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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]

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.

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]

This study aimed to determine which dietary factors were associated with habitual sleep duration in pre/peri- and post-menopausal women. Data from the 2007–2008 National Health and Nutrition Examination Survey were used (N = 1,783). Habitual sleep duration was categorized as very short (<5 h), short (5–6 h), normal (7–8 h), and long (≥9 h). Diet assessment was performed following validated procedures. In pre/peri-menopausal women (n = 1,116), controlling for the confounders, fewer number of foods, less intake of protein, carbohydrates, thiamin (B1), food folate, total choline, phosphorus, sodium, potassium, and selenium were significantly associated with a higher risk for very short sleep. Being on a low-salt diet was related to a lower risk for long sleep. In comparison, in post-menopausal women (n = 667), controlling for the confounders, more sugar intake, less intake of phosphorus and zinc were related to a higher risk for short sleep. There were novel associations between diet and sleep duration, particularly among pre/peri-menopausal women. Future research is needed to confirm those causal relationships. [ABSTRACT FROM AUTHOR]

Abstract: Sleep is a biological imperative associated with cardiometabolic disease risk. As such, a thorough discussion of the sociocultural and demographic determinants of sleep is warranted, if not overdue. This paper begins with a brief review of the laboratory and epidemiologic evidence linking sleep deficiency, which includes insufficient sleep and poor sleep quality, with increased risk of chronic cardiometabolic diseases such as obesity, diabetes and hypertension. Identification of the determinants of sleep deficiency is the critical next step to understanding the role sleep plays in human variation in health and disease. Therefore, the majority of this paper describes the different biopsychosocial determinants of sleep, including age, gender, psychosocial factors (depression, stress and loneliness), socioeconomic position and race/ethnicity. In addition, because sleep duration is partly determined by behavior, it will be shaped by cultural values, beliefs and practices. Therefore, possible cultural differences that may impact sleep are discussed. If certain cultural, ethnic or social groups are more likely to experience sleep deficiency, then these differences in sleep could increase their risk of cardiometabolic diseases. Furthermore, if the mechanisms underlying the increased risk of sleep deficiency in certain populations can be identified, interventions could be developed to target these mechanisms, reduce sleep differences and potentially reduce cardiometabolic disease risk. [Copyright &y& Elsevier]

Sleep represents a set of biological functions necessary for the maintenance of life. Performing these functions, though, requires that an individual engage in behaviors, which are affected by social and environmental factors. Race/ethnicity and socioeconomic position represent categories of factors that likely play a role in the experience of sleep in the community. Previous studies have suggested that racial/ethnic minorities and the socioeconomically disadvantaged may be more likely to experience sleep patterns that are associated with adverse health outcomes. It is possible that disparities in sleep represent a pathway by which larger disparities in health emerge. This review (1) contextualizes the concept of race/ethnicity in biomedical research, (2) summarizes previous studies that describe patterns of sleep attainment across race/ethnicity groups, (3) discusses several pathways by which race/ethnicity may be associated with sleep, (4) introduces the potential role of socioeconomic position in the patterning of sleep, and (5) proposes future research directions to address this issue. [ABSTRACT FROM AUTHOR]

