The solid curve is a dual harmonic function tted through all
of the data points. The horizontal dashed line represents the
anticipated 0.54 h average delay drift of the pacemaker between the
pre- and post-stimulus phase assessments.
and after a 6.7-h bright light stimulus (10,000 lux)

timed at various times of day. The x-axis represents
the timing of the light stimulus. The melatonin midpoint
phase is dened as 22 h and core body temperature minimum phase is estimated at 0 h. (The midpoint of melatonin secretion usually occurs just after the midpoint of
a regular sleep episode in adult humans sleeping 8 h
[35]). Responses to the bright light stimulus are shown
on the y-axis as a phase shift.
In general, the human system responds in a systematic and predictable manner: light during the end of
the daytime and beginning of the nighttime (before the
estimated core body temperature minimum) shifts circadian rhythms later (phase delay); bright light during the
end of the nighttime or at the beginning of the daytime
(after the estimated core body temperature minimum)
shifts circadian rhythms earlier (phase advance)
[34,36]. (It is important to note that a PRC to light for
adolescent humans has not yet been described and
may dier from the adult PRC.) This exibility of the
system allows animals, including humans, to entrain to
the 24-h solar day. The entrainment process diers
among individuals because some manifest an oscillatory
period shorter than 24 h and some longer than 24 h. The
intrinsic period of healthy human adolescents averages
24.27 h [37]. The majority of humans entrain by a small
phase advance each day and a small-proportion entrain
by a small phase delay [38]. According to the adult
human light PRC, morning exposure to light will facili-
The homeostatic sleep/wake system is thought to be

relatively independent of circadian timing. A simple
way to characterize the process is that sleep pressure
increases the longer one is awake and dissipates as one
sleeps. Slow wave sleep (SWS, stages 3 and 4) and electroencephalographic (EEG) slow wave activity (SWA,
power in the 0.754.5 Hz range) have been used as physiological markers for sleep pressure. Thus, SWA is
high at the beginning of the nocturnal sleep episode
when sleep pressure is greatest, and SWA shows an
exponential decline across the nights successive nonrapid eye movement (NREM) episodes [3941]. Furthermore, as wake is extended, SWA increases during subsequent sleep episodes, proportional to prior wake
duration [4143]. The homeostatic process is also
reected in changes in the theta and alpha components
of the waking EEG as a function of sleep and wake
durations [44].
Models describing the interaction between sleep/
wake homeostasis and the circadian timing system are
used to describe sleep/wake regulation. Borbely [39]
was the rst to describe a model to identify the interaction between these two systems in the Two Process
Model of Sleep Regulation, a model that was later
rened by Borbely and others [40,4547]. He called the
circadian component Process C and the homeostatic
sleep/wake component Process S. A schematic of the
two interacting processes is shown in Fig. 2. Sleep occurs
when Process S reaches an upper threshold and wake
occurs when Process S is below a lower threshold. Process C controls the thresholds and has been termed the
somnostat, drawing an analogy to a thermostat [40].
According to this model, sleep is initiated at one circadian phase and wake is initiated at a dierent circadian
phase. Accordingly, the frequency of the sleep/wake
cycle depends on the distance between the two thresholds or phases.
Another variation of the model [48] casts the two systems in opposition to one another for describing sleep/
wake regulation. In this model, a circadian (clockdependent) alerting process opposes a wake-dependent
sleep-promoting process to maintain wakefulness across
the daytime [48]. Dijk and Czeisler [49] propose a
similar opponent process to describe the maintenance
606

Two-Process Model of Sleep Regulation
Upper Threshold
(Sleep Initiation)
Lower Threshold
(Wake Initiation)
WAKE
SLEEP
00:00 08:00
Time
WAKE
SLEEP
00:00 08:00
Fig. 2. A schematic of the Two-Process Model of Sleep Regulation

adapted from Daan and colleagues (1984) [40]. Bold lines represent
Process S: sleep pressure accumulates during waking and dissipates
during sleep. Process C regulates the timing of sleep so that when sleep
pressure surpasses an upper threshold, sleep is initiated and, when
sleep pressure falls below a lower threshold, wake is initiated. Process S
and Process C align so that sleep is timed from midnight to 0800 h, a
typical adult sleep schedule.
of nocturnal sleep in humans. As sleep pressure dissipates across the night, sleep is protected by the circadian
timing system, which achieves maximal levels of sleep
propensity during the second half of the habitual sleep
period.
Our laboratory has used the two-process model as a
framework to study adolescent sleep/wake regulation
[50,51]. We review studies that have investigated pubertal changes of the circadian and homeostatic sleep systems. These data may provide us with additional
insight into the observed sleep/wake behavioral changes
of adolescents.
5. Circadian timing and sleep/wake homeostasis during
adolescent development
5.1. Process C
The circadian timing system undergoes developmental changes during adolescence. Although sleep/wake
patterns have long been known to delay in adolescents,
behavioral factors (e.g., social and scholastic obligations) were assumed to be entirely responsible. The
notion that circadian timing may change was noted by
Carskadon and colleagues in a study of circadian phase
preference in young adolescents [52]. Phase preference,
or morningness/eveningness is a behavioral construct
related to the time of day best suited for waking behavior. Carskadon and colleagues found that phase preference was correlated with self-assessed pubertal
development, especially in girls [52]. Subsequent studies
conrmed that more mature and older adolescents prefer later timing of activities than younger, less mature
adolescents [22,53]. Adolescents with evening and morning phase preference also show dierences in patterns of
sleep/wake; those with evening preference report later

