Sleep regularity and body mass index: findings from a prospective study of first-year college students.

STUDY OBJECTIVES: Using data from a large, prospective study of sleep in first-year college students, we examined whether students' sleep regularity is associated with body mass index (BMI) and BMI change (∆BMI) during their first college semester. In a subset of participants, we also tested whether dim light melatonin onset (DLMO) phase and DLMO-bedtime phase angle are associated with BMI and ∆BMI. METHODS: Analyses included data from 581 students (mean age = 18.7 ± 0.5 years; 58% female; 48% non-white) who had their height and weight assessed at the start of classes (T1) and end of 9 weeks. Participants completed online daily sleep diaries from which total sleep time (TST) and the sleep regularity index (SRI) were calculated. Among participants who completed a DLMO protocol (n = 161), circadian phase was quantified by DLMO and circadian alignment by DLMO-bedtime phase angle. Data were analyzed with linear regressions that controlled for sex and average TST. RESULTS: Average SRI was 74.1 ± 8.7 (range: 25.7; 91.6). Average BMI at T1 was 22.0 ± 3.5 and participants gained 1.8 ± 2.4 kg (range: -7.2; 11.4); 39% gained 2-5 kg, 8% gained >5 kg. Lower SRI was associated with greater BMI at T1 (B = -0.06 [95% CI: -0.09; -0.02], p = 0.001) but not with ∆BMI (p = 0.062). Average TST was not significantly associated with BMI or ∆BMI, nor were circadian phase and alignment in the subsample (p's > 0.05). CONCLUSIONS: Sleep regularity is an understudied but relevant sleep dimension associated with BMI during young adulthood. Our findings warrant future work to examine longer-term associations between sleep regularity and weight gain.

Association of Poor Sleep Burden in Middle Age and Older Adults With Risk for Delirium During Hospitalization.

BACKGROUND: Delirium is a distressing neurocognitive disorder recently linked to sleep disturbances. However, the longitudinal relationship between sleep and delirium remains unclear. This study assessed the associations of poor sleep burden, and its trajectory, with delirium risk during hospitalization. METHODS: About 321 818 participants from the UK Biobank (mean age 58 ± 8 years [SD]; range 37-74 years) reported (2006-2010) sleep traits (sleep duration, excessive daytime sleepiness, insomnia-type complaints, napping, and chronotype-a closely related circadian measure for sleep timing), aggregated into a sleep burden score (0-9). New-onset delirium (n = 4 775) was obtained from hospitalization records during a 12-year median follow-up. About 42 291 (mean age 64 ± 8 years; range 44-83 years) had repeat sleep assessment on average 8 years after their first. RESULTS: In the baseline cohort, Cox proportional hazards models showed that moderate (aggregate scores = 4-5) and severe (scores = 6-9) poor sleep burden groups were 18% (hazard ratio = 1.18 [95% confidence interval: 1.08-1.28], p < .001) and 57% (1.57 [1.38-1.80], p < .001), more likely to develop delirium, respectively. The latter risk magnitude is equivalent to 2 additional cardiovascular risks. These findings appeared robust when restricted to postoperative delirium and after exclusion of underlying dementia. Higher sleep burden was also associated with delirium in the follow-up cohort. Worsening sleep burden (score increase ≥2 vs no change) further increased the risk for delirium (1.79 [1.23-2.62], p = .002) independent of their baseline sleep score and time lag. The risk was highest in those younger than 65 years at baseline (p for interaction <.001). CONCLUSION: Poor sleep burden and worsening trajectory were associated with increased risk for delirium; promotion of sleep health may be important for those at higher risk.

Objective Assessment of Daytime Napping and Incident Heart Failure in 1140 Community-Dwelling Older Adults: A Prospective, Observational Cohort Study.