Objectives: The association between inadequate sleep and type 2 diabetes has garnered much attention, but little is known about sleep and type 1 diabetes (T1D). Our objectives were to conduct a systematic review and meta-analysis comparing sleep in persons with and without T1D, and to explore relationships between sleep and glycemic control in T1D.Methods: Studies were identified from Medline and Scopus. Studies reporting measures of sleep in T1D patients and controls, and/or associations between sleep and glycemic control, were selected.Results: A total of 22 studies were eligible for the meta-analysis. Children with T1D had shorter sleep duration (mean difference [MD] = -26.4 minutes; 95% confidence interval [CI] = -35.4, -17.7) than controls. Adults with T1D reported poorer sleep quality (MD in standardized sleep quality score = 0.51; 95% CI = 0.33, 0.70), with higher scores reflecting worse sleep quality) than controls, but there was no difference in self-reported sleep duration. Adults with TID who reported sleeping >6 hours had lower hemoglobin A1c (HbA1c) levels than those sleeping ≤6 hours (MD = -0.24%; 95% CI = -0.47, -0.02), and participants reporting good sleep quality had lower HbA1c than those with poor sleep quality (MD = -0.19%; 95% CI = -0.30, -0.08). The estimated prevalence of obstructive sleep apnea (OSA) in adults with TID was 51.9% (95% CI = 31.2, 72.6). Patients with moderate-to-severe OSA had a trend toward higher HbA1c (MD = 0.39%, 95% CI = -0.08, 0.87).Conclusion: T1D was associated with poorer sleep and high prevalence of OSA. Poor sleep quality, shorter sleep duration, and OSA were associated with suboptimal glycemic control in T1D patients. [ABSTRACT FROM AUTHOR]

Background: Prior studies report less favorable sleep characteristics among non-Whites as compared with non-Hispanic Whites. However, few population-based studies have used objective measures of sleep duration, especially in more than two racial/ethnic groups. We tested whether objectively estimated sleep duration and self-reported sleep quality varied by race and whether differences were at least partially explained by the variability in clinical, psychological, and behavioral covariates.Methods: Adults aged 35-64 years who self-identified as White, Black, Asian, or Hispanic were randomly sampled from Chicago, IL, and the surrounding suburbs. Our analytic sample included adults who had an apnea-hypopnea index <15 after one night of screening and who completed seven nights of wrist actigraphy for determination of sleep duration, sleep percentage, minutes of wake after sleep onset, and sleep fragmentation (n = 495). Daytime sleepiness was estimated using the Epworth Sleepiness Scale (ESS), and sleep quality was estimated from the Pittsburgh Sleep Quality Index (PSQI).Results: Following statistical adjustment for age, gender, education, work schedule (ie, day vs. night shift), smoking status, depressive symptoms, body mass index (BMI), hypertension, and diabetes, sleep duration (minutes) was significantly (all p < 0.01) shorter in Black (mean = 399.5), Hispanic (mean = 411.7), and Asian (mean = 409.6) participants than in White participants (mean = 447.4). All remaining sleep characteristics were significantly less favorable among Black participants as compared with White participants. Asian participants also reported significantly more daytime sleepiness than did White participants.Conclusions: Differences in sleep characteristics by race/ethnicity are apparent in a sample of adults with a low probability of sleep apnea and following adjustment for known confounders. [ABSTRACT FROM AUTHOR]

Objective To determine the association between objectively measured sleep and 10-year changes in estimated glomerular filtration rate (eGFR). Methods From 2003 to 2005, an ancillary sleep study was conducted at the Chicago site of the Coronary Artery Risk Development in Young Adults (CARDIA) study. Community-based black and white adults (aged 32–51 years) wore a wrist actigraph for up to six nights to record sleep duration and fragmentation. Sleep quality was measured with the Pittsburgh Sleep Quality Index (PSQI). Participants without history of cardiovascular or chronic kidney diseases, proteinuria, or hypertension at the 2000–2001 CARDIA examination were followed over 10 years ( n  = 463). eGFR was estimated from serum creatinine (eGFR Cr ) at the 2000–2001, 2005–2006, and 2010–2011 CARDIA examinations, whereas cystatin-C-estimated eGFR (eGFR Cys ) was measured at the 2000–2001 and 2005–2006 examinations. Generalized estimating equation regression and linear models estimated the associations of each sleep parameter with changes in eGFR Cr and eGFR Cys , controlling for cardiovascular and renal risk. Results Sleep parameters were not related to 5-year change in eGFR Cys . However, each 1 h decrease in sleep duration was significantly associated with a 1.5 mL/min/1.73 m 2 higher eGFR Cr [95% confidence interval (CI), 0.2–2.7], and each one-point increase in PSQI was significantly associated with a 0.5 mL/min/1.73 m 2 higher eGFR Cr (95% CI, 0.04–0.9) over 10 years. Conclusion In this community-based sample, shorter sleep and poorer sleep quality were related to higher kidney filtration rates over 10 years. [ABSTRACT FROM AUTHOR]

