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The aim of the study is to investigate effects of physical exertion on cognitive deficits from sleep loss under conditions that mimic a firefighting scenario.Twenty-four male participants completed a crossover study design with 3 conditions: total sleep deprivation, sleep disruption (three 60-minute awakenings), and rested control. Participants then completed 50 minutes of a physical exertion task involving treadmill exercise in a heated room while wearing firefighter protective clothing. Vigilant attention and task-switching performance were assessed pre- and post-sleep manipulation and pre- and post-physical exertion. Vigilant attention was also assessed mid-physical exertion.Total sleep deprivation and sleep disruption increased attentional lapses and task-switching RT. Total sleep deprivation additionally reduced task-switching accuracy. Performance after physical exertion improved only for task-switching RT after total sleep deprivation.Physical exertion selectively mitigated task-switching RT deficits from the most severe sleep loss condition, total sleep deprivation.

We examined whether interindividual differences in naturalistic sleep patterns correlate with any deviations from typical brain aging.Our sample consisted of 251 participants without current psychiatric diagnoses (9-25 years; mean [standard deviation] = 17.4 ± 4.52 yr; 58% female) drawn from the Neuroimaging and Pediatric Sleep Databank. Participants completed a T1-weighted structural magnetic resonance imaging scan and 5-7 days of wrist actigraphy to assess naturalistic sleep patterns (duration, timing, continuity, and regularity). We estimated brain age from extracted structural magnetic resonance imaging indices and calculated brain age gap (estimated brain age-chronological age). Robust regressions tested cross-sectional associations between brain age gap and sleep patterns. Exploratory models investigated moderating effects of age and biological gender and, in a subset of the sample, links between sleep, brain age gap, and depression severity (Patient-Reported Outcomes Measurement Information System Depression).Later sleep timing (midsleep) was associated with more advanced brain aging (larger brain age gap), β = 0.1575, pLater midsleep may be one behavioral cause or correlate of more advanced brain aging, particularly among males. Future studies should examine whether advanced brain aging and individual differences in sleep precede the onset of suboptimal cognitive-emotional outcomes in adolescents.

Identifying proximal risk factors for suicidal ideation that are modifiable and relevant for adolescents and young adults is critical for suicide prevention. This study used an intensive monitoring approach to examine whether objectively- and subjectively- measured sleep characteristics predict next-day suicidal ideation occurrence and intensity through affective reactivity to interpersonal events in young people at high risk for suicide.Participants included 59 (13-23 years; 76% White; 75% female) adolescents and young adults undergoing intensive outpatient program treatment for depression and suicidality. Participants completed daily ratings of suicidal ideation, sleep quality, and affective reactivity to positive and negative interpersonal events for up to 3 months (M = 56 days, SD = 24.13). Actigraphy captured behavioral sleep duration and timing. Multilevel modeling was used to evaluate within-person fluctuations in sleep and affective reactivity as predictors of suicidal ideation, and multilevel mediation tested the indirect effects of sleep on suicidal ideation via affective reactivity to interpersonal events.Results indicate significant indirect effects of objectively measured sleep duration and subjective sleep quality on next-day suicidal ideation via affective reactivity to negative and positive interpersonal events, respectively. Shorter-than-usual sleep predicted the presence and intensity of next-day suicidal ideation via heightened affective reactivity to negative interpersonal events. Worse sleep quality than usual predicted next-day suicidal ideation via reduced affective reactivity to positive interpersonal events.Affectivity reactivity is a proximal mechanism through which sleep indices may influence risk for suicidal thinking on a daily basis. Findings highlight the utility of targeting sleep and emotion regulation in suicide prevention among adolescents and young adults at high-risk for suicide.

Study Objectives Adolescence is characterized by significant brain development, accompanied by changes in sleep timing and architecture. It also is a period of profound psychosocial changes, including the initiation of alcohol use; however, it is unknown how alcohol use affects sleep architecture in the context of adolescent development. We tracked developmental changes in polysomnographic (PSG) and electroencephalographic (EEG) sleep measures and their relationship with emergent alcohol use in adolescents considering confounding effects (e.g. cannabis use). Methods Adolescents (n = 94, 43% female, age: 12–21 years) in the National Consortium on Alcohol and Neurodevelopment in Adolescence (NCANDA) study had annual laboratory PSG recordings across 4-years. Participants were no/low drinkers at baseline. Results Linear mixed effect models showed developmental changes in sleep macrostructure and EEG, including a decrease in slow wave sleep and slow wave (delta) EEG activity with advancing age. Emergent moderate/heavy alcohol use across three follow-up years was associated with a decline in percentage rapid eye movement (REM) sleep over time, a longer sleep onset latency (SOL) and shorter total sleep time (TST) in older adolescents, and lower non-REM delta and theta power in males. Conclusions These longitudinal data show substantial developmental changes in sleep architecture. Emergent alcohol use during this period was associated with altered sleep continuity, architecture, and EEG measures, with some effects dependent on age and sex. These effects, in part, could be attributed to the effects of alcohol on underlying brain maturation processes involved in sleep–wake regulation.

BackgroundGrowing evidence indicates that sleep characteristics predict future substance use and related problems. However, most prior studies assessed a limited range of sleep characteristics, studied a narrow age span, and included few follow-up assessments. Here, we used six annual assessments from the National Consortium on Alcohol and Neurodevelopment in Adolescence (NCANDA) study, which spans adolescence and young adulthood with an accelerated longitudinal design, to examine whether multiple sleep characteristics in any year predict alcohol and cannabis use the following year.MethodsThe sample included 831 NCANDA participants (423 females; baseline age 12-21years). Sleep variables included circadian preference, sleep quality, daytime sleepiness, the timing of midsleep (weekday/weekend), and sleep duration (weekday/weekend). Using generalized linear mixed models (logistic for cannabis; ordinal for binge severity), we tested whether each repeatedly measured sleep characteristic (years 0-4) predicted substance use (alcohol binge severity or cannabis use) the following year (years 1-5), covarying for age, sex, race, visit, parental education, and previous year's substance use.ResultsGreater eveningness, more daytime sleepiness, later weekend sleep timing, and shorter sleep duration (weekday/weekend) all predicted more severe alcohol binge drinking the following year. Only greater eveningness predicted a greater likelihood of any cannabis use the following year. Post-hoc stratified exploratory analyses indicated that some associations (e.g., greater eveningness and shorter weekend sleep duration) predicted binge severity only in female participants, and that middle/high school versus post-high school adolescents were more vulnerable to sleep-related risk for cannabis use.ConclusionsOur findings support the relevance of multiple sleep/circadian characteristics in the risk for future alcohol binge severity and cannabis use. Preliminary findings suggest that these risk factors vary based on developmental stage and sex. Results underscore a need for greater attention to sleep/circadian characteristics as potential risk factors for substance use in youth and may inform new avenues to prevention and intervention.