Background Disrupted nighttime sleep has been associated with heart failure (HF). However, the relationship between daytime napping, an important aspect of sleep behavior commonly seen in older adults, and HF remains unclear. We sought to investigate the association of objectively assessed daytime napping and risk of incident HF during follow-up. Methods and Results We studied 1140 older adults (age, 80.7±7.4 [SD] years; female sex, 867 [76.1%]) in the Rush Memory and Aging Project who had no HF at baseline and were followed annually for up to 14 years. Motor activity (ie, actigraphy) was recorded for ≈10 days at baseline. We assessed daytime napping episodes between 9 am and 7 pm objectively from actigraphy using a previously published algorithm for sleep detection. Cox proportional hazards models examined associations of daily napping duration and frequency with incident HF. Eighty-six participants developed incident HF, and the mean onset time was 5.7 years (SD, 3.4; range, 1-14). Participants who napped longer than 44.4 minutes (ie, the median daily napping duration) showed a 1.73-fold higher risk of developing incident HF than participants who napped <44.4 minutes. Consistently, participants who napped >1.7 times/day (ie, the median daily napping frequency) showed a 2.20-fold increase compared with participants who napped <1.7 times/day. These associations persisted after adjustment for covariates, including nighttime sleep, comorbidities, and cardiovascular disease/risk factors. Conclusions Longer and more frequent objective napping predicted elevated future risk of developing incident HF. Future studies are needed to establish underlying mechanisms.

Day-to-day associations between sleep characteristics and affect in community dwelling adults.

Despite the high co-occurrence of sleep and mood disturbances, day-to-day associations between sleep characteristics (sleep duration, continuity, and timing) and dimensions of mood (positive affect and negative affect) remain unclear. The present study aimed to test whether there is a daily, bidirectional association between these sleep characteristics and affective states, while addressing methodological limitations in the extant literature by using actiography and ecological momentary assessment methods. Participants were community dwelling, midlife adults (aged 30-54 years, N = 462, 47% male) drawn from the Adult Health and Behavior Project-Phase 2 study. Participants' sleep patterns were assessed with actiography over a 7-day monitoring period, and on 4 of those days, participants completed an ecological momentary assessment protocol that included hourly assessments of positive affect and negative affect during their wake intervals. Using hierarchical linear modelling, we tested whether participants' sleep characteristics on a given night predicted next-day affect and vice versa. We also explored whether nocturnal sleep characteristics would differentially associate with affect at different times of day (morning, afternoon, and evening) while controlling for multiple health behaviours. We found that when participants reported higher positive affect on a given day, they slept later that night (B = 0.22, p = .010). Although we found no other statistically significant associations in our primary analyses (all p > .05), we found several sleep-affect associations specific to time of day (B ranges: 0.01-0.18, all p ≤ .02), which warrants further study. Overall, our findings suggest that healthy adults may be resilient to daily fluctuations in their sleep and mood.

Fragmentation of Rest/Activity Patterns in Community-Based Elderly Individuals Predicts Incident Heart Failure.

STUDY OBJECTIVES: Heart failure has previously been linked to sleep disorders that are often associated with frequent disturbances to human rest/activity patterns. We tested whether fragmentation of sustained rest/activity patterns derived from actigraphic recordings at baseline predicts incident heart failure in community-based elderly individuals. METHODS: We studied 1099 community-based elderly adults participating in the Rush Memory and Aging Project who had baseline motor activity monitoring up to 11 days and were followed annually for up to 14 years. Fragmentation was assessed using previously validated indexes, derived from the probability of transitions once sustained rest or activity has been established. Heart failure was recorded via a clinical interview during the annual follow-up. Cox proportional hazards models were constructed to examine the relationship between rest fragmentation index and incident heart failure. Covariates grouped in terms of demographics, lifestyle factors and co-morbidities and cardiovascular risk factors/diseases were included. RESULTS: Increased rest fragmentation (but not activity fragmentation) was associated with higher risk for incident heart failure. Specifically, a subject with a rest fragmentation at the 90th percentile showed a 57% increased risk of developing incident heart failure compared to a subject at the 10th percentile in this cohort. This effect was equivalent to that of being over a decade older. These observations were consistent after adjusting for all covariates. CONCLUSION: Increased rest fragmentation, a potential surrogate for sleep fragmentation, is independently associated with a higher risk of developing heart failure in community-based elderly adults during up to 14 years of follow-up. Further work is required to examine the specific contributions from daytime napping versus nighttime sleep periods in the elderly, as well as the underlying autonomic and cardio-dynamic pathways that may explain the effects on heart function.

Nocturnal heart rate variability moderates the association between sleep-wake regularity and mood in young adults.

