J Youth Adolescence (2015) 44:518–542
DOI 10.1007/s10964-014-0160-5
EMPIRICAL RESEARCH
The Effects of Age, Gender, Hopelessness, and Exposure
to Violence on Sleep Disorder Symptoms and Daytime Sleepiness
Among Adolescents in Impoverished Neighborhoods
Mary Grace Umlauf • Anneliese C. Bolland •
Kathleen A. Bolland • Sara Tomek •
John M. Bolland
Received: 27 April 2014 / Accepted: 15 July 2014 / Published online: 29 July 2014
 Springer Science+Business Media New York 2014
Abstract Although sleep problems are associated with
negative outcomes among adolescents, studies have not
focused on sleep disorder symptoms among adolescents
living in impoverished neighborhoods and how sleep prob-
lems may be related to two factors common in those envi-
ronments: hopelessness and exposure to violence. This study
used data from the longitudinal Mobile Youth Survey (MYS;
N = 11,838, 49 % female, 93 % African-American) to
examine trajectories of sleep problems by age (10–18 years)
among impoverished adolescents as a function of gender,
feelings of hopelessness, and exposure to violence. The
results indicate that sleep problems associated with trau-
matic stress decline with age, with four notable distinctions.
First, the steepest decline occurs during the early adolescent
years. Second, the rate of decline is steeper for males than for
females. Third, exposure to violence impedes the rate of
M. G. Umlauf  J. M. Bolland
The University of Alabama, Tuscaloosa, AL, USA
J. M. Bolland
e-mail: jbolland@ua.edu
A. C. Bolland
Institute for Social Science Research, The University of
Alabama, Tuscaloosa, AL 35487-0216, USA
e-mail: acbolland@as.ua.edu
K. A. Bolland (&)
School of Social Work, The University of Alabama, Tuscaloosa,
AL 35487-0314, USA
e-mail: kbolland@sw.ua.edu
S. Tomek
Department of Educational Studies in Psychology, Research
Methodology, and Counseling, The University of Alabama,
Tuscaloosa, AL 35487-0232, USA
e-mail: stomek@bamaed.ua.edu
123
decline for all adolescents, but more dramatically for females
than for males. Fourth, the rate of decline is smallest for
adolescents with feelings of hopelessness who also had been
exposed to violence. To explore the generalizability of these
results to other types of sleep disorders, we analyzed cross-
sectional data collected from a subsample of 14- and
15-year-old MYS participants (N = 263, 49 % female,
100 % African-American) who completed a sleep symptoms
questionnaire. Four results from the cross-sectional analysis
extend the findings of the longitudinal analysis. First, the
cross-sectional results showed that symptoms of apnea,
insomnia, nightmares, and restless legs syndrome or periodic
limb movement disorder (RLS/PLMD), as well as daytime
sleepiness, increase as a function of hopelessness. Second,
symptoms of insomnia, RLS, and nightmares, as well as
daytime sleepiness, increase as function of exposure to
violence. Third, symptoms of insomnia and RLS/PLMD are
greater under conditions of combined hopelessness and
exposure to violence than for either condition alone. Fourth,
symptoms of RLS/PLMD are worst for females who have
been exposed to violence and experience hopelessness.
Overall, the findings suggest that hopelessness and exposure
to violence have negative independent and multiplicative
effects on adolescent sleep, particularly for females.
Understanding the causal factors associated with inadequate
sleep in impoverished adolescents is important for three
reasons. First, sleep is an important aspect of adolescent
development. Second, inadequate sleep has severe conse-
quences for adolescent morbidity, mortality, and overall
quality of life. Third, impoverished adolescents are at the
most severe risk for poor outcomes, and improvement in
their sleep may produce large gains.
Keywords Adolescence  Sleep  Violence 
Hopelessness  Poverty  Stress
J Youth Adolescence (2015) 44:518–542
Introduction
Sleep disruption is highly prevalent among adolescents,
with grave consequences both for the individual and for
society. The National Sleep Foundation (2006) reported
that 45 % of adolescents do not get sufficient sleep on
school nights and that high school seniors are short by an
average of 11.7 h of sleep per week. Insufficient sleep and
daytime sleepiness have, in turn, been identified as con-
tributing to somatic, psychological, and behavioral prob-
lems that are of particular concern among adolescents.
Overall, sleep disruption among adolescents has severe
societal costs in terms of decreased productivity and
diminished quality of life (Martiniuk et al. 2009; Ohayon
2005; Colten and Altevogt 2006). Sleep is particularly
important for brain maturation among children and youth,
and sleep deprivation in adolescents has a potent negative
effect on behavior, emotion, and attention (Dahl and Lewin
2002). Studies have found that insufficient sleep is asso-
ciated with fighting, bullying, and shoplifting (Holmberg
and Hellberg 2008); self-harm (Martiniuk et al.); and
aggression, anger, and impulsivity (Dahl 2006; Ireland and
Culpin 2006; Umlauf et al. 2011).
Many factors may contribute to problematic sleep among
adolescents. One that has been largely overlooked, however,
is poverty, particularly in distressed urban neighborhoods
(Bolland 2003; Bolland et al. 2007). Life in these neighbor-
hoods is fraught with danger, with violence rates as much as
six times higher than in middle-class neighborhoods (Bolland
et al.). With violence comes psychological distress, often
manifested as post-traumatic stress and feelings of hopeless-
ness, which have serious consequences for sleep. For exam-
ple, a recent report from the National Health Interview Study
documented the importance of neighborhood influences and
minority status on sleep. One striking conclusion of the study
was that inner city residents and African Americans had
higher risks for short sleep (Hale and Do 2007). Other studies
have reported, but without explanation, that African Ameri-
cans have worse sleep and lower sleep quality, longer sleep
latency, and more napping than members of other ethnic
groups in the United States (see Durrence and Lichstein 2006,
for a review). Such differences have been described as ‘‘sleep
disparities’’ associated with poverty and ethnic and minority
populations (Patel et al. 2010). These findings are important
with respect to impoverished adolescents because of the high
correlation between race and poverty.
In the current study of inner city adolescents, we exam-
ined how sleep might be affected by exposure to violence and
hopelessness, in addition to developmental status and gender.
We employed two analytic strategies. First, we conducted a
longitudinal analysis of trajectories of sleep symptoms
among a large sample of adolescents (10–18 years old) using
a measure of sleep dysfunction associated with traumatic
519
stress. Second, we conducted a cross-sectional analysis of a
subsample of 14- and 15-year olds using survey measures of
sleep disorders and daytime sleepiness. In the following
sections, we briefly discuss why it is important to consider
how age, gender, exposure to violence, and feelings of
hopelessness affect adolescent sleep patterns and quality.
Adolescent Development, Gender, and Sleep
Hormonal, somatic, and behavioral changes have been
suggested as defining characteristics of adolescence (Brand
and Kirov 2011; Hagenauer and Lee 2013). Over the
course of adolescence, bedtime gets later (Fukuda and
Ishihara 2001). This change reflects a naturally occurring
shift in the circadian cycle of sleep and wakefulness
(Carskadon et al. 1993; Jenni et al. 2005). Regardless of
their preference for a later bedtime, adolescents’ individual
need for sleep does not change (Carskadon 2011). School
and social schedules do not match this circadian delay,
however, causing adolescents to often get less sleep than
they need (Ohayon et al. 2000). As a result, many ado-
lescents report daytime sleepiness.
It is clear that the adolescent brain is characterized by its
plasticity, with extensive remodeling, including pruning of
synapses (Buchmann et al. 2011; Tarokh et al. 2010). A
large body of electroencephalographic (EEG) research
demonstrates that low frequency brain waves (which are
associated with sleep) decline during adolescence, parallel to
the synaptic pruning (Baker et al. 2012; Campbell et al.
2011; Feinberg and Campbell 2013; Tarokh et al.). Evidence
of gender differences in these EEG studies is inconsistent
(c.f., Baker et al., Campbell et al.) and it has been suggested
that observed gender differences are likely caused by
pubertal hormones (Hagenauer and Lee). Theory suggests
that age and gender effects on sleep during adolescence
should be consistent. However, this has not been the case.
Although sleep quality appears to be unrelated to age
(Sadeh et al. 2000), specific sleep disorders can vary or be
stable across adolescence. For example, snoring (a symptom
of obstructive sleep apnea) does not appear to change with
age during childhood (Anuntaseree et al. 2001; Lumeng and
Chervin 2008), nor does restless legs syndrome (RLS; Yil-
maz et al. 2011). Sleepwalking declines with age (Ohayon
et al. 2000), but in most studies insomnia appears to increase
with age (Liu and Zhou 2002; Ohayon et al.). However, at
least two studies suggested that insomnia decreases with age
(Klackenberg 1982; Laberge et al. 2001).
Similarly, inconsistent gender differences have been
reported (see Dewald et al. 2010 for a review) for adoles-
cent snoring (Lumeng and Chervin 2008), insomnia (Hy-
sing et al. 2013), and periodic limb movement during sleep
(Sadeh et al. 2000; Yilmaz et al. 2011). Nightmares
(Schredl and Reinhard 2011), however, appear to be more
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common among adolescent females than males. When they
have been tested, age-by-gender interactions have not been
statistically significant (Hysing et al.; Laberge et al. 2001).
To some extent, inconsistencies in empirical findings may
be methodological. Sleep quality, duration, and disorders
can be measured objectively using EEG, polysomnography
(PSG), and actigraphy, and subjectively using symptom
reports or observation of sleep. Not surprisingly, the cor-
respondence between objective and subjective measures is
not always high (Tremaine et al. 2010). Typically, sleep
studies, particularly those using objective measures, have
small sample sizes, leading to a lack of statistical power
that may be a factor in the inconsistent findings (Lumeng
and Chervin). Different measures have been collected
cross-sectionally and longitudinally, and ages have been
combined in different ways. Further, Dewald et al. sug-
gested that some inconsistent gender effects may be a
function of the pubertal status of the females sampled,
which can be affected by the age ranges studied. In the end,
the degree to which changes in sleep are more inter-indi-
vidual or intra-individual is not clear (Baker et al. 2012). In
light of these inconsistencies, more research into the effects
of gender and development on adolescent sleep is war-
ranted. In addition to exploring gender and development as
main effects, however, factors that may moderate the
relationship between these factors and sleep should be
explored.
Poverty, Exposure to Violence, and Adolescent Sleep
Very few studies have focused on sleep among impover-
ished adolescents. Some studies have, however, included
such adolescents in their samples, which allows the effects
of poverty on sleep to be assessed. These studies have
concluded that adolescents living in poverty experience
more sleep problems than those with greater economic
resources (El-Sheikh et al. 2010; Hale et al. 2010; Marco
et al. 2012; Singh and Kenney 2013). A variety of expla-
nations for poorer sleep outcomes in impoverished popu-
lations have been offered, including greater stress (Hill
et al. 2009; Ross and Mirowsky 2001); parents working
evening and night shifts, shared sleeping spaces, and per-
ceived neighborhood crime and danger (Owens et al.
2006); neighborhood noise and lighting (Hill et al.); and a
lack of daily routine (Evans et al. 2005).
Perhaps the most consistently studied of these factors is
stress (e.g., Sadeh 1996). Dahl and Lewin (2002) argue,
‘‘social stresses evoke powerful feelings of threat and sleep
disruption, but feelings of love, caring, and social con-
nection create a sense of safety and promote sleep’’
(p. 176). Pynoos et al. (1987) demonstrated this argument
in their examination of a sniper attack at an elementary
school playground. They reported that children who
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visually witnessed the attack and/or knew the child who
was killed were more traumatized than those who either did
not know the child or who were not on the playground that
day, leading them to greater sleep problems. The preva-
lence of multiple psychophysiological stressors is a hall-
mark of poverty (Evans and English 2002; Evans and Kim
2012), and the violence common in poor neighborhoods is
one such stressor for children and adolescents (Bolland
et al. 2007; Scarpa 2003). Even adolescents who have not
been direct victims of violence may frequently witness
violence, and witnessing violence may lead to even greater
psychological harm than victimization itself (Bolland et al.
2005). Thus, exposure to violence is potentially one of the
more important sources of stress in impoverished neigh-
borhoods, and one that may have implications for sleep.
Hopelessness and Adolescent Sleep
Hopelessness has been defined as ‘‘an expectation that
highly desired outcomes will not occur or that negative
ones will occur…, and that nothing is going to change
things for the better…’’ (Joiner and Wagner 1995, p. 778).
Hopelessness is rampant among inner-city adolescents
(Bolland 2003; Bolland et al. 2007), developing as a
function of disruptive events and lack of connectedness to
other people or things (Bolland et al. 2005). Chronic
stressors tend to contribute to increased hopelessness
(Dohrenwend 2006; Landis et al. 2007), and their impact is
likely cumulative (Pynoos and Nader 1988). Hopelessness
reflects a lack of future orientation, and as such it has
developmental qualities (Bolland et al. 2007), declining
with age through adolescence. Given that many stressors
are associated with an impoverished environment, and that