Background and aim Short sleep duration and poor quality sleep are associated with coronary heart disease (CHD) mortality; however, the underlying pathophysiologic process remains unclear. Sleep apnea may confound the association because of its relationship with formation of thrombi, the vascular occlusive process in CHD. We tested whether sleep duration and quality were associated with prothrombotic biomarkers in adults with a low probability of apnea. Methods We included adults aged 35-64years recruited from the community and who had an apnea hypopnea index <15 after one night of screening (n=506). Sleep duration and maintenance were determined from 7days of wrist actigraphy; daytime sleepiness was estimated using the Epworth Sleepiness Scale. Factor VIII (FVIII), von Willebrand factor (vWF), thrombin antithrombin (TAT) complexes, and plasminogen activator inhibitor-1 (PAI-1) were measured in fasting blood. Results Sleep duration, maintenance, and daytime sleepiness were not associated with FVIII, vWf, or TAT. Sleep maintenance was modestly inversely associated with higher levels of log-transformed PAI-1 (β=-0.07, standard error (SE)=0.03 per 4.8%, p=0.04) following adjustment for demographic characteristics, cardiovascular risk factors, and body mass index (BMI). Conclusions Mild impairment in sleep was modestly associated with activation of coagulation; further study is needed to evaluate the role of fibrinolytic factors in sleep-mediated coronary thrombosis. [ABSTRACT FROM AUTHOR]

Abstract: Short sleep duration is associated with weight gain and obesity, diabetes, cardiovascular disease, psychiatric illness, and performance deficits. Likewise, long sleep duration is also associated with poor physical and mental health. The role of a healthy diet in habitual sleep duration represents a largely unexplored pathway linking sleep and health. This study evaluated associations between habitual sleep parameters and dietary/nutritional variables obtained via the National Health and Nutrition Examination Survey (NHANES), 2007–2008. We hypothesized that habitual very short (<5h) short (5–6h) and long (9+h) sleep durations are associated with intake of a number of dietary nutrient variables. Overall, energy intake varied across very short (2036kcal), short (2201kcal), and long (1926kcal) sleep duration, relative to normal (2151kcal) sleep duration (p =0.001). Normal sleep duration was associated with the greatest food variety (17.8), compared to very short (14.0), short (16.5) and long (16.3) sleep duration (p <0.001). Associations between sleep duration were found across nutrient categories, with significant associations between habitual sleep duration and proteins, carbohydrates, vitamins and minerals. In stepwise analyses, significant contributors of unique variance included theobromine (long sleep RR=0.910, p <0.05), vitamin C (short sleep RR=0.890, p <0.05), tap water (short sleep RR=0.952, p <0.001; very short (<5h) sleep RR=0.941, p <0.05), lutein+zeaxanthin (short sleep RR=1.123, p <0.05), dodecanoic acid (long sleep RR=0.812, p <0.05), choline (long sleep RR=0.450, p =0.001), lycopene (very short (<5h) sleep RR=0.950, p <0.05), total carbohydrate (very short (<5h) sleep RR=0.494, p <0.05; long sleep RR=0.509, p <0.05), selenium (short sleep RR=0.670, p <0.01) and alcohol (long sleep RR=1.172, p <0.01). Overall, many nutrient variables were associated with short and/or long sleep duration, which may be explained by differences in food variety. Future studies should assess whether these associations are due to appetite dysregulation, due to short/long sleep and/or whether these nutrients have physiologic effects on sleep regulation. In addition, these data may help us better understand the complex relationship between diet and sleep and the potential role of diet in the relationship between sleep and obesity and other cardiometabolic risks. [Copyright &y& Elsevier]