sleep schedules than those with morning phase preference [52,53]. Adult studies show that the temporal alignment between sleep and circadian timing diers between
morning and evening types; morning types sleep at a
later circadian phase compared to evening types
[54,55]. These studies provide some evidence that sleep
regulation mechanisms may dier between phase preference types. Furthermore, these studies leave open the possibility that the adolescent phase preference shift toward
eveningness is indicative of underlying changes to mechanisms regulating sleep and wake during pubertal development. Indeed, laboratory studies provide evidence to
suggest that the circadian timing system changes during
puberty: pubertal stage is positively associated with later
circadian timing when sleep (dark) is held xed [51,56].
One of the themes of our laboratorys research program is to understand the factors that contribute to
the developmental circadian phase delay during adolescence. We have hypothesized that changes in light sensitivity, the endogenous circadian period, and/or the
homeostatic sleep system may play a role in the developmental circadian and sleep behavior changes.
Our studies have investigated these hypotheses by
studying adolescents at dierent levels of maturity,
indexed by Tanner stage. Tanner stage is a rating of
pubertal development and based on secondary sexual
characteristics, including pubic hair growth and distribution, stage of genital development for boys, and stage
of breast development for girls [57].
The human light PRC (Fig. 1) predicts the circadian
timing systems response to light; however, the amplitude of this response may dier between individuals
and during development. One possible explanation for
the adolescent phase delay is a change in light sensitivity. Preliminary results do not support this hypothesis;
evening (23000000 h) light sensitivity and morning
(03000400 h) light sensitivity do not dier between
Tanner 1/2 (pre- to early pubertal) and Tanner 3/4/5
(mid- to post-pubertal) participants. Both early pubertal
and mid-/late pubertal youngsters showed similar melatonin suppression responses and, thus, light sensitivity
as a result of 150 and 500 lux of white broad spectrum
light [37].
Developmental dierences may not have manifested
because of the amount of variability in the melatonin
suppression response. These individual dierences may
be due to dierences in daytime light exposure between
individuals. More bright light exposure during the daytime decreases the response to a subsequent light exposure as assessed by melatonin suppression [58].
Furthermore, in this study, time in bed was held xed
to 10 h per night for both Tanner groups, which is
another possible explanation for the lack of developmental dierences in melatonin suppression. Ten hours
is not the typical amount of time spent in bed, especially
for the older group, and recent work shows that less
total sleep time may attenuate the phase shifting
response [59,60]. In other words, if adolescents are studied on their natural schedules, it is possible that older
adolescent may show a weaker response to light compared to younger adolescents. Dampening the response
to the phase advance portion of the light PRC may hinder synchronization.
Additional research is needed to understand
responses to light during adolescent development. Furthermore, given that the circadian timing system is most
sensitive to short-wavelength light (460 nm) [61,62],
further investigation of sensitivity to dened light bandwidths may help us understand how the circadian timing
system and its sensitivity to external zeitgebers may or
may not change during adolescence.
A developmental delay of circadian phase during
adolescence may also be related to a lengthening of
the intrinsic period of the circadian clock, that is, a
longer internal day length. In a preliminary analysis,
Carskadon and colleagues measured period in 27 adolescents aged 915 years, showing an average of
24.27 h [63]. The sample size was not adequate to test
dierences across Tanner stage; however, intrinsic period was signicantly longer than the average in adults,
as measured by others [51,6365]. Reports show that
entrained circadian phase in young adults was positively
associated with circadian period; a later circadian phase
was related to a longer period [66,67]. Furthermore,
recent work showed that a longer intrinsic period was
associated with a circadian timing system that more
readily phase delayed in constant conditions [68]. Preliminary data from adolescents and drawing parallels in
the adult literature leaves open the potential that a
longer period during adolescence could lead to a developmental circadian delay. This hypothesis still needs to
be tested with more participants across pubertal
development.
5.2. Process S
Recent modeling work of Jenni and colleagues [69]
provides data to support developmental changes to Process S. Using model simulation techniques of SWA,
results showed a slower accumulation of Process S during wake in mature adolescents (Tanner 5) compared to
pre- or early pubertal adolescents (Tanner 1 and 2)
under conditions of sleep deprivation. Furthermore,
the upper threshold (asymptote) for Tanner 5 participants was higher compared to Tanner 1 and 2 participants; the dierence between the thresholds was larger
for the Tanner 5 youngsters compared to Tanner 1
and 2. Further support for the slowing of Process S
comes from sleep latency data, which shows Tanner 1
participants falling asleep faster in the evening (2230
and 0030 test points) compared to Tanner 5 participants
607
[70]. In other words, sleep pressure may build at a faster

rate for the pre-pubertal adolescent, allowing sleep onset
to occur more rapidly than for the mature adolescent.
By contrast, the dissipation of Process S during sleep
does not dier between pre-/early pubertal and mature
adolescents [7173].
In summary, evidence to date supports hypotheses
that circadian mechanisms change across adolescent
development, including a change toward evening circadian phase preference and later circadian phase. Furthermore, adolescents may tend to have a longer
intrinsic period compared to adults. Slower accumulation of homeostatic sleep pressure during puberty also
permits the older adolescent to stay awake longer and,
thus, delay the sleep/wake (dark/light) cycle. Therefore,
in addition to environmental factors, underlying
changes in the circadian and sleep systems accompanying pubertal development may also be associated with
later sleep/wake schedules often observed in adolescents.
Puberty is associated with enormous change to the
neuroendocrine milieu. To date, however, it is unclear
how these changes interact with specic sleep regulation
mechanisms [74].
6. Delayed sleep phase syndrome (DSPS)
The developmental changes in the circadian and sleep
systems we have described may be exaggerated in adolescents who receive a diagnosis of delayed sleep phase
syndrome (DSPS). DSPS is a disorder with a typical
onset in the second decade of life or earlier [75]. Weitzman, Czeisler, and colleagues [76,77] rst described
delayed sleep phase insomnia as a distinct syndrome
characterized by a cluster of features including a chronic
inability to fall asleep and wake at a desired clock time,
consistency in reported sleep times at later hours than
other individuals, and otherwise normal sleep when
measured by all-night polysomnography if the delayed
schedule is allowed. An important characteristic of the
syndrome is that patients are able to initiate and maintain sleep on their normal delayed schedule; diculties
manifest only when they attempt to synchronize their
sleep schedule with requirements of normal everyday
schedules of society. As a result, patients with DSPS
are locked into a sleep schedule that is out of phase with
usual work and school requirements. Other consequences of DSPS include sleep loss, disturbed sleep,
excessive daytime sleepiness, and impaired waking
function.
The 2005 International Classication of Sleep Disorders (ICSD)-Revised lists DSPS (now called Delayed
Sleep Phase Disorder) within a set of Circadian Rhythm
Sleep Disorders and provides three general criteria for a
circadian rhythm disorder: (1) a persistent or recurrent
pattern of sleep disturbances resulting from a misalignment of endogenous rhythm and external factors that
608
aect the timing or duration of sleep; (2) sleep disruption that leads to insomnia and/or excessive daytime
sleepiness; and (3) impaired social, occupational, or
other spheres of functioning related to the sleep disturbance. The ICSD notes that objective ndings typically
show a delay demonstrated by diary and actigraphy of
sleep onset until 01000600 h, with wake-up time in late
morning or early afternoon, especially on weekends and
vacations; normal sleep from all-night polysomnography on the delayed schedule and prolonged sleep latency
on a conventional schedule; measures of circadian phase
(e.g., temperature recording or DLMO) that indicate a
phase delay; scores on a morningness/eveningness
(phase preference) questionnaire in the denite evening
type range. Dierential diagnosis issues include the
importance of distinguishing DSPS, particularly in adolescents, from normal sleep patterns where a delayed
schedule is maintained without distress or impaired
functioning. Social and behavioral factors, such as late
evening activities, school avoidance, and social or family
dysfunction, may have a role in the development and
maintenance of a syndromic delay. In addition, dierentiation of DSPS from other insomnias rests on the nding that sleep initiation and maintenance are normal
when the patient is allowed to sleep on his or her preferred schedule. Finally, the excessive daytime sleepiness
in these patients occurs on mornings on which they must
arise earlier than preferred; sleepiness abates if the preferred sleep schedule is allowed.
Prevalence estimates of DSPS range widely. The 1997
edition of the ICSD [78], estimated that 510% of
patients with insomnia complaints seen in sleep clinics
have DSPS. The 2005 ICSD-Revised [79] places this gure at 10%. Other reports based on questionnaires, telephone sampling, or mixed subjective and objective
measures estimate the prevalence of DSPS in the general
population anywhere between 0.13% and 3.1% [80]. A
recent study, based on interviews structured to question
Diagnostic and Statistical Manual of Mental Disorders,
Fourth edition (DSM-IV) criteria in 1124 European
adolescents aged 1518 years, reported a relatively low
rate (0.4%) of adolescents with some circadian disorder
[81]. The rate was 0.2% in a companion sample of young
adults, ages 1924 years. The authors noted that a larger
number of adolescents reported some indicators of circadian rhythm disorders, such as dierences between
real and desired sleep schedule, extra sleep on days o,
and diculties getting up in the morning, although they
did not report negative daytime consequences requisite
for DSPS classication. Furthermore, this study was
completed in Europe, where later school start times
(08000830 h) than in many areas of the United States
may better t the normally delaying patterns of adolescence and involve less distress related to poor sleep. The
prevalence rate for at least one symptom of insomnia in
the adolescent sample was 30%, and the most commonly
reported symptom was non-restorative sleep, followed