upward mobility for people living in poverty is limited
(South and Crowder 1997), hopelessness itself may be
chronic, with both trait-like and state-like qualities (Beck
et al. 1990; Blackburn et al. 1986).
Only one study (Sadeh et al. 1995) has rigorously
examined the relationship between hopelessness and sleep,
finding that hopelessness interferes with sleep (measured
by actigraphy). Two other studies (McKnight-Eily et al.
2011; Perez et al. 2010) using self-reported sleep measures
and a single question that combined hopelessness and
sadness found similar results. In addition, Whisman and
Pinto (1997) found a small positive correlation between
hopelessness and a single insomnia question from the Beck
Depression Inventory. A number of studies, however, have
examined the relationship between depression (a close
cousin of hopelessness) and sleep. While the PSG results
for children and adolescents are equivocal (see Ivanenko
et al. 2005, for a review), there does seem to be a rela-
tionship between depression and prolonged sleep latency
(e.g., Dahl et al. 1996). Subjective reports of sleep show a
J Youth Adolescence (2015) 44:518–542
clearer relationship to depression, with depressed adoles-
cents reporting poorer sleep quality (Roberts et al. 1995).
The implications of these results for hopelessness should be
interpreted cautiously, however, because hopelessness and
depression are not synonymous. On the one hand, hope-
lessness is considered to be a subtype of depression
(Abramson et al. 1989), and the two are correlated in both
youths (Whisman and Pinto 1997) and adults (Mystakidou
et al. 2009). On the other hand, depression is a mood dis-
order related to feelings in the here and now, whereas
hopelessness is related to beliefs about the future. More-
over, depression is definitionally confounded with sleep
(e.g., insomnia is considered to be a symptom of
depression).
Interactive Effects of Exposure to Violence,
Hopelessness, Age, and Gender on Sleep
Several studies (Bolland et al. 2005; Mrug and Windle
2010; Wanklyn et al. 2012) have examined the relationship
between exposure to violence and hopelessness, finding
that exposure to violence predicts hopelessness. While it is
intriguing to speculate whether hopelessness mediates or
moderates the relationship between exposure to violence
and sleep, research has not directly addressed this question.
However, through examination of traumatic stress and
depression as proxies for exposure to violence and hope-
lessness respectively, some insights into the relationship
among hopelessness, exposure to violence, and sleep can
be gained. Babson et al. (2011) found that traumatic stress
affects sleep quality even after controlling for depression.
Using PSG, Woodward et al. (1996) found that veterans
with both posttraumatic stress disorder and major depres-
sive disorder showed small but noticeable differences in
sleep architecture from those with PTSD but no depression.
Similarly, Williamson et al. (1995) found that depressed
adolescents who had experienced stressful life events
exhibited sleep architecture different from those who had
not experienced such events. Carter and Grant (2011)
found that hopelessness combined interactively with life
events and with daily hassles to affect both depression and
anxiety. In a similar way, Kliewer et al. (2004) found that
protective factors interacted with exposure to violence to
predict depression. These results suggest that protective
and risk factors (e.g., hopelessness) may interact with acute
stressors (e.g., exposure to violence), to affect sleep quality
(although notably, Carter and Grant did not find that this
particular interaction affected depression). Although the
results from these studies should be interpreted cautiously
as support for the discussion at hand, they suggest the
wisdom of further study of the issues.
Gender interacts with both traumatic stress and depres-
sion (as potential proxies for exposure to violence and
521
hopelessness) to affect sleep, although the exact nature of
the interactions is open to debate. For example, whereas
studies of adults (Banack et al. 2014) have shown that
women suffering from depression report worse sleep
quality than men suffering from depression, PSG results for
both youth (Robert et al. 2006) and adults (Armitage 2007;
Armitage et al. 2000a, b) show depressed males to be at
greater risk than depressed females for poor sleep. Also
using PSG, Richards et al. (2013) reported that PTSD
affected sleep architecture differently for males and
females. A review of other literature (Kobayashi et al.
2012) finds that females with PTSD experience poorer
sleep than males with PTSD.
A series of studies has demonstrated that gender 9 age
and gender 9 age 9 depression interactions affect sleep
microarchitecture (Armitage et al. 2006; Armitage et al.
2000a, b; Robert et al. 2006). The presence of these
interactions puts in sharp relief the risk of excluding them.
For example, studies have found very inconsistent results
relating to developmental status and PTSD (Agustini et al.
2011; Copeland et al. 2007; Kar et al. 2007). Contractor
et al. (2013) suggested that these conflicting results may be
due to different symptom clusters being more relevant for
different ages, but they also warned that conflicting results
may be due to failure to include relevant moderating
variables in the analysis. A similar cautionary criticism
applies to the conflicting results regarding age, gender, and
adolescent sleep discussed earlier in this paper.
The Current Study
Summarizing the preceding discussion, it is clear that sleep
disruption is prevalent among adolescents and that several
factors may contribute to problematic sleep. How those
factors contribute to sleep problems, especially for
impoverished adolescents is less clear. At a demographic
level, for example, although age and gender have been
linked to sleep quality, inconsistent results regarding the
directions of age and gender effects have been reported.
Two of our research questions, therefore, address age and
gender. First, how does age affect adolescent sleep? Sec-
ond, how does gender affect adolescent sleep? Feelings of
hopelessness and stress, both of which are associated with
poverty, appear to interfere with sleep quality, although
few studies have examined the relationships among
impoverished adolescents. Our third and fourth research
questions, then, address these two factors. Third, how do
feelings of hopelessness affect adolescent sleep? Fourth,
how does exposure to violence and the stress it creates
affect adolescent sleep? Additionally, sleep research sug-
gests that predictive factors may interact in complex ways
to affect sleep. Our fifth research question addresses these
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potential interactions. How do age, gender, feelings of
hopelessness, and exposure to violence interact to affect
adolescent sleep? Finally, research has shown that poverty
contributes to poor sleep. Notably, we did not explicitly
address poverty in the research questions. Rather, poverty
is a constant in the research design, which focuses on
factors associated with (but not invariant with respect to)
poverty. By limiting the variance around socioeconomic
status, we were able to more accurately examine the effects
of hopelessness and exposure to violence on adolescent
sleep without the risk of residual confounding.
We framed this study to address research questions,
rather than to test hypotheses, for two reasons. First, the
literature is not sufficiently consistent, in most cases, to
allow us to specify the direction that statistical relation-
ships might take. Second, the majority of research on
adolescent sleep has not examined impoverished popula-
tions, so there was little to guide the direction of hypoth-
eses regarding sleep among impoverished adolescents.
We conducted two analyses to address the research
questions. In our initial analysis, we used data from the
Mobile Youth Survey (MYS), a multiple cohort longitudinal
study of poverty and adolescent risk conducted in Mobile,
Alabama between 1998 and 2011. In this analysis, we used a
narrow measure of sleep problems, examining trouble
sleeping and nightmares that occur when bad things happen
to a family member or friend. Even though the measure is
narrow, bad things happen to family members and friends
with sufficient regularity in impoverished neighborhoods
that this measure may address an important aspect of sleep
quality for these adolescents. In a follow-up analysis, we
used additional survey data collected from a subsample of
14- and 15-year-old MYS participants in 2010–2011. These
data were merged with the MYS measures of hopelessness
and exposure to violence so that we could explore the gen-
eralizability of the initial results to a wider range of sleep
disorder symptoms, albeit within a truncated age range.
Methods
Setting and Sample
This study employed data collected as part of the MYS, a
multiple cohort longitudinal study of poverty and adolescent
risk. Details of sample recruitment, sample characteristics,
and survey administration are provided elsewhere (Bolland
et al. 2013) and will be reported only briefly here. The MYS
was conducted in Mobile, Alabama between 1998 and 2011.
The Mobile Metropolitan Statistical Area (MSA), with a
total population of over 540,000, is dominated by the city of
Mobile, with a population of approximately 200,000. In
2000, 46.1 % of Mobile’s population was African American
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and 1.4 % was of Hispanic descent; 22.4 % lived in poverty.
The median household income in 2000 was $31,445.
Prichard, a city of nearly 30,000, borders Mobile on its north
side. In 2000, 83.3 % of Prichard’s population was African
American and 0.6 % was of Hispanic descent; 44.1 % lived
in poverty. Prichard’s median household income in 2000 was
$19,544. In 1990, 42 % of African Americans in the MSA
lived in high-poverty census tracts, placing Mobile third in
the nation in this measure of concentrated poverty (Jar-
gowsky 1997).
Over 12,000 adolescents between the ages of 9.75 and
19.25 (at time of enrollment) participated in the MYS. The
University of Alabama Institutional Review Board
approved the study and parental consent was obtained for
all research participants. Recruitment and survey admin-
istration took place each year during the summer. During
early years of the survey, recruiters knocked on randomly-
selected doors in pre-identified neighborhoods to recruit
age-appropriate adolescents to participate. During sub-
sequent years, recruiters went to homes where enrollees
lived, recruiting them to participate again and recruiting
any additional age-appropriate adolescents living in the
home. Each year, adolescents who heard about the survey
and came to the survey location were allowed to enroll,
provided that they met the age criteria, lived in a neigh-
borhood where data were being collected, and had parental
consent. Approximately 93.5 % described themselves as
African American, 6 % as mixed race, and \1 % as Cau-
casian or Asian. School records indicated that considerably
\1 % were of Hispanic descent. Approximately 51 % of
respondents were male (range across waves = 47.8–53.8),
and approximately 90 % reported that they received free or
reduced-cost lunch. Analysis of a small sample of free/
reduced-cost lunch applications for the 2005–2006 school
year shows average monthly household income of
approximately $400.
Enrollees in the MYS were encouraged to continue
participating in the annual surveys until they reached
19.25 years of age. The typical enrollee was surveyed 2.92
times (range = 1–10 times). Year-to-year retention aver-
aged approximately 70 %. Analyses showed that the MYS
sample is representative of all comparably aged youths in
the target neighborhoods, and that missing data due to
dropout can be considered missing at random (Bolland
2012). Each summer following 1998, a new cohort was
recruited to supplement already enrolled participants, as
described in the preceding paragraph. In 1999, this new
cohort accounted for 49.4 % of all participants (this is not
surprising, given that some of those recruited in 1998 did
not participate because the study was new and they were
not sure the researchers could be trusted; by 1999, trust had
increased and they chose to participate). After 1999,
between 23.1 % (2004) and 35.5 % (2009) of the
J Youth Adolescence (2015) 44:518–542
participants each year represented a new cohort. The mean
age of participants at the time of enrollment was
13.01 years (range across waves = 12.31–13.56), with a
median within-wave standard deviation equal to 2.67.
Each summer, respondents were surveyed in a neigh-
borhood facility (e.g., nearby elementary school, community
center) in groups of about 15, with the survey questions read
aloud and individuals marking responses on printed scan-
nable questionnaires. Respondents who appeared to have
difficulty keeping up were invited to be surveyed individu-
ally or in groups of no more than two to four. A typical
survey administration took 90 min, and respondents were
paid $10 (1998–2005) or $15 (2006–2011) in appreciation
for their time.
During the 2010 and 2011 MYS data collection periods, a
subsample of MYS participants (aged 14 and 15; 49.4 %
female; 92.7 % African American, 7.3 % mixed race) was
recruited without replacement to participate in an additional
survey that focused on sleep problems, habits, and outcomes
(MYS-Sleep Study). This subsample was recruited from
selected MYS survey groups, chosen to be representative of
the kinds of neighborhoods where the MYS was conducted
(e.g., public housing and non-public housing). During the
second year of data collection, only adolescents who had not
participated the first year were allowed to participate. The
participation rate for the MYS-Sleep Study was nearly
100 % of those recruited (N = 263). Interviews were con-
ducted in participants’ homes where parental consent was
obtained. Trained interviewers read questions aloud and
recorded the respondents’ answers. Each participant was
given $5 for his/her time to complete the 45-min interview.
Sleep items were taken from a number of established sleep
questionnaires, including the Sleep-50 inventory (Spoor-
maker et al. 2005). Each sleep study participant also con-
tributed MYS data the year of the sleep interview, and the
