Behavioral-social rhythms and cardiovascular disease risk in retired night shift workers and retired day workers.

OBJECTIVE: Stability in the timing of key daily routine behaviors such as working/doing housework, sleeping, eating, and engaging in social interactions (i.e., behavioral-social rhythms) contributes to health. This study examined whether behavioral-social rhythms were associated with CVD risk factors in retired night shift workers and retired day workers and explored whether past night shift work exposure moderated this association. METHODS: 154 retired older adults participated in this study. Multiple logistic regression models were used to examine associations between behavioral-social rhythms and CVD risk factors. Independent variables included Social Rhythm Metric (SRM)-5 score and actigraphy rest-activity rhythm intra-daily variability (IV) and inter-daily stability (IS). Dependent variables were metabolic syndrome prevalence and its five individual components. RESULTS: More regular behavioral-social rhythms were associated with lower odds of prevalent metabolic syndrome (SRM: OR = 0.57, 95% CI [0.35, 0.88]; IV: OR = 4.00, 95% CI [1.86, 8.58]; IS: OR = 0.42, 95% CI [0.24, 0.73]) and two of its individual components: body mass index (SRM: OR = 0.56, 95% CI [0.37, 0.85]; IV: OR = 2.84, 95% CI [1.59, 5.07]; IS: OR = 0.42, 95% CI [0.26, 0.68]) and high-density lipoprotein cholesterol (SRM: OR = 0.49, 95% CI [0.30, 0.80]; IV: OR = 2.49, 95% CI [1.25, 4.96]; IS: OR = 0.35, 95% CI [0.19, 0.66]). Past shift work history did not moderate the association between behavioral-social rhythms and metabolic syndrome. CONCLUSIONS: Behavioral-social rhythms were related to CVD risk factors in retired adults regardless of prior night shift work exposure. Older retired workers may benefit from education and interventions aiming to increase behavioral-social rhythm regularity.

Do sleep and circadian characteristics predict alcohol use in adult drinkers?

BACKGROUND: While sleep and circadian rhythms are recognized contributors to the risk for alcohol use and related problems, few studies have examined whether objective sleep and circadian measures can predict future alcohol use in humans, and no such studies have been conducted in adults. This study examined whether any baseline sleep and/or circadian characteristics of otherwise healthy adults predicted their alcohol use over the subsequent 12 months. METHODS: Participants (21-42 years) included 28 light and 50 heavy drinkers. At baseline, a comprehensive range of self-reported and objective sleep/circadian measures was assessed via questionnaires, wrist actigraphy, and measurement of dim light melatonin onset and circadian photoreceptor responsivity. Following this, the number of alcoholic drinks per week and binge drinking episodes per month were assessed quarterly over the subsequent 12 months. Anticipated effects of alcohol (stimulation, sedation, and rewarding aspects) were also assessed quarterly over the 12 months. Analyses included generalized linear mixed-effects models and causal mediation analysis. RESULTS: Across the range of measures, only self-reported insomnia symptoms and a longer total sleep time at baseline predicted more drinks per week and binges per month (ps <0.02). There was a trend for the anticipated alcohol effect of wanting more alcohol at the 6-month timepoint to mediate the relationship between insomnia symptoms at baseline and drinks per week at 12 months (p = 0.069). CONCLUSIONS: These results suggest that in otherwise healthy adults, insomnia symptoms, even if subclinical, are a significant predictor of future drinking, and appear to outweigh the influence of circadian factors on future drinking, at least in otherwise healthy adults. Insomnia symptoms may be a modifiable target for reducing the risk of alcohol misuse.

Circadian photoentrainment varies by season and depressed state: associations between light sensitivity and sleep and circadian timing.

