Quick bibliography: Reviews/recent articles on the importance of adequate sleep for good physical and mental health.
*Dewald, J. F., Meijer, A. M., Oort, F. J., Kerkhof, G. A., & Bögels, S. M. (2010). The influence of sleep quality, sleep duration and sleepiness on school performance in children and adolescents: A meta-analytic review. Sleep Medicine Reviews, 14(3), 179-189. [Cited by]
“Insufficient sleep, poor sleep quality and sleepiness are common problems in children and adolescents being related to learning, memory and school performance. The associations between sleep quality, sleep duration, sleepiness and school performance were examined in three separate meta-analyses including influential factors (e.g., gender, age, parameter assessment) as moderators. All three sleep variables were significantly but modestly related to school performance. Effect sizes were larger for studies including younger participants which can be explained by dramatic prefrontal cortex changes during (early) adolescence. Concerning the relationship between sleep duration and school performance, age effects were even larger in studies that included more boys than in studies that included more girls, demonstrating the importance of differential pubertal development of boys and girls.”
*Harrison, Y., & Horne, J. A. (2000). The impact of sleep deprivation on decision making: A review. Journal of Experimental Psychology. Applied, 6(3), 236-249. [PDF] [Cited by]
“Few sleep deprivation (SD) studies involve realism or high-level decision making, factors relevant to managers, military commanders, and so forth, who are undergoing prolonged work during crises. Instead, research has favored simple tasks sensitive to SD mostly because of their dull monotony. In contrast, complex rule-based, convergent, and logical tasks are unaffected by short-term SD, seemingly because of heightened participant interest and compensatory effort. However, recent findings show that despite this effort, SD still impairs decision making involving the unexpected, innovation, revising plans, competing distraction, and effective communication. Decision-making models developed outside SD provide useful perspectives on these latter effects, as does a neuropsychological explanation of sleep function. SD presents particular difficulties for sleep-deprived decision makers who require these latter skills during emergency situations.”
“Sleep is a behavioral phenomenon conserved among mammals and some invertebrates, yet the biological functions of sleep are still being elucidated. In humans, sleep time becomes shorter, more fragmented, and of poorer quality with advancing age. Epidemiologically, the development of age-related neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease is associated with pronounced sleep disruption, whereas emerging mechanistic studies suggest that sleep disruption may be causally linked to neurodegenerative pathology, suggesting that sleep may represent a key therapeutic target in the prevention of these conditions. In this review, we discuss the physiology of sleep, the pathophysiology of neurodegenerative disease, and the current literature supporting the relationship between sleep, aging, and neurodegenerative disease.”
*Irwin, M. R. (2019). Sleep and inflammation: Partners in sickness and in health. Nature Reviews. Immunology, 19(11), 702-715. [Cited by]
“The discovery of reciprocal connections between the central nervous system, sleep and the immune system has shown that sleep enhances immune defenses and that afferent signals from immune cells promote sleep. One mechanism by which sleep is proposed to provide a survival advantage is in terms of supporting a neurally integrated immune system that might anticipate injury and infectious threats. However, in modern times, chronic social threats can drive the development of sleep disturbances in humans, which can contribute to the dysregulation of inflammatory and antiviral responses. In this Review, I describe our current understanding of the relationship between sleep dynamics and host defense mechanisms, with a focus on cytokine responses, the neuroendocrine and autonomic pathways that connect sleep with the immune system and the role of inflammatory peptides in the homeostatic regulation of sleep. Furthermore, I discuss the therapeutic potential of harnessing these reciprocal mechanisms of sleep–immune regulation to mitigate the risk of inflammatory and infectious diseases.”
*Wang, C., & Holtzman, D. M. (2020). Bidirectional relationship between sleep and Alzheimer’s disease: Role of amyloid, tau, and other factors. Neuropsychopharmacology, 45(1), 104-120. [Cited by]
“As we age, we experience changes in our nighttime sleep and daytime wakefulness. Individuals afflicted with Alzheimer’s disease (AD) can develop sleep problems even before memory and other cognitive deficits are reported. As the disease progresses and cognitive changes ensue, sleep disturbances become even more debilitating. Thus, it is imperative to gain a better understanding of the relationship between sleep and AD pathogenesis. We postulate a bidirectional relationship between sleep and the neuropathological hallmarks of AD; in particular, the accumulation of amyloid-β (Aβ) and tau. Our research group has shown that extracellular levels of both Aβ and tau fluctuate during the normal sleep−wake cycle. Disturbed sleep and increased wakefulness acutely lead to increased Aβ production and decreased Aβ clearance, whereas Aβ aggregation and deposition is enhanced by chronic increased wakefulness in animal models. Once Aβ accumulates, there is evidence in both mice and humans that this results in disturbed sleep. New findings from our group reveal that acute sleep deprivation increases levels of tau in mouse brain interstitial fluid (ISF) and human cerebrospinal fluid (CSF) and chronic sleep deprivation accelerates the spread of tau protein aggregates in neural networks. Finally, recent evidence also suggests that accumulation of tau aggregates in the brain correlates with decreased nonrapid eye movement (NREM) sleep slow wave activity. In this review, we first provide a brief overview of the AD and sleep literature and then highlight recent advances in the understanding of the relationship between sleep and AD pathogenesis. Importantly, the effects of the bidirectional relationship between the sleep−wake cycle and tau have not been previously discussed in other reviews on this topic. Lastly, we provide possible directions for future studies on the role of sleep in AD. ”
*Zhou, Q., Zhang, M., & Hu, D. (2019). Dose-response association between sleep duration and obesity risk: A systematic review and meta-analysis of prospective cohort studies. Sleep and Breathing, 23(4), 1035-1045. [Cited by]
“The association between sleep duration and obesity risk remains unclear. We performed an updated meta-analysis to quantify a potential dose-response relation between sleep duration and risk of obesity. PubMed and Embase were searched for prospective cohort studies examining the association between sleep duration and risk of obesity that were published up to October 28, 2017. Random effects models were used to evaluate the pooled relative risks (RRs) and 95% confidence intervals (CIs) for the association of sleep duration and obesity. Restricted cubic splines were used to model the dose-response association. The meta-analysis included 12 studies (16 reports). We found a reverse J-shaped relation between sleep duration and obesity, with the lowest risk at 7–8-h sleep per day. Compared with 7-h sleep duration per day, the pooled relative risks for obesity were 1.09 (95% CI 1.05–1.14) for each 1-h decrement among individuals who slept < 7 h per day and 1.02 (95% CI 0.99–1.05) for each 1-h increment of sleep duration among individuals with longer sleep duration. Short sleep duration significantly increased the risk of obesity. Compared with 7-h sleep duration per day, the risk of obesity increases 9% for each 1-h decrease in sleep duration. ”
For additional research about sleep and its impacts on physical and mental health, please see the Science Primary Literature Database.
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