MYS and MYS-Sleep data were matched by participant
identification number for analyses.
Measures
Demographic Variables
Age and gender (0 = male, 1 = female) were both self-
reported measures from the MYS.
Exposure to Violence (ExViol)
We measured exposure to violence with two MYS ques-
tions: ‘‘Have you ever seen someone being cut, stabbed, or
shot?’’ (no, yes); ‘‘During the past 90 days, did you see
someone being cut, stabbed, or shot?’’ (no, yes just once,
yes more than once). Responses to these questions were
combined into a frequency/recency scale (0 = never;
523
1 = not during the past 90 days; 2 = once during the past
90 days; 3 = more than once during the past 90 days; see
Bolland et al. 2007 for details).
Witnessing violence was a relatively frequent event
(across waves, the median incidence of reports that
respondents had seen someone cut or shot at least once
during the past 3 months was equal to 26.3 %). Witnessing
violence was also reasonably consistent across time, with
the median 12-month correlation (r12) equal to .29
(p \ .001). Longer-term correlations (through 72 months)
were also statistically significant (e.g., median r24 = .26,
p \ .001; median r36 = .22, p \ .001).
Sleep Problems
Two MYS items address sleep problems that occur as a
function of traumatic stress. One item is phrased, ‘‘How
often do you have bad dreams about bad things that have
happened to family members or friends?’’ and the other is,
‘‘How often do you have trouble sleeping when bad things
happen to family members or friends?’’ Responses to both
questions were almost never = 0; sometimes = 1, very
often = 2. We combined these two questions into an
additive scale (0–4), where a higher number indicates
greater problems. Internal reliability is only moderate
(median within-wave a = .62, range = .51–.66), as would
be expected for a scale with only two items. The correla-
tions between the two items, however, are robust (median
within-wave r = .45, range = .34–.50).
The typical MYS respondent reported that sleep prob-
lems associated with traumatic stress occurred sometimes
(median within-wave M = 1.85; median within-wave
SD = 1.18). Certainly, there was plenty of opportunity for
post-traumatic stress within this population, with the
median within-wave percentage reporting that a friend or
relative had been cut or shot during the past year equal to
34.0 %. Other types of events involving a family member
of friend that might lead to post-traumatic stress for the
adolescent include illness or death, arrest, school suspen-
sion or expulsion, losing a job, and so forth. The cross-time
consistency for sleep problems was somewhat lower than
that for exposure to violence, with median r12 = .24
(p \ .001). The cross-time consistency for longer intervals
was also less consistent than for exposure to violence
(median r24 = .20, p \ .001; median r36 = .17, p \ .001).
Like exposure to violence, consistency in sleep problems
remained statistically significant through 72 months.
Hopelessness
The measure of hopelessness was five questions adapted
from the Hopelessness Scale for Children (Kazdin et al.
1983), selected for their high item-total correlations.
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Respondents were asked to disagree (0) or agree (1) with
each of the five statements. One example is, ‘‘All I see
ahead of me are bad things, not good things’’ and another
is, ‘‘I might as well give up because I can’t make things
better for myself.’’ A sixth statement (‘‘I do not expect to
live a very long life’’) was added, based on the low
expectations of survival held by many inner-city adoles-
cents (e.g., DuRant et al. 1994). The six items constitute an
additive 6-point (0–6) Brief Hopelessness Scale. The
internal reliability of the scale is acceptable (median
within-wave a = .75, range = .70–.83).
Although hopelessness values were not high in an
absolute sense (median within-wave M = 1.45; median
within-wave SD = 1.73), they are very high compared
with other adolescent populations (Bolland et al. 2007).
Hopelessness was somewhat more consistent than the two
previous scales, with median r12 = .33 (p \ .001). The
hopelessness correlations remained statistically significant
through 84 months (median r24 = .27, p \ .001; median
r36 = .24, p \ .001; median r48 = .23, p \ .001).
Sleep Disorder Symptoms
The Sleep-50 inventory was used to assess for symptoms of
common sleep disorders and for daytime sleepiness
(Spoormaker et al. 2005). In contrast to many other sleep
inventories, the Sleep-50 screens for nine sleep disorders
found in the Diagnostic and Statistical Manual of Mental
Disorders, revised 4th edition. The 50 items yield nine
subscales. Seven of the subscales are associated with spe-
cific sleep disorders (apnea, insomnia, narcolepsy, RLS,
circadian rhythm disorder, sleepwalking, and nightmares),
one addresses risk factors for poor sleep, and one addresses
daytime sleepiness. The subscales generally have good
internal reliability (Cronbach a ranges from .46 to .78, see
Table 2) and test–retest reliability, and they show strong
correspondence to clinical diagnoses (j = .77).
Our method for calculating the sleep disorder subscales
was altered from the original formula developed by
Spoormaker et al. (2005). As in the original survey, each
question allowed four response options describing the
intensity of a particular symptom during the past 4 weeks
(not at all, somewhat, rather much, very much). We,
however, coded the responses 0, 1, 2, 3, respectively,
instead of 1, 2, 3, 4. The responses from each participant
were summed within each subscale to create subscale
scores. Maximum values for each subscale vary from 6
(circadian rhythm) to 27 (insomnia).
One additional change was made to the original con-
ceptualization of the Sleep-50 subscales. Spoormaker
et al. (2005) originally conceptualized the final item
(‘‘Generally, I sleep badly’’) as a component of a separate
sleepiness subscale. However, their factor analysis
123
J Youth Adolescence (2015) 44:518–542
demonstrated that this item was a better fit with the
insomnia subscale. We therefore included that item in the
insomnia subscale.
Analysis Plan
The longitudinal analysis used the framework suggested by
Singer and Willett (2003) for estimating random and fixed
growth effects in longitudinal data. This analysis used the
complete MYS data for respondents aged 10–18, with two
exclusions. First, respondents at time t who showed an
overall pattern of response inconsistency at time t (see
Bolland et al. 2007 for a discussion) were excluded from
this study. Second, respondents who contributed only a
single data point were excluded from this study. This
yielded a final sample of 7,945 respondents with a total of
27,595 observations.
We estimated an unconditional means model, with no
predictors (Model 1); an unconditional growth model
(Model 2), with both linear (age) and quadratic (age2)
growth terms; a conditional growth model which added
gender (and gender interactions) to Model 2 as a time-
invariant covariate (Model 3); a conditional growth model
which added hopelessness (and hopelessness interactions)
to Model 3 as a time-varying covariate (Model 4); and a
conditional growth model which added exposure to vio-
lence (and exposure to violence interactions) to Model 4 as
a time-varying covariate (Model 5). Model 1 estimates only
the intercept as a random factor. Models 2 and 3 treat
intercept and agelin as random effects. Model 4 adds
hopelessness and agelin 9 hopelessness as random effects.
Finally, Model 5 adds ExViol and agelin 9 ExViol as
additional random effects. With the exception of Model 5,
each analysis estimated a full factorial model. Because of
the number of terms and the potential confounding
among correlated terms in Model 5, two four-way inter-
actions (agelin 9 gender 9 ExViol 9 hopelessness; agequad 9
gender 9 ExViol 9 hopelessness) were eliminated from the
full-factorial model. In addition, several possible random
effects (e.g., agequad, agequad 9 ExViol, ExViol 9 hope-
lessness) were not estimated because the complexity they
created resulted in an estimated G matrix that was not
positive definite. All longitudinal models were estimated
using SAS PROC MIXED with an unstructured covariance
matrix.
In the follow-up cross-sectional analysis, a MANOVA
model was estimated using SAS PROC GLM, with sleep
disorders and sleepiness (measured by subscales of the
Sleep-50 inventory) as the multivariate dependent vari-
ables, and gender, ExViol, and hopelessness (as measured
by the MYS) as independent variables. An ANOVA model
was estimated for the nightmare subscale of the Sleep-50
inventory with the same independent variables.
J Youth Adolescence (2015) 44:518–542
In any analysis that includes the multiplicative combi-
nation of continuous variables X1 and X2 as an X1 9 X2
interaction, X1 and X2 are likely to covary with X1 9 X2. To
alleviate collinearity concerns, Aiken and West (1991) have
suggested centering X1 and X2 such that M = 0. We used this
approach to center hopelessness and exposure to violence for
all of the analyses. For consistency, we also centered gender.
Results
Longitudinal Analysis of MYS Data
The correlations among the variables employed in the mul-
tivariate analysis are reported in the lower-half diagonal in
Table 1. These correlations reflect all data meeting the
inclusion criteria for the longitudinal analysis. As such, they
include repeated observations from most respondents, so
they are weighted toward those respondents who contributed
the most data points and should be interpreted cautiously.
Although most are statistically significant, the coefficients
are very modest. Only the age-sleep problems correlation
coefficient is larger than .15. The correlation between
exposure to violence and sleep problems is not statistically
different for males (across years, median r = .107) and
females (across years, median r = .161), nor is the correla-
tion between hopelessness and sleep problems (across years,
median r = .067 for males; median r = .089 for females).
Table 2 shows the parameter estimates (^ c for fixed
effects, r^2 for random effects), standard errors of the
estimates, and summary and fit statistics for the five growth
curve models. In the unconditional means model (Model
1), the significant intercept (p \ .01) indicates that in this
population the mean self-rating for sleep problems (1.84) is
significantly different from zero. The intraclass correlation
(q) equals .19, indicating that the vast majority of the
variance is due to within-subject variation rather than to
between-subject variation. The unconditional growth
model (Model 2) showed a significant improvement over
Model 1: the difference in the -2 log likelihood goodness
of fit statistic for the two models (906.7), which has a v2
distribution where df = the change in number of parame-
ters for the two models, is statistically significant
(Dv2 = 906.7, df = 4, p \ .01). The pseudo R2 (.06)
indicates a modest increase in variance explained by add-
ing the growth factors. The linear age parameter is negative
and statistically significant (p \ .01), indicating decreasing
sleep problems with age. The quadratic age parameter is
positive and statistically significant (p \ .01), indicating a
deceleration of the age effect during later adolescence. The
significant variance around the linear growth parameter,
however, indicates room for improvement.
525
Model 3 adds gender differences to all level 1 effects.
The addition of gender significantly improved model fit
(Dv2 = 85.4, df = 3, p \ .01), although the increase in
variance explained is negligible. The non-significant gen-
der main effect indicates that both male and female ado-
lescents have similar levels of sleep problems at age 10.
However, the statistically significant gender 9 agelin
(p \ .01) and gender 9 agequad (p \ .05) effects indicate
differential growth across adolescence for the two genders.
Again, the statistically significant variance components
indicate room for improvement.
Model 4 adds hopelessness to all level-1 effects, and to
level-2 as a main effect and in interaction with agelin. The
addition of these terms significantly improved model fit
(Dv2 = 111.9, df = 12, p \ .01); the increase in variance
explained (change in pseudo R2 = .032) was again modest.
The significant hopelessness main effect (p \ .001) indi-
cates that at age 10, hopelessness is positively related to
sleep problems. None of the hopelessness interactions,
however, is statistically significant. As before, the statisti-
cally significant variance components indicate room for
improvement.
Exposure to violence was the last effect added to the
analysis (see Model 5). The addition of the ExViol terms
significantly improved model fit (Dv2 = 475.4, df = 21,
p \ .01). Increase in variance explained (change in pseudo
R2 = .023) is again modest. The overall variance explained
by the model, however, is moderate (pseudo R2 = .117).
The significant main effect for exposure to violence
(p \ .01) indicates that at age 10, adolescents who expe-
rienced more frequent and/or recent exposure to violence
reported greater sleep problems than those who had not
experienced violence either frequently or recently. The
significant hopelessness 9 ExViol interaction (p \ .01)
indicates a differential relationship between hopelessness
and sleep problems depending on level of ExViol.
Although there is no relationship between hopelessness and
sleep problems for adolescents with high exposure to vio-
lence, there is a positive relationship between hopelessness
and sleep problems for adolescents with low exposure to
violence. None of the other interactions between exposure
to violence, hopelessness, and gender were statistically
significant, indicating no differential relationships with
sleep problems.
Table 2 also reports effect sizes. Following Peugh
(2010) and Singer and Willett (2003), we calculated effect
size as the proportional reduction in variance (PRV). This
actually yields two measures of effect size. The first
measure is the reduction in variance around the intercept
and the second is the reduction in variance around the
slope. The results showed a moderate proportional reduc-
tion in intra-individual variance (pseudo R2 for Model
2 = .062) for growth (the effect size for growth combines
123
 526