Sleep changes over the human life span, and it does so across multiple dimensions. We used individual-level cross-sectional data to characterize age trends and sex differences in actigraphy and self-report sleep dimensions across the healthy human life span.The Pittsburgh Lifespan Sleep Databank consists of harmonized participant-level data from sleep-related studies conducted at the University of Pittsburgh (2003-2019). We included data from 1065 (n = 577 female; 21 studies) Pittsburgh Lifespan Sleep Databank participants aged 10 to 87 years without a major psychiatric, sleep, or medical condition. All participants completed wrist actigraphy and the self-rated Pittsburgh Sleep Quality Index. Main outcomes included actigraphy and self-report sleep duration, efficiency, and onset/offset timing, and actigraphy variability in midsleep timing.We used generalized additive models to examine potentially nonlinear relationships between age and sleep characteristics and to examine sex differences. Actigraphy and self-report sleep onset time shifted later between ages 10 and 18 years (23:03-24:10 [actigraphy]; 21:58-23:53 [self-report]) and then earlier during the 20s (00:08-23:40 [actigraphy]; 23:50-23:34 [self-report]). Actigraphy and self-report wake-up time also shifted earlier during the mid-20s through late 30s (07:48-06:52 [actigraphy]; 07:40-06:41 [self-report]). Self-report, but not actigraphy, sleep duration declined between ages 10 and 20 years (09:09-07:35). Self-report sleep efficiency decreased over the entire life span (96.12-93.28), as did actigraphy variability (01:54-01:31).Awareness of age trends in multiple sleep dimensions in healthy individuals-and explicating the timing and nature of sex differences in age-related change-can suggest periods of sleep-related risk or resilience and guide intervention efforts.

PURPOSE OF REVIEW: Suicide is currently the second leading cause of death among youth. Identification of modifiable near-term risk factors can inform suicide prevention strategies. One promising, readily assessed factor is sleep. We critically review the literature on sleep and suicidal thoughts and behaviors among youth. RECENT FINDINGS: Most studies examining the youth sleep-suicidality relationship are from epidemiological samples in which both sleep problems and suicidality were assessed over variable timeframes using limited items from scales not designed to measure these constructs. Nonetheless, these data overwhelmingly support an association between suicidality and a range of sleep difficulties (e.g., insomnia, short/long sleep, weekend oversleep), above and beyond depressive symptoms. Limited studies include clinical samples or prospective designs. We review potential mechanisms and present a developmentally-informed integrative model. SUMMARY: Literature supports a clear association between sleep difficulties and youth suicidality. Future directions include prospective longitudinal studies and targeted prevention efforts.

Studies have established a clear relationship between subjective sleep problems and the continuum of suicidality in adolescents. These studies are primarily cross-sectional in nature and conducted with epidemiological and depressed clinical samples. More recent studies focus on prospective data. Herein, we provide an update on current studies on the sleep-suicide association among youth. To further the critical mission of youth suicide prevention, future directions include more nuanced study of sleep employing a sleep health framework, longitudinal studies employing both objective and subjective sleep measures, fine-grained temporal associations between these constructs and their fluctuations over time, as well as enhanced understanding of the mechanisms underlying these associations.

Sleep and circadian rhythm disruptions are symptoms of, and hypothesized underlying mechanisms in, seasonal depression. Discrepant observational findings and mixed responses to sleep/circadian-based treatments suggest heterogenous sleep and circadian disruptions in seasonal depression, despite these disruptions historically conceptualized as delayed circadian phase and hypersomnia. This study used a data-driven cluster analysis to characterize sleep/circadian profiles in seasonal depression to identify treatment targets for future interventions. Biobehavioral measures of sleep and circadian rhythms were assessed during the winter in individuals with Seasonal Affective Disorder (SAD), subsyndromal-SAD (S-SAD), or nonseasonal, never depressed controls (total sample N = 103). The following variables were used in the cluster analysis: circadian phase (from dim light melatonin onset), midsleep timing, total sleep time, sleep efficiency, regularity of midsleep timing, and nap duration (all from wrist actigraphy). Sleep and circadian variables were compared across clusters and controls. Despite limited sleep/circadian differences between diagnostic groups, there were two reliable (Jaccard Coefficients0.75) sleep/circadian profiles in SAD/S-SAD individuals: a 'Disrupted sleep' cluster, characterized by irregular and fragmented sleep and an 'Advanced' cluster, characterized by early sleep and circadian timing and longer total sleep times (7.5 h). Clusters did not differ by depression severity. Midsleep correlated with DLMO (r = 0.56), irregularity (r = 0.3), and total sleep time (r = -0.27). Sleep and circadian disruptions in seasonal depression are not uniformly characterized by hypersomnia and circadian phase delay. Presence of distinct sleep and circadian subgroups in seasonal depression may predict successful treatment response. Prospective assessment and tailoring of individual sleep and circadian disruptions may reduce treatment failures.

BackgroundHypersomnolence has been considered a prominent feature of seasonal affective disorder (SAD) despite mixed research findings. In the largest multi-season study conducted to date, we aimed to clarify the nature and extent of hypersomnolence in SAD using multiple measurements during winter depressive episodes and summer remission.MethodsSleep measurements assessed in individuals with SAD and nonseasonal, never-depressed controls included actigraphy, daily sleep diaries, retrospective self-report questionnaires, and self-reported hypersomnia assessed via clinical interviews. To characterize hypersomnolence in SAD we (1) compared sleep between diagnostic groups and seasons, (2) examined correlates of self-reported hypersomnia in SAD, and (3) assessed agreement between commonly used measurement modalities.ResultsIn winter compared to summer, individuals with SAD (n = 64) reported sleeping 72 min longer based on clinical interviews (p < 0.001) and 23 min longer based on actigraphy (p = 0.011). Controls (n = 80) did not differ across seasons. There were no seasonal or group differences on total sleep time when assessed by sleep diaries or retrospective self-reports (p's > 0.05). Endorsement of winter hypersomnia in SAD participants was predicted by greater fatigue, total sleep time, time in bed, naps, and later sleep midpoints (p's < 0.05).ConclusionDespite a winter increase in total sleep time and year-round elevated daytime sleepiness, the average total sleep time (7 h) suggest hypersomnolence is a poor characterization of SAD. Importantly, self-reported hypersomnia captures multiple sleep disruptions, not solely lengthened sleep duration. We recommend using a multimodal assessment of hypersomnolence in mood disorders prior to sleep intervention.

Objective Youth who have a parent with recurrent depression are at high risk for mental health problems. There is a need to identify transdiagnostic and clinically actionable mechanisms that explain higher rates of psychopathology among high-risk youth. The present study sought to examine whether offspring of depressed parents exhibit greater parent- and self-reported sleep disturbance, shorter sleep duration, and later sleep midpoint compared to youth without any parental psychopathology. Method Participants included 82 youth, including 41 youth (ages 9–13; mean age = 11.07 years; 46% female) deemed to be at high-risk based on having a parent with a recurrent depression history, and 41 (mean age = 11.16 years; 49% female) at low-risk based on having parents without any history of psychopathology. Youth and their parents completed measures of youth sleep disturbance, and youth completed measures of sleep duration and midpoint using a daily sleep diary for 9 days. Results Offspring of parents with depression exhibited more sleep disturbance (e.g., problematic nighttime behaviors and daytime sleepiness) than low-risk youth as reported by both parents and youth. For parent-reported sleep disturbance, there were also sex differences. High-risk girls had more sleep disturbance than high-risk boys or low-risk girls. There were no group differences for daily sleep duration and midpoint. Conclusion Sleep disturbance may be an important area for assessment among offspring of parents with depression. Our findings highlight one potential transdiagnostic risk factor that may emerge among high-risk youth, and sex-specific differences in sleep disturbance, which have implications for prevention and intervention.