by diculties in initiating sleep.
DSPS is associated with a wide range of problems,
including inability to work or attend school, which can
lead to job loss, truancy, school failure [75,77,82], daytime sleepiness, social diculties, and depressed mood
[75,83]. Thorpy and colleagues [75] reported more than
half of adolescent DSPS patients in their study had features of depression as measured by the Beck Depression
Index (BDI), Minnesota Multiphasic Personality Inventory (MMPI), or psychological evaluation; 6 of the 22
patients had prior treatment for depression. Ferber
[84] suggested that adolescent DSPS patients might
include some who are clinically depressed and resistant
to treatment and others who are cooperative to treatment and not depressed. The direction of eects for
these aective disorders is not clear. Alcohol, drug,
and substance use and abuse may also occur.
Original speculations regarding the etiology of DSPS
included abnormalities of the circadian timing system,
such as long intrinsic period or a weak phase advance
portion of the light PRC [76,77]. Subsequent work has
expanded possible mechanisms to include the sleep
homeostatic system, systems coordinating circadian
and sleep processes, behavior, psychological traits and
features, genetic processes, and combined eects. In
addition to the hallmark delays of sleep onset and oset,
patients also manifest delayed timing of melatonin secretory patterns and core body temperature nadir [85,86].
A recent study by Aoki and colleagues [87] reported
increased suppression of melatonin to light exposure in
DSPS patients versus controls; they suggest that hypersensitivity to evening light may be a precipitating or
maintaining factor for the phase delay in DSPS. Ozaki
and colleagues [86] reported a longer interval between
body temperature nadir and sleep oset in DSPS
patients compared to controls as well as longer sleep episodes, ndings since replicated in two studies [88,89].
Ozaki and colleagues [86] suggested that the inability
of DSPS patients to phase advance normally might
result from not being exposed to the advance portion
of their light PRC due to their elongated sleep episodes.
Of note is that the interval between body temperature
nadir and sleep oset is shorter in normal controls with
an evening preference [54,55] but longer in DSPS
patients, suggesting a discontinuity along the morningness/eveningness dimension. In any case, the interface
between circadian and homeostatic processes appears
to be disturbed or irregular in DSPS patients.
Another line of experimental investigation implicates
decits in sleep/wake homeostasis in the etiology of
DSPS. Uchiyama and colleagues [90], for example, studied DSPS patients and healthy controls using a constant
routine followed by an ultra-short sleep/wake cycle protocol. Results showed reduced sleep in patients versus
controls following sleep deprivation. These researchers
suggested that DSPS patients may have poor ability to

compensate for lost sleep and, thus, have diculty falling asleep even when they wake early or have shortened
sleep. Watanabe and colleagues [89] also reported dierence between DSPS patients and controls on several
polysomnographic sleep variables, including SWS, further indicating involvement of the homeostatic system.
These ndings indicate that DSPS may involve
abnormalities of the circadian timing system or the
sleep/wake homeostatic process. Circadian period,
phase, and entrainment mechanisms, as well as the
capacity of the sleep homeostat have all been implicated
in the etiology of this disorder. Because this disorder has
the highest prevalence during adolescence and school
performance is often compromised, the issue of eective
treatment takes on added importance.
Three techniques are typically used to treat DSPS:
chronotherapy, phototherapy, and exogenous melatonin
administration. We note, however, that few studies have
tested these treatments for DSPS in adolescents. The
rst treatment proposed for DSPS was chronotherapy,
which requires the patient to delay bedtime and wakeup time by 3 h per day until the desired sleep schedule
is reached. At this point, the patient is advised to maintain the desired sleep/wake schedule seven days per week
[77].
Bright light therapy, or phototherapy, is another
technique used to treat DSPS. Light timed at the end
of the patients night over consecutive days phase
advances the circadian timing system. Because the timing of light administration is critical for the ecacy of
phototherapy, measuring initial circadian phase in constant conditions is necessary. Using the light PRC as a
guide, light is then timed relative to the individuals circadian phase. Light intensity appears to phase advance
the circadian timing system in a doseresponse manner;
thus, brighter light (9500 lux) induces greater phase
shifts in comparison to normal indoor lighting
(180 lux) [91]. Unfortunately, as Wyatt [80] notes,
there is no duration response curve; the optimal number of hours and consecutive days of light exposure has
not been determined.
Exogenous melatonin administration is another proposed treatment for DSPS. Melatonin is thought to have
both a chronobiotic (phase shifting) and soporic (sleepinducing) eect on humans. Melatonin administration
must be timed relative to circadian phase as Lewys
[92] melatonin PRC demonstrates; melatonin administered approximately 13 h before DLMO phase induces
a phase advance shift. Studies show a phase shift in the
advance direction in adult DSPS patients using exogenous melatonin administration (0.35.0 mg) [9395].
Sedative eects of exogenous melatonin are reliably
observed in adults during the late morning to early evening hours when circulating endogenous melatonin levels
are low [96105]. By contrast, if melatonin is adminis-
609
tered when circulating levels of the hormone are above

the basal daytime levels, the sleep-promoting inuence
of the hormone is attenuated or absent [106109]. Therefore, DSPS patients may benet from the sedative eects
of melatonin administered a few hours before DLMO
phase (when circulating melatonin levels are low) when
attempting to phase advance the circadian timing
system.
7. Conclusions
Developmental delays in sleep/wake behavior across
adolescence are associated with extrinsic and intrinsic
factors. Investigations of circadian timing mechanisms
and homeostatic sleep processes may provide insights
into biological underpinnings of behavioral changes.
Future research is needed to identify whether DSPS is
an exaggeration of a typical developmental delay or
whether the pathophysiology of DSPS has other pathways. Furthermore, ecacy studies of chronotherapy,
phototherapy, and exogenous melatonin treatments of
DSPS in adolescents are needed.
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Sleep Medicine xxx (2010) xxxxxx
Contents lists available at ScienceDirect
Sleep Medicine
journal homepage: www.elsevier.com/locate/sleep
Review Article
Electronic media use and sleep in school-aged children and adolescents: A review
Neralie Cain, Michael Gradisar *
School of Psychology, Flinders University, Adelaide, SA, Australia
a r t i c l e
i n f o
Article history:
Received 3 December 2009
Received in revised form 15 February 2010
Accepted 19 February 2010
Available online xxxx
Keywords:
Child
Adolescent
Sleep
Media
Technology
Television
Computer
a b s t r a c t
Electronic media have often been considered to have a negative impact on the sleep of children and adolescents, but there are no comprehensive reviews of research in this area. The present study identified 36
papers that have investigated the relationship between sleep and electronic media in school-aged children and adolescents, including television viewing, use of computers, electronic gaming, and/or the internet, mobile telephones, and music. Many variables have been investigated across these studies, although
delayed bedtime and shorter total sleep time have been found to be most consistently related to media
use. A model of the mechanisms by which media use may affect sleep is presented and discussed as a
vehicle for future research.
! 2010 Elsevier B.V. All rights reserved.
During recent decades, research investigating the sleep patterns

and habits of children and adolescents has become increasingly
more prevalent. In these age groups, sleep is considered particularly important for learning and memory, as well as having implications for emotional regulation and behaviour [1,2]. More
specifically, insufficient sleep and poor sleep quality have been
associated with impairments in declarative, procedural and working memory performance, as well as poor concentration, which
logically translates into poor academic performance [13].
It is now well known that there is an inverse relationship between sleep duration and age. For example, Iglowstein and colleagues reported that children move from getting a mean of 11 h
sleep at age 6, to 9.6 h at age 11, to 8.1 h at age 16 [4], and these
values are consistent with those reported by other authors [57].
Interestingly, the total sleep duration of children and adolescents
also seems to be decreasing over time, with young people today
receiving less sleep than their counterparts from previous generations [4,5]. But why is it that children and adolescents are getting
less sleep?
In the late 1970s it was postulated that the age-related decrease
in sleep duration was due to a biological decrease in sleep need
[8]. But when adolescents were given the opportunity to sleep for
10 h each day in the Stanford sleep camp studies, there was no difference in duration of sleep obtained by adolescents at different
* Corresponding author. Address: c/o School of Psychology, Flinders University,
GPO Box 2100, Adelaide, SA 5001, Australia. Tel.: +61 8 8201 2324; fax: +61 8 8201
3877.
E-mail address: [email protected] (M. Gradisar).
ages or pubertal stages [8]. This suggests that environmental factors (such as decreased parental monitoring) and psychosocial factors (such as increased use of electronic media) have a
considerable influence on the amount of sleep obtained by adolescents [8]. Nevertheless, despite popular press [811] and the common practice for clinicians to emphasise the negative impact of
electronic media on sleep, there have been no comprehensive reviews of empirical research in this area.1 The current papers aims
are to (1) describe the evolution of technology and how this may
be impacting child and adolescent sleep, (2) review relevant research
to date, and (3) provide future directions for both research and clinical practice.
1. Literature search and inclusion criteria