123
Table 1 Correlations among sleep disorder symptoms and MYS variables
2 3 4 5 6 7 8 9 10 11 12 13 14

Sleep disorder symptomsa

1 Apnea .535*** .439*** .461*** .212*** .261*** .242*** .383*** .444*** – .023 .100 .125** .138**
2 Insomnia .575*** .479*** .334*** .277*** .380*** .466*** .599*** – .057 .080 .216*** .229***
3 Narcolepsy .417*** .348*** .427*** .307*** .416*** .559*** – .061 .073 .119* .298***
4 RLS/PLMDb .139** .297*** .281*** .259*** .438*** – .003 .086 .085 .083
5 Circadian rhythm .171*** .144** .088 .376*** – .031 .102 .090 .236***
6 Sleepwalking .392*** .332*** .413*** – .035 .146** .040 .166***
7 Nightmares (item) .664*** .424*** – .139** .076 .131** .234***
8 Nightmares (scale) .367*** – .037 .051 .042 .213**
9 Sleepiness – .091 .165*** .168*** .223***
MYS variables
10 Agec – – – –
11 Gender .007 -.103 -.077 .154**
12 Hopelessness -.118*** -.110*** .013 -.004
13 Exposure to violence .032*** -.075*** .061*** .212***
14 Sleep problems -.159*** .063*** .061*** .128***
Sample size for each correlation varied depending on missing data for each pair of variables
Correlations above the diagonal were calculated for the MYS sleep subsample (N = 247 except the Nightmare Scale, where N = 160); correlations below the diagonal were calculated for the
entire MYS sample aggregated across waves of data (N = 27,595) that met the inclusion criteria for the growth curve analysis
a
Sleep disorder symptoms were measured by Sleep-50 subscales
b
Restless legs syndrome/periodic limb movement disorder
c
Correlations with age were not calculated for the sleep subsample, because age is homogeneous (14, 15)
* p \ .10; ** p \ .05; *** p \ .01
J Youth Adolescence (2015) 44:518–542
 Table 2 Estimated model parameters for unconditional means model and growth models of sleep problems across adolescence (N = 7,945; 27,595 observations)
Fixed effects Model 1 Model 2 Model 3 Model 4 Model 5 Effect size
c^ ðsec^Þ c^ ðsec^Þ c^ ðsec^Þ c^ ðsec^Þ c^ ðsec^Þ Intercept Slope

Intercept 1.843 (0.009)*** 2.283 (0.020)*** 2.284 (0.020)*** 2.274 (0.020)*** 2.298 (0.020)***
Agelin -0.173 (0.010)*** -0.175 (0.010)*** -0.166 (0.010)*** -0.169 (0.010)***
Agequad 0.012 (0.001)*** 0.012 (0.001)*** 0.011 (0.001)*** 0.011 (0.001)***
Gender 0.024 (0.040) 0.019 (0.040) 0.028 (0.040) .001 .001
Hopelessness 0.038 (0.011)*** 0.029 (0.011)** .003 .000
ExViol 0.172 (0.020)*** .024 .046
Gender 9 hopelessness 0.021 (0.022) 0.023 (0.023) .000 .002
J Youth Adolescence (2015) 44:518–542

Gender 9 ExViol -0.029 (0.040) .001 .001

Hopelessness 9 ExViol -0.040 (0.011)*** .000 .000
Gender 9 hopelessness 9 ExViol 0.006 (0.009) .000 .000
Gender 9 agelin 0.060 (0.020)*** 0.067 (0.021)*** 0.069 (0.021)*** .007 .012
Gender 9 agequad -0.005 (0.002)** -0.006 (0.002)** -0.006 (0.002)**
Hopelessness 9 agelin -0.007 (0.006) -0.003 (0.006) .002 .001
Hopelessness 9 agequad 0.001 (0.001) 0.000 (0.001)
ExViol 9 agelin -0.004 (0.011) .001 .000
ExViol 9 agequad 0.000 (0.001)
Gender 9 hopelessness 9 agelin 0.002 (0.012) 0.003 (0.012) .000 .003
Gender 9 hopelessness 9 agequad -0.001 (0.001) -0.001 (0.001)
Gender 9 ExViol 9 agelin 0.042 (0.022)* .000 .000
Gender 9 ExViol 9 agequad -0.005 (0.003)**
Hopelessness 9 ExViol 9 agelin 0.016 (0.006) **
Hopelessness 9 ExViol 9 agequad -0.002 (0.001) **
527

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 Table 2 continued
528

Random Effects Model 1 Model 2 Model 3 Model 4 Model 5 Effect size

123
r^2 ðser^2 Þ r^2 ðser^2 Þ r^2 ðser^2 Þ r^2 ðser^2 Þ r^2 ðser^2 Þ Intercept Slope

Intercept 0.271 (.010)*** 0.405 (0.026)*** 0.403 (0.026)*** 0.496 (0.037)*** 0.329 (0.026)***
Agelin 0.007 (0.001)*** 0.007 (0.001)*** 0.009 (0.002)*** 0.009 (0.002)***
Hopelessness 0.101 (0.020)*** 0.025 (0.006)***
ExViol 0.075 (0.019)***
Hopelessness 9 agelin 0.001 (0.001)* 0.000 (0.000)*
ExViol 9 agelin 0.001 (0.001)*
Cov(intercept, agelin) -0.031 (0.005)*** -0.031 (0.005)*** -0.044 (0.007)*** -0.029 (0.006)***
Cov(intercept, hopelessness) -0.125 (0.025)*** -0.029 (0.009)***
Cov(intercept, ExViol) -0.031 (0.014)**
Cov(intercept, hopelessness 9 agelin) 0.016 (0.006)*** 0.003 (0.002)
Cov(intercept, ExViol 9 agelin) 0.005 (0.004)
Cov(agelin, hopelessness) 0.013 (0.005)** -0.003 (0.002)
Cov(agelin, ExViol) 0.013 (0.005)**
Cov(agelin, hopelessness 9 agelin) -0.002 (0.001)** 0.001 (0.000)
Cov(agelin, ExViol 9 agelin) -0.002 (0.001)**
Cov(hopelessness, ExViol) -0.006 (0.007)
Cov(hopelessness, hopelessness 9 agelin) -0.009 (0.004)** -0.002 (0.001)*
Cov(ExViol, ExViol 9 agelin) -0.009 (0.004)**
Cov(hoplessness, ExViol 9 agelin) 0.003 (0.002)*
Cov(ExViol, hopelessness 9 agelin) 0.001 (0.002)
Cov(hopelessness 9 agelin, ExViol 9 agelin) -0.000 (0.000)
Residual 1.139 (0.011)*** 1.068 (0.012)*** 1.067 (0.012)*** 1.032 (0.012)*** 1.006 (0.012)***
Summary and fit statistics
q^ 0.192
Pseudo R2e 0.062 0.063 0.094 0.117
-2 log likelihood 86,466.2 85,559.5 85,474.1 85,362.2 84,886.8
AIC 86,472.2 85,573.5 85,494.1 85,408.2 84,974.8
BIC 86,493.1 85,622.3 85,563.9 85,568.8 85,282.0
* p \ .10; ** p \ .05; *** p \ .01
J Youth Adolescence (2015) 44:518–542
J Youth Adolescence (2015) 44:518–542 529