Background Restricting time in bed improves insomnia symptoms, but the neural mechanisms for this effect are unknown. Total and partial acute sleep restriction may be useful paradigms for elucidating these effects. We examined the impact of acute sleep restriction on cerebral glucose metabolism during non-rapid eye movement (NREM) sleep in individuals with primary insomnia (n = 17) and good sleep (n = 19). Methods Participants underwent [18F]fluorodeoxyglucose positron emission tomography scans during baseline and recovery NREM sleep following one night of partial or total sleep restriction. We compared group differences in baseline-recovery changes, as well as main effects of group and condition (baseline vs. recovery NREM sleep), for relative regional cerebral metabolic rate for glucose (rCMRglc), whole-brain glucose metabolism, and sleep quality. Results Relative rCMRglc was significantly lower during recovery NREM sleep compared to baseline in the left frontoparietal cortex, medial frontal cortex, posterior cingulate cortex, and thalamus, with no significant group differences. Good sleepers, but not insomnia patients, had lower whole-brain glucose metabolism during recovery NREM sleep compared to baseline. Acute sleep restriction improved sleep quality in individual with insomnia. Subgroup analyses including only participants who underwent partial sleep restriction yielded the same pattern of findings. Conclusion Individuals with insomnia and good sleepers showed similar relative rCMRglc responses to acute sleep restriction. Brain regions showing the greatest baseline-recovery changes in both groups included regions previously shown to have smaller sleep-wake differences in patients with primary insomnia. Acute sleep restriction, and by extension sleep restriction therapy, may impact regional metabolic alterations that characterize insomnia.

Study Objectives Structural brain maturation and sleep are complex processes that exhibit significant changes over adolescence and are linked to many physical and mental health outcomes. We investigated whether sleep–gray matter relationships are developmentally invariant (i.e. stable across age) or developmentally specific (i.e. only present during discrete time windows) from late childhood through young adulthood. Methods We constructed the Neuroimaging and Pediatric Sleep Databank from eight research studies conducted at the University of Pittsburgh (2009–2020). Participants completed a T1-weighted structural MRI scan (sMRI) and 5–7 days of wrist actigraphy to assess naturalistic sleep. The final analytic sample consisted of 225 participants without current psychiatric diagnoses (9–25 years). We extracted cortical thickness and subcortical volumes from sMRI. Sleep patterns (duration, timing, continuity, regularity) were estimated from wrist actigraphy. Using regularized regression, we examined cross-sectional associations between sMRI measures and sleep patterns, as well as the effects of age, sex, and their interaction with sMRI measures on sleep. Results Shorter sleep duration, later sleep timing, and poorer sleep continuity were associated with thinner cortex and altered subcortical volumes in diverse brain regions across adolescence. In a discrete subset of regions (e.g. posterior cingulate), thinner cortex was associated with these sleep patterns from late childhood through early-to-mid adolescence but not in late adolescence and young adulthood. Conclusions In childhood and adolescence, developmentally invariant and developmentally specific associations exist between sleep patterns and gray matter structure, across brain regions linked to sensory, cognitive, and emotional processes. Sleep intervention during specific developmental periods could potentially promote healthier neurodevelopmental outcomes.

Most adolescents get less than the recommended 8-10 hr of sleep per night. Functional deficits from lack of sleep include disruption of working memory. Adult neuroimaging studies of sleep deprivation suggest diminished responses in task-related brain networks if performance degrades, but compensatory increased responses with maintained performance. This study utilized functional magnetic resonance imaging to examine compensatory and diminished brain responses in adolescents during working memory performance, comparing chronic sleep restriction and healthy sleep duration. Thirty-six healthy adolescents, 14-17 years old, experienced a 3-week protocol: (a) sleep phase stabilization; (b) sleep restriction (~6.5 hr nightly); and (c) healthy sleep duration (~9 hr nightly). After each sleep manipulation, we acquired functional magnetic resonance imaging with an NBack working memory task with four difficulty levels (0 to 3-back). NBack performance degraded with higher task difficulty, but without a detectable effect of sleep duration. ANOVA revealed main effects of both NBack difficulty and sleep in widespread brain networks. Planned contrasts showed that, compared with healthy sleep, sleep restriction resulted in greater medial prefrontal activation and weaker activation in the precuneus for the most difficult task condition. During sleep restriction, we found compensatory functional responses in brain regions that process sensory input and vigilance. However, adolescents also showed impaired performance and diminished brain responses during the hardest task level under a week of chronic sleep restriction. Chronic sleep restriction during adolescence is common. Understanding the impact of ongoing functional compensation and performance breakdown during this developmental period can have important implications for learning and educational strategies.

ImportanceStructural brain maturation and sleep are complex processes that exhibit significant changes over adolescence and are linked to healthy physical and mental development. The precise timing and magnitude of these changes influence function throughout the lifespan. However, the relationships between gray matter structure and sleep patterns during adolescence are not fully understood. A detailed characterization of brain-sleep associations during this sensitive period is crucial for understanding factors contributing to optimal neurodevelopmental trajectories in adolescence.ObjectiveTo investigate whether sleep-gray matter relationships are developmentally-invariant (i.e., stable across age) or developmentally-specific (i.e., only present during discrete time windows) from late childhood through young adulthood.SettingThe Neuroimaging and Pediatric Sleep Databank was constructed from 8 research studies conducted at the University of Pittsburgh between 2009 and 2020.ParticipantsThe final sample consisted of 240 participants without current psychiatric diagnoses (9-25 years), and with good quality sleep tracking and structural MRI (sMRI) data.DesignParticipants completed a sMRI scan and 5-7 days of wrist actigraphy to assess naturalistic sleep. We examined cross-sectional associations between sMRI measures and sleep patterns, as well as the effects of age, sex, and their interaction with sMRI measures on sleep.Main Outcome(s) and Measure(s)Using Freesurfer software, we extracted cortical thickness and subcortical volumes from T1-weighted MRI. Sleep patterns (duration, timing, continuity, regularity) were estimated from wrist actigraphy.ResultsShorter sleep duration, later sleep timing, and poorer sleep continuity were associated with a stable pattern of thinner cortex and altered subcortical volumes in diverse brain regions across adolescence. In a discrete subset of regions (e.g., posterior cingulate), thinner cortex was associated with these sleep patterns from late childhood through early-to-mid adolescence, but not in late adolescence and young adulthood.Conclusions and RelevanceIn childhood and adolescence, developmentally-invariant and developmentally-specific associations exist between sleep patterns and gray matter structure, in a wide array of brain regions linked to many sensory, cognitive, and emotional processes. Sleep intervention during specific developmental periods could potentially promote healthier neurodevelopmental outcomes.KEY POINTSQuestionDoes age modulate associations between gray matter structure and actigraphic sleep patterns across adolescent development?FindingsThis cross-sectional study reports stable associations between regional gray matter structure and shorter duration, later timing, and poorer continuity of sleep from ages 9 to 25 years-old, as well as developmentally-specific associations that are present only from late childhood to early-to-mid adolescence.MeaningStronger coupling of gray matter and sleep patterns from late childhood to early-to-mid adolescence potentially implicates this discrete developmental window as a period of vulnerability to adverse sleep-brain interactions. Sleep intervention during this developmental stage may support healthier neurodevelopmental trajectories.

A retinal subsensitivity to environmental light may trigger Seasonal Affective Disorder (SAD) under low wintertime light conditions. The main aim of this study was to assess the responses of melanopsin-containing retinal ganglion cells in participants (N= 65) diagnosed with unipolar SAD compared to controls with no history of depression. Participants attended a summer visit, a winter visit, or both. Retinal responses to light were measured using the post-illumination pupil response (PIPR) to assess melanopsin-driven responses in the non-visual light input pathway. Linear mixed-effects modeling was used to test a group*season interaction on the Net PIPR (red minus blue light response, percent baseline). We observed a significant group*season interaction such that the PIPR decreased from summer to winter significantly in the SAD group while not in the control group. The SAD group PIPR was significantly lower in winter compared to controls but did not differ between groups in summer. Only 60% of the participants underwent an eye health exam, although all participants reported no history of retinal pathology, and eye exam status was neither associated with outcome nor different between groups. This seasonal variation in melanopsin driven non-visual responses to light may be a risk factor for SAD, and further highlights individual differences in responses to light for direct or indirect effects of light on mood.