STUDY OBJECTIVES: Altered light sensitivity may be an underlying vulnerability for disrupted circadian photoentrainment. The photic information necessary for circadian photoentrainment is sent to the circadian clock from melanopsin-containing intrinsically photosensitive retinal ganglion cells (ipRGCs). The current study tested whether the responsivity of ipRGCs measured using the post-illumination pupil response (PIPR) was associated with circadian phase, sleep timing, and circadian alignment, and if these relationships varied by season or depression severity. METHODS: Adult participants (N = 323, agem = 40.5, agesd = 13.5) with varying depression severity were recruited during the summer (n = 154) and winter (n = 169) months. Light sensitivity was measured using the PIPR. Circadian phase was assessed using Dim Light Melatonin Onset (DLMO) on Friday evenings. Midsleep was measured using actigraphy. Circadian alignment was calculated as the DLMO-midsleep phase angle. Multilevel regression models covaried for age, gender, and time since wake of PIPR assessment. RESULTS: Greater light sensitivity was associated with later circadian phase in summer but not in winter (ß = 0.23; p = 0.03). Greater light sensitivity was associated with shorter DLMO-midsleep phase angles (ß = 0.20; p = 0.03) in minimal depression but not in moderate depression (SIGHSAD < 6.6; Johnson-Neyman region of significance). CONCLUSIONS: Light sensitivity measured by the PIPR was associated with circadian phase during the summer but not in winter, suggesting ipRGC functioning in humans may affect circadian entrainment when external zeitgebers are robust. Light sensitivity was associated with circadian alignment only in participants with minimal depression, suggesting circadian photoentrainment, a possible driver of mood, may be decreased in depression year-round, similar to decreased photoentrainment in winter.

Sleep-Related Predictors of Risk for Alcohol Use and Related Problems in Adolescents and Young Adults.

PURPOSE: Growing evidence supports sleep and circadian rhythms as influencing alcohol use and the course of alcohol use disorder (AUD). Studying sleep/circadian-alcohol associations during adolescence and young adulthood may be valuable for identifying sleep/circadian-related approaches to preventing and/or treating AUD. This paper reviews current evidence for prospective associations between sleep/circadian factors and alcohol involvement during adolescence and young adulthood with an emphasis on the effects of sleep/circadian factors on alcohol use. SEARCH METHODS: The authors conducted a literature search in PsycInfo, PubMed, and Web of Science using the search terms "sleep" and "alcohol" paired with "adolescent" or "adolescence" or "young adult" or "emerging adult," focusing on the title/abstract fields, and restricting to English-language articles. Next, the search was narrowed to articles with a prospective/longitudinal or experimental design, a sleep-related measure as a predictor, an alcohol-related measure as an outcome, and confirming a primarily adolescent and/or young adult sample. This step was completed by a joint review of candidate article abstracts by two of the authors. SEARCH RESULTS: The initial search resulted in 720 articles. After review of the abstracts, the list was narrowed to 27 articles reporting on observational longitudinal studies and three articles reporting on intervention trials. Noted for potential inclusion were 35 additional articles that reported on studies with alcohol-related predictors and sleep-related outcomes, and/or reported on candidate moderators or mediators of sleep-alcohol associations. Additional articles were identified via review of relevant article reference lists and prior exposure based on the authors' previous work in this area. DISCUSSION AND CONCLUSIONS: Overall, the review supports a range of sleep/circadian characteristics during adolescence and young adulthood predicting the development of alcohol use and/or alcohol-related problems. Although sleep treatment studies in adolescents and young adults engaging in regular and/or heavy drinking show that sleep can be improved in those individuals, as well as potentially reducing alcohol craving and alcohol-related consequences, no studies in any age group have yet demonstrated that improving sleep reduces drinking behavior. Notable limitations include relatively few longitudinal studies and only two experimental studies, insufficient consideration of different assessment timescales (e.g., day-to-day vs. years), insufficient consideration of the multidimensional nature of sleep, a paucity of objective measures of sleep and circadian rhythms, and insufficient consideration of how demographic variables may influence sleep/circadian-alcohol associations. Examining such moderators, particularly those related to minoritized identities, as well as further investigation of putative mechanistic pathways linking sleep/circadian characteristics to alcohol outcomes, are important next steps.