To identify papers for this review, a literature search was performed using the PsycInfo and PubMed databases with a variety
of search terms (e.g., media AND sleep; computer AND sleep).
Articles were also identified from the reference lists of these papers. Included articles described original research studies that
measured both an aspect of media use or ownership and an aspect
of sleep. Articles were only included if they contained participants
aged approximately 517 years and were available in English. Published abstracts, unpublished theses and dissertations, and articles
1
We are aware of one previous review [12]; however, only 9 academic articles
were discussed (compared to 36 in the current review) and this included studies
involving infants and toddlers, as well as school-aged children and adolescents.
1389-9457/$ - see front matter ! 2010 Elsevier B.V. All rights reserved.
doi:10.1016/j.sleep.2010.02.006
Please cite this article in press as: Cain N, Gradisar M. Electronic media use and sleep in school-aged children and adolescents: A review. Sleep Med (2010),
doi:10.1016/j.sleep.2010.02.006
N. Cain, M. Gradisar / Sleep Medicine xxx (2010) xxxxxx
lescents who reported getting 68 h sleep and those who reported

getting 35 h sleep [20].
Individual media items in a child or adolescents bedroom have
also been associated with sleep disturbance. The presence of a television in a child or adolescents bedroom has been related to delayed bedtimes [17,19], less time in bed [19], shorter total sleep
time [14,15,18], increased bedtime resistance [18], and higher
overall level of sleep disturbance [16,18]. But one study found no
significant relationship between total sleep time and having a television in the bedroom [20]. The presence of a computer or electronic
gaming console in a child or adolescents bedroom has been associated with delayed bedtime [17,19], less time in bed [19], shorter
total sleep time [14,17], and increased prevalence of disorders of
bedtime resistance, delayed sleep onset, sleep anxiety, parasomnias, and sleep-disordered breathing [14]. Mobile telephones in bedrooms pose an additional problem as they alert the individual to
incoming calls or text messages. In a recent study in Belgium, adolescents who reported being woken up at least occasionally by text
messages were significantly more tired than adolescents never woken by text messages [21]. Importantly, simply having a mobile or
fixed-line telephone in the bedroom has been related to delayed
bedtime on weekend days and a discrepancy of more than 1 h between weekday and weekend bedtimes [17]. Despite this research
being correlational (the implications of which will be discussed in
further detail later), these results suggest that technology should
be kept out of bedrooms in order to promote good sleep among
children and adolescents. The following sections will explore research relating to children and adolescents use of these media
items (in or outside the bedroom), beginning with the most researched: television.
that primarily focused on age groups outside the range specified

above were excluded from this review.
Using these criteria, 36 research articles were identified. Of
these, 20 related to television viewing, 15 related to the use of
computers, electronic gaming, and/or the internet, 7 related to mobile telephones, and 2 related to music (although some papers
examined the influence of more than one media type).
2. Bedroom media presence and sleep

According to the National Sleep Foundations 2006 Sleep in
America Poll, almost all American adolescents (97%) had at least
one electronic media device in their bedroom [13]. These items included such things as music players (90%), televisions (57%), video
game consoles (43%), mobile (42%) or fixed-line telephones (34%),
computers (28%), and internet access (21%). Older adolescents
had more media devices in their bedrooms than younger adolescents, with a median of two devices for 6th8th graders and four
devices for 9th12th graders [13]. In line with this, studies with
primary school children have revealed lower prevalence rates of
1843% for televisions in bedrooms [1418], 1820% for computers
or video games [14,17], and 14% for mobile phones [17]. Other
studies have found gender differences, with adolescent boys being
more likely than adolescent girls to have a television or computer
game console in their bedroom [19].
The National Sleep Foundation found that adolescents who had
four or more media devices in their bedrooms got significantly less
sleep on both school nights and non-school nights than adolescents who had three media devices or less [13]. These adolescents
were also more likely to have fallen asleep at school or while doing
homework at least a few times per week, felt too tired or sleepy
during the day, and more likely to think that they have a sleep
problem. Adolescents with more media devices in their bedroom
also drank more caffeinated beverages during the day and were
more likely to be evening types (i.e., having a preference for
going to bed late and getting up late) than adolescents with fewer
media devices in their bedroom. Considering that the percentage of
children who watch television or play video games before bed is
significantly higher among children who have a television or video
game console in their bedroom [17], it is likely that bedroom media presence has an indirect effect on sleep (see Fig. 1). Consistent
with this hypothesis, adolescents (aged 1218 years) who reported
getting more than 8 h sleep per night have been found to engage in
less technology-related activities after 9 pm compared with ado-
3. Television viewing and sleep

Television broadcasting began in the late 1930s in Britain and
the early 1940s in America, followed later by countries such as Japan in 1953 and Australia in 1956 [22]. Following the Second
World War, television experienced a popularity boom in the
1950s and 1960s as televisions became more affordable, but even
then, key stations only broadcasted for several hours per day
[22,23]. Television viewing became more flexible from the 1980s,
with the introduction of video cassette recorders, and 1990s, with
cable television and the large clear images associated with digital
broadcasting [23]. Even today, large wide-screen television sets
Socio-Economic Status?
Increased
Daytime
Media Use
Electronic
Media Device
in Bedroom
Age?
Possible Mechanism???
Increased PreBedtime
Media Use
Media use directly displaces

sleep
Media use causes increased
mental/emotional/
physiological arousal
Bright light exposure delays
the Circadian Rhythm
Sleep
Problems
Impaired
Daytime
Functioning
Parental Control?
Fig. 1. A graphical representation of the potential impact of electronic media on sleep.
doi:10.1016/j.sleep.2010.02.006
vision had a negative effect on their childs sleep [18]. These figures
are important, considering that much of the research reviewed in
this paper relies on parent-report data (see Section 7 for further
discussion of this issue).
In terms of television viewing in the evening or at bedtime, it
has been reported that as many as 82% of American adolescents
watch television after 9 pm and 34% watch DVDs or videos [20].
Watching television in the evenings has been associated with significantly shorter total sleep time on both weekends and weekdays
[33,34] and with a generally higher frequency of sleep problems
compared with children not watching television after 9 pm [30].
Similarly, children and adolescents who often or occasionally
watch television in the evening have significantly later bedtimes
and wake-up times on weekdays and/or weekend days [17,34].
Television viewing at bedtime has also been found to be significantly correlated with sleepwake transition disorders, disorders
of excessive somnolence, and overall sleep problem severity in
children aged 56 years [31]. A discrepancy of more than 1 h between weekday and weekend bedtimes has also been associated
with watching television before bedtime [17]. Subjective reports
from adolescents are also consistent with these findings [35].
The results presented in Table 1 reveal that many different variables have been investigated in relation to television viewing and
sleep among school-aged children. As yet, however, there is little
consensus regarding which aspects of sleep may be related to television viewing. The most consistent results to date seem to be decreased total sleep time, prolonged sleep onset latency, and
delayed bedtime. More research is clearly needed to determine
whether or not other aspects of sleep are also related to television
viewing.
It is important to note that all of the abovementioned studies
are correlational and that empirical evidence in this area is rare.
In a small experimental study, 11 boys (aged 1214 years) were
exposed to 1 h of a subjectively exciting movie, approximately 2
3 h prior to bedtime [36]. Their sleep was then monitored using
both subjective and objective measures (i.e., sleep diary and polysomnography, respectively). Compared to a control evening when
they did not watch television or play video games at all, participants had significantly lower sleep efficiency (i.e., percentage
of time in bed that the individual was actually asleep) on the
are becoming increasingly more affordable and more prevalent,

