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We aim to examine the association of sleep duration, sleep quality, late chronotype, and circadian misalignment with glycemic control and risk of complications in young adults with youth-onset type 2 diabetes followed in the Treatment Options for Type 2 Diabetes in Adolescents and Youth (TODAY) study. Self-reported sleep duration, quality, timing, and circadian misalignment were assessed via a modified Pittsburgh Sleep Quality Index (PSQI) questionnaire, and chronotype was assessed via the Morningness-Eveningness Questionnaire (MEQ). We examined diabetes complications including loss of glycemic control (defined as hemoglobin A1c ≥8%), hypertension, dyslipidemia, albuminuria, and diabetic peripheral neuropathy. Multivariable logistic regression models were constructed to assess associations between sleep and circadian measures with outcomes of interest, such as loss of glycemic control and diabetes complications. A total of 421 participants (34.2% male), mean age 23.6 ± 2.5 yr, mean body mass index (BMI) of 36.1 ± 8.3 kg/m2, and mean diabetes duration of 10.0 ± 1.5 yr were evaluated. Self-reported short sleep duration, daytime sleepiness, and sleep quality were not associated with loss of glycemic control or diabetes complications. Late self-reported bedtime (after midnight) on work/school nights, rather than self-expressed chronotype or circadian misalignment, was independently associated with loss of glycemic control. An association was seen between late bedtimes and albuminuria but was attenuated after adjusting for depression. In conclusion, late bedtime on work/school days, rather than short sleep duration, daytime sleepiness, or poor sleep quality, was independently associated with loss of glycemic control in this longitudinal cohort of young adults with youth-onset type 2 diabetes. NEW & NOTEWORTHY: The prevalence of type 2 diabetes in youth is increasing at an alarming rate. Identifying potentially modifiable factors modulating glycemic control is critically important to reduce micro and macrovascular complications. In a large cohort of youth-onset type 2 diabetes, self-reported late bedtime on work/school days was independently associated with loss of glycemic control in this longitudinal cohort of young adults with youth-onset type 2 diabetes. [ABSTRACT FROM AUTHOR]

Circadian disruption is pervasive and can occur at multiple organizational levels, contributing to poor health outcomes at individual and population levels. Evidence points to a bidirectional relationship, in that circadian disruption increases disease severity and many diseases can disrupt circadian rhythms. Importantly, circadian disruption can increase the risk for the expression and development of neurologic, psychiatric, cardiometabolic, and immune disorders. Thus, harnessing the rich findings from preclinical and translational research in circadian biology to enhance health via circadian-based approaches represents a unique opportunity for personalized/precision medicine and overall societal well-being. In this Review, we discuss the implications of circadian disruption for human health using a bench-to-bedside approach. Evidence from preclinical and translational science is applied to a clinical and population-based approach. Given the broad implications of circadian regulation for human health, this Review focuses its discussion on selected examples in neurologic, psychiatric, metabolic, cardiovascular, allergic, and immunologic disorders that highlight the interrelatedness between circadian disruption and human disease and the potential of circadian-based interventions, such as bright light therapy and exogenous melatonin, as well as chronotherapy to improve and/or modify disease outcomes., Circadian (circa, 'about,' and diem, 'day') rhythms are endogenous oscillations with an approximately 24-hour cycle. Circadian rhythms in physiology and behavior are organized by a central 'master' clock, the suprachiasmatic [...]

Summary: Previous research has demonstrated that exposure to light preceding and during sleep is associated with poor sleep, but most research to date has utilized either experimental or cross‐sectional designs. The current study expands upon prior studies by using a microlongitudinal design that examines the night‐to‐night associations between light and sleep health in a diverse sample of adults (pre‐registered at osf.io/k5zgv). US adults aged 18–87 years from two parent studies (N = 124) wore an actiwatch for up to 10 nights. Light variables estimated from actigraphy include both average exposure and time above light threshold of 10 (TALT10) and 40 (TALT40) lux both during sleep and for the 1‐hr preceding sleep. Actigraphy‐based sleep variables included sleep offset, duration, percentage and fragmentation index. Higher average light exposure during sleep was associated with a later sleep‐offset time, lower sleep percentage and higher fragmentation index (all p < 0.01). More minutes of TALT10 during sleep was associated with later sleep timing, lower sleep percentage and higher fragmentation index (all p < 0.01), and greater TALT40 during sleep was associated with lower sleep percentage. Light exposure was not related to sleep duration. In summary, greater light exposure during sleep was related to poorer sleep continuity and later wake time. The lack of association between light and sleep duration may be the result of compensating for sleep disruption by delaying wake time. Multi‐level interventions to consistently reduce light levels during sleep should be considered. [ABSTRACT FROM AUTHOR]