Effect of daily discrimination on naturalistic sleep health features in young adults.

OBJECTIVE: Racial inequities in sleep health are well documented and may be partially attributable to discrimination experiences. However, the effects of acute discrimination experiences on same-night sleep health are understudied. We quantified naturalistic discrimination experiences captured using ecological momentary assessment (EMA) and examined whether reporting discrimination on a given day predicted sleep health that night. METHOD: Participants completed baseline assessments and a 17-day EMA protocol, with text prompts delivered four times daily to collect discrimination experiences. Seven different daily sleep characteristics were ascertained each morning. Discrimination reasons (e.g., because of my racial identity) were reported by participants and categorized into any, racial, or nonracial discrimination. Outcomes included the seven sleep diary characteristics. We fit generalized linear mixed effects models for each sleep outcome and discrimination category, controlling for key covariates. RESULTS: The analytic sample included 116 self-identified Black and White individuals (48% Black, 71% assigned female at birth, average age = 24.5 years). Among Black participants, race-based discrimination was associated with a 0.5-hr reduction in total sleep time (TST). Among White individuals, nonracial discrimination was associated with a 0.6-hr reduction in TST, an earlier sleep offset, and reduced sleep efficiency (partly attributable to more nighttime awakenings). CONCLUSIONS: Young adults may sleep worse on nights after experiencing discrimination, and different types of discrimination affect different sleep outcomes for Black and White individuals. Future studies may consider developing treatments that account for different sleep vulnerabilities for people experiencing discrimination on a given day. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Pre-pandemic circadian phase predicts pandemic alcohol use among adolescents.

Later circadian timing during adolescence is linked to worse sleep, more severe depression and greater alcohol involvement, perhaps due to circadian misalignment imposed by early school schedules. School schedules shifted later during the COVID-19 pandemic, ostensibly reducing circadian misalignment and potentially mitigating problems with depression and alcohol. We used the pandemic as a natural experiment to test whether adolescent drinkers with later circadian timing showed improvements in sleep, depression and alcohol involvement. Participants were 42 adolescents reporting alcohol use. We assessed circadian phase via dim light melatonin onset prior to the pandemic, then conducted remote assessments of sleep, depressive symptoms and alcohol use during the pandemic. Mixed-effects models were used to test for pandemic effects, covarying for age, sex, time since baseline evaluation, and current school/work status. Adolescents with later circadian timing reported less sleep than other teens on school nights, both before and during the pandemic. Although school night sleep increased during the pandemic (F = 28.36, p < 0.001), those increases were not greater for individuals with later circadian timing. Individuals with later circadian timing reported larger increases in alcohol use than other teens during the pandemic (X2 = 36.03, p < 0.001). Depressive symptoms increased during the pandemic (X2 = 46.51, p < 0.001) but did not differ based on circadian timing. Consistent with prior reports, adolescents with later circadian timing obtained less sleep, and later school schedules facilitated increased sleep duration. Nonetheless, individuals with later circadian timing reported the sharpest increases in alcohol use, suggesting that circadian timing contributes to risk for alcohol use beyond the effects of insufficient sleep.

The association between cortical gyrification and sleep in adolescents and young adults.