with many homes now having multiple sets [18].
Although early research found no significant correlation between television viewing and evening sleep duration for schoolaged children [24], a number of subsequent studies have found a
relationship between television viewing and a variety of sleep variables (see Table 1). For example, one study found that the number
of hours of television watched per day predicted increased bedtime
resistance in children aged 410 years, after controlling for demographic variables of age, gender, and socio-economic status [18].
Comparing children who watched less than 2 h of television each
weekday, children who watched more than 2 h of television each
weekday had increased sleep onset latency, increased sleep anxiety, increased night waking, and increased total sleep disturbance
[18]. In a longitudinal study, the number of hours of television
viewing at age 14 was associated with increased sleep problems
at follow-up (age 1622) [25]. In addition, adolescents who chose
to reduce their television viewing to less than 1 h per day were less
likely to experience sleep problems at follow-up. Other studies
have found television use to be associated with less time in bed
on weekdays [19], delayed bedtime on both weekdays and weekend days [14,19,2628], later wake-up time or out-of-bed time
[14,19,26], increased sleep onset latency [14,29,30], shorter sleep
duration [14,26,27,31], and sleep disorders involving bedtime
resistance, sleep anxiety, and/or parasomnias [14,18,30,31]. This
appears to be a worldwide phenomenon, with research now available from Australia, Europe, Asia, and North America.
In addition to active television viewing, one study also examined the relationship between passive television viewing and sleep
among 5- to 6-year-old children [31]. The authors found that the
amount of time the television was switched on during the childs
waking hours was significantly correlated with decreased total
sleep duration. Furthermore, passive television exposure was associated with disorders of initiating and maintaining sleep and overall sleep problem severity.
In an Indian survey of parental opinions about the effect of television on childrens sleep it was reported that 18% of parents believed their child (aged 310 years) had a decreased or disturbed
sleep pattern as a result of television viewing [32]. In contrast, an
American study found that only 6.5% of parents believed that tele-
Table 1
Relationship between television viewing and sleep variables.
Authors
Age (years)
Weissbluth et al. [24]

Tynjala et al. [28]
Gupta et al. [32]
Owens et al. [18]
Van den Bulck [35]
Saarenpaa-Heikkila et al. [27]
Toyran et al. [30]
Thorleifsdottir et al. [34]
516
1116
510
410
1718
917
69
610
1115
1619
1317
1217
1215
613
1415
1213
56
511
511
1219
612
Johnson et al. [25]

Van den Bulck [19]
Gaina et al. [42]
BaHammam et al. [33]
Fuligni and Hardway [43]
Gaina et al. [29]
Paavonen et al. [31]
Li et al. [14]
Adam et al. [26]
Oka et al. [17]
TIB
TST
SOL
WASO
GTB
WUT
DS/T
BR
SA
Parasomnias
SWT
DES
Overall sleep disturbance
X
U
X
U
U
U
U
U
U
X
U
U
U
U
U
U
U
U
U
U
U
U
U
U
U
U
U
U
U
U
X
U
X
U
U
U
U
U
U
U
Note: U = examined in study (significant relationship between variables); X = examined in study (non-significant); TIB = shorter time in bed; TST = shorter total sleep time;
SOL = longer sleep onset latency; WASO = more night waking; GTB = delayed bedtime; WUT = delayed wake-up time; DS/T = daytime sleepiness or tiredness; BR = bedtime
resistance; SA = sleep anxiety; SDB = sleep-disordered breathing; SWT = sleepwake transition disorders; DES = disorders of excessive somnolence.
doi:10.1016/j.sleep.2010.02.006
any sleep disorders (e.g., bedtime resistance, sleep anxiety, parasomnias) [14] and, in contrast to another study [19], found no significant relationship with wake-up times on weekdays or weekend
days nor with weekday bedtimes or daytime sleepiness.
When considering the use of computers or electronic games in
the evening or at night it has been reported that 55% of American
adolescents access the internet and 24% play computer games after
9 pm [20]. Playing video games or using a computer before bed has
been associated with later bedtimes [17,37], shorter total sleep
duration [17,33,37], later wake-up time on weekend days [17], increased daytime tiredness [37], and poorer overall sleep quality
[45]. A discrepancy of more than 1 h between weekday and weekend bedtimes and a discrepancy of more than 2 h between weekday and weekend wake-up times have also been associated with
playing video games before bed [17].
In terms of internet use, three studies have obtained consistent
results despite measuring internet use in different ways. Van den
Bulck measured the amount of time that adolescents spent using
the internet at any time of day [19], Oka and colleagues categorized
children according to whether or not they used the internet before
bed two or more times per week [17], while Yen and colleagues
used a self-report questionnaire to assess symptoms of internet
addiction [46]. Taken together, this research revealed that internet
use is related to delayed bedtimes [17,19], delayed weekend wakeup times or out-of-bed times [17,19], shorter total sleep times
[17,46], shorter time in bed on weekdays [19], higher levels of
tiredness [19], and higher levels of subjective insomnia [46] (see
Table 3). A discrepancy of more than 2 h between weekday and
weekend wake-up times was also associated with using the internet before bed [17].
In a small experimental study (described earlier), participants
were exposed to 1 h of video-game play approximately 23 h prior
to bedtime [36]. Compared to a control evening, participants had
significantly longer sleep onset latencies on the experimental night
and experienced significant changes in their sleep architecture,
with less time spent in slow-wave sleep. But there was no difference in overall sleep efficiency or time spent awake after sleep onset. A second experimental study involved 22 male participants
aged 1215 years who participated in three experimental conditions: playing a violent video game, playing a non-violent video
game, neither playing video games nor watching exciting television programs [47]. Games were played for 2 h, ending half an hour
before bedtime, and a comprehensive questionnaire and sleep
diary was also completed on each occasion. There were no significant differences between the two game-playing conditions for any
sleep item. Compared to the control night, however, participants
went to bed significantly later on both gaming nights and, after
playing the non-violent game, participants reported that it was significantly easier to fall asleep, and their out-of-bed time the following morning was significantly earlier. Weaver and colleagues
conducted a similar experimental study involving 13 male adolescents (aged 1418 years) and found that, compared to a passive
DVD viewing control condition, pre-sleep video game playing resulted in a small increase in sleep onset latency and a small decrease in subjective sleepiness [48]. But in contrast to previous
studies, there were no changes in sleep architecture.
experimental night. But there was no effect on any other sleep