Objectives Few studies have sought to evaluate how screen media use relates to symptoms of sleep-wake disturbances. To extend these prior studies in a large sample of children, this study examined associations of different types of screen media with symptom severity of different classes of sleep-wake disturbances. This study was preregistered here. Design This study utilized the baseline cross-sectional survey administered within the Adolescent Brain Cognitive Development Study (ABCD; Release 2.0). Participants ABCD recruited over 11,000 U.S. children age 9–10 across 21 study sites using an epidemiologically-informed school-based recruitment strategy. Measurements Children reported typical weekend and weekday use of TV, video, video game, social media, texting, and video chat, and parents completed reports of the child's symptom severity of sleep-wake disturbances via the Sleep Disturbance Scale for Children. Results Greater screen media use, TV, video, and video game use, was associated with decreased sleep duration, increased sleep onset latency as well as greater excessive sleepiness, insomnia, and overall sleep disturbance symptom severity. Use of these screen medias were also associated with clinically relevant sleep problems. Ethnoracial differences emerged in screen use and sleep, but did not moderate the association between screen use and sleep. Conclusions Greater use of screen medias was not just associated with longer sleep onset latency and shorter sleep duration, but also increased severity of multiple types of sleep-wake disturbances. Future research should use longitudinal designs to determine the direction of these associations in adolescent populations.

Purpose The aim of the study was to investigate associations between sleep disturbances and mental health in adolescents. Methods Data are from a national sample of 11,670 U.S. participants (5,594 females, aged 9–10 years, 63.5% white) in the Adolescent Brain Cognitive Development study. Initial longitudinal analyses were conducted for a subset of the sample (n = 4,951). Measures of youth sleep disturbance (disorders of initiating and maintaining sleep, sleep–wake transition disorders, and disorders of excessive somnolence) and “typical” total sleep time (number of hours slept on most nights in the past 6 months) were obtained from the parent-report Sleep Disturbance Scale (Data Release 2.0). Parent-report measures of youth mental health (depression, internalizing, and externalizing behaviors) from the Child Behavior Checklist and typical screen time were included. Results At baseline, greater sleep disturbance and shorter total sleep time were associated with greater internalizing, externalizing, and depression scores. After controlling for baseline mental health symptoms, baseline sleep disturbance significantly predicted depression and internalizing and externalizing scores at 1-year follow-up. A significant interaction with sex indicated that the association between disorders of excessive somnolence and depression 1 year later was steeper for girls, compared with boys (p Conclusions Sleep disturbances predicted future mental health, particularly depression in this young sample, highlighting the potential to harness sleep as a tool to mitigate the persistence of depression across early adolescence and potentially prevent an adolescent onset of major depressive disorder.

Introduction Social media (SM) use has been increasingly recognized as a potential contributor to poor sleep. Few studies have examined SM use and sleep using ecological momentary assessment (EMA), compared different types of media use (SM, television, gaming), or examined whether youth at high and low familial risk for depression are differentially affected by SM use. Methods The current study included 76 youth (46% female; Mean age = 11.28 years) who were recruited based on parental history of recurrent depression (N = 35 high risk; N = 41 low risk) in the United States. Youth completed a 9-day EMA protocol, which included current activity at time of prompt and daily sleep onset and offset times. Regression and multilevel models were conducted to examine the effects of media use on sleep. Results Results indicated that youth who used more SM (mean and number of days) went to sleep later, but did not have shorter sleep duration. Youth with more SM use also had higher levels of variability of both sleep timing and sleep duration across the 9-day period. There were no effects of gaming or TV on sleep, and youth at high risk for depression did not have differences in SM use or its effects on sleep compared to low-risk youth. Conclusions These findings indicate a unique impact of SM use on sleep timing and variability for youth (regardless of risk status), which may suggest a unique and modifiable pathway through which SM use contributes to poor health.

Identifying objectively measurable seasonal changes in 24-hour activity patterns (rest-activity rhythms or RARs) that occur in seasonal affective disorder (SAD) could help guide research and practice towards new monitoring tools or prevention targets. We quantified rest-activity rhythms (RARs) from actigraphy data using non-parametric and extended cosine based approaches, then compared RARs between people with SAD and healthy controls in the summer (n=70) and winter seasons (n=84). We also characterized the within-person seasonal RAR changes that occurred in the SAD (n=19) and control (n=26) participants who contributed repeated measures. Only controls had significant winter increases in RAR fragmentation (intra-daily variability; in controls mean winter-summer changes (log scale) = 0.05, 0.21 standard deviation, p = 0.03). In SAD participants only, estimated evening settling times (down-mesor) were an average of 30 minutes earlier in the winter compared with the summer (1-hour standard deviation, p=0.045). These RAR characteristics correlated with greater fatigue (Spearman |r|=0.36) but not depression symptom severity. Additional research is needed to ascertain why healthy controls, but not people with SAD, appear to have increased RAR fragmentation in the winter. People with SAD lacked this increase in RAR fragmentation, and instead had earlier evening setting in the winter. Prospective and intervention studies with greater temporal resolution are warranted to ascertain how these seasonal behavioral differences relate to fatigue pathophysiology in SAD. Future research is needed to determine whether extending the winter active period, even in relatively fragmented bouts, could help reduce the fatigue symptoms common in SAD.

Sleep homeostasis and circadian function are important maintaining factors for optimal health and well-being. Conversely, sleep and circadian disruptions are implicated in a variety of adverse health outcomes, including substance use disorders. These risks are particularly salient during adolescence. Adolescents require 8 to 10 hours of sleep per night, although few consistently achieve these durations. A mismatch between developmental changes and social/environmental demands contributes to inadequate sleep. Homeostatic sleep drive takes longer to build, circadian rhythms naturally become delayed, and sensitivity to the phase-shifting effects of light increases, all of which lead to an evening preference (i.e., chronotype) during adolescence. In addition, school start times are often earlier in adolescence and the use of electronic devices at night increases, leading to disrupted sleep and circadian misalignment (i.e., social jet lag). Social factors (e.g., peer influence) and school demands further impact sleep and circadian rhythms. To cope with sleepiness, many teens regularly consume highly caffeinated energy drinks and other stimulants, creating further disruptions in sleep. Chronic sleep loss and circadian misalignment enhance developmental tendencies toward increased reward sensitivity and impulsivity, increasing the likelihood of engaging in risky behaviors and exacerbating the vulnerability to substance use and substance use disorders. We review the neurobiology of brain reward systems and the impact of sleep and circadian rhythms changes on addiction vulnerability in adolescence and suggest areas that warrant additional research.

Objective Theoretical models posit that stressors contribute to the onset and maintenance of bipolar disorder in adolescence through disruptions in stress physiology, but physiological response to stressors has not been evaluated in adolescents with bipolar illness. The present study tests the hypothesis that adolescents with bipolar disorder will have greater reactivity to a laboratory social stress task than healthy adolescents. Method Adolescents with bipolar illness (n = 27) and healthy adolescents (n = 28) completed a modified version of the Trier Social Stress Task. Stress response was assessed using high frequency heart rate variability (HF-HRV), heart rate (HR), mean arterial blood pressure (MAP), salivary cortisol, and subjective stress. Multilevel models were used to test for group differences in resting-state physiology, and stress reactivity and recovery. Results Adolescents with bipolar disorder had greater reactivity in HF-HRV (z = 3.32), but blunted reactivity in MAP (z = −3.08) and cortisol (z = −2.60), during the stressor compared to healthy adolescents. They also had lower resting HF-HRV (z = −3.49) and cortisol (z = −2.86), and higher resting HR (z = 3.56), than healthy adolescents. Conclusions These results indicate that bipolar disorder is associated with disruptions in autonomic and endocrine response to stress during adolescence, including greater HF-HRV reactivity. Further research should evaluate whether these individual differences in stress physiology precede and predict the onset of mood episodes.

