Role of Sleep Timing in Caloric Intake and BMI

Cohort studies about the sleep duration on the risk of death among Chinese older adults are still lacking. The aim of this study was to examine whether extremely long or short sleep duration was associated with mortality in Chinese adults aged 65 years or older. We included participants aged 65 years or older in 2011 at baseline in 23 provinces from the Chinese Longitudinal Healthy Longevity Survey who were followed up in 2014/2018 in China. Sleep duration was categorized as short sleep duration (< 7 hours) and long sleep duration (> 8 hours). We used the Cox proportional hazards model and restricted cubic spline analysis to explore the association between sleep duration and mortality. Among 9578 participants, short sleep duration was associated with an 11% higher risk of death (adjusted hazard ratio [aHR]: 1.11; 95% confidence interval [CI]: 1.02-1.20) and long sleep duration was associated with a 24% higher risk of death (aHR: 1.24; 95% CI: 1.15-1.34), after adjustment for all covariates. There was a U-shaped association between sleep duration and all-cause mortality (nonlinear, P < .0001). Stratified analyses showed that the risk was higher among older people who smoked and with a higher level of education both for short and long sleepers than for those who never smoked and were illiterate (P value for interaction < .05). There was a U-shaped association between sleep duration and all-cause mortality in Chinese older adults, especially in more educated individuals and smokers. Du M, Liu M, Liu J. The association between sleep duration and the risk of mortality in the Chinese older adults: a national cohort study. J Clin Sleep Med. 2021;17(9):1821-1829.

The aims were (1) to investigate differences by ethnicity and socioeconomic status (SES) in objective measures of sleep in children aged 7-9 years and (2) determine whether measures of sleep predict child achievement in reading or mathematics after controlling for ethnicity and SES. Four groups of parent-child dyads were recruited: Māori, low-SES schools (n = 18); Māori, high-SES schools (n = 17); New Zealand European, low-SES schools (n = 18); New Zealand European, high-SES schools (n = 17). Child sleep was measured by actigraphy. Parents and teachers reported child daytime sleepiness and behavior, and children completed a self-report of anxiety symptoms. Teachers also reported on child achievement in reading and mathematics. Children from low-SES schools went to bed later on school nights (F[1,68] = 12.150, P = .001) and woke later (F[1,68] = 15.978, P < .001) than children from high-SES schools but had similar sleep duration. There were no differences related to ethnicity. Children from low-SES schools were almost 3 times more likely to be below national standards for mathematics. Children not meeting academic standards in mathematics had a later sleep start time, lower sleep period efficiency, and a decreased total sleep time. However, when SES and sleep period efficiency were modeled together neither were found to significantly influence achievement in mathematics. In this study, SES influenced sleep timing but not the quality and quantity of sleep in 7- to 9-year-old children, and a significant independent effect of sleep efficiency on learning could not be demonstrated.

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 (&amp;#914;= -.222; p =.005). Earlier sleep timing (&amp;#914;= -.186; p &amp;lt; .001) and shorter sleep duration(&amp;#914;= -.103; p &amp;lt; .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 (&amp;#914;= -.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 (&amp;lt; 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: To examine if sleep timing (combination of bedtime and wake up time) is associated with energy intake and physical activity/sedentary behaviour in obese adolescents. Methods: Participants included in this cross-sectional examination were 26 (13 females) obese volunteers (BMI ≥ 95th percentile) with a mean age of 13.6 ± 0.5 years and valid data on self-reported sleep, food intake (dietary record), physical activity and sedentary time (accelerometer), screen time (self-reported), and anthropometry (BMI). We categorized participants as “late sleepers” (midpoint of sleep >3:30 a.m., n=13) and participants as “normal sleepers” (midpoint of sleep ≤ 2:30 a.m., n=13). Results: As expected, wake-up time and bedtime were different between sleep timing groups (p<0.01); however, total sleep duration was the same (9.23 ± 1.14 vs. 9.16 ± 1.28 hours for normal and late sleepers, respectively, p=0.88). There was no significant BMI difference between late sleepers and normal sleepers. Total daily caloric intake was 27% higher in late sleepers (425 kcal) compared to normal sleepers (p=0.04). Using a linear regression model in the whole sample we observed that later sleep timing was associated with greater total caloric intake, independent of age, sex, BMI, moderate-to-vigorous physical activity (MVPA) and sleep duration (β=368.6, p=0.01). No association was found between sleep timing and MVPA or sedentary time. However, later sleep timing was related to greater screen time, independent of age, sex, BMI and sleep duration (β=105.7, p<0.01). Conclusion: The present study is the first to report that later bedtime is associated with greater caloric intake and screen time in obese adolescents independent of total sleep duration.