STUDY OBJECTIVES: Healthy sleep is important for adolescent neurodevelopment, and relationships between brain structure and sleep can vary in strength over this maturational window. Although cortical gyrification is increasingly considered a useful index for understanding cognitive and emotional outcomes in adolescence, and sleep is also a strong predictor of such outcomes, we know relatively little about associations between cortical gyrification and sleep. We aimed to identify developmentally invariant (stable across age) or developmentally specific (observed only during discrete age intervals) gyrification-sleep relationships in young people. METHODS: A total of 252 Neuroimaging and Pediatric Sleep Databank participants (9-26 years; 58.3% female) completed wrist actigraphy and a structural MRI scan. Local gyrification index (lGI) was estimated for 34 bilateral brain regions. Naturalistic sleep characteristics (duration, timing, continuity, and regularity) were estimated from wrist actigraphy. Regularized regression for feature selection was used to examine gyrification-sleep relationships. RESULTS: For most brain regions, greater lGI was associated with longer sleep duration, earlier sleep timing, lower variability in sleep regularity, and shorter time awake after sleep onset. lGI in frontoparietal network regions showed associations with sleep patterns that were stable across age. However, in default mode network regions, lGI was only associated with sleep patterns from late childhood through early-to-mid adolescence, a period of vulnerability for mental health disorders. CONCLUSIONS: We detected both developmentally invariant and developmentally specific ties between local gyrification and naturalistic sleep patterns. Default mode network regions may be particularly susceptible to interventions promoting more optimal sleep during childhood and adolescence.

Performance evaluation of the open-source Yet Another Spindle Algorithm sleep staging algorithm against gold standard manual evaluation of polysomnographic records in adolescence.

GOAL AND AIMS: To evaluate an automatic sleep scoring algorithm against manual polysomnography sleep scoring. FOCUS METHOD/TECHNOLOGY: Yet Another Spindle Algorithm automatic sleep staging algorithm. REFERENCE METHOD/TECHNOLOGY: Manual sleep scoring. SAMPLE: 327 nights (151 healthy adolescents), from the NCANDA study. DESIGN: Participants underwent one-to-three overnight polysomnography recordings, one consisting of an event-related-potential paradigm. CORE ANALYTICS: Epoch by Epoch and discrepancy analyses (Bland Altman plots) were conducted on the overall sample. ADDITIONAL ANALYTICS AND EXPLORATORY ANALYSES: Epoch by Epoch and discrepancy analysis were repeated separately on standard polysomnography nights and event-related potential nights. Regression models were estimated on age, sex, scorer, and site of recording, separately on standard polysomnography nights and event-related potential nights. CORE OUTCOMES: The Yet Another Spindle Algorithm sleep scoring algorithm's average sensitivity of 93.04% for Wake, 87.67% for N2, 84.46% for N3, 86.02% for rapid-eye-movement, and 40.39% for N1. Specificity was 96.75% for Wake, 97.31% for N1, 88.87% for N2, 97.99% for N3, and 97.70% for rapid-eye-movement. The Matthews Correlation Coefficient was highest in rapid-eye-movement sleep (0.85) while lowest in N1 (0.39). Cohen's Kappa mirrored Matthews Correlation Coefficient results. In Bland-Altman plots, the bias between Yet Another Spindle Algorithm and human scoring showed proportionality to the manual scoring measurement size. IMPORTANT ADDITIONAL OUTCOMES: Yet Another Spindle Algorithm performance was reduced in event-related-potential/polysomnography nights for N3 and rapid-eye-movement. According to the Matthews Correlation Coefficient, the Yet Another Spindle Algorithm performance was affected by younger age, male sex, recording sites, and scorers. CORE CONCLUSION: Results support the use of Yet Another Spindle Algorithm to score adolescents' polysomnography sleep records, possibly with classification outcomes supervised by an expert scorer.

The association between cortical gyrification and sleep in adolescents and young adults.

Study objectives: Healthy sleep is important for adolescent neurodevelopment, and relationships between brain structure and sleep can vary in strength over this maturational window. Although cortical gyrification is increasingly considered a useful index for understanding cognitive and emotional outcomes in adolescence, and sleep is also a strong predictor of such outcomes, we know relatively little about associations between cortical gyrification and sleep. Methods: Using Local gyrification index (lGI) of 34 bilateral brain regions and regularized regression for feature selection, we examined gyrification-sleep relationships in the Neuroimaging and Pediatric Sleep databank (252 participants; 9-26 years; 58.3% female) and identified developmentally invariant (stable across age) or developmentally specific (observed only during discrete age intervals) brain-sleep associations. Naturalistic sleep characteristics (duration, timing, continuity, and regularity) were estimated from wrist actigraphy. Results: For most brain regions, greater lGI was associated with longer sleep duration, earlier sleep timing, lower variability in sleep regularity, and shorter time awake after sleep onset. lGI in frontoparietal network regions showed associations with sleep patterns that were stable across age. However, in default mode network regions, lGI was only associated with sleep patterns from late childhood through early-to-mid adolescence, a period of vulnerability for mental health disorders. Conclusions: We detected both developmentally invariant and developmentally specific ties between local gyrification and naturalistic sleep patterns. Default mode network regions may be particularly susceptible to interventions promoting more optimal sleep during childhood and adolescence.