During the course of adolescence, reductions occur in cortical thickness and gray matter (GM) volume, along with a 65% reduction in slow wave (delta) activity during sleep (SWA) but empirical data linking these structural brain and functional sleep differences, is lacking. Here we investigated specifically whether age-related differences in cortical thickness and GM volume and cortical thickness accounted for the typical age-related difference in slow wave (delta) activity (SWA) during sleep. 132 healthy participants (age: 12–21 years) from the National Consortium on Alcohol and NeuroDevelopment in Adolescence (NCANDA) study were included in this cross-sectional analysis of baseline polysomnographic, electroencephalographic (EEG) and magnetic resonance imaging (MRI) data. By applying mediation models we identified a large, direct effect of age on SWA in adolescents, which explained 45% of the variance in ultra-SWA (0.3 to 1Hz) and 52% of the variance in delta-SWA (1Hz to

Author(s): Hasler, Brant P; Franzen, Peter L; de Zambotti, Massimiliano; Prouty, Devin; Brown, Sandra A; Tapert, Susan F; Pfefferbaum, Adolf; Pohl, Kilian M; Sullivan, Edith V; De Bellis, Michael D; Nagel, Bonnie J; Baker, Fiona C; Colrain, Ian M; Clark, Duncan B | Abstract: BackgroundAbundant cross-sectional evidence links eveningness (a preference for later sleep-wake timing) and increased alcohol and drug use among adolescents and young adults. However, longitudinal studies are needed to examine whether eveningness is a risk factor for subsequent alcohol and drug use, particularly during adolescence, which is marked by parallel peaks in eveningness and risk for the onset of alcohol use disorders. This study examined whether eveningness and other sleep characteristics were associated with concurrent or subsequent substance involvement in a longitudinal study of adolescents.MethodsParticipants were 729 adolescents (368 females; age 12 to 21nyears) in the National Consortium on Alcohol and Neurodevelopment in Adolescence study. Associations between the sleep variables (circadian preference, sleep quality, daytime sleepiness, sleep timing, and sleep duration) and 3 categorical substance variables (at-risk alcohol use, alcohol bingeing, and past-year marijuana use [y/n]) were examined using ordinal and logistic regression with baseline age, sex, race, ethnicity, socioeconomic status, and psychiatric problems as covariates.ResultsAt baseline, greater eveningness was associated with greater at-risk alcohol use, greater bingeing, and past-year use of marijuana. Later weekday and weekend bedtimes, but not weekday or weekend sleep duration, showed similar associations across the 3 substance outcomes at baseline. Greater baseline eveningness was also prospectively associated with greater bingeing and past-year use of marijuana at the 1-year follow-up, after covarying for baseline bingeing and marijuana use. Later baseline weekday and weekend bedtimes, and shorter baseline weekday sleep duration, were similarly associated with greater bingeing and past-year use of marijuana at the 1-year follow-up after covarying for baseline values.ConclusionsFindings suggest that eveningness and sleep timing may be under recognized risk factors and future areas of intervention for adolescent involvement in alcohol and marijuana that should be considered along with other previously identified sleep factors such as insomnia and insufficient sleep.

Introduction Hypersomnolence is commonly reported in Major Depressive Disorder with Seasonal Pattern (Seasonal Affective Disorder; SAD). However, self-reported hypersomnolence may conflate long sleep duration, daytime sleepiness, fatigue, increased time in bed, or maladaptive sleep cognitions, undermining treatment efforts. Methods Eighty-eight participants ages 18-65 years old were recruited during the winter (SAD = 43, Control = 45). Depression severity was assessed by a clinician rated interview, and self-reported hypersomnolence was determined by assessing self-reported sleep duration. Participants wore an Actiwatch for 4-14 days and completed self-report measures of daytime sleepiness and fatigue. We performed a hierarchical linear regression to determine which factors best explain self-reported winter hypersomnolence: actigraphic total sleep time (TST), time in bed (TIB), depression severity, sleepiness, or fatigue. Due to collinearity of TST and TIB, we separated those variables into two models predicting hypersomnolence. Results SAD participants endorsed greater hypersomnolence than controls during the winter (B = .714; p < .001). In model 1, TST (OR(1,14) = .024, p Conclusion We found evidence for the multifaceted etiology of self-reported hypersomnolence. Daytime sleepiness, sleep duration, time in bed, and the shared variance between fatigue and depression severity all explained self-reported hypersomnolence. Treatment of hypersomnolence should include actigraphy, and should be individually tailored based on presentation. Support NIMH K.A.R. MH103303

Introduction Social media use is a risk factor for poor sleep among adolescents. It remains unclear whether social media use before bed impacts later sleep timing or whether youth turn to social media because of sleep problems, which impacts sleep timing. No study to date has examined this relationship using prospective designs and objective sleep measures among high-risk adolescents, who may be particularly vulnerable to social media use. Methods As a preliminary test of this relationship, 25 adolescents and young adults in an intensive outpatient program for depression and suicidality completed baseline measures of social media use and wore actiwatches for up to three months. Social media use included: 1) minutes of use within 2 hours of going to sleep, and 2) frequency of social media use due to difficulty falling or staying asleep. To examine social media as a predictor of sleep timing over the next month, actigraphic measures of sleep timing (i.e., onset) were used in the first month after baseline. Results Multilevel modeling indicated that higher levels of social media use in the 2 hours before bed (mean = 46.94 minutes) predicted later sleep timing (B = .02; SE = .01; p= .003). Similarly, higher frequency of social media use due to perceived sleep problems predicted later sleep timing (B = .22; SE = .11; p= .04). Models covaried for age, gender, and prior-day depressed mood. When simultaneously entered, only minutes of social media use in the 2 hours before bed significantly predicted later sleep timing. Conclusion Findings suggest that the relationship between social media use and sleep timing among adolescents with depression and suicidality may be driven by both social media use before bed and media use due to sleep problems. Research assessing objective social media use and daily relationships are needed to further disentangle this relationship. Support Jessica L Hamilton is supported by a T32 fellowship from NHLBI (HL082610; PI: Buysse). This research is supported by grants from the American Foundation for Suicide Prevention and University of Pittsburgh Clinical and Translational Science Institute.