Higher plasma levels of leptin have been associated with increased cardiometabolic risk. The aim of this study was to investigate the association between short duration of sleep and hyperleptinemia in Taiwanese adults. We examined the association between duration of sleep and hyperleptinemia in 254 men and women recruited from the physical examination center at a regional hospital in southern Taiwan. Hyperleptinemia was defined as a plasma leptin level of 8.13 ng/mL and above. Short sleep duration was defined as < 6.5 h/day. Multiple logistic regression analysis was used to assess the association between short duration of sleep and hyperleptinemia. In females, short duration of sleep (< 6.5 h/day; OR = 2.15, 95% CI = 0.99-4.78), greater hip circumference (OR = 3.00, CI = 1.13-8.78), higher percent body fat (OR = 1.75, CI = 1.07-2.95), and higher white blood cell counts (OR = 1.67, CI = 1.26-2.28) were associated with an increased risk of hyperleptinemia. In males, greater body weight was significantly associated with an increased risk of hyperleptinemia (OR = 3.55, 95% CI = 1.46-10.23). There was also a trend of association (p = 0.096) between short duration of sleep and an increased risk of hyperleptinemia (OR = 4.98, 95% CI = 0.80-42.40). In this study of healthy Taiwanese adults, short duration of sleep was significantly associated with hyperleptinemia in women, and the association was independent of adiposity.

We aimed to explore the pairwise interactions between sleep disturbance, abnormal sleep duration, and abnormal sleep timing on the odds of suicidal ideation (SI) among U.S. adults. Data of 13,307 adults from the 2015–2020 National Health and Nutrition Examination Survey were analyzed. Sleep duration was categorized into short (<7 hours), normal (7–9 hours), and long sleep duration (≥9 hours). Sleep timing was categorized into normal [22:00–23:00), late (≥23:00), and early sleep timing (<22:00). SI was assessed through the ninth item of the Patient Health Questionnaire 9. Multivariate logistic regression and likelihood ratio tests were conducted to evaluate the associations of sleep disturbance, duration, and timing with SI odds and the pairwise interactions between them. After adjusting for confounders, sleep disturbance, late sleep timing, and long sleep duration were significantly associated with higher odds of SI, with the ORs of 2.36 (1.62–3.43), 1.88 (1.30–2.72), and 1.85 (1.06–3.22), respectively. Sleep duration showed context-dependent associations with SI: short sleep duration was linked to higher SI odds only in the presence of sleep disturbance or early sleep timing, whereas long sleep duration was associated with greater SI odds overall, with stronger effects among those with sleep disturbance or late sleep timing. Significant interactions were observed (p for interaction = 0.03 for each). The association between abnormal sleep duration and the odds of SI was modified by sleep disturbance and abnormal sleep timing. Not applicable.

To examine associations between objectively measured sleep duration and sleep timing with odds ofcompletion of an in vitro fertilization (IVF) cycle. This prospective cohort study enrolled 48 women undergoing IVF at a large tertiary medical center between 2015 and 2017. Sleep was assessed by wrist-worn actigraphy, 1-2 weeks prior to initiation of the IVF cycle. Reproductive and IVF cycle data and demographic and health information were obtained from medical charts. Sleep duration, midpoint, and bedtime were examined in relation to IVF cycle completion using logistic regression models, adjusted for age and anti-Müllerian hormone levels. A sub-analysis excluded women who worked non-day shifts to control for circadian misalignment. The median age of all participants was 33 years, with 29% of women >35 years. Ten women had an IVF cycle cancelation prior to embryo transfer. These women had shorter sleep duration, more nocturnal awakenings, lower sleep efficiency, and later sleep timing relative to those who completed their cycle. Longer sleep duration was associated with lower odds of uncompleted IVF cycle (OR = 0.88; 95%CI 0.78, 1.00, per 20-min increment of increasedsleep duration). Women with later sleep midpoint and later bedtime had higher odds of uncompleted cycle relative to those with earlier midpoint and earlier bedtime; OR = 1.24; 95%CI 1.09, 1.40 and OR = 1.33; 95%CI 1.17, 1.53 respectively, for 20-min increments. These results were independent of age, anti-Müllerian hormone levels, or sleep duration, and remained significant after exclusion of shift-working women. Shorter sleep duration and later sleep timing increase the odds of uncompleted cycles prior to embryo transfer.