agelin and agequad; we also combined agelin and agequad in

estimating effect sizes for any interactions with growth).
ExViol had a small-to-moderate sized effect on the inter-
cept, and exposure to violence and gender 9 growth had a
small-to-moderate sized effect on the slope. All the other
effect sizes were small or very small.
Figure 1a, b plots the trajectories derived from Model 5,
the former for low levels of hopelessness and the latter for
high levels of hopelessness (low and high hopelessness as
well as low and high ExViol are plotted at levels one
standard deviation below and one standard deviation above
the means of the respective variables). Gender interacts
with both agelin (p \ .01) and agequad (p \ .05) to predict
sleep problems, with declines in sleep problems across age
steeper for males than for females. In addition, gender 9
ExViol 9 agequad is a significant predictor of sleep prob-
lems (p \ .05) and the gender 9 ExViol 9 agelin interac-
tion trends toward significance (p \ .10). Sleep problems
among males with high exposure to violence appear to
decline more steeply than those of females with high
exposure to violence during early adolescence, while sleep
problems among males with low levels of violence decline
more steeply than sleep problems for comparable females
during later years of adolescence. Finally, the hopeless-
ness 9 ExViol 9 agelin and the hopelessness 9 ExViol 9
agequad interactions are both significant predictors of sleep
problems (both ps \ .05). Across genders, the high expo- Fig. 1 Sleep problems associated with traumatic stress as a function
sure to violence trajectories for low and high levels of of age, gender, and exposure to violence for adolescents with low
hopelessness are nearly coincident. In contrast, for ado- levels of hopelessness (a) and high levels of hopelessness (b)
lescents with low violence exposure, the high hopelessness
trajectories decline more sharply than the low hopelessness remained the same as specified earlier. Finally, the gen-
trajectories, at least during the early adolescent years. der 9 ExViol interaction, which was not statistically sig-
To further explore how the main effects and interactions nificant at age 10, trends toward significance at age 12
among gender, hopelessness, and exposure to violence (p \ .10), achieves statistical significance at ages 13, 14,
affect sleep problems, we created eight new data sets with and 15 (p \ .05), and trends toward significance at age 16
age re-centered at 11, 12, …, 18. We then estimated Model (p \ .10). At each of these ages, increased exposure to
5 eight times, with centered age equal to the intercepts. violence had a larger effect on sleep problems for females
This allowed us to determine the statistical significance of than for males.
gender, hopelessness, ExViol, gender 9 hopelessness, As a final analysis, we considered the possibility that
gender 9 ExViol, hopelessness 9 ExViol, and gender 9 hopelessness may mediate the relationship we found
hopelessness 9 ExViol at each age (see Biesanz et al. 2004 between exposure to violence and sleep problems. To
for a rationale). This analysis showed that although gender explore this possibility, we used a truncated version of the
is not significant at age 10, it does become statistically criteria for establishing mediation developed by Baron and
significant at age 11 and remains so through age 18 (all Kenny (1986). They argued that a necessary condition for
ps \ .05). Hopelessness, which was statistically significant mediation between the predictor variable X, the outcome
at age 10, remains so through age 17 (all ps \ .05). variable Y, and the mediator Z is that the relationship
Exposure to violence, which was statistically significant at between X and Y must be weakened when Z is included in
age 10, remains so through age 18 (all ps \ .01). All these the equation. To test this, we reran the analyses, adding
effects remained positive, indicating that their relationship exposure to violence and interactions in Model 4 and
to sleep remains the same as previously specified. The adding hopelessness and interactions in Model 5. Contrary
hopelessness 9 ExViol interaction, which was statistically to the requirements for establishing mediation, most
significant at age 10, remained so through age 12 (all parameter estimates involving ExViol actually increased
ps \ .05). Again, the functional form of the interaction with the addition of the hopelessness variables (e.g., the

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parameter estimate for the ExViol main effect increased
from .156 to .172; the parameter estimate for the gen-
der 9 ExViol 9 agelin interaction increased from .037 to
.042). Thus, there is no evidence of mediation in this
relationship.
Cross-Sectional Analysis of Sleep Disorder Symptoms
Because the longitudinal analysis used a narrow sleep
measure, we re-examined the research questions using the
Sleep-50 subscales to obtain more robust measures of sleep
disorders. These analyses used data from the MYS sleep
subsample, which was limited to one wave of data from 14-
to 15-year olds. With only one wave of data, we could not
address any aspects of age or development.
The means and variances for all Sleep-50 subscales
(except risk factors) are reported in Table 3. In addition,
Table 3 reports the internal consistency (Cronbach a) and
the percentage of respondents reporting high scores (i.e., a
mean response of more than 1 across subscale items). The
first finding of note is that several subscales have very low
prevalence of high scores. Specifically, fewer than 10 % of
the respondents had an average response of ‘‘somewhat’’ or
higher to the questions comprising the apnea and sleep-
walking subscales, and between 10 and 15 % of the
respondents had an average response of ‘‘somewhat’’ or
higher to the questions comprising the narcolepsy and the
RLS/periodic limb movement disorder (RLS/PLMD) sub-
scales. The subscale means were very similar to those
reported by Gaultney (2010) for college students. However,
using Spoormaker et al.’s (2005) risk cutpoints, we found
somewhat higher risk rates for insomnia (14.7 vs. 12 %)
and very much higher risk rates for apnea (14.8 vs. 4 %),
narcolepsy (57.3 vs. 16.0 %), RLS/PLMD (28.1 vs. 8.0 %),
circadian rhythm disorder (23.4 vs. 7.0 %), and sleep-
walking (5.3 vs. 0.4 %). The risk rate for nightmares is also
much higher than the 2.0 % reported by Gaultney; exactly
how much higher is a function of whether our estimate is
based on only respondents who experienced nightmares
(29.9 %) or all respondents (47.3 %). The Cronbach a
values for the subscales were comparable to those reported
by Spoormaker et al. (2005; reported in Table 3) for all the
subscales except sleepwalking.
Given these similarities, we might conclude that these
subscales are all valid measures of sleep disorders. However,
two of the subscales seem problematic. First, the two-item
circadian rhythm subscale has low internal consistency
(a = .46). The internal consistency is likely low because the
subscale includes only two items (we eliminated the shift
work question from the subscale). Even so, the correlation
between the two items is not high (r = .30). Second, the
internal consistency of the narcolepsy subscale is relatively
low (a = .55). While this, by itself, does not necessarily
indicate a validity problem, its prevalence rate does. Our
finding that 10.5 % of respondents received a high score is
similar to the risk prevalence reported by Gaultney (2010),
but both of these numbers deviate greatly from the estimated
prevalence among adults in the United States (.0004–.001)
reported by Stores (1999). Only about half of the cases
reported by Stores present during childhood. It is therefore
likely that the Sleep-50 narcolepsy subscale is confounded
with the daytime sleepiness subscale (c.f., Luginbuehl et al.
2008). Indeed, the correlation between the two subscales in
the MYS sleep sample is high (r = .56).

Table 3 Descriptive statistics for sleep disorder symptoms

Sleep disorder symptoms Items N Ma SD High score (%)b At-risk (%)c Cronbach ad

Apnea 8 230 3.457 2.943 7.8 14.8 .535 (.51)

Insomnia 9 225 6.809 5.017 24.4 14.7 .744 (.85)
Narcolepsy 5 246 2.529 2.552 13.4 57.3 .548 (.52)
RLS/PLMD 4 249 1.819 2.385 12.0 28.1 .678 (.70)
Circadian rhythm 2 244 2.266 1.182 44.7 23.4 .461 (.47)
Sleepwalking 3 245 0.947 1.502 5.3 5.3 .507 (.84)
Nightmare (1 item) 1 234 0.790 0.970 17.9 17.9
Nightmare (subscale) 4 148 4.608 3.461 47.3 47.3 .766
Sleepiness 6 240 5.371 4.404 32.9 32.9 .777 (.86)
Sleep disorder symptoms were measured by the Sleep-50 subscales; Statistics were based on respondents who answered all questions constituting
each subscale
a
Subscale scores were adjusted such that the lowest possible score was zero. Individual items were scored as follows: 0 = not at all;
1 = somewhat; 2 = rather much; 3 = very much
b
Percent of respondents with a mean response [1.0 (‘‘somewhat’’) to questions comprising the subscale
c
Percent of respondents with a mean response exceeding the cutpoint specified Spoormaker et al. (2005) for meeting at-risk criterion
d
Numbers in parentheses are Cronbach a coefficients reported by Spoormaker et al. (2005)