variables, including sleep onset latency and time spent awake after
sleep onset.
Many children and adolescents watch television in the evenings
for the purpose of aiding sleep onset [18,37]. For example, one
study found that 76.5% of their sample (495 children aged 4
10 years) had television viewing as part of their usual bedtime routines [18]. As seen in Table 2, use of television has been associated
with reduced total sleep time, longer sleep onset latency, delayed
bedtime, increased bedtime resistance, increased sleep anxiety,
and an increased level of overall sleep disturbance. It has not been
significantly associated with parasomnias or time spent awake
after sleep onset.
When considering daytime consequences, one study found no
significant correlations between any of their television viewing
variables and daytime sleepiness in children aged 410 years
[18]. But others found television use to be associated with increased daytime sleepiness or tiredness in adolescents aged 12
17 years [19,27]. The use of television as a sleep aid was also associated with increased tiredness in this age group [37]. As the American Academy of Sleep Medicine stressed the importance of
daytime dysfunction in the context of sleep disturbance [38], further research is clearly needed on the impact of television viewing
on the daytime consequences of poor sleep.
Overall, it appears that television viewing among children and
adolescents should be limited, especially in the evenings. Two
hours per day has been suggested as a recommended maximum
for school-aged children [39]. Furthermore, consistent with common sleep hygiene recommendations, it appears that televisions
should be kept out of bedrooms in order to create an environment
conducive to sleep.
4. Use of computer or electronic games and sleep
Computer and electronic games were introduced to the public in
the early 1970s; however, their popularity surged in the late 1980s
and 1990s with the rapid progression of gaming technology and
several major video gaming companies competing for prominence
[23]. In the 2000s, while the use of computer game software declined considerably (as more games were produced solely for gaming consoles), internet gaming surged in popularity as more
individuals gained access to this technology [23]. For example, the
Australian Bureau of Statistics reported that the number of households with access to a home computer doubled from 1998 to
2008, and the number of households with internet access increased
fivefold over the same time period [40]. Canadian data also showed
an increase in household internet access from 2001 to 2005 [41].
Frequent use of computer or electronic games has been associated with later bedtimes on weekend days [14,19,26], longer sleep
onset latency [29,42], later out-of-bed times on weekend days [19],
earlier out-of-bed times on weekdays [19], shorter total sleep time
or less time in bed [14,19,26,43,44], and higher levels of daytime
tiredness [19] (see Table 3). These results persist even after controlling for demographic and activity variables and presence of a
gaming computer in the bedroom [14,19]. One study, however,
also found that computer use was not significantly correlated with
Table 2
Relationship between sleep variables and use of television as a sleep aid.
Authors
Age (years)
TST
SOL
WASO
Owens et al. [18]

Eggermont and Van den Bulck [37]
410
1217
U
U
GTB
U
BR
SA
Parasomnias
Daytime sleepiness/tiredness
Overall sleep disturbance
X
U
Note: U = examined in study (significant relationship between variables); X = examined in study (non-significant); TST = shorter total sleep time; SOL = longer sleep onset
latency; WASO = more night awakenings; GTB = delayed bedtime; BR = bedtime resistance; SA = sleep anxiety.
doi:10.1016/j.sleep.2010.02.006

Table 3
Relationship between sleep variables and use of computer, internet, or electronic games.
Authors
Age (years)
TIB
Van den Bulck [19]

Gaina et al. [42]
BaHammam et al. [33]
Eggermont and Van den Bulck [37]
Fuligni and Hardway [43]
Gaina et al. [29]
Li et al. [14]
Mesquita and Reimao [45]
Punamaki et al. [44]
Adam et al. [26]
Oka et al. [17]
Yen et al. [46]
1217
1215
613
1217
1415
1213
511
1518
1218
511
612
1218
TST
SOL
GTB
WUT
BR
SA
Parasomnias
Daytime sleepiness/tiredness
Overall sleep quality
U
U
U
U
U
U
X
U
U
U
U
U
U
U
U
U
U
Note: U = examined in study (significant relationship between variables); X = examined in study (non-significant); TIB = less time in bed; TST = shorter total sleep time;
SOL = longer sleep onset latency; GTB = delayed bedtime; WUT = later weekend wake-up time; BR = bedtime resistance; SA = sleep anxiety.
Overall, it appears that time playing computer or electronic

games should be limited both during the day and in the evening
for school-aged children and adolescents. Consistent with recommendations regarding television viewing, a cut-off of 2 h of
game-playing per day has been suggested as being appropriate
[29], but results from a recent experimental study suggest that it
may be important to distinguish between violent and non-violent
games, as it appears that playing non-violent games in the evening
may produce positive effects on sleep [47]. Research regarding
internet use has suggested that excessive use at any time of day
may be related to negative consequences for sleep, although no
recommendations have yet been made regarding frequency or
duration of use.
5. Mobile telephone use and sleep
Since first being tested in the late 1970s, mobile telephone technology has developed rapidly [23]. Telephones are now not only
used for making and receiving calls, but also for text-messaging
(introduced in the early 1990s) [23], accessing the internet (introduced in the early 2000s) [23], playing games, listening to music,
and storing other personal information (e.g., calendar). Due to
the rapid development of technology in this area, it should be
noted that studies performed on mobile phone use may not have
included all of the above.
Mobile phone use among Finnish adolescents has been associated with shorter sleep duration [44]. Similarly, Japanese adolescents aged 1315 who use their mobile telephone every day
were found to be more evening-typed and have later wake-up
times and shorter total sleep duration [49]. They also reported
being less satisfied with their current sleep duration than students
who did not use a mobile telephone every day [49]. Furthermore,
adolescents who reported using their telephone for more than
20 min at a time reported staying in bed longer after waking up
on weekend mornings and having more frequent daytime naps

compared to students who used their telephone for shorter durations [49]. Another Japanese study, however, later found no significant difference between adolescents with short sleep onset
latency (i.e., less than 10 min) and long sleep onset latency (i.e.,
more than 10 min) for mobile telephone ownership or mobile telephone use [42]. A more recent study of Taiwanese adolescents also
found no relationship between problematic mobile phone usage
(based on symptoms of addiction or dependence) and total sleep
time or subjective insomnia [46]. Swedish researchers found a
borderline significant relationship between daytime tiredness
and mobile phone use, but found no significant relationship between self-reported sleep disturbance and mobile phone use [50].
When considering use of mobile telephones at bedtime or during the night, a recent study found that 34% of American adolescents reported text messaging and 44% reported talking on the
telephone after 9 pm [20]. Furthermore, up to one-third of adolescents reported being woken up by incoming text messages at least
once per month [21]. This appears to be more of a problem with
increasing age, as older adolescents (mean age 16 years) were woken up by text messages significantly more often than younger
adolescents (mean age 13 years) [21]. Mobile phone use after
lights out (which includes both incoming and outgoing calls
and text messages) was also found to be related to increased tiredness measured concurrently [21] and 1 year later [51]. In particular, adolescents who used mobile telephones between midnight
and 3 am were most likely to be very tired (3.9 times more than
adolescents who never used mobile telephones after lights out)
[51].
While it is clear that children and adolescents use mobile telephones in the evening and at night, the impact of this use on their
sleep and daytime functioning is less clear. As seen in Table 4, results in this area appear to be less consistent than in other areas of
electronic media discussed in this paper. Given the wide-ranging
Table 4
Relationship between sleep variables and mobile telephone use.
Authors
Age (years)
TST
Harada et al. [49]

Van den Bulck [21]
Gaina et al. [42]
Punamaki et al. [44]
Van den Bulck [51]
Soderqvist et al. [50]
Yen et al. [46]
1315
1217
1215
1218
1217
1519
1218
SOL
WUT
Evening
type
Dissatisfied with
sleep
Nap
frequently
Daytime sleepiness/
tiredness
Subjective
insomnia
U
X
U
U
U
X
X
X
Note: U = examined in study (significant relationship between variables); X = examined in study (non-significant); TST = shorter total sleep time; SOL = longer sleep onset
latency; WUT = later weekend wake-up time.
doi:10.1016/j.sleep.2010.02.006
activities a mobile phone provides and its portability this could become the most frequently used media device (day and night) and
thus should be an essential item assessed in future studies.
6. Music and sleep