Effects of emerging alcohol use on developmental trajectories of functional sleep measures in adolescents.

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.

Elusive hypersomnolence in seasonal affective disorder: actigraphic and self-reported sleep in and out of depressive episodes.

BACKGROUND: Hypersomnolence 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. METHODS: Sleep 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. RESULTS: In 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). CONCLUSION: Despite 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.

Morning perception of sleep, stress, and mood, and its relationship with overnight physiological sleep: findings from the National Consortium on Alcohol and Neurodevelopment in Adolescence (NCANDA) study.

This cross-sectional study investigated objective-subjective sleep discrepancies and the physiological basis for morning perceptions of sleep, mood, and readiness, in adolescents. Data collected during a single in-laboratory polysomnographic assessment from 137 healthy adolescents (61 girls; age range: 12-21 years) in the United States National Consortium on Alcohol and Neurodevelopment in Adolescence (NCANDA) study were analysed. Upon awakening, participants completed questionnaires assessing sleep quality, mood, and readiness. We evaluated the relationship between overnight polysomnographic, electroencephalographic, sleep autonomic nervous system functioning measures, and next morning self-reported indices. Results showed that older adolescents reported more awakenings, yet they perceived their sleep to be deeper and less restless than younger adolescents. Prediction models including sleep physiology measures (polysomnographic, electroencephalographic, and sleep autonomic nervous system) explained between 3% and 29% of morning sleep perception, mood, and readiness indices. The subjective experience of sleep is a complex phenomenon with multiple components. Distinct physiological sleep processes contribute to the morning perception of sleep and related measures of mood and readiness. More than 70% of the variance (based on a single observation per person) in the perception of sleep, mood, and morning readiness is not explained by overnight sleep-related physiological measures, suggesting that other factors are important for the subjective sleep experience.

Preliminary evidence that misalignment between sleep and circadian timing alters risk-taking preferences.

Decision-making has been shown to suffer when circadian preference is misaligned with time of assessment; however, little is known about how misalignment between sleep timing and the central circadian clock impacts decision-making. This study captured naturally occurring variation in circadian alignment (i.e., alignment of sleep-wake timing with the central circadian clock) to examine if greater misalignment predicts worse decision-making. Over the course of 2 weeks, 32 late adolescent drinkers (aged 18-22 years; 61% female; 69% White) continuously wore actigraphs and completed two overnight in-laboratory visits (Thursday and Sunday) in which both dim-light melatonin onset (DLMO) and behavioural decision-making (risk taking, framing, and strategic reasoning tasks) were assessed. Sleep-wake timing was assessed by actigraphic midsleep from the 2 nights prior to each in-laboratory visit. Alignment was operationalised as the phase angle (interval) between average DLMO and average midsleep. Multilevel modelling was used to predict performance on decision-making tasks from circadian alignment during each in-laboratory visit; non-linear associations were also examined. Shorter DLMO-midsleep phase angle predicted greater risk-taking under conditions of potential loss (B = -0.11, p = 0.06), but less risk-taking under conditions of potential reward (B = 0.14, p = 0.03) in a curvilinear fashion. Misalignment did not predict outcomes in the framing and strategic reasoning tasks. Findings suggest that shorter alignment in timing of sleep with the central circadian clock (e.g., phase-delayed misalignment) may impact risky decision-making, further extending accumulating evidence that sleep/circadian factors are tied to risk-taking. Future studies will need to replicate findings and experimentally probe whether manipulating alignment influences decision-making.