Introduction Seasonal affective disorder (SAD) increases risk for attention-deficit/hyperactivity disorder (ADHD), although the mechanism linking SAD and ADHD is unknown. Prior research has identified insomnia and delayed sleep phase in both ADHD and SAD. We hypothesized that sleep duration and timing in SAD would be associated with the severity of ADHD symptoms. Methods Adults with SAD (n = 45) and subsyndromal SAD (S-SAD; n = 18) aged 19-66 years from Pittsburgh, PA., were assessed for ADHD symptoms, self-report sleep quality, depression severity, and daytime sleepiness in the Winter. Participants wore an Actiwatch for 4-14 days, from which we calculated sleep-onset latency, total sleep time, sleep midpoint, and sleep efficiency. We conducted a hierarchical multivariate linear regression to determine if sleep characteristics predict ADHD symptom severity in our sample while controlling for depressive symptoms. Age and gender were added in Step 1, seasonal depression severity in Step 2, actigraphy-based total sleep time, sleep onset latency, midpoint, and efficiency in Step 3, and self-reported sleep quality and daytime sleepiness in Step 4. Results Participants mostly scored in the “likely” or “highly likely” ADHD range (87.30%, n=55), higher than the national prevalence rate (4.4%). When controlling for age, gender, and depression severity, only shorter actigraphy-based total sleep time was associated with higher ADHD symptom severity (β=-0.30, p Conclusion Our results suggest that individuals with SAD who experience daytime sleepiness and/or possibly shorter actigraphy-based sleep duration experience higher ADHD symptom severity. Treatments like Trans-C or CBT-I to improve daytime sleepiness and sleep duration may be indicated for SAD patients who present with comorbid ADHD symptoms. Support NIMH K.A.R. MH103303

OBJECTIVE Sleep disruption contributes to the pathophysiology of mental disorders, particularly bipolar illness, but the biobehavioral mechanisms of this relationship are insufficiently understood. This study evaluated sleep duration, timing, and variability as prospective predictors of parasympathetic nervous system activity during rest and social stress in adolescents with bipolar disorder, reflecting sleep-related interference in stress regulatory systems that may confer vulnerability to mood episodes. METHOD Participants were adolescents with bipolar disorder (n = 22) and healthy adolescents (n = 27). Sleep duration and timing were measured by actigraphy for 1 week before a laboratory social stress task, during which high-frequency heart rate variability (HF-HRV) was indexed using electrocardiography. Multilevel models were used to evaluate group, sleep characteristics, and their interactions as predictors of initial HF-HRV and change in HF-HRV during rest and stress. RESULTS Associations between group and changes in HF-HRV during stress were moderated by sleep duration mean (z = 2.24, p = .025) and variability (z = -2.78, p = .006). There were also main effects of mean sleep duration on initial HF-HRV during rest (z = -5.37, p < .001) and stress (z = -2.69, p = .007). Follow-up analyses indicated that, in bipolar adolescents during stress, shorter and longer sleep durations were associated with lower initial HF-HRV (z = -5.44, p < .001), and greater variability in sleep duration was associated with less change in HF-HRV (z = -2.18, p = .029). CONCLUSIONS Sleep durations that are relatively short or long, which are characteristic of mood episodes, are associated with parasympathetic vulnerability to social stress in adolescents with bipolar disorder. Obtaining regular sleep of moderate duration may favorably affect responses to stress in bipolar youth.

Introduction Insufficient sleep impairs cognitive function which results in costly errors. Firefighter shifts regularly exceed 24-hrs with little to no sleep. Nevertheless, firefighters must maintain and flexibly shift attention in high-pressure scenarios. Firefighters also engage in strenuous physical exertion during fire suppression activities. However, it is unclear whether physical exertion acts as another stressor, exasperating cognitive deficits due to insufficient sleep, or whether physical exertion enhances arousal to reduce cognitive deficits. Moreover, the effects of physical exertion may depend on the type of cognitive process and extent of sleep loss. We examined the effect of physical exertion on vigilant attention and task-switching in firefighters who underwent sleep-deprivation or sleep-disruption. Methods Participants were 17 healthy young adult males who participated in a within-subjects crossover design with three experimental lab visits: sleep-deprivation, sleep-disruption (woken 3 times for 60-min each), and normal sleep. The next day, participants completed a 50-min treadmill exercise task in a heated room in firefighter protective clothing. Participants completed a vigilant attention task (Psychomotor Vigilance Task, PVT) and a task-switching task five to nine times each visit. The five timepoints of interest–before and after the sleep manipulation night, before and after the treadmill exercise task, and recovery (approximately 180-min following exercise)–were examined using linear mixed effects models. Results We analyzed lapses (reaction times [RT]>500ms) on the PVT and switch-trial RT and accuracy on the task-switching task for sleep-deprivation and sleep-disruption conditions relative to normal sleep. Sleep-disruption, p=.001, and sleep-deprivation, p Conclusion Physical exertion reduced task-switching and attentional deficits caused by insufficient sleep, with more benefits observed during recovery. We found no evidence for performance decrements due to physical exertion. Physical exertion may interact with the extent of sleep loss–primarily benefitting performance under conditions of total sleep-deprivation. Support (if any) DSF Charitable Foundation and University of Pittsburgh Clinical and Translational Science Institute UL1TR001857.

Introduction Sleep continuously changes over the human lifespan and it does so across multiple dimensions, including duration, timing, efficiency, and variability. Although studies focused on specific developmental periods have shown age-related changes in sleep, methodological differences make it difficult to synthesize information across studies to fully understand precisely when these sleep changes occur. Our goal was to use individual-level actigraphy and self-report sleep data from a single site to characterize age trends and sex differences in actigraphy and self-report sleep dimensions across the healthy human lifespan. To accomplish this goal, we developed the Pittsburgh Lifespan Sleep Databank (PLSD), a large aggregate databank of participants from sleep research studies conducted at the University of Pittsburgh. Methods In the present analysis, we included N=1,070 PLSD participants from 21 studies without a major psychiatric, sleep, or medical condition. We used Generalized Additive Models to examine flexible, potentially non-linear relationships between age and sleep dimensions (actigraphy and self-report duration, efficiency, and timing; actigraphy variability) from ages 10 to 87. We also examined whether these sleep characteristics differed by sex across the lifespan. Results The most dramatic age-related trends were observed in sleep timing. Actigraphy and self-report sleep onset time shifted later between ages 10–18 and then shifted earlier again during the 20s. Actigraphy and self-report wake-up time also shifted earlier during the mid-20s through late 30s. Self-report duration became shorter from approximately ages 10–20. Self-report sleep efficiency and actigraphy variability both decreased over the entire lifespan. Relative to males, females tended to have earlier self-report sleep onset, higher actigraphy sleep efficiency, and longer actigraphy duration. Conclusion By focusing on lifespan sleep rather than specific age segments of the samples, we can provide a unified assessment of age-related changes and sex differences from childhood through older adulthood. An understanding of age trends and sex differences in sleep in healthy individuals – and explicating the timing and nature of these difference – can be used to identify periods of sleep-related risk or resilience and guide intervention efforts. Support (if any) University of Pittsburgh Clinical and Translational Science Institute (UL1TR001857).

STUDY OBJECTIVES To investigate age-related differences in polysomnographic and sleep electroencephalographic (EEG) measures, considering sex, pubertal stage, ethnicity, and scalp topography in a large group of adolescents in the National Consortium on Alcohol and NeuroDevelopment in Adolescence (NCANDA). METHODS Following an adaptation/clinical screening night, 141 healthy adolescents (12-21 y, 64 girls) had polysomnographic recordings, from which sleep staging and EEG measures were derived. The setting was the SRI International Human Sleep Laboratory and University of Pittsburgh Pediatric Sleep Laboratory. RESULTS Older age was associated with a lower percentage of N3 sleep, accompanied by higher percentages of N2, N1, and rapid eye movement (REM) sleep. Older boys compared with younger boys had more frequent awakenings and wakefulness after sleep onset, effects that were absent in girls. Delta (0.3-4 Hz) EEG power in nonrapid eye movement NREM sleep was lower in older than younger adolescents at all electrode sites, with steeper slopes of decline over the occipital scalp. EEG power in higher frequency bands was also lower in older adolescents than younger adolescents, with equal effects across electrodes. Percent delta power in the first NREM period was similar across age. African Americans had lower EEG power across frequency bands (delta to sigma) compared with Caucasians. Finally, replacing age with pubertal status in the models showed similar relationships. CONCLUSIONS Substantial differences in sleep architecture and EEG were evident across adolescence in this large group, with sex modifying some relationships. Establishment and follow-up of this cohort allows the investigation of sleep EEG-brain structural relationships and the effect of behaviors, such as alcohol and substance use, on sleep EEG maturation.