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The upper half matrix in Table 1 reports correlations
among the sleep disorder symptoms (measured by the
Sleep-50 subscales) and the MYS variables used in the
cross-sectional analyses. The correlations among the sub-
scales are substantial (median r = .426), perhaps reflecting
common medical (e.g., Gusbeth-Tatomir et al. 2007) and
psychiatric antecedents of different sleep disorders (e.g.,
Roth et al. 2006). While some studies (Luginbuehl et al.
2008) have shown lower correlations among sleep disor-
ders than we found, others have shown higher correlations
than reported in Table 1 (Roth et al.).
To determine how sleep disorders were affected by
gender, hopelessness, and exposure to violence, we esti-
mated a MANOVA model using selected Sleep-50 sub-
scales. Across respondents, 3.03 % of the responses to the
questions comprising these subscales were missing. To
remove the potential bias that elimination of cases with
missing data would create (38.4 % of cases would have
been eliminated), we used a Markov Chain Monte Carlo
process to impute 11 data sets (SAS PROC MI). To test
whether the missing data were missing at random (a critical
assumption in multiple imputation), we calculated corre-
lations between missingness in the Sleep-50 subscales and
relevant MYS variables (gender, age, hopelessness,
response inconsistency, presence of a father figure, sleep
problems associated with traumatic stress, overall trau-
matic stress, belief in the inevitability of violence, worry,
and self-worth; these were also used to impute missing
values). Only five of the eighty correlations were statisti-
cally significant, which is almost exactly what would be
expected by chance with a = .05. Thus, the assumption
that the missing data are missing at random appears rea-
sonable. As would be expected with low rates of missing
data and 11 imputations, the relative efficiency (Rubin
1987) of the imputation process is high across the outcome
measures (in all cases RE [ .99).
Table 4 MANOVA results testing the association between sleep disorder symptoms and gender, hopelessness, and exposure to violence
(ExViol; N = 247)
Corrected model Mediana
Wilkes K Approximate F(6, 235)
Gender .963 1.49
Hopelessness .953 1.93
ExViol .927 3.07
Gender 9 hopelessness .973 1.07
Gender 9 ExViol .976 0.96
Hopelessness 9 ExViol .951 2.00
Gender 9 hopelessness 9 ExViol .937 2.63
a
Median values across 11 imputations
b
Range of values across 11 imputations
531
We chose to eliminate three subscales from the MA-
NOVA analysis. The circadian rhythm and narcolepsy
subscales were eliminated for the reasons discussed pre-
viously. We also eliminated the nightmare subscale,
because only respondents who responded positively to the
nightmare screen question were asked to answer the other
nightmare questions. As a result, it would not have been
reasonable to impute responses to these questions from the
other data, nor would it have been reasonable to eliminate
from the MANOVA analysis the 115 cases that responded
negatively to the screening question. As an alternative, we
conducted a separate univariate ANOVA for this subscale.
We did, however, include the single nightmare screener
item in the MANOVA analysis.
We estimated a full factorial MANOVA model (with
gender, hopelessness, and exposure to violence as inde-
pendent variables) for the five subscales and the nightmare
item, using SAS PROC GLM in conjunction with SAS PROC
MIANALYZE. Table 4 reports median values of Wilk’s K
across the 11 imputed data sets, along with approximate
F statistics and associated probability levels, for each of the
effects. Because of the exploratory nature of the study, we
used a relatively liberal a level (.10) to determine which
effects to explore in univariate analyses. Based on this
criterion, we conducted further analyses of hopelessness,
exposure to violence, hopelessness 9 ExViol, and gender 9
hopelessness 9 ExViol.
Table 5 reports the results of the univariate analyses for
all six variables (five subscales and the nightmare item) as
well as the R2 and statistical significance for each corrected
model. Of initial note, the insomnia, sleepwalking, night-
mare, and daytime sleepiness models are all statistically
significant. Although not large, the variance explained (R2)
by these models is consequential.
With respect to individual effects, hopelessness was a
significant and positive predictor of apnea, daytime
Rangeb
p Wilkes K p
.181 .956–.968 .135–.310
.077 .950–.961 .059–.156
.007 .919–.936 .003–.015
.381 .968–.976 .265–.454
.453 .969–.980 .288–.578
.067 .947–.962 .045–.170
.017 .931–.949 .010–.058
123
 532 J Youth Adolescence (2015) 44:518–542

.019
.037
.031
.001
.015
.001
.001
Table 5 Univariate general linear model slope coefficients, standard errors, and semi-partial g2 values for apnea, insomnia, RLS/PLMD, nightmares, sleepwalking, and daytime sleepiness

Daytime sleepiness
sleepiness (both ps \ .01), insomnia, and RLS/PLMD

g2
(both ps \ .05), and the positive relationship between

5.586 (0.276)***

0.532 (0.174)***
0.764 (0.274)***
hopelessness and nightmares trended toward significance

Slope coefficients and standard errors were derived from 11 multiple imputations of the original dataset. R , F(7,239), and semi-partial g statistics are medians calculated across the 11 imputed datasets
1.177 (0.553)**

1.072 (0.547)*
0.164 (0.349)

0.073 (0.167)
0.166 (0.336)
(p \ .10). Exposure to violence was a significant and
3.22**
.086
positive predictor of insomnia, daytime sleepiness (both
b (seb) ps \ .01), apnea, and nightmares (both ps \ .05), and the
positive relationship between exposure to violence and
.023
RLS/PLMD trended toward significance (p \ .10). The
.014
.022
.000
.010
.003
.007
g2

hopelessness 9 ExViol interaction was a positive predictor

of insomnia (p \ .05), and the positive relationship trended
0.793 (0.064)***
0.305 (0.125)**

0.142 (0.063)**
Nightmaresc

0.072 (0.039)*

-0.023 (0.080) toward significance for RLS/PLMD (p \ .10). Figure 2a

0.190 (0.124)
-0.029 (0.037)
0.102 (0.076)
shows the effect of hopelessness 9 ExViol on insomnia (in
2.71**
.073

this and all of the following figures, high hopelessness and

b (seb)

ExViol are calculated at one standard deviation above their

respective means, and low levels of hopelessness and
.001
.010
.000
.009
.003
.009
.017

ExViol are calculated at one standard deviation below their

g2

means). At low levels of hopelessness, exposure to vio-

1.044 (0.109)***

lence had a small positive effect on insomnia, whereas at

-0.265 (0.130)**
0.115 (0.217)
0.110 (0.068)
-0.001 (0.107)
-0.206 (0.137)
0.166 (0.214)
-0.094 (0.065)
Sleepwalking

high levels of hopelessness, exposure to violence had a

large positive effect on insomnia. The effect of hopeless-
2.09**
.058

b (seb)

ness 9 ExViol on RLS/PLMD was functionally similar but

less dramatic. Finally, the three-way gender 9 hopeless-
ness 9 ExViol interaction predicted sleepwalking
.002
.019
.013
.007
.007
.013
.015

(p \ .05), and the relationship trended toward significance

g2

for RLS/PLMD (p \ .10). Figure 2b shows the effect of

1.942 (0.156)***

0.210 (0.098)**

the three-way interaction on RLS/PLMD. For adolescents

0.279 (0.154)*

0.161 (0.094)*
0.353 (0.189)*
2
0.229 (0.313)

0.255 (0.194)
0.415 (0.308)

(both males and females) with low levels of hopelessness

RLS/PLMDb

and males with high levels of hopelessness, exposure to

b (seb)
.042

violence had little impact on RLS/PLMD. For females with

1.51

high levels hopelessness, however, exposure to violence

.012
.018
.054
.002
.015
.016
.007

had a large positive impact on RLS/PLMD. Figure 2c

g2

shows the relationship between gender 9 hopeless-

The nightmare statistics were based on the single-item nightmare frequency measure
7.467 (0.326)***

1.208 (0.323)***

ness 9 ExViol and sleepwalking. Males with high levels

0.434 (0.205)**

1.284 (0.646)**
0.395 (0.197)**
1.160 (0.653)*

0.321 (0.413)

0.524 (0.394)

of hopelessness showed a small positive change in sleep-

walking as a function of exposure to violence, whereas
Insomnia

b (seb)
3.34***

females with high levels of hopelessness showed a small

.089

negative change in sleepwalking as a function of exposure

.003
.019
.019
.001
.007
.008
.005

to violence. Exposure to violence had a negligible impact

g2

Restless legs syndrome/periodic limb movement disorder

on sleepwalking for males with low levels of hopelessness.

In contrast, exposure to violence had a large positive
3.757 (0.198)***

0.259 (0.128)***
0.423 (0.198)**
0.378 (0.395)

0.125 (0.256)
0.461 (0.394)
0.146 (0.123)
0.271 (0.245)

impact on sleepwalking for females with low levels of

hopelessness. Although generally effect sizes (semi-partial
b (seb)
Apneaa

g2) were low, exposure to violence explained over 5 % of

.041
1.47

the variance in insomnia, and both hopelessness and

* p \ .10; ** p \ .05; *** p \ .01

exposure to violence explained over 3 % of the variance in

Gender 9 hopelessness 9 ExViol

daytime sleepiness.
As a final analysis, we estimated a univariate ANOVA
Hopelessness 9 ExViol
Gender 9 hopelessness

model for the nightmare subscale (N = 140). None of the

effects was statistically significant. While this could per-
Gender 9 ExViol
Corrected model

haps be explained by the relatively small sample for this

Hopelessness
(N = 247)

