Sleep extension and cardiometabolic health: what it is, possible mechanisms and real-world applications.

Short sleep duration is associated with heightened cardiometabolic disease risk and has reached epidemic proportions among children, adolescents and adults. Potential mechanisms underlying this association are complex and multifaceted, including disturbances in circadian timing, food intake and appetitive hormones, brain regions linked to control of hedonic eating, physical activity, an altered microbiome and impaired insulin sensitivity. Sleep extension, or increasing total sleep duration, is an emerging and ecologically relevant intervention with significant potential to advance our understanding of the mechanisms underlying the association between short sleep duration and the risk of cardiometabolic disease. If effective, sleep extension interventions have potential to improve cardiometabolic health across the lifespan. Existing data show that sleep extension is feasible and might have potential cardiometabolic health benefits, although there are limitations that the field must overcome. Notably, most existing studies are short term (2-8 weeks), use different sleep extension strategies, analyse a wide array of cardiometabolic health outcomes in different populations and, frequently, lack adequate statistical power, thus limiting robust scientific conclusions. Overcoming these limitations will require fully powered, randomized studies conducted in people with habitual short sleep duration and existing cardiometabolic risk factors. Additionally, randomized controlled trials comparing different sleep extension strategies are essential to determine the most effective interventions. Ongoing and future research should focus on elucidating the potential cardiometabolic health benefits of sleep extension. Such studies have high potential to generate crucial knowledge with potential to improve health and quality of life for those struggling with short sleep duration.

Circadian misalignment disrupts biomarkers of cardiovascular disease risk and promotes a hypercoagulable state.

The circadian system regulates 24-h time-of-day patterns of cardiovascular physiology, with circadian misalignment resulting in adverse cardiovascular risk. Although many proteins in the coagulation-fibrinolysis axis show 24-h time-of-day patterns, it is not understood if these temporal patterns are regulated by circadian or behavioral (e.g., sleep and food intake) cycles, or how circadian misalignment influences these patterns. Thus, we utilized a night shiftwork protocol to analyze circadian versus behavioral cycle regulation of 238 plasma proteins linked to cardiovascular physiology. Six healthy men aged 26.2 ± 5.6 years (mean ± SD) completed the protocol involving two baseline days with 8-h nighttime sleep opportunities (circadian alignment), a transition to shiftwork day, followed by 2 days of simulated night shiftwork with 8-h daytime sleep opportunities (circadian misalignment). Plasma was collected for proteomics every 4 h across 24 h during baseline and during daytime sleep and the second night shift. Cosinor analyses identified proteins with circadian or behavioral cycle-regulated 24-h time-of-day patterns. Five proteins were circadian regulated (plasminogen activator inhibitor-1, angiopoietin-2, insulin-like growth factor binding protein-4, follistatin-related protein-3, and endoplasmic reticulum resident protein-29). No cardiovascular-related proteins showed regulation by behavioral cycles. Within the coagulation pathway, circadian misalignment decreased tissue factor pathway inhibitor, increased tissue factor, and induced a 24-h time-of-day pattern in coagulation factor VII (all FDR < 0.10). Such changes in protein abundance are consistent with changes observed in hypercoagulable states. Our analyses identify circadian regulation of proteins involved in cardiovascular physiology and indicate that acute circadian misalignment could promote a hypercoagulable state, possibly contributing to elevated cardiovascular disease risk among shift workers.

Night-time sleep duration and postpartum weight retention in primiparous women.

Objectives: Approximately 75% of women weigh more at 1-year postpartum than pre-pregnancy. More than 47% retain >10 lbs at 1-year postpartum, which is associated with adverse health outcomes for mother and child. Disturbed sleep may contribute to risk of postpartum weight retention (PWR) as short sleep duration is associated with increased risk of obesity. Thus, we investigated whether night-time sleep duration is associated with risk for excessive PWR. We also explored night-time sleep duration and change in postpartum waist circumference. Methods: This is an ancillary analysis from a prospective cohort study. Participants were healthy primiparous adults with a singleton birth. Excessive PWR at 1-year postpartum was defined as ≥7% of pre-pregnancy weight. Log-binomial and linear regression assessed associations between night-time sleep duration at 6 months postpartum and PWR at 1-year postpartum. Linear regression assessed the association between night-time sleep duration and change in postpartum waist circumference. Results: Mean age of participants (N = 467) was 29.51 (SD ±â€…4.78) years. Night-time sleep duration by actigraphy or self-report was not associated with risk for excessive PWR (risk ratio 0.96, [95%CI 0.87-1.06]; risk ratio 0.95 [95%CI 0.83-1.07], respectively) or change in waist circumference. Conclusion: Night-time sleep duration at 6 months postpartum was not associated with PWR at 1-year postpartum. Mixed findings among our results and previous research could be due to our focus on night-time sleep, and differences in sleep measurement methods and timeframes across studies. More comprehensively assessing sleep, including multiple sleep dimensions, may help advance our understanding of potential links between sleep and PWR. Trial Registration: The parent study, Motherhood and Pelvic Health (MAP Study), is registered at https://clinicaltrials.gov/ct2/show/NCT02512016, NCT02512016.

Biomarkers linking habitual short sleep duration with risk of cardiometabolic disease: current progress and future directions.

Approximately one in three adults in the United States sleeps less than the recommended 7 h per night. Decades of epidemiological data and data from experimental sleep restriction studies demonstrate short sleep duration is associated with adverse cardiometabolic risk, including risk of type 2 diabetes and cardiovascular disease. However, the precise mechanisms underlying this risk are not fully elucidated and there is a lack of sleep-based interventions designed to mitigate such risk. One strategy to overcome these limitations is to develop biomarkers that link habitual short sleep duration with adverse cardiometabolic risk. Such biomarkers could inform biochemical mechanisms, identify new targets for interventions, support precision medicine by identifying individuals most likely to benefit from sleep-based interventions, and ultimately lead to improved cardiometabolic health in people with habitual short sleep durations. Early progress demonstrates proof-of-principle that omics-based technologies are a viable approach to create biochemical signatures (biomarkers) of short sleep duration, primarily derived from acute studies of experimental sleep restriction. Yet, much work remains. Notably, studies that translate early findings from experimental sleep restriction to free-living adults with habitual short sleep duration have high potential to advance the field. Such studies also create an exciting opportunity for larger randomized controlled trials that simultaneously identify biomarkers of habitual short sleep duration and evaluate the efficacy of sleep-based interventions. Ultimately, early progress in developing molecular biomarkers of short sleep duration combined with the prior decades of progress in the sleep and metabolism fields provide the foundation for exciting progress in the biomarker development space.