The human circadian system plays a vital role in many physiological processes, and circadian rhythms are found in virtually all tissues and organs. The disruption of circadian rhythms may lead to adverse health outcomes. Evidence from recent population‐based studies was reviewed because they represent real‐world behavior and can be useful in developing future studies to reduce the risk of adverse health conditions, including cardiovascular diseases, obesity, and diabetes mellitus, which may occur because of circadian disruption. An electronic search in PubMed and Web of Science (2012–2022) was performed. Selected articles were based on specific inclusion and exclusion criteria. Five factors that may disrupt circadian rhythm alignment are discussed: shift work, late chronotype, late sleep timing, sleep irregularity, and late meal timing. Evidence from observational studies of these circadian disruptors suggests potential detrimental effects on cardiometabolic health, including higher BMI/obesity, higher blood pressure, greater dyslipidemia, greater inflammation, and diabetes. Future research should identify the specific underlying pathways in order to mitigate the health consequences of shift work. Furthermore, optimal sleep and mealtimes for metabolic health can be explored in intervention studies. Lastly, it is important that the timing of external environmental cues (such as light) and behaviors that influence circadian rhythms are managed. [ABSTRACT FROM AUTHOR]

Diabetes is highly prevalent and is associated with dietary behaviors. Time-restricted eating, which consolidates caloric intake to a shortened eating duration, has demonstrated improvement in metabolic health. Timing of eating could also impact metabolism. Our objective was to examine whether the timing of eating was associated with metabolic health independently of eating duration. Data (n = 7619) are from four cycles (2005–2012) of the National Health and Nutrition Examination Survey (NHANES), a nationally representative U.S. survey that included surveys, physical examinations, and dietary recalls. The primary exposures are eating duration and eating start time estimated from two non-consecutive dietary recalls. Primary outcomes were fasting glucose and estimated insulin resistance using the homeostatic model assessment method (HOMA-IR). The mean (95% CI) eating duration was 12.0 h (11.9–12.0) and the mean (95% CI) start time was 8:21 (8:15–8:26). Earlier eating start time was significantly associated with lower fasting glucose and estimated insulin resistance but eating interval duration was not. Every hour later that eating commenced was associated with approximately 0.6% higher glucose level and 3% higher HOMA-IR (both p < 0.001). In this cross-sectional study, earlier eating start time was associated with more favorable metabolic measures, indicating that meal timing is another important characteristic of dietary patterns that may influence metabolism. [ABSTRACT FROM AUTHOR]

Sleep hygiene recommendations discourage eating before bedtime; however, the impact of mealtime on sleep has been inconsistent. We examined gender-stratified associations between eating or drinking <1, <2 and <3 h before bedtime, sleep duration and wake after sleep onset (WASO >30 min). This study utilised 2003–2018 data from the American Time Use Survey, a nationally representative sample of USA residents aged ≥15 years. Participants recorded weekday/weekend activities during a 24-h period. Age-specific sleep duration and WASO were estimated categorically and continuously. Eating or drinking were identified from all activities recorded <1, <2 and <3 h before bedtime. Mean ± se sleep duration was 8·0 ± 0·006 h, and 6% of participants ate or drank <1 h prior to weekdays bedtime. Overall, eating or drinking <1 h prior to bedtime was associated with longer weekdays sleep duration. Women and men who ate or drank <1 h before bedtime, v. those who did not, had 35 min (95% CI (30,39)) and 25 min (95 % CI (21,29)) longer sleep duration, respectively, as well as increased odds of WASO; women (OR=2·03, 95% CI (1·66,2·49)) and men (OR=2·64, 95% CI (2·08,3·36)). As the interval of eating or drinking prior to bedtime expanded, odds of short and long sleep durations and WASO decreased. This population-based data linked eating or drinking <1 h before bedtime to longer sleep duration, but increased WASO. Eating or drinking further from bedtime lowers the odds of short and long sleep duration and WASO. Causal pathways are difficult to discern, though inefficient sleep after late-night eating could increase WASO and trigger compensatory increases in sleep duration. [ABSTRACT FROM AUTHOR]