Surprisingly, the effect of music on the sleep of children and
adolescents has rarely been studied, despite the fact that electronic
transmission of music has followed a similar developmental timeline to that of television. FM radio transmission began in the 1960s,
with audio cassettes and compact discs developed in the 1980s,
followed later by portable MP3 players in the late 1990s [23].
A recent study found that 42% of American adolescents reported
listening to music on an MP3 player after 9 pm [20], and the National Sleep Foundation reported that 90% of adolescents have a
music player in their bedroom [13]. But only two studies have explored the effectiveness of music as a sleep aid among school-aged
children and adolescents. In a cross-sectional correlational study
use of music as a sleep aid was related to later bedtime on weekdays, less sleep on weekdays, and increased tiredness among adolescents aged 1217 years [37]. But it was not significantly related
to bedtime or total sleep time on weekend days [37]. In an experimental study with participants in the 5th grade, participants were
randomly allocated to either receive sedative classical music at
naptime and bedtime for three weeks or not to receive music during this time [52]. The researcher found that children in the experimental group had better subjective global sleep quality over time
than those in the control group [52]. They also experienced
improvements in subjective sleep efficiency and subjective sleep
duration, and there was a significant decrease over time in the percentage of children who were considered poor sleepers [52]. The
intervention received by the experimental group, however, also involved a component of relaxation training, as the children in this
group were instructed to monitor their breathing and relax their
muscles as they listened to the music. Therefore, it cannot be concluded that the effects on sleep were purely a result of listening to
music. Considering the widespread use of music players in the
evening, more research is needed to ascertain the effects of different types of music on sleep.
7. Study limitations
The research studies reviewed here are plagued by a number of
limitations. The first limitation is that only three experimental
studies were found [36,47,52]. Instead, most report on cross-sectional correlational studies, which means that causal direction is
difficult to ascertain. It is possible that children and adolescents
who use technology in the evening do so because they do not need
as much sleep as their peers or because they already have a delayed sleep pattern and cannot fall asleep at their designated bedtime. For example, in a household where a parent encourages his/
her teenager to go to bed at 10 pm, the delayed adolescent may go
to his/her bedroom (but not feel sleepy) and occupy time by using
his/her mobile telephone, computer or television until feeling sleepy enough to go to bed several hours later. Another factor, such as
parenting style or the presence of childhood behavioural problems,
may also impact both media use and sleep problems among younger children. For example, a child who exhibits difficult behaviours
may be encouraged to watch television to give the parents a break
and keep the child occupied. Consistent with this hypothesis, research has revealed that sleep problems are common among children with behaviour problems [53] and some studies have found
that children with behavioural and emotional problems spend
more time watching television [54].
Of the 36 studies reviewed, 21 used self-report data, 10 used

parent-report data, 5 used both parent and self-report data, and
2 studies used objective data obtained from polysomnography
(in addition to self-report measures). Of the self- and parent-report
data, 17 collected data using general questions (such as rating how
often a certain sleep problem occurs or estimating total sleep time
without reference to other sleep parameters), 13 asked participants to estimate sleep parameters (e.g., estimated bedtimes,
wake-up times, sleep onset latencies), and only 6 asked about actual sleep parameters for a given night (e.g., sleep diary). It is evident from these observations there has been very little consistency
between studies in the method and/or content of sleep information
obtained. Furthermore, parent-reports of sleep parameters may
not be an accurate way of measuring the sleep habits of older children and adolescents [55,56]. In future studies, sleep should be
measured using self-report estimates of sleep parameters (including go-to-bed time, sleep onset latency, time spent awake after
sleep onset, wake-up time, and out-of-bed time, each estimated
separately for weekdays and weekend days) or using records of
these parameters taken from sleep diaries. Subjective reports such
as these have been validated against objective sleep measures (e.g.,
actigraphy) in adolescent populations [57]. Considering the importance of daytime consequences of sleep problems, ratings of daytime functioning (e.g., sleepiness) at different times of day should
also be included.
Consideration must be given to whether or not differences reported in these studies are meaningful, even if they are statistically
significant. In some cases, the difference between groups in bedtime or wake-up time was only 1015 min [17,34]. While this difference was statistically significant, we must consider whether a
bedtime delay of 10 min produces a clinically significant impairment in total sleep quality or daytime consequences. Alternatively,
it may be clinically important to consider the impact of media on
the discrepancy between weekday and weekend sleep patterns
for adolescents, as a discrepancy of more than 2 h between weekday and weekend wake-up times has been considered clinically
significant by other researchers and clinicians [38]. It should be
noted that this has been considered by one group of researchers,
who reported that a wake-up time discrepancy of this size was
associated with playing video games or using the internet before
bed more than two nights per week [17].
Different age ranges have been used in the studies reviewed
here. As many developmental changes occur with sleep patterns
and sleep habits during the school years, especially with the onset
of puberty, it may be more informative to use smaller age ranges.
For example, one group of researchers acknowledged that it is
likely that the effects of both active TV viewing and passive TV
exposure are largely age-dependent (p. 158) [31]. There are also
differences in the type and extent of electronic media use among
children of different ages [44] and it is likely that parental control
of media use also changes with age. Finally, it has been found that
time spent using a computer on weekend days mediates the relationship between age and weekend total sleep time, suggesting
that the interrelationship between age, media use, and sleep is
likely to be complex [26].
Studies summarised in this paper come from a variety of countries and cultures. It is possible that there are cultural differences
in the magnitude of the effect of media on sleep, as there are cultural differences in technology available (e.g., households in the
United States are more likely to have cable television, students
in Japan are more likely to have mobile telephones that can also
be used for internet access and television viewing) [17] and also
differences in sleep habits between cultures [58]. Cultural differences have been found in the use of media devices by boys and
girls, with girls using computers more than boys in Brazil, but boys
using computers more than girls in the United States [45].
doi:10.1016/j.sleep.2010.02.006
8. Possible mechanisms
A number of mechanisms have been proposed by which media
use might impact sleep quality or quantity. First, media use may
directly displace sleep or other activities related to good sleep hygiene (such as physical activity). Second, media use in the evenings
may cause children to become physiologically aroused, making it
more difficult for them to relax prior to bedtime. A number of studies have found increases in physiological arousal associated with
playing computer games [47,5962], and with the advent of more
physical computer gaming technology (such as the Nintendo Wii)
this issue becomes increasingly more relevant. Third, evening
exposure to bright light from television or computer screens may
suppress melatonin and consequently delay the circadian rhythm
[63]. Finally, electromagnetic radiation from mobile telephones
has been found to change sleep architecture [64,65] and delay melatonin production [66].
It is beyond the scope of this paper to comprehensively review
the support for and against the model presented in Fig. 1. Furthermore, it is acknowledged that much of the research in this area has
been correlational in nature and, consequently, the causal directions presented in the proposed model are largely speculative. In
addition to the results relating to the potential mechanisms described above, however, studies providing preliminary support
for other aspects of the model have already been mentioned in this
review. For example, the percentage of children who watch television or play video games before bed has been found to be higher
among children who have a television or video game console in
their bedroom [17] and the relationship between age and weekend
total sleep time has been found to be mediated by time spent using
a computer [26]. It would be useful for future studies to comprehensively test this model, using research designs that move beyond
the correlational analyses which are prevalent in this area.
9. Conclusions
Despite the aforementioned limitations, it appears that the use
of electronic media by children and adolescents does have a negative impact on their sleep, although the precise effects and mechanisms remain unclear. Across different media types, the most
consistent results have been obtained regarding delayed bedtime
and shorter total sleep time associated with excessive media use.
In future research, it would be good to develop and test a model
of the mechanisms by which media use affects sleep (such as that
presented in Fig. 1). This would provide further evidence to inform
clinicians, parents, young people, and the popular press and will
likely become even more relevant as technology continues to develop in the future.
Looking towards the future, the research community faces the
challenge of keeping up with advances in technology. For example,
studies on mobile telephones have so far only considered making
and receiving calls and sending and receiving text messages. Mobile telephone technology, on the other hand, has evolved at such
a rate that many people now use their mobile telephone to access
the internet, send and receive emails, engage in social networking,
listen to music, and play games. Furthermore, as television and
computer screens become increasingly larger and bright light
exposure from screens is considered to influence melatonin production, future studies may need to incorporate variables which
would not have been considered in previous research.
Eventually, guidelines about the duration and timing of electronic media use should be developed for children and adolescents
of different ages and these should be made known to the public.
Considering the evidence to date it appears that watching television and using other media devices at bedtime should generally
be discouraged [31]. Parents should also be informed that simply