STUDY OBJECTIVES: Sleep-wake regularity (SWR) is often disrupted in college students and mood disorders are rife at this age. Disrupted SWR can cause repetitive and long-term misalignment between environmental and behavioral cycles and the circadian system which may then have psychological and physical health consequences. We tested whether SWR was independently associated with mood and autonomic function in a healthy adult cohort. METHODS: We studied 42 college students over a 3 week period using daily sleep-wake diaries and continuous electrocardiogram recordings. Weekly SWR was quantified by the interdaily stability of sleep-wake times (ISSW) and mood was assessed weekly using the Beck Depression Inventory-II. To assess autonomic function, we quantified the high-frequency (HF) power of heart rate variability (HRV). Linear mixed effects models were used to assess the relationship between repeated weekly measures of mood, SWR, and HF. RESULTS: Low weekly ISSW predicted subsequent poor mood and worsening mood independently of age, sex, race, sleep duration, and physical activity. Although no association was found between ISSW and HF, the ISSW-mood association was significantly moderated by nocturnal HF, i.e. reported mood was lowest after a week with low ISSW and high HF. Prior week mood scores did not significantly predict the subsequent week's ISSW. CONCLUSIONS: Irregular sleep-wake timing appears to precede poor mood in young adults. Further work is needed to understand the implications of high nocturnal HRV in those with low mood and irregular sleep-wake cycles.

Sleep duration partially accounts for race differences in diurnal cortisol dynamics.

OBJECTIVE: Emerging research demonstrates race differences in diurnal cortisol slope, an indicator of hypothalamic-pituitary-adrenocortical (HPA)-axis functioning associated with morbidity and mortality, with African Americans showing flatter diurnal slopes than their White counterparts. Sleep characteristics are associated with both race and with HPA-axis functioning. The present report examines whether sleep duration may account for race differences in cortisol dynamics. METHOD: Participants were 424 employed African American and White adults (mean age = 42.8 years, 84.2% White, 53.6% female) with no cardiovascular disease (Adult Health and Behavior Project-Phase 2 [AHAB-II] cohort, University of Pittsburgh). Cortisol slope was calculated using 4 salivary cortisol readings, averaged over each of 4 days. Demographic (age, sex), psychosocial (socioeconomic status [SES], affect, discrimination), and health behaviors (smoking, alcohol use, physical activity) variables were used as covariates, and sleep (self-report and accelerometry) was also assessed. RESULTS: African Americans had flatter slopes than Whites (F(1, 411) = 10.45, B = .02, p = .001) in models adjusting for demographic, psychosocial, and health behavior covariates. Shorter actigraphy-assessed total sleep time was a second significant predictor of flatter cortisol slopes (F(1, 411) = 25.27, B = -.0002, p < .0001). Total sleep time partially accounted for the relationship between race and diurnal slope [confidence interval = .05 (lower = .014, upper .04)]. CONCLUSIONS: African Americans have flatter diurnal cortisol slopes than their White counterparts, an effect that may be partially attributable to race differences in nightly sleep duration. Sleep parameters should be considered in further research on race and cortisol. (PsycINFO Database Record

Social Jetlag, Chronotype, and Cardiometabolic Risk.

CONTEXT: Shift work, which imposes a habitual disruption in the circadian system, has been linked to increased incidence of cardiometabolic diseases, and acute circadian misalignment alters various metabolic processes. However, it remains unclear whether day-to-day circadian dysregulation contributes to these risks beyond poor sleep and other behavioral characteristics. OBJECTIVE: Individuals differ in circadian phase preference, known as chronotype, but may be constrained by modern work obligations to specific sleep schedules. Individuals experience social jetlag (SJL) due to a habitual discrepancy between their endogenous circadian rhythm and actual sleep times imposed by social obligations. Here, we examined whether chronotype and/or SJL associate with components of cardiovascular disease risk beyond the known effects of sleep disturbances, poor health behaviors, and depressive symptomatology. DESIGN: Participants were healthy, midlife adults who worked part- or full-time day shifts (n = 447; mean age, 42.7 [range, 30-54] y; 53% female; 83% white). Chronotype was assessed with the Composite Scale of Morningness. SJL was quantified as the difference (in minutes) between the midpoints of actigraphy-derived sleep intervals before work vs non-workdays. RESULTS: Multiple regression analyses showed that SJL related to a lower high-density lipoprotein-cholesterol level, higher triglycerides, higher fasting plasma insulin, insulin resistance, and adiposity (P < .05), even after adjustment for subjective sleep quality, actigraphy-derived sleep characteristics, depressive symptomatology, and health behaviors. Evening chronotype associated with lower high-density lipoprotein-cholesterol after adjustment for covariates. CONCLUSION: Our findings suggest that a misalignment of sleep timing is associated with metabolic risk factors that predispose to diabetes and atherosclerotic cardiovascular disease.