Introduction Sleep duration and circadian misalignment have been linked to fertility and fecundability. However, sleep in women undergoing IVF has rarely been examined. This study investigated the role of sleep duration and timing with completion of an IVF cycle. Methods Prospective study of women undergoing IVF at a tertiary medical center between 2015 and 2017. Sleep was assessed by wrist-worn actigraphy 1–2 weeks prior to the initiation of their IVF cycle. Reproductive profile, IVF cycle details, demographic and health information were obtained from medical charts. Sleep duration, midpoint and bedtime were examined in relation to IVF cycle completion using logistic regression models, adjusted for age and anti-Müllerian hormone levels. A sub-analysis excluded women who worked non-day shifts to control for circadian misalignment. Results A total of 48 women were studied. Median age was 33y (range 25–42), with 29% of women older than 35 years. Ten women had an IVF cycle cancellation prior to embryo transfer. These women had shorter sleep duration, more nocturnal awakenings, lower sleep efficiency, and later sleep timing in comparison to those who completed their cycle. Twenty-minute increases in sleep duration were associated with lower odds of an uncompleted IVF cycle (OR = 0.88; 95% CI 0.78, 1.00). Women with later sleep midpoints and later bedtime had higher odds of an uncompleted cycle relative to those with earlier midpoints and earlier bedtime; OR=1.24; 95% CI 1.09, 1.40 and OR=1.33; 95% CI 1.17, 1.53 respectively, per 20-minute increments. These results were independent of age, levels of anti-Müllerian hormone, or sleep duration, and remained unchanged after exclusion of shift-working women. Conclusion This study demonstrated the influence of sleep duration and sleep timing on the odds of an uncompleted IVF cycle prior to embryo transfer. Sleep is a modifiable behavior that may contribute to IVF cycle success. Support (if any):

To investigate associations between adolescent sleep duration and timing, and blood leukocyte DNA methylation, one type of epigenetic modification that may respond to changes in sleep. Cross-sectional epigenome-wide analysis of DNA methylation was conducted to identify sleep-related CpG sites in 269 females and 233 males (14.4 ± 2.1 years on average) from the ELEMENT cohort study, in Mexico City. Sleep duration and midpoint on weekdays and weekends were assessed using 7-day wrist actigraphy (Actigraph GTX-BT), and DNA methylation in blood leukocytes was measured using the Illumina Infinium Methylation EPIC BeadChip. Linear regression was conducted to assess the relationship between sleep variables and DNA methylation at each array locus, adjusting for demographic confounders, batch effects, and cell types. Differentially methylated regions (DMRs) were assessed using ipDMR, and subsequent pathway analysis of relevant genes was conducted. At false discovery rate-adjusted p-value (Q) < .05, there was one inverse site-specific association between sleep midpoint on weekends and cg04070324 (not annotated to a specific gene) among males only (Q = 0.02). However, DMR analysis in the full sample revealed 1875 total significant DMRs at Q < 0.05, and there was little overlap of DMRs associated with sleep duration versus midpoint. Sex-stratified analysis revealed more associations among males than females (e.g. 3284 DMRs compared to 1346). Based on pathway enrichment analysis, the male-specific pathways for sleep duration were related to DNA and metabolism, whereas for sleep midpoint they were related to developmental processes. Epigenome-wide analysis identified distinct associations with sleep duration and timing, especially among male adolescents.

