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Study objectivesSleep duration has been associated with risk of dementia and stroke, but few studies have investigated the relationship between sleep duration and brain MRI measures, particularly in middle age.MethodsIn a prospective cohort of 613 black and white adults (mean age = 45.4 years) enrolled in the Coronary Artery Risk Development in Young Adults (CARDIA) study, participants reported typical sleep duration, dichotomized into moderate sleep duration (> 6 to ≤ 8 h) and short sleep duration (≤ 6 h) at baseline (2005-2006). Five years later, we obtained brain MRI markers of white matter including fractional anisotropy, mean diffusivity, and white matter hyperintensities.ResultsCompared to moderate sleepers, short sleepers had an elevated ratio of white matter hyperintensities to normal tissue in the parietal region (OR = 2.31, 95% CI: 1.47, 3.61) adjusted for age, race/sex, education, hypertension, stroke/TIA, depression, smoking status, and physical activity. White matter diffusivity was also higher, approximately a 0.2 standard deviation difference, in frontal, parietal, and temporal white matter regions, among those reporting shorter sleep duration in (P < 0.05 for all).ConclusionsShort sleep duration was associated with worse markers of white matter integrity in midlife. These mid-life differences in white matter may underlie the link between poor sleep and risk of dementia and stroke.

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]

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]