Chronotype predicts positive affect rhythms measured by ecological momentary assessment.

Evening chronotype, a correlate of delayed circadian rhythms, is associated with depression. Altered positive affect (PA) rhythms may mediate the association between evening chronotype and depression severity. Consequently, a better understanding of the relationship between chronotype and PA may aid in understanding the etiology of depression. Recent studies have found that individuals with evening chronotype show delayed and blunted PA rhythms, although these studies are relatively limited in sample size, representativeness and number of daily affect measures. Further, published studies have not included how sleep timing changes on workday and non-workdays, or social jet lag (SJL) may contribute to the chronotype-PA rhythm link. Healthy non-depressed adults (n = 408) completed self-report affect and chronotype questionnaires. Subsequently, positive and negative affects were measured hourly while awake for at least two workdays and one non-workday by ecological momentary assessment (EMA). Sleep variables were collected via actigraphy and compared across chronotype groups. A cosinor variant of multilevel modeling was used to model individual and chronotype group rhythms and to calculate two variables: (1) amplitude of PA, or the absolute amount of daily variation from peak to trough during one period of the rhythm and (2) acrophase, or the time at which the peak amplitude of affect rhythms occurred. On workdays, individuals with evening chronotype had significantly lower PA amplitudes and later workday acrophase times than their morning type counterparts. In contrast to predictions, SJL was not found to be a mediator in the relationship between chronotype and PA rhythms. The association of chronotype and PA rhythms in healthy adults may suggest the importance of daily measurement of PA in depressed individuals and would be consistent with the hypothesis that evening chronotype may create vulnerability to depression via delayed and blunted PA rhythms.

Shorter sleep duration is associated with decreased insulin sensitivity in healthy white men.

STUDY OBJECTIVES: Short sleep has been linked to increased risk for type 2 diabetes and incident cardiovascular disease and acute sleep restriction impairs insulin-mediated glucose disposal. Here, we examined whether indices of glucose metabolism vary with naturally occurring differences in sleep duration. DESIGN AND MEASURES: Subjects were midlife, nondiabetic community volunteers (N = 224; mean age 44.5 ± 6.6 y [range: 30-54]; 52% female; 89% white). Laboratory measures of insulin sensitivity (Si) and acute secretion (AIRg), glucose effectiveness (Sg), and disposition index (Di) were obtained from a 180-min, intravenous glucose tolerance test. RESULTS: Shorter self-reported sleep duration (in hours) was associated with lower Si (P = 0.043), although an interaction of sleep duration with participant race (ß = -0.81, P = 0.002) showed this association significant only in whites. Moreover, sex-stratified analyses revealed that shorter sleep duration predicted lower Si in white men (ß = 0.29, P = 0.003) but not in white women (P = 0.22). Findings were similar for AIRg. The relationship between sleep duration and AIRg was moderated by race as well as sex, such that shorter sleep duration associated with greater insulin release only in white men (ß = -0.28, P = 0.004). Sleep duration was unrelated to Sg and Di (P's > 0.05). CONCLUSIONS: Our findings suggest that shorter sleep duration may impair insulin sensitivity and beta-cell function in nondiabetic white men, possibly contributing to later type 2 diabetes and cardiovascular disease.

The role of beliefs and attitudes about sleep in seasonal and nonseasonal mood disorder, and nondepressed controls.