Introduction Sleep health is linked to dietary choices, and skipping breakfast is associated with risk of negative health outcomes in adolescents. However, there is a lack of research on whether dimensions of sleep at night predict adolescents eating breakfast the next day. We investigated within- and between-person associations of multiple aspects of sleep with adolescent breakfast consumption. Methods Data were collected from a subset of the age 15 wave of the Fragile Families and Child Wellbeing Study (n=590). Teens wore an actigraphy device and completed daily surveys for ~1 week (mean=5.9 days). Surveys assessed subjective sleep quality (low–high) and consumption of breakfast (no/yes). Mixed models assessed whether actigraphy-measured sleep timing (onset, midpoint, and offset) and subjective sleep quality predicted odds of breakfast consumption in both within- and between-person models. A curvilinear association between sleep duration and breakfast consumption was also assessed. Irregularity of sleep duration and timing were tested as additional predictors, calculated as SD per person (in between-person models only). Analyses included random intercepts for participants and covariates: school day, boredom, loneliness, happiness, depressive symptoms, sex, race/ethnicity, body mass index, and household income. Results Within-person analyses revealed a significant curvilinear association between sleep duration and breakfast consumption, such that on nights when teens slept shorter or longer than their average, they had lower odds of eating breakfast the next day (p=.005). Additionally, on nights when teens had a later sleep midpoint or offset than their usual, they tended to skip breakfast the next day (both p&amp;lt;.05). Between-person models showed that teens who on average had later sleep timing (onset, midpoint, and offset) and who reported lower sleep quality had lower odds of eating breakfast (all p&amp;lt;.04). Lastly, teens with greater irregularity of sleep duration and sleep timing (midpoint and offset) had lower odds of eating breakfast (all p&amp;lt;.009). Conclusion Findings indicate that multiple dimensions of adolescent sleep health, including long and short sleep duration, later sleep timing, and poorer sleep quality, are associated with lower odds of eating breakfast. These sleep and dietary behaviors in adolescence may consequently impact future metabolic health. Support (if any) R01HD073352

Objective/Background Short and long sleep duration, later sleep midpoint, and greater intra-individual sleep variability are associated with lower physical activity, but previous research lacks objective and concurrent assessment of sleep and physical activity. This cross-sectional study examined whether sleep duration, midpoint, and variability in duration and midpoint were related to wrist actigraphy-measured physical activity. Participants Participants were 2156 Hispanics/Latinos in the Hispanic Community Health Study/Study of Latinos (HCHS/SOL) Sueño Ancillary Study. Methods Participants wore Actiwatch devices to measure sleep and physical activity via the wrist for ≥5 days. Physical activity was defined as minutes/day in the upper quartile of the sampling distribution’s non-sleep activity, capturing light to vigorous physical activity. Results An inverse linear relationship between sleep duration and physical activity was found such that each additional sleep hour related to 29 fewer minutes of physical activity (B = −28.7, SE = 3.8), p < .01). Variability in sleep midpoint was also associated with physical activity; with each 1-hr increase in variability there were 24 more minutes of physical activity (B = 24.2, SE = 5.6, p < .01). In contrast, sleep midpoint and variability in duration were not associated with physical activity. Sensitivity analyses identified an association of short sleep duration and greater variability in sleep duration with greater accelerometry-derived moderate-to-vigorous physical activity measured at the HCHS/SOL baseline (M = 2.1 years before the sleep assessment). Conclusions Findings help clarify inconsistent prior research associating short sleep duration and sleep variability with greater health risks but also contribute novel information with simultaneous objective assessments.

Background:Adequate sleep duration is a prevention factor for pediatric obesity, but the role of timing is still unclear.Objectives:To investigate associations of sleep duration and timing with BMI in a large pediatric database.Methods:Medical chart and survey data were collected from 29,409 children aged 2-18 years who attended well-child visits between Jan 2019 and Dec 2023 (repeated-measures cross-sectional design). Logistic and linear mixed effects regression models accounting for repeated measures estimated odds of overweight/obesity and continuous BMI-for-age CDC-based percentiles for each additional/later hour of sleep duration, midpoint (median of bedtime and wake time), and bedtime, adjusted for potential confounders and stratified by age groups.Results:Among young children (2-5y), shorter sleep duration but not sleep timing was related to higher odds of overweight/obesity (21% higher odds with 95% CI: 3% to 36%). In mid-childhood (6-12 y), shorter sleep duration and later midpoint were associated with higher odds of overweight/obesity (18%, 95%CI = 9%, 26%; 32%, 95%CI = 17%, 49%). Among adolescents (13-18 y), each hour of later sleep midpoint equated to 12% higher odds of living with overweight/obesity (95% CI: 1% to 23%). Linear models were similar.Conclusions:Shorter sleep duration at younger ages and later sleep timing in adolescence was associated with higher BMI.