analysis, little variance in nightmare intensity was

Parameter

Intercept
Gender

ExViol

explained by the model (median R2 = .022 across impu-

2

tations); given the effect sizes observed in the multivariate

R
F

b
a

123
J Youth Adolescence (2015) 44:518–542
analysis (e.g., the ExViol–insomnia relationship), the sta-
tistical power for this analysis was between .7 and .8.
Discussion
Although the study of sleep has enjoyed a dramatic
increase in recent years, the study of sleep among adoles-
cents has lagged behind. This seems counterintuitive,
because adolescence is a time when many developmental
changes occur and consequent changes in sleep patterns
and problems could be observed. On the other hand, situ-
ational factors may interact with development to affect
sleep, making it difficult to separate these two effects. This
creates the potential for inconsistent findings regarding
adolescent sleep.
Poverty, Age, and Sleep
The relationship between age and sleep during adolescence
is one example of this inconsistency. Almost all extant
studies of adolescent sleep have found that quantity of
sleep declines over adolescence, but there is little consen-
sus regarding the developmental progression of sleep
problems during this period. The first finding from our
longitudinal analysis—sleep problems decline during
Fig. 2 a Insomnia as a function of hopelessness and exposure to violence. b RLS/PLMD as a function of gender, hopelessness, and exposure to
violence. c Sleepwalking as a function of gender, hopelessness, and exposure to violence
533
adolescence—would initially seem to further complicate
the long list of inconsistent results. However, our focus on
poverty actually helps clarify these inconsistent results.
Life in impoverished neighborhoods is stressful for
adolescents living in them. One important stressor in
impoverished neighborhoods is violence. Compared with
non-impoverished neighborhoods, impoverished neighbor-
hoods are considerably more violent (Bolland et al. 2007;
Richters and Martinez 1993), and some have been likened
to war zones (Garbarino et al. 1992; Osofsky 1995). Other
potential stressors associated with life in poverty include
high arrest rates (Warner and Coomer 2003), school failure
(Ludwig et al. 2001), food insecurity (Rose 1999), and poor
physical health (Newacheck et al. 2003). The violence and
other stressors in impoverished neighborhoods have been
associated with several negative psychological outcomes,
including post-traumatic stress disorder (Cooley-Quille
et al. 2001) and hopelessness (Bolland et al. 2007).
A particularly important example of how stress and poor
health disproportionately affect sleep in poor neighbor-
hoods is asthma and related upper-respiratory disorders.
Stress and allergens (e.g., mold, dust mites) associated with
substandard housing common in low-income neighbor-
hoods (Bradman et al. 2005) contribute to asthma (Wright
et al. 1998), with estimates of asthma rates among
impoverished urban youth over 20 % higher than among
123
534
non-poor urban youth (Aligne et al. 2000). Asthma, in turn,
interferes significantly with sleep (Jensen et al. 2013).
Duncan (1996) summarized findings showing that the
effects of stress decline with age through early adulthood.
Exactly why this is the case, or how physical and psy-
chological morbidity interact with development to affect
sleep, is unclear. But at some point, stressful events seem
to have diminishing psychological consequences. Two
explanations present themselves. One explanation is that
adolescents who experience stress develop coping strate-
gies to lessen its effects. There is consensus that coping is
influenced by development, although how coping capaci-
ties and strategies change through childhood and adoles-
cence is not yet clear (Zimmer-Gembeck and Skinner
2011). While many coping strategies are positive (e.g.,
problem solving, support seeking), others may be negative
(e.g., giving up on once-desired outcomes).
A second explanation is that adolescents become less
reactive to stressors. This may reflect psychological con-
ditioning (e.g., adolescents become used to, and even come
to expect, negative events, so those events are no longer as
stressful). But it may also reflect a physiological response.
Stressors of all types trigger the immediate production of
cortisol, a hormone that stimulates a fight or flight response
(e.g., increase in heart and breathing rate, selected dilation
and constriction of blood vessels, liberation of metabolic
energy sources). While this reaction is essential for adap-
tation to the challenges of daily life, it can create allostatic
overload (McEwen 2004) if it is not turned off or if it is
turned on too often. The result is blunted stress reactivity,
where cortisol production is reduced and stressful events
generate little reaction. Not surprisingly, blunted stress
reactivity is more common among impoverished popula-
tions than in populations with more resources (Haushofer
et al. 2011).
Reduced stress reactivity, whether psychological or
physiological in nature, helps explain why the conse-
quences of stress decline with age, particularly in impov-
erished neighborhoods. Consider, for example, stressors
related to violence. An old adage holds that violence breeds
violence (Curtis 1963). As adolescents are increasingly
exposed to violence, they may turn to violence as a way of
solving problems. Given that the violence-breeds-violence
loop is cumulative, exposure to violence should increase
with age. The stress associated with any new exposure
should decrease, however, due to better coping, condi-
tioning, and/or blunted stress reactivity. Given that these
stressful incidents accumulate with age, sleep problems
may also decrease with age—a conclusion that reflects our
findings.
Additional examples of cumulative experiences with
stressful events abound in impoverished neighborhoods. In
each case it is reasonable to expect that as the events
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J Youth Adolescence (2015) 44:518–542
become typical rather than unexpected, the experience of
stress might diminish. Being arrested, for example, is
something that many adolescents living in impoverished
neighborhoods expect, but nonetheless the first time it
happens is likely to be the most stressful. As arrest records
accumulate, the stress with any new arrest may decrease.
As another example, during early adolescence, when even
students in impoverished neighborhoods expect to gradu-
ate, school failure is stressful. By mid-adolescence, how-
ever, that expectation may have diminished, and with it, the
stress of school failure may also diminish. Finally, the
incidence of asthma has been shown to decline from
childhood through the adolescent years (Strachan et al.
1996).
All of these observations lead us to conclude that, during
adolescence, psychological health may increase even when
stressors increase, and this is exactly what we found. For
example, the correlation between age and hopelessness
reported for the MYS sample in Table 1 is negative (also
see Bolland et al. 2007). Similarly, using a growth curve
framework, Church et al. (2012) found that feelings of self-
worth increase through adolescence for the MYS sample.
In contrast, Fredriksen et al. (2004) reported a negative
trajectory for self-esteem among a sample of mostly non-
impoverished, European American adolescents in Chicago.
Taken together, these results suggest that age may have an
effect on psychological functioning for impoverished
adolescents that is different from its effect for non-
impoverished adolescents. And given that stress, hope-
lessness, and physical health (e.g., asthma) all have an
impact on sleep quality, the inconsistencies associated with
age and adolescent sleep noted in the introduction can be at
least partially resolved.
Poverty, Gender, and Sleep
A second finding of note involves gender. Although other
studies failed to demonstrate a gender by age effect (e.g.,
Hysing et al. 2013; Laberge et al. 2001) on sleep, our
longitudinal analyses showed that the trajectories of sleep
problems associated with traumatic stress are different for
males and females, with males showing a more dramatic
decline in these trajectories than females. Although the
cross-sectional results did not show a multivariate main
effect across sleep disorders for gender, this null finding
may warrant greater investigation. Notably, all the uni-
variate analyses of sleep disorders except apnea and day-
time sleepiness showed either a main effect for sleepiness
or a three-way interaction among gender, hopelessness, and
exposure to violence. For each of those disorders, females
demonstrated more sleep problems than males. For the
single-item nightmare symptom, we observed a significant
gender effect—although this result should be interpreted
J Youth Adolescence (2015) 44:518–542
cautiously since the multivariate test of the gender effect
was not statistically significant. This finding is consistent
with studies showing higher rates of nightmares in females
than in males (Schredl and Reinhard 2011).
Again, the poverty in the MYS sample may help explain
why in our sample, compared to males, female adolescents
experienced more sleep problems related to traumatic
stress. The explanation invokes gender differences in
response to stress and stressors. Additionally, given the
greater number of stressors inherent in impoverished
neighborhoods, the explanation suggests that impoverished
females should have greater sleep problems than impov-
erished males. Females are more likely than males to report
traumatic stress following exposure to traumatic events
(Green et al. 1991), and the overall prevalence of PTSD is
nearly two times higher than for adolescent males (Kilpa-
trick et al. 2003). Given the high incidence and prevalence
of traumatic events and other stressors in impoverished
neighborhoods, we should expect females living in poverty
to show more psychological distress than males in similar
circumstances (c.f., Copeland and Gorey 2012; Richman
and Jonassaint 2008). This conclusion is also consistent
with findings showing that males with blunted stress
reactivity are more likely than females to manifest psy-
chopathic (O’Leary et al. 2007) and sociopathic (Portnoy
et al. 2014) traits. Given that females have more severe
reactions to traumatic events they observe, we also should
not be surprised to discover gender differences in both the
progression of asthma (Venn et al. 1998) and how it affects
sleep (Jensen et al. 2013).
From Theoretical to Empirical
In the previous discussion, we presented theoretical support
for our findings about the influence of age and gender on
adolescent sleep. In our analyses, we examined two con-
ditions associated with poverty: exposure to violence and
hopelessness. We found in both the longitudinal analysis
and the cross-sectional analysis that hopelessness, exposure
to violence, and the hopelessness by exposure to violence
interaction negatively affect sleep. This latter finding is
consistent with results obtained by Green et al. (1991)
showing that among adolescents, depression is a risk factor
for PTSD following a traumatic event (see also Duncan
1996, for a review of the literature). We also found a sig-
nificant three-way interaction among age, gender, and
exposure to violence in the longitudinal analysis, suggest-
ing that the sleep trajectories of females were more nega-
tively affected by exposure to violence than those of males,
particularly during the early adolescent years. This finding
is partially consistent with the cross-sectional results,
which showed that females with both high levels of
hopelessness and exposure to violence are most susceptible
535
to RLS/PLMD symptoms. The cross-sectional results for
nightmare frequency are not so clear. They showed, how-
ever, that high exposure to violence had the strongest
negative effect on nightmares for females (which is con-
sistent with the longitudinal results). Notably, though, none
of the three predictor variables, either alone or in combi-
nation, affected the severity of nightmares. The results for
sleepwalking showed that exposure to violence had the
strongest negative effect on females with low levels of
hopelessness. This is counterintuitive (with respect to
hopelessness level) and requires further exploration. In
general, though, the similarity of the longitudinal results
and the cross-sectional results suggests that the longitudi-
nal findings with respect to age can potentially be gen-
eralized to more specific (and clinically recognized) sleep
disorders.
Common Etiology of Sleep Disorders
The etiology of sleep disorders is the subject of ongoing
investigation. While results are not definitive, underactive
dopaminergic pathways in the central nervous system have
been linked to both insomnia (Finan and Smith 2013) and
RLS (Allen 2004). Dopamine deficiency and its impact on
sleep have been attributed to genetic factors (Bodenmann
et al. 2009; Roman et al. 2004) and to iron deficiency
(Earley et al. 2000). Although sleep disorders have also
been tied to stress (e.g., Ohayon and Roth 2002; Pynoos
et al. 1987), the effect of stress on dopamine has seldom
been explored in the context of sleep. Yet, this seems to be
particularly important, particularly in adolescence.
Reviewing the effects of stress on dopamine signaling
during adolescence, Sinclair et al. (2014) concluded that
the effect is much greater than during later life. Moreover,
they also concluded that sex hormones, both alone and in
conjunction with stress hormones, affect dopamine sig-
naling in adolescents. These findings provide an additional
explanation for why exposure to violence, and the stress it
creates, may affect sleep disorders among impoverished
minority adolescents, and why the results are more
accentuated for females than for males. Given that the
relationship between stress and dopamine signaling
decreases with age, it might also help explain why we
found that sleep problems decline with age. This area of
research is in its relative infancy, and much more research
needs to be conducted before these questions can be
answered definitively. It does seem useful, however, to
pursue the relationship between exposure to violence and
stress. For example, research should explore how exposure
to violence affects production of cortisol and how exposure
to violence interacts with other aspects of poverty (e.g.,
allergens) that also stimulate cortisol production.
123
536
Implications
Our results have several important implications related to
research and practice. First, with respect to research, the
results show that context is critical in the interpretation of
sleep results. Sleep does not occur in a vacuum. It occurs
among people who are involved in activities of daily life,
complete with the daily hassles and stressors that are part
of their lives. Life thus represents the bookends of sleep:
what went on before, and what is expected after. Our
results and discussion suggest the importance of poverty as
a part of life that surrounds sleep, but certainly there are
other conditions and situations that may also affect sleep
(e.g., immigrant status). While the literature has been quite
thorough in examining how specific risk and protective
factors (e.g., exercise, weekends, depression) may affect
sleep, it has been less thorough in describing how risk and
protective factors associated with certain life conditions or
situations accumulate or interact to affect sleep. Further,
Bronfenbrenner (1979) suggests that experience in any
given context may interact with characteristics of the
individual to affect all aspects of life—with implications
for development and sleep.
A second research implication involves the causes and
consequences of poor sleep. A number of studies (Holley
et al. 2011; Moore et al. 2009; Umlauf et al. 2011; for a
review, see Gregory and Sadeh 2012) show that poor sleep
quality is associated with both emotional (e.g., depression)