Activity patterns related to depression symptoms in stressed dementia caregivers.

OBJECTIVES: Self-reported activity restriction is an established correlate of depression in dementia caregivers (dCGs). It is plausible that the daily distribution of objectively measured activity is also altered in dCGs with depression symptoms; if so, such activity characteristics could provide a passively measurable marker of depression or specific times to target preventive interventions. We therefore investigated how levels of activity throughout the day differed in dCGs with and without depression symptoms, then tested whether any such differences predicted changes in symptoms 6 months later. DESIGN, SETTING, PARTICIPANTS, AND MEASUREMENTS: We examined 56 dCGs (mean age = 71, standard deviation (SD) = 6.7; 68% female) and used clustering to identify subgroups which had distinct depression symptom levels, leveraging baseline Center for Epidemiologic Studies of Depression Scale-Revised Edition and Patient Health Questionnaire-9 (PHQ-9) measures, as well as a PHQ-9 score from 6 months later. Using wrist activity (mean recording length = 12.9 days, minimum = 6 days), we calculated average hourly activity levels and then assessed when activity levels relate to depression symptoms and changes in symptoms 6 months later. RESULTS: Clustering identified subgroups characterized by: (1) no/minimal symptoms (36%) and (2) depression symptoms (64%). After multiple comparison correction, the group of dCGs with depression symptoms was less active from 8 to 10 AM (Cohen's d ≤ -0.9). These morning activity levels predicted the degree of symptom change on the PHQ-9 6 months later (per SD unit ß = -0.8, 95% confidence interval: -1.6, -0.1, p = 0.03) independent of self-reported activity restriction and other key factors. CONCLUSIONS: These novel findings suggest that morning activity may protect dCGs from depression symptoms. Future studies should test whether helping dCGs get active in the morning influences the other features of depression in this population (i.e. insomnia, intrusive thoughts, and perceived activity restriction).

Naturalistic Sleep Patterns are Linked to Global Structural Brain Aging in Adolescence.

PURPOSE: We examined whether interindividual differences in naturalistic sleep patterns correlate with any deviations from typical brain aging. METHODS: 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). RESULTS: Later sleep timing (midsleep) was associated with more advanced brain aging (larger brain age gap), ß = 0.1575, puncorr = .0042, pfdr = .0167. Exploratory models suggested that this effect may be driven by males, although the interaction of gender and brain age gap did not survive multiple comparison correction (ß = 0.2459, puncorr = .0336, pfdr = .1061). Sleep duration, continuity, and regularity were not significantly associated with brain age gap. Age did not moderate any brain age gap-sleep relationships. In this psychiatrically healthy sample, depression severity was also not associated with brain age gap or sleep. DISCUSSION: Later 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.

Sleep and circadian rhythm profiles in seasonal depression.

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 Coefficients >0.75) 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.

Homeostatic response to sleep deprivation and circadian rhythmicity are intact in older adults with insomnia.

STUDY OBJECTIVES: We examined whether homeostatic sleep drive and circadian rhythmicity differ in older adults with insomnia (OAI) compared to older good sleepers (GS). METHODS: OAI (n = 37) and GS (n = 30) participated in a 60-h in-lab study with sleep deprivation and constant routine paradigms. Homeostatic sleep drive was assessed by examining the effect of sleep deprivation on delta EEG power and theta EEG power, and repeated sleep latency tests. Circadian rhythm was assessed with salivary melatonin (phase and amplitude), core body temperature (phase, amplitude, and mesor), and sleep latency during a constant routine paradigm. Mixed models were used to assess interactions of group (OAS vs GS) with homeostatic sleep and circadian effects. RESULTS: Compared to GS, OAI showed a greater linear increase in waking theta power during sleep deprivation, but the two groups did not show differential responses to sleep deprivation in delta EEG, or in repeated sleep latency tests. The two groups did not differ in circadian phase or amplitude of melatonin or core body temperature rhythms. OAI had a significantly elevated core body temperature mesor compared to GS. CONCLUSIONS: Homeostatic response to sleep deprivation was intact in OAI compared to GS; theta EEG power suggested a greater homeostatic response in OAI. Circadian rhythm amplitude and phase were similar in OAI compared to GS. Elevated body temperature mesor in OAI may indicate elevated physiological arousal. These findings suggest that effective treatments for insomnia in older adults may leverage intact sleep and circadian regulatory mechanisms, rather than repair defective sleep and circadian regulation.