Introduction Postpartum anxiety is understudied and underdiagnosed in postpartum women, despite being more common than postpartum depression. Given associations between postpartum anxiety and adverse maternal and infant outcomes, it is crucial to identify patterns and predictors of postpartum anxiety. We examined the associations between sleep duration and timing and postpartum anxiety over 6 months following delivery. Methods Pregnant women (n=147; 30-39 weeks) with a history of depression completed the Pittsburgh Sleep Quality Index (PSQI), Edinburgh Postnatal Depression Scale, and Generalized Anxiety Disorder Scale-7 monthly following delivery for 6 months. Sleep duration and timing were extracted from the PSQI. Sleep timing was calculated as the midpoint between sleep onset and offset. In a multilevel model, sleep duration and timing were person-mean centered at level 1 (month level) and grand-mean centered at level 2 (participant level). Level 1 included main effects of time, sleep duration and timing, and interactions between time and person-mean centered sleep duration and timing and time and grand-mean centered sleep duration and timing. Level 2 included main effects of sleep duration and timing. Depression symptoms were included as a covariate at both levels. Results The intraclass correlation for anxiety symptoms was .46, supporting the use of a multilevel model. Anxiety symptoms increased over time (p&amp;lt;.001). Months with shorter sleep duration were associated with higher concurrent anxiety symptoms (p&amp;lt;.001). The effect of sleep duration on anxiety symptoms varied over time, such that those with shorter sleep duration reported higher anxiety symptoms than those with longer sleep duration in early postpartum months, whereas anxiety symptoms increased during later postpartum months regardless of sleep duration. Sleep timing was not significantly associated with anxiety symptoms (p&amp;gt;.05). Conclusion Postpartum anxiety increased over time, suggesting such symptoms are not transient features of the immediate postpartum period and highlighting the need to identify predictors. Shorter sleep duration may signal risk for elevated postpartum anxiety on a monthly timescale, particularly during early postpartum months. Treatments aimed at promoting sleep to improve postpartum anxiety may be most effective if targeted at early postpartum months. Future research should replicate these findings with objective sleep measures. Support (if any) Happiest Baby, Inc.; NIH T32 HL149646

Combined effects of sleep timing and nighttime sleep duration on non-alcoholic fatty liver disease

Introduction Adequate sleep is essential for cognitive and emotion-related functioning, and 9 to 12 hr of sleep is recommended for children ages 6 to 12 years and 8 to 10 hr for children ages 13 to 18 years. However, national survey data indicate that older youth sleep for fewer hours and fall asleep later than younger youth. This shift in sleep duration and timing corresponds with a sharp increase in onset of emotion-related problems (e.g., anxiety, depression) during adolescence. Given that both sleep duration and timing have been linked to emotion-related outcomes, the present study tests the effects of sleep duration and timing, and their interaction, on resting-state functional connectivity (RS-FC) of corticolimbic emotion-related neural circuitry in children and adolescents. Methods A total of 63 children and adolescents (6–17 years, 34 females) completed a weekend overnight sleep journal and a 10-min resting-state functional magnetic resonance imaging scan the next day (Sunday). Whole-brain RS-FC of the amygdala was computed, and the effects of sleep duration, timing (i.e., midpoint of sleep), and their interaction were explored using regression analyses. Results Overall, we found that older youth tended to sleep later and for fewer hours than younger youth. Controlling for age, shorter sleep duration was associated with lower RS-FC between the amygdala and regions implicated in emotion regulation, including ventral anterior cingulate cortex, precentral gyrus, and superior temporal gyrus. Interestingly, midpoint of sleep was associated with altered connectivity in a distinct set of brain regions involved in interoception and sensory processing, including insula, supramarginal gyrus, and postcentral gyrus. Our data also indicate widespread interactive effects of sleep duration and midpoint on brain regions implicated in emotion regulation, sensory processing, and motor control. Conclusion These results suggest that both sleep duration and midpoint of sleep are associated with next-day RS-FC within corticolimbic emotion-related neural circuitry in children and adolescents. The observed interactive effects of sleep duration and timing on RS-FC may reflect how homeostatic and circadian process interact in the brain and explain the complex patterns observed with respect to emotional health when considering sleep duration and timing. Sleep-related changes in corticolimbic circuitry may contribute to the onset of emotion-related problems during adolescence.