and behavioral (e.g., violence and aggression) problems.
Many (although not all) of these studies are cross-sectional,
and they are not able to determine directionality of these
relationships. Longitudinal studies, however, suggest that
the relationship is likely bidirectional (Baglioni et al. 2010;
Shanahan et al. 2014). This suggests that without some
type of intervention, sleep problems and the emotional and
behavioral problems they are associated with will only get
worse over time. Why, then, do our results show that sleep
problems decline with age?
An explanation relies on coping mechanisms as well as
psychological or physiological models of blunted stress
response. Thus, as the cumulative impact of stress and
sleep deprivation increases, the adolescent’s mind and
body develop ways of reducing the impact of the stressors.
But while these coping mechanisms may benefit sleep, they
do not benefit the life chances of the adolescent. Unfortu-
nately, the coping strategy many impoverished adolescents
develop involves giving up on things that were once
important to them (e.g., success in school). The physio-
logical response is even worse, in that by dampening cor-
tisol production the adolescent may not react at all to stress.
This increases the potential for harm (i.e., finding oneself
in a dangerous situation and not benefiting from the fight or
flight response). Thus, sleep quality should not be viewed
123
J Youth Adolescence (2015) 44:518–542
as the canary in the mineshaft (as long as the person is
sleeping well, other aspects of his or her life also are likely
well), for an impoverished adolescent whose life is in
shambles may sleep like a baby. The relationship between
sleep quality and overall quality of life therefore requires
further investigation.
In addition, the factors that affect sleep may well affect
other aspects of adolescence. For example, hopelessness
and exposure to violence may affect delinquency. Delin-
quency, in turn, may affect hopelessness and exposure to
violence. As suggested previously, this bidirectional rela-
tionship may be subject to gender and age effects (Becker
et al. 2012). Therefore, the explanations we present should
be viewed as applicable to adolescent development in
general and the behaviors that accompany development,
rather than uniquely to adolescent sleep.
A third implication involves practice. Because the
response to stress is potentially blunted with age, the bid-
irectionality of the relationship between sleep and emo-
tional and behavioral problems may affect impoverished
youths most during the early years of their adolescence.
This conjecture, however, requires further research to
inform practice. If it is true, then early adolescence is the
time when interventions can be most efficacious. Fortu-
nately, both hopelessness and stress associated with expo-
sure to violence are potentially mutable, even among
adolescents living in poverty. Exactly how to reduce these
psychologically devastating conditions, particularly among
those living in poverty, is underexplored. But given the
consequences of the poor sleep that they contribute to (e.g.,
poor school performance, violence and aggression, somatic
and mental health problems), this is an area that we cannot
afford to ignore. Moreover, given the risk of poor life
outcomes for adolescents living in poverty, any improve-
ment in sleep is likely to yield significant rewards.
A fourth implication also involves practice. We found
clear age and gender effects, suggesting that interventions,
whether aimed directly at sleep or at the contextual factors
that influence sleep, should be targeted to age and gender
differences. In addition, interventions should be sensitive
to the environment in which their target population lives.
The results we presented address some of these issues, but
much more research is needed. Our research should be
considered a starting point rather than an ending point.
Strengths and Limitations
The main strengths of this study are its longitudinal nature
with annual waves of data collection, its size, the range of
ages it examines, and its focus on an understudied and
important population. In cross-sectional studies, assess-
ment of group differences (e.g., between age differences)
assumes that the groups are equivalent (e.g., 13- and
J Youth Adolescence (2015) 44:518–542
14-year olds are equivalent except for their ages). This is
an often-tenuous assumption; even using covariates to
statistically equalize groups assumes that relevant covari-
ates have been identified and measured. In the present
study, we were able to model intra-individual variability
across as many as ten annual observation points per
respondent, using each study participant as his or her own
control. As a result, we can be more certain that results
(e.g., age effects) are truly due to developmental factors.
The strength of the findings associated with age (6.2 % of
the intra-individual variance explained by the two age
variables) attests to that conclusion. Perhaps not coinci-
dentally, the two other cited articles that found a negative
slope for age (Klackenberg 1982; Laberge et al. 2001) both
used longitudinal data. In addition, the sample for the
longitudinal analysis is quite large. While that creates the
potential for finding statistical significance without prac-
tical clinical significance, it also allows us to examine
effects that are not possible to explore with smaller sam-
ples. For example, a smaller sample may not have been
able to demonstrate a three-way interaction between gen-
der, exposure to violence, and age. While the effect size is
small, this result potentially points us to further study of
gender differences in the area of sleep. Of course, the
narrow sleep measure used in the longitudinal analysis
limits the generalizability of the longitudinal findings.
Whereas the correlations between the longitudinal sleep
measure and the Sleep-50 apnea, RLS/PLMD, and sleep-
walking subscales are low (see Table 1), the correlations
between the longitudinal measure and the Sleep-50
insomnia, narcolepsy, circadian rhythm, nightmare, and
daytime sleepiness subscales are more robust, suggesting
that they may tap some underlying construct. Although the
cross-sectional analyses do not benefit from the large
sample or the age range of the longitudinal analysis, they
do have more valid measures of sleep and sleep disorders.
Our focus on impoverished adolescents is a strength in
two ways. First, this population is understudied, and little is
known about the sleep patterns of these youth and how they
are affected by the challenges of growing up in an
impoverished environment. Our findings point out the
importance for sleep of factors that typically have low
prevalence and incidence in more affluent populations (i.e.,
exposure to violence, feelings of hopelessness). Put another
way, the findings point to the importance of context in
studying sleep (and presumably in studying other biologi-
cal and psychological phenomena). The divergent findings
in the sleep literature might be less inconsistent if context
were more carefully controlled. Second, poverty is both a
philosophical and a practical concern that should be the
focus of more study. In 2014, 22 % of children in the
United States lived in families with incomes below the
federal poverty level. Philosophically, it can be argued that
537
the social disenfranchisement of such a large population is
the greatest threat to democracy in America. At a practical
level, children of poverty account for a disproportionate
segment of crime and incarceration, public assistance, and
health costs in the United States. Without a better under-
standing of the unique challenges that this population faces,
we, as a society, can make few inroads into alleviating
either the philosophical or the practical costs associated
with poverty. This study is one small step in that direction.
A clear limitation of this study relates to observed effect
sizes. While some of the effects (e.g., age in the longitu-
dinal analysis) are of medium size in Cohen’s (1988)
parlance, and others fall into the upper range of small (e.g.,
exposure to violence in the longitudinal analysis; exposure
to violence in the univariate cross-sectional analysis of
insomnia; exposure to violence and hopelessness in the
univariate cross-sectional analysis of daytime sleepiness),
most of the statistically significant effects have small or
very small effect sizes. Thus, the results of these analyses
should be interpreted with caution.
Another limitation of the study, which also is a potential
strength, involves its socioeconomically homogeneous
sample from a single geographical location. This certainly
limits the external validity of the results. However, the
homogeneity of the sample also potentially increases the
internal validity of the results by effectively controlling for
unmeasured variable bias and reducing residual con-
founding. This, in turn, has implications for interpreting
effect sizes.
In any study where an exogenous variable (Z) is corre-
lated with the independent variable (X) and the dependent
variable (Y), the relationship between X and Y is con-
founded if Z is not included in the model (Kaufman and
Cooper 2001; Kaufman and Poole 2000); the X–Y rela-
tionship is also confounded if Z is in the model but is
mismeasured. More specifically, if both the factors that
affect sleep (X) and sleep itself (Y) are correlated with
socioeconomic status (Z), for example, then failure to
control adequately for SES will result in residual con-
founding between predictive factors and sleep, potentially
exaggerating the magnitude of any observed statistical
relationship. Unfortunately, socioeconomic status is an
ethereal concept, and neither its meaning nor its measure-
ment is easily understood (Braveman et al. 2005; Oakes
and Rossi 2003; Shavers 2007). Beyond the usual mea-
sured components of income, education, and occupation,
SES also includes a number of other components, including
housing situation, neighborhood characteristics, experi-
ences, and wealth. As a result, SES is often mismeasured or
incompletely measured, resulting in overestimation of
effect sizes and statistical significance of the X–Y relation-
ship. Our study, by severely restricting range in SES,
produces potentially more accurate effect sizes (i.e., the
123
538
true effect of X on Y when the confounding effects of SES
are removed).
Finally, it is important to note limitations with sleep
questionnaires. First, they do not yield clinical diagnoses.
In addition, they are subject to measurement error and
validity issues. A comparison of sleep diaries and sleep
measures based on actigraphy, for example, showed mod-
erate correlations among males for total sleep time
(r = .58) but very low correlations for wake time following
sleep onset (r = .06; Tremaine et al. 2010). This limitation
can be resolved only by comparing survey results with
those generated by PSG conducted in the usual sleep
environment (home monitoring). While this has been done
in a very few studies, the use of comprehensive PSG, or
even actigraphy, has not been implemented among
impoverished adolescents.
Conclusion
Negative consequences of inadequate quantity and quality
of sleep have been well established, but less research has
been conducted into causes of poor sleep among adoles-
cents. Sleep disparities have been associated with poverty
and with ethnic and minority populations, but without
emphasis on adolescents (Patel et al. 2010). This study
addresses these gaps by examining how contextual factors
associated with poverty influence sleep among low-income
adolescents. Two findings stand out. First, exposure to
violence and feelings of hopelessness—two factors com-
mon among adolescents living in impoverished neighbor-
hoods—have negative effects on adolescent sleep, both
independently and multiplicatively. Second, younger ado-
lescents and female adolescents–particularly those who are
exposed to violence—are especially at risk for poor sleep.
These findings are consistent with research that demon-
strates the influence of contextual factors on both the
magnitude and patterns of adolescent behaviors and out-
comes (e.g., Bolland 2003; Lynam et al. 2000; Meier et al.
2008). We explored how age and gender differences in
stress reactivity may explain our results, suggesting that
additional research is needed to further clarify sleep
problems among impoverished adolescents. Because feel-
ings of hopelessness and ways that adolescents process and
react to violent events are both important determinants of
poor sleep and potentially mutable, we suggest that
research be directed toward solutions to these two prob-
lems. Research-informed interventions can then be the
cornerstones of programs developed to address quality of
life issues within this population, including the improve-
ment of sleep quality.
123
J Youth Adolescence (2015) 44:518–542
Acknowledgments The research reported here was partially sup-
ported by the National Institutes of Health Office for Research on
Minority Health through a cooperative agreement administered by the
National Institute for Child Health and Human Development
(HD30060); a grant from the Center for Substance Abuse Treatment,
Substance Abuse and Mental Health Services Administration
(TI13340); a grant from the National Institute on Drug Abuse
(DA017428); a grant from the Southern Nursing Research Society;
The University of Alabama; the Cities of Mobile and Prichard; the
Mobile Housing Board; and the Mobile County Health Department.
Author contributions MGU conceived the study, participated in its
design and coordination, and drafted the manuscript; ACB partici-
pated in study design; managing data; and participated in drafting of
the manuscript; KAB participated in drafting of the manuscript and
interpreting of results; ST participated in analysis and interpretation
of the data; and JMB participated in the study design and coordina-
tion, drafted the manuscript, and participated in analysis and inter-
pretation of the data. All authors read and approved the final
manuscript.
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Mary Grace Umlauf, RN, PhD, FAAN is a professor emerita at The
University of Alabama. She received her doctorate in Nursing from
The University of Texas at Austin. Her research has included sleep,
sleep disorders, adolescent, adult and geriatric health, as well as
nursing faculty development in the Middle East and Japan as a
Fulbright Scholar.
Anneliese C. Bolland, PhD is an assistant research scientist in the
Institute for Social Science Research at The University of Alabama.
She received her doctorate in Educational Research from The
University of Alabama. She has experience organizing and managing
large, longitudinal datasets. Her research interests include hard-to-
reach populations and factors that affect them.
Kathleen A. Bolland, PhD is an assistant professor in the School of
Social Work at The University of Alabama. She received her
doctorate in Social Work from The University of Alabama. Her areas
of research interest include adolescents at risk, program evaluation,
and assessment of student learning outcomes. She was involved in the
administration of the Mobile Youth Survey.
Sara Tomek, PhD is an assistant professor in Educational Research
in the College of Education at The University of Alabama. She
received her doctorate in Psychology from The University of Illinois.
She is a statistical methodologist, working within psychology and
education, and she currently is working on numerous longitudinal
studies using the Mobile Youth Survey data.
John M. Bolland, PhD is a professor emeritus at The University of
Alabama. He received his doctorate in Political Science from The
Ohio State University. He designed and served as principal investi-
gator of the Mobile Youth Survey, and he supervised MYS data
collection each year. His research interests include urban poverty and
adolescents at risk.
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