Sleep and circadian differences between light and heavy adult alcohol drinkers.

BACKGROUND: Numerous studies have reported that eveningness is associated with increased alcohol consumption. However, biological markers of circadian timing, such as dim light melatonin onset (DLMO) and circadian photoreceptor responsivity (post-illumination pupil response, PIPR), have rarely been assessed in the context of habitual alcohol consumption. This study aimed to examine sleep, circadian timing, and photoreceptor responsivity in adult alcohol drinkers. METHODS: Participants (21 to 45 years) included 28 light and 50 heavy drinkers. The 8-day study consisted of a week of ad lib sleep monitored with wrist actigraphy, followed by a 9-h laboratory session with a photoreceptor responsivity and circadian phase assessment. RESULTS: The heavy drinkers obtained on average 28 more minutes of sleep (p = 0.002) and reported more eveningness than the light drinkers (p = 0.029). There was a trend for a shorter DLMO-midsleep interval (p = 0.059) in the heavy drinkers, reflecting a tendency for them to sleep at an earlier circadian phase. The PIPR in the heavy drinkers was significantly smaller than in the light drinkers (p = 0.032), suggesting reduced circadian photoreceptor responsivity in the heavy drinkers. A larger PIPR was significantly associated with a later DLMO in the light drinkers (r = 0.44, p = 0.019), but this relationship was absent in the heavy drinkers (r = -0.01, p = 0.94). CONCLUSIONS: These results are consistent with earlier reports of more eveningness and a shorter DLMO-midsleep interval being associated with heavier alcohol drinking. The novel finding of reduced circadian photoreceptor responsivity in heavy drinkers is consistent with prior rodent studies. Future studies should explore the impact of habitual alcohol consumption on other measures of circadian photoreceptor responsivity.

Associations between specific sleep and circadian characteristics and alcohol use disorder criteria and problems.

Given the significant heterogeneity of alcohol use disorder (AUD) and the increasing priority to understand individual profiles of AUD, pursuing symptom-level examinations of AUD is important. Disturbances in sleep and circadian rhythms have demonstrated robust associations with alcohol consumption and AUD, yet little research has examined these associations at the symptom- or problem-levels and research to date has focused on one or two sleep/circadian characteristics. We sought to investigate the associations between (a) specific AUD symptoms and (b) domains of alcohol-related problems, and multiple sleep characteristics, collected at a daily level in the naturalistic environment. Young adult drinkers were recruited from the community (N = 159, Mage = 23.9, 58.5% female, 6.3% Asian, 35.9% Black or African American, 51.6% White, 5.0% multiracial) and completed a baseline visit as well as up to 18 days of naturalistic assessment. Several sleep/circadian characteristics, including eveningness, later midsleep timing, and shorter total sleep time, were consistently associated with the hazardous use symptom, above and beyond alcohol consumption. Eveningness (beta[SE] = 0.21[0.00], p <.01) was a significant predictor of the alcohol-related problem domain of role interference. Exploratory analyses did not find significant associations between sleep/circadian characteristics and cannabis-related problems. The relationship between sleep/circadian characteristics and AUD and related problems may be driven by a narrower set of symptoms, such as hazardous use and role interference. This may be due to shared mechanistic dysfunction in domains such as reward processing or cognitive control. Thus, these alcohol-related symptoms and problems may be addressed through transdiagnostic treatment approaches that target these underlying mechanisms.