Background: In addition to quantity and quality, meal timing and eating duration are additional dietary characteristics that impact cardiometabolic health. Given that cardiometabolic health disparities exist among racial and ethnic groups, we examined whether meal timing and eating duration are additional diet-related differences among racial and ethnic groups. Methods: Participants (n = 13,084) were adults (≥20 years) from the National Health and Nutrition Examination (NHANES, 2011–2018) Survey. Times of first and last meal and the interval between them (eating duration) were derived from two 24-h dietary recalls. Multiple linear regression analyses compared these variables among race and ethnicity after adjusting for potential confounders. Results: Compared to non-Hispanic White adults, the first mealtime was significantly later for Mexican American (23 min), Non-Hispanic Asian (15 min), Non-Hispanic Black (46 min), and Other Hispanic (20 min) and Other Racial (14 min) adults (all p < 0.05). Mexican American and Non-Hispanic Asian adults had a significantly different last mealtime by 13 min earlier and 25 min later, respectively, compared to Non-Hispanic White adults. Compared to Non-Hispanic White adults, the mean eating duration was shorter for other Hispanic (20 min), Mexican American (36 min), and Non-Hispanic Black (49 min) adults. Conclusions: Meal timing and eating duration are additional dietary characteristics that vary significantly among racial and ethnic groups. [ABSTRACT FROM AUTHOR]

A study was conducted to establish the relationship between short sleep duration and the increased risk of coronary artery calcification. Results indicated that longer measured sleep did reduce the risk of calcification.

The association between sleep and adolescent growth and developmental stage is examined in a large sample of adolescents ages 12-16 years from a nationally representative longitudinal study. The results, which are based on a large sample size, guarantee further examination with more objective measures into the association between sleep and growth and development among adolescents.

Non‐communicable diseases, including diabetes, are partly responsible for the deceleration of improvements of life expectancy in many countries. Diabetes is also associated with sleep disturbances. Our aim was to determine whether sleep disturbances, particularly in people with diabetes, were associated with increased mortality risk. Data from the UK Biobank were analysed (n = 487,728, mean follow‐up time = 8.9 years). The primary exposure was sleep disturbances, assessed through the question: Do you have trouble falling asleep at night or do you wake up in the middle of the night? The primary outcome was mortality. We also dichotomized sleep disturbances into "never/sometimes" versus "usually" (frequently), and combined with the presence/absence of diabetes: 24.2% of participants reported "never/rarely" experiencing sleep disturbances, 47.8% "sometimes" and 28.0% "usually". In age‐ and sex‐adjusted models, frequent sleep disturbances were associated with an increased risk of all‐cause mortality (hazard ratio [HR], 1.31; 95% confidence interval [CI], 1.26–1.37), which remained significant in the fully adjusted model (HR 1.13, 95% CI 1.09–1.18). The presence of both diabetes and frequent sleep disturbances was associated with greater risk of all‐cause mortality than either condition alone. In the fully adjusted model, the hazard ratio for all‐cause mortality was 1.11 (95% CI, 1.07–1.15) for frequent sleep disturbances alone, 1.67 (95% CI, 1.57–1.76) for diabetes alone and 1.87 for both (95% CI, 1.75–2.01). Frequent sleep disturbances (experienced by more than one quarter of the sample) were associated with increased risk of all‐cause mortality. Mortality risk was highest in those with both diabetes and frequent sleep disturbances. Complaints of difficulty falling or staying asleep merit attention by physicians. [ABSTRACT FROM AUTHOR]