Objectives We conducted a pilot study of a sleep health promotion program for college students. The aims of the study were to (1) determine the feasibility of the program and (2) explore changes in sleep knowledge and sleep diary parameters. Design Open trial of a sleep health promotion program for college students. Setting A small liberal arts university in southwestern Pennsylvania. Participants University students (primarily female). Intervention Active intervention components included individualized e-mail feedback based on each participant's baseline sleep diary and an in-person, group format presentation on sleep health. Measurements Participants completed online questionnaires and sleep diaries before and after the health promotion intervention. Online questionnaires focused on sleep knowledge and attitudes toward sleep, as well as Patient Reported Outcomes Measurement Information System sleep and psychosocial assessments. Results Of participants who completed some aspects of the study, 89% completed at least one intervention component (in-person lecture and/or sleep diary). Participants reported significant improvement in sleep knowledge and changes in sleep diary parameters (decreased sleep onset latency and time spent in bed, resulting in greater sleep efficiency). Sleep duration also increased by 30 minutes among short sleepers who obtained Conclusions Preliminary evaluation of a brief program to promote sleep health suggests that it is feasible and acceptable to implement, and that it can favorably alter sleep knowledge and behaviors reported on the sleep diary in college students. Controlled trials are warranted.

STUDY OBJECTIVES To investigate the relationship between K-complexes (KCs) and cardiac functioning. METHODS Forty healthy adolescents aged 16-22 y (19 females) participated in the study. Heart rate (HR) fluctuations associated with spontaneous and evoked KCs were investigated on two nights, one with (event-related potential night) and one without auditory tones presented across the night. RESULTS There was a clear biphasic cardiac response to evoked and spontaneous KCs, with an initial acceleration in HR followed by a deceleration (P < 0.001). HR acceleration occurred immediately to KCs in response to tones presented in the first third of the interbeat interval, but was delayed a beat when the tone occurred later in the cardiac cycle (P < 0.05). Sex differences were also evident. Pretone baseline HR was higher, and the magnitude of the HR response was blunted and delayed, in female compared to male adolescents (P < 0.001). Also, pretone baseline HR was lower when a tone elicited a KC compared to when it did not (P < 0.001), suggesting that KCs are possibly more likely to be elicited by external stimuli in states of reduced cardiac activation. CONCLUSIONS The strict dependency observed between KCs and cardiac control indicates a potential role of KCs in modulating the cardiovascular system during sleep. Sex differences in the KC-cardiac response indicate the sensitivity of this measure in capturing sex differences in cardiac regulatory physiology.

Introduction The post-illumination pupil response (PIPR) is a measure of the responsivity of intrinsically photosensitive retinal ganglion cells (ipRGCs), and reflects the cell biology of the photoentrainment pathway projecting from the retina to the circadian clock. Adequate signaling from the ipRGCs in the retina to the circadian clock is necessary to result in robust circadian output which we hypothesize would increase inter-daily stability (IS), a non-parametric modeling technique that examines stability of rest activity rhythms across successive days. Methods Participants were aged 18–66 years and recruited from the greater Pittsburgh area during the Winter with Seasonal Affective Disorder who completed both actigraphy and pupillometry (n = 16). PIPR measures were collected after a 1 second red or blue light pulse, and are calculated as the Net difference between red and blue at multiple time frames: at 6 seconds post stimulus (PIPR 6), from 10–30 seconds post-stimulus (PIPR 20), or from 10–40 seconds post-stimulus (PIPR 30). Using actigraphy, inter-daily stability (IS) was calculated as the amount of overall variability in the recording that is accounted for by the typical 24-hour profile, and reflects stability of the mean 24-h profile day-to-day. Results Inter-daily stability (IS) was associated with Net PIPR 20 (Β = 0.561; p = .031) and Net PIPR 30 (Β = 0.551; p = .034; all Β’s are standardized), but not Net PIPR 6 (Β = 0.298; p = .304). Retinal irradiance was calculated for each participant based on age and pupil diameter, to account for age-related differences in transmission of the stimulus to the retina. All raw Net PIPR values were adjusted for calculated retinal irradiance, and gender and time since wake were included as covariates. Conclusion Inter-daily stability (IS) values indicate greater stability of 24-hour activity profiles across days. If reduced responsivity to entraining pulses of light is associated with day-to-day instability in activity rhythms, as shown here, we might expect that amplifying entraining light through environmental changes or bright light therapy would normalize inter-daily stability in SAD, or the reverse, stabilizing activity profiles across days could improve depression and/or normalize retinal ipRGC responsivity. Support NIMH K.A.R. MH103303

Introduction Studies consistently demonstrate a link between subjective sleep disturbances and the continuum of suicidality, although this evidence primarily comes from retrospective, cross-sectional studies using limited items to assess sleep. Longitudinal assessment of well-defined and measured sleep/wake behaviors with high-risk individuals are needed to enhance the specificity of near-term suicide risk detection and render concrete targets for suicide prevention. Methods Participants (N=46) included ultra-high-risk adolescents (N=29 ages 12-18) and college students (N=17 ages 18-24). For up to 12 weeks, participants wore an actigraph to yield objective data on sleep/wake, and concurrently completed daily cellphone-based ratings of subjective sleep and suicidality. Generalized estimating equations were used to examine the association between sleep parameters (subjective and objective) and the odds of next-day suicidal outcomes (i.e., passive death wish [PDW], suicidal ideation, suicidal intent) controlling for age, gender, and depression severity. Results Significant quadratic relationships were observed between actigraphy-derived total sleep time (TST) and probability of next-day PDW (Z=3.7, p=0.0002), suicidal ideation (Z=2.1, p=0.04), and suicidal intent (Z=2.78, p=0.006), with increasing suicidality at low and high values of TST. Low sleep efficiency (20 minutes) with next-day suicidal intent (OR=3.00, Z=2.37, p=0.018). Conclusion Poor sleep health may signal increasing suicide risk, and are modifiable risk factors. We document a significant temporal association whereby objectively-derived short and long TST and low sleep efficiency, as well as subjective sleep quality and sleep onset latency, predicts next day’s suicidality. Further understanding of the temporal association between sleep and suicidality may hold promise to inform real-time monitoring and preventive strategies. Interventions targeting these factors may therefore help reduce suicidality in high-risk youth. Support American Foundation for Suicide Prevention; University of Pittsburgh Clinical and Translational Science Institute

Introduction Insufficient sleep, circadian misalignment, and altered eating patterns are linked to depression. Despite the temporal association between the sleep/wake and feed/fast cycles, it is unclear how depression severity influences this relationship. Methods Sixty-eight participants ages 18-65 years across the depression continuum wore an Actiwatch for 5-17 nights and reported daily meal times (730 nights total). Multilevel models tested previous night’s sleep timing and duration as predictors of the length of the next day’s eating window. Within-person sleep duration and timing were entered as Level 1 predictors to account for nightly variation in sleep. Between-person sleep duration and timing were entered as Level 2 predictors. A three-way interaction between depression severity and Level 2 sleep duration/timing was entered. Covariates included age, gender, and day (weeknight/weekend). Results Across participants, average later sleep timing predicted a longer eating window (Β= -.222; p =.005). Earlier sleep timing (Β= -.186; p < .001) and shorter sleep duration(Β= -.103; p < .001) relative to a person’s average each predicted a longer next-day eating window. A three-way interaction was found between sleep duration, timing, and depression (Β= -.159; p = .002). At shorter sleep durations, individuals with higher depression severity had a positive relationship between sleep timing and eating window length, and individuals with low depression had a negative relationship between sleep timing and eating window length. Conclusion At shorter sleep durations (< 6.5 hr), individuals with high depression and later sleep timing or low depression and early sleep timing had the longest eating windows, which have been linked to adverse metabolic health. Future experiments should test short sleep duration, sleep timing, and depression as potential causes of lengthened eating windows to determine if targeting sleep duration and timing could improve adverse metabolic markers in depression. Support NIMH K.A.R. MH103303