BACKGROUND: Unhelpful sleep-related cognitions play an important role in insomnia and major depressive disorder, but their role in seasonal affective disorder has not yet been explored. Therefore, the purpose of this study was to determine if individuals with seasonal affective disorder (SAD) have sleep-related cognitions similar to those with primary insomnia, and those with insomnia related to comorbid nonseasonal depression. METHODS: Participants (n=147) completed the Dysfunctional Beliefs and Attitudes about Sleep 16-item scale (DBAS-16) and the Structured Interview Guide for the Hamilton Depression Rating Scale, Seasonal Affective Disorder Version (SIGH-SAD), which assesses self reported sleep problems including early, middle, or late insomnia, and hypersomnia in the previous week. All participants were assessed in winter, and during an episode for those with a depressive disorder. RESULTS: Individuals with SAD were more likely to report hypersomnia on the SIGH-SAD, as well as a combined presentation of hypersomnia and insomnia on the Pittsburgh Sleep Quality Index (PSQI). The SAD group reported DBAS-16 scores in the range associated with clinical sleep disturbance, and DBAS-16 scores were most strongly associated with reports of early insomnia, suggesting circadian misalignment. LIMITATIONS: Limitations include the self-report nature of the SIGH-SAD instrument on which insomnia and hypersomnia reports were based. CONCLUSIONS: Future work could employ sleep- or chronobiological-focused interventions to improve clinical response in SAD.

Melanopsin, photosensitive ganglion cells, and seasonal affective disorder.

In two recent reports, melanopsin gene variations were associated with seasonal affective disorder (SAD), and in changes in the timing of sleep and activity in healthy individuals. New studies have deepened our understanding of the retinohypothalamic tract, which translates environmental light received by the retina into neural signals sent to a set of nonvisual nuclei in the brain that are responsible for functions other than sight including circadian, neuroendocrine and neurobehavioral regulation. Because this pathway mediates seasonal changes in physiology, behavior, and mood, individual variations in the pathway may explain why approximately 1-2% of the North American population develops mood disorders with a seasonal pattern (i.e., Major Depressive and Bipolar Disorders with a seasonal pattern, also known as seasonal affective disorder/SAD). Components of depression including mood changes, sleep patterns, appetite, and cognitive performance can be affected by the biological and behavioral responses to light. Specifically, variations in the gene sequence for the retinal photopigment, melanopsin, may be responsible for significant increased risk for mood disorders with a seasonal pattern, and may do so by leading to changes in activity and sleep timing in winter. The retinal sensitivity of SAD is hypothesized to be decreased compared to controls, and that further decrements in winter light levels may combine to trigger depression in winter. Here we outline steps for new research to address the possible role of melanopsin in seasonal affective disorder including chromatic pupillometry designed to measure the sensitivity of melanopsin containing retinal ganglion cells.

Melanopsin gene variations interact with season to predict sleep onset and chronotype.

The human melanopsin gene has been reported to mediate risk for seasonal affective disorder (SAD), which is hypothesized to be caused by decreased photic input during winter when light levels fall below threshold, resulting in differences in circadian phase and/or sleep. However, it is unclear if melanopsin increases risk of SAD by causing differences in sleep or circadian phase, or if those differences are symptoms of the mood disorder. To determine if melanopsin sequence variations are associated with differences in sleep-wake behavior among those not suffering from a mood disorder, the authors tested associations between melanopsin gene polymorphisms and self-reported sleep timing (sleep onset and wake time) in a community sample (N = 234) of non-Hispanic Caucasian participants (age 30-54 yrs) with no history of psychological, neurological, or sleep disorders. The authors also tested the effect of melanopsin variations on differences in preferred sleep and activity timing (i.e., chronotype), which may reflect differences in circadian phase, sleep homeostasis, or both. Daylength on the day of assessment was measured and included in analyses. DNA samples were genotyped for melanopsin gene polymorphisms using fluorescence polarization. P10L genotype interacted with daylength to predict self-reported sleep onset (interaction p < .05). Specifically, sleep onset among those with the TT genotype was later in the day when individuals were assessed on longer days and earlier in the day on shorter days, whereas individuals in the other genotype groups (i.e., CC and CT) did not show this interaction effect. P10L genotype also interacted in an analogous way with daylength to predict self-reported morningness (interaction p < .05). These results suggest that the P10L TT genotype interacts with daylength to predispose individuals to vary in sleep onset and chronotype as a function of daylength, whereas other genotypes at P10L do not seem to have effects that vary by daylength. A better understanding of how melanopsin confers heightened responsivity to daylength may improve our understanding of a broad range of behavioral responses to light (i.e., circadian, sleep, mood) as well as the etiology of disorders with seasonal patterns of recurrence or exacerbation.