having electronic media devices in the bedroom can negatively affect their childrens sleep.
10. Research priorities
It is recommended that future research should concentrate on
the following areas:
1. Using experimental methods to better establish causal links
between electronic media use and sleep.
2. Including the latest technologies (e.g., portable electronic
devices) in future studies.
3. Assessing the statistical and clinical significance of research
findings that relate to measures of sleep quality, sleep quantity,
and sleep timing.
4. Attempting to test the mechanisms involved in the relationships between electronic media use and sleep.
Financial support
N/A.
Conflicts of interest
Nil.
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doi:10.1016/j.sleep.2010.02.006
B. Clinical Sleep Science - X. Normal Physiology of Sleep and Normal Variants
0920
CIRCADIAN PHASE PIIEIERENCE, SLEEP PATTEINS AND
PERCEIVED HEALTI{ IN ADOLESCENTS
Snlith Ll 't, Boncl TLt :, RalJa' TI , Shcu ke' Iil,lt -t, Carskacbn ll'[A] :
rDeparturent of Psychiatry ancl Hurnan Behavror, Alperr Medical
School of Brorvn University, Providence, RI, United States,:Sleep
Research Laboratory, Bradley Hospital, Providence, RI. United States.
rDepartrnent of Medicine, Alper-t Medical School of Brorvn University,
Plovrdence, RI, United States, rDeparnent of Psychology. University
of Arizona, Tucson, AZ, United States
Introduction: Both circadian phase plelercnce and
inadeqr.rate sleep
have been associated rvith clinical and fnctional outcolnes. The impact
ofcircadian pliase prelerence on sleep patterns in adolescents in relation
to perceived health and health outcoures is less u'ell explorecl. The prev
ent study exanlines associations among circadian phase prelerence, total
sleep tirne. and perceived health in a saurple ofadolescents.
Methods: 145 parricipants recruited from a large sarnple olstudents recently admitted to college (agcs l7 - 21, urean age oflS years;68 rnales)
completed an online questionnaire to assess sleep, rnood, and other behaviors. Circadian phase prelerence rvas rneasured using the Hornestberg Momingness-Eveningness Questionnaire (lvlEQ); parricipants
rvere categorized into three groups based on the original scoring criteria;
rnomin-q types (n:21), neLrtral types (n: 84). and evening types (n:
40). Perceived health was taken from a single itent ("Horv rvor.rld you
charactedze your general health?") on a scale of I to 5 (1 : "excellent,"
5 : "poor"). Sleep pattems on school nights and non-school nights over
the past two rveeks rvere assessed using iteurs frour ari adolescenl sleep
habits sun'ey.
Results: As a continuous variable, higher MEQ score (associated rvith
rronringness) was related to better perceived health (R! : .034, P < .05);
however; rvhen self-r'eported school night total sleep tirne rvas entered
into the regression equation, VEQ score rvas no longer a significant predictor of perceived health (ARr =.005, P >.1). Analyses of MEQ as
a categorical variable levealed that evening types reported a later bed
time on school nights (rnean: l2:36arn, SD = 1.07hrs) than rnoming
(mean = ll:34prn, SD:0.96hrs) and neutal types (rnean - ll:44pm,
SD = 0.86hrs), but wake tirnes did not difler arnong MEQ groups (mean
: 6:44arn, SD : 0.69hrs). Evening-types reporled less total sleep tirle
on school nights (mean - 6.79hrs. SD: 1.69) than morning (mean:
8.03hrs, SD: Li7) and neutral types (urean = 7.69hrs, SD = L34).
Conclusion: Adolescents rvho sell-identify as evening types sleep less
than morning types or neutral types on school nights due to later bedtines and sirnilar wake tirnes. Evening types perceive their health as
worse than their moming type counteqrafis; this darity is accounted
for by the difference in total sleep time on school nights betrveen the
groups.
Support (IfAny): This rvork rvas supporled by the National Institute for
Mental Health (grant R0l MH079179). Tilenn Raffray is supported by
the ELrropean Sleep Center, Paris Ftance and I'lnstitut Servier, Neuillysu-Seine, France.
SLEEP, Volume 33, Abstract Supplement,20l0
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Journal of Adolescent Health 46 (2010) 124132

Sleep Patterns and Predictors of Disturbed Sleep in a Large Population

Department of Psychology, Virginia Commonwealth University, Richmond, Virginia

Sleep quality; Sleep disturbance; Adolescence; Stress; Mood; College students

Little doubt exists among health professionals about the

with an increased risk of work absenteeism and accidents [1], as

H.G. Lund et al. / Journal of Adolescent Health 46 (2010) 124132

it physically harder to maintain earlier bedtimes [6,7].

and the remaining 3% identified as other or elected not to

H.G. Lund et al. / Journal of Adolescent Health 46 (2010) 124132

and anger [27]. The shortened version includes a list of 30

weekend behaviors. Multivariate analysis of variance was

H.G. Lund et al. / Journal of Adolescent Health 46 (2010) 124132

Sleep quality, mood, and health

College Jr. College Sr.

a week. Over one-third of students cited other reasons

College Jr. College Sr.

bedtimes and risetimes during the week than did females,

Poor sleep quality was associated with significantly higher

H.G. Lund et al. / Journal of Adolescent Health 46 (2010) 124132

Total sleep time

12:21 a.m. 74 min

23.8 min, 19.2 min

8:05 a.m.,76 min

7.02 hours, 1.15 hours

PSQI Pittsburgh Sleep Quality Index.

Predictors of sleep quality

tional 3%, and morningness/eveningness (MES) accounting

H.G. Lund et al. / Journal of Adolescent Health 46 (2010) 124132

1 < 3,4 2 < 4

1,2 < 3,4

and weekend bedtimes and risetimes) in this report were

oping depressive mood disorder [31,32]. Also, as in any

H.G. Lund et al. / Journal of Adolescent Health 46 (2010) 124132

Stayed up to 3 a.m. >13/week

Sleepiness and performance

the neuroendocrine system. Developmental changes in the

Of particular concern is the tendency for older adolescents

H.G. Lund et al. / Journal of Adolescent Health 46 (2010) 124132

[5] Wolfson AR, Carskadon MA. Understanding adolescents sleep

H.G. Lund et al. / Journal of Adolescent Health 46 (2010) 124132

[31] Breslau N, Roth T, Rosenthal L, Andreski P. Sleep disturbances and

Sleep Medicine 8 (2007) 602612

Sleep, circadian rhythms, and delayed phase in adolescence

Corresponding author. Tel.: +1 401 421 9440; fax: +1 401 453

S.J. Crowley et al. / Sleep Medicine 8 (2007) 602612

Weekday Rise Timea

Middle School Years (11-13 years old)

High School Years (14-19 years old)

include watching TV, playing video games, and using

Another consistent nding is that the reported rise

S.J. Crowley et al. / Sleep Medicine 8 (2007) 602612

in September averaged about 1.5 h earlier than in

S.J. Crowley et al. / Sleep Medicine 8 (2007) 602612

tate entrainment in humans who have an intrinsic period

and after a 6.7-h bright light stimulus (10,000 lux)

The homeostatic sleep/wake system is thought to be

S.J. Crowley et al. / Sleep Medicine 8 (2007) 602612