Objective Sleep changes substantially during adolescence; however, our understanding of age-related differences in specific electroencephalographic waveforms during this developmental period is limited. Method Sigma power, spindle characteristics and cognitive data were calculated for fast (∼13 Hz) central and slow (∼11 Hz) frontal sleep spindles for a large cross-sectional sample of adolescents (N = 134, aged 12–21 years, from the National Consortium on Alcohol and NeuroDevelopment in Adolescence (NCANDA) study). Results Older age (and advanced pubertal development) was associated with lower absolute sigma power and greater fast spindle density, with spindles having a shorter duration and smaller amplitude and occurring at a faster average frequency than at a younger age. Spindle characteristics were not directly associated with cognition. An indirect relationship (age * density) provided some evidence for an association between better episodic memory performance and greater spindle density only for younger adolescents. Conclusion Spindle characteristics in adolescents differed according to age, possibly reflecting underlying differences in thalamo-cortical connectivity, and may play a role in episodic memory early in adolescence. Significance Sleep spindles may serve as a marker of adolescent development, likely reflecting brain maturational status. Investigating specific spindle characteristics, in addition to sigma power, is necessary to fully characterize spindles during adolescence.

Objective To conduct a pilot randomized trial of Interpersonal and Social Rhythm Therapy plus Data-Informed Referral (IPSRT + DIR) versus DIR-alone for adolescents at-risk for bipolar disorder (BP). Method Eligible participants included youth (12–18) with a BP parent; youth with BP were excluded. Participants (n = 42) were randomized to receive IPSRT + DIR to treat any psychiatric disorders present at baseline, or DIR-alone. A blind evaluator assessed outcomes at baseline, 3- and 6-months. Participants wore an actigraph to measure sleep/wake patterns for 7 days at baseline and 6-months. Primary outcomes included mood and non-mood symptoms and sleep disturbance. Results Youth randomized to IPSRT + DIR attended approximately half of scheduled IPSRT sessions. Although 33% of DIR-alone youth were referred for mental health services at intake (another 33% were already engaged in services), none initiated new services over follow-up. No youth developed new-onset mood disorder over follow-up. Self- and parent-reported mood and non-mood psychiatric symptoms did not distinguish the groups, although youth in DIR-alone tended to have higher baseline scores on most measures. Per clinician ratings, 1 youth receiving IPSRT + DIR displayed subthreshold hypo/manic symptoms, versus 2 receiving DIR-alone (OR = 14.7, p = 0.03), possibly signaling less subthreshold hypo/manic symptoms, and for fewer weeks (χ2= 11.06, p = 0.0009), over 6-months with IPSRT + DIR. We found a small effect for youth in the IPSRT + DIR group to evidence more WASO at pre-treatment, but less at follow-up (cohen's d = 0.28). Limitations Small sample size limits statistical power, and we are unable to definitively attribute group differences to IPSRT versus greater clinical contact. Ability to examine distal/rare (i.e., BP onset) outcomes was limited. Conclusions Adolescents at-risk for BP present challenges to psychosocial treatment engagement and retention. IPSRT merits further study as an acceptable intervention for at-risk youth, though necessary frequency and intensity to affect outcomes should be examined. The potential to delay or prevent subthreshold hypo/manic symptoms via enhanced sleep continuity is an area for further examination. Future studies with larger samples and extended follow-up can help determine whether IPSRT may delay or prevent syndromal hypo/mania in youth at-risk.

Sleep discrepancies are common in primary insomnia (PI) and include reports of longer sleep onset latency (SOL) than measured by polysomnography (PSG) or "negative SOL discrepancy." We hypothesized that negative SOL discrepancy in PI would be associated with higher relative glucose metabolism during nonrapid eye movement (NREM) sleep in brain networks involved in conscious awareness, including the salience, left executive control, and default mode networks.PI (n = 32) and good sleeper controls (GS; n = 30) completed [18F]fluorodeoxyglucose positron emission tomography (FDG-PET) scans during NREM sleep, and relative regional cerebral metabolic rate for glucose (rCMRglc) was measured. Sleep discrepancy was calculated by subtracting PSG-measured SOL on the PET night from corresponding self-report values the following morning. We tested for interactions between group (PI vs. GS) and SOL discrepancy for rCMRglc during NREM sleep using both a region of interest mask and exploratory whole-brain analyses.Significant group by SOL discrepancy interactions for rCMRglc were observed in several brain regions (pcorrected.05 for all clusters). In the PI group, more negative SOL discrepancy (self-reportedPSG-measured SOL) was associated with significantly higher relative rCMRglc in the right anterior insula and middle/posterior cingulate during NREM sleep. In GS, more positive SOL discrepancy (self-reportedPSG-measured SOL) was associated with significantly higher relative rCMRglc in the right anterior insula, left anterior cingulate cortex, and middle/posterior cingulate cortex.Although preliminary, these findings suggest regions of the brain previously shown to be involved in conscious awareness, and the perception of PSG-defined states may also be involved in the phenomena of SOL discrepancy.

PURPOSE. We assessed sex- and age-dependent differences in a cross-sectional analysis of cardiac autonomic nervous system (ANS) regulation during sleep in adolescents. METHODS. Nocturnal heart rate (HR) and heart rate variability (HRV) metrics, reflecting ANS functioning, were analyzed across the night and within undisturbed rapid-eye movement (REM) and non-REM (NREM) sleep in 149 healthy adolescents (12–22y; 67 female) from the National Consortium on Alcohol and Neurodevelopment in Adolescence (NCANDA). RESULTS. Nocturnal HR was slower in older, more pubertally-advanced boys than younger boys. In girls, HR did not vary according to age or maturity, although overall HRV and vagal modulation declined with age. While younger boys and girls had similar HR, the male-female HR difference increased by ~2.4bpm every year (p

Human and animal studies indicate that reward function is modulated by the circadian clock that governs our daily sleep/wake rhythm. For example, a robust circadian rhythm exists in positive affect, which is lower in the morning hours and peaks in the afternoon. A handful of functional neuroimaging studies suggest that systematic diurnal variation exists in brain activity related to other functions, but no published human studies have examined daily variation in the neural processing of reward. In the present study, we attempt to advance this literature by using functional neuroimaging methods to examine time-of-day changes in the responsivity of the reward circuit. Using a within-person design and a functional magnetic resonance imaging (fMRI) monetary reward task, we compared morning and afternoon reward-related brain activation in a sample of healthy young adults within 24 h. Region of interest analyses focused on the striatum, and we hypothesized greater reward activation in the afternoon, concordant with the circadian peak in positive affect. Results were consistent with our hypothesis. In addition, we counterbalanced the order of morning and afternoon scans in order to explore the short-term stability of the neural response. Whole-brain analyses showed a markedly higher reactivity to reward throughout the brain in the first scan relative to the second scan, consistent with habituation to the monetary reward stimuli. However, these effects did not appear to explain the time-of-day findings. In summary, we report the first preliminary evidence of circadian variation in the neural processing of reward. These findings have both methodological and theoretical implications.