Exposure to Artificial Light At Night (ALAN) results in a disruption of the circadian system, which is deleterious to health. In industrialized countries, 75% of the total workforce is estimated to ...have been involved in shift work and night work. Epidemiologic studies, mainly of nurses, have revealed an association between sustained night work and a 50–100% higher incidence of breast cancer. The potential and multifactorial mechanisms of the effects include the suppression of melatonin secretion by ALAN, sleep deprivation, and circadian disruption.
Shift and/or night work generally decreases the time spent sleeping, and it disrupts the circadian time structure. In the long run, this desynchronization is detrimental to health, as underscored by a large number of epidemiological studies that have uncovered elevated rates of several diseases, including cancer, diabetes, cardiovascular risks, obesity, mood disorders and age-related macular degeneration. It amounts to a public health issue in the light of the very substantial number of individuals involved. The IARC has classified shift work in group 2A of “probable carcinogens to humans” since “they involve a circadian disorganization”. Countermeasures to the effects of ALAN, such as melatonin, bright light, or psychotropic drugs, have been proposed as a means to combat circadian clock disruption and improve adaptation to shift and night work. We review the evidence for the ALAN impacts on health. Furthermore, we highlight the importance of an in-depth mechanistic understanding to combat the detrimental properties of exposure to ALAN and develop strategies of prevention.
The effects of acute sleep deprivation on β-amyloid (Aβ) clearance in the human brain have not been documented. Here we used PET and 18F-florbetaben to measure brain Aβ burden (ABB) in 20 healthy ...controls tested after a night of rested sleep (baseline) and after a night of sleep deprivation. We show that one night of sleep deprivation, relative to baseline, resulted in a significant increase in Aβ burden in the right hippocampus and thalamus. These increases were associated with mood worsening following sleep deprivation, but were not related to the genetic risk (APOE genotype) for Alzheimer’s disease. Additionally, baseline ABB in a range of subcortical regions and the precuneus was inversely associated with reported night sleep hours. APOE genotyping was also linked to subcortical ABB, suggesting that different Alzheimer’s disease risk factors might independently affect ABB in nearby brain regions. In summary, our findings show adverse effects of one-night sleep deprivation on brain ABB and expand on prior findings of higher Aβ accumulation with chronic less sleep.
Circadian (∼24-hour) timing systems pervade all kingdoms of life and temporally optimize behavior and physiology in humans. Relatively recent changes to our environments, such as the introduction of ...artificial lighting, can disorganize the circadian system, from the level of the molecular clocks that regulate the timing of cellular activities to the level of synchronization between our daily cycles of behavior and the solar day. Sleep/wake cycles are intertwined with the circadian system, and global trends indicate that these, too, are increasingly subject to disruption. A large proportion of the world's population is at increased risk of environmentally driven circadian rhythm and sleep disruption, and a minority of individuals are also genetically predisposed to circadian misalignment and sleep disorders. The consequences of disruption to the circadian system and sleep are profound and include myriad metabolic ramifications, some of which may be compounded by adverse effects on dietary choices. If not addressed, the deleterious effects of such disruption will continue to cause widespread health problems; therefore, implementation of the numerous behavioral and pharmaceutical interventions that can help restore circadian system alignment and enhance sleep will be important.
Delirium occurs frequently in critically ill patients and has been associated with both short-term and long-term consequences. Efforts to decrease delirium prevalence have been directed at ...identifying and modifying its risk factors. One potentially modifiable risk factor is sleep deprivation. Critically ill patients are known to experience poor sleep quality with severe sleep fragmentation and disruption of sleep architecture. Poor sleep while in the intensive care unit is one of the most common complaints of patients who survive critical illness. The relationship between delirium and sleep deprivation remains controversial. However, studies have demonstrated many similarities between the clinical and physiologic profiles of patients with delirium and sleep deprivation. This article aims to review the literature, the clinical and neurobiologic consequences of sleep deprivation, and the potential relationship between sleep deprivation and delirium in intensive care unit patients. Sleep deprivation may prove to be a modifiable risk factor for the development of delirium with important implications for the acute and long-term outcome of critically ill patients.
Study Objectives: Sleep plays a pivotal role in the off-line processing of emotional memory. However, much remains unknown for its immediate vs. long-term influences. We employed behavioral and ...electrophysiological measures to investigate the short- and long-term impacts of sleep vs. sleep deprivation on emotional memory. Methods: Fifty-nine participants incidentally learned 60 negative and 60 neutral pictures in the evening and were randomly assigned to either sleep or sleep deprivation conditions. We measured memory recognition and subjective affective ratings in 12- and 60-h post-encoding tests, with EEGs in the delayed test. Results: In a 12-h post-encoding test, compared to sleep deprivation, sleep equally preserved both negative and neutral memory, and their affective tones. In the 60-h post-encoding test, negative and neutral memories declined significantly in the sleep group, with attenuated emotional responses to negative memories over time. Furthermore, two groups showed spatial-temporally distinguishable ERPs at the delayed test: while both groups showed the old-new frontal negativity (300-500 ms, FN400), sleep-deprived participants additionally showed an old-new parietal, Late Positive Component effect (600-1000 ms, LPC). Multivariate whole-brain ERPs analyses further suggested that sleep prioritized neural representation of emotion over memory processing, while they were less distinguishable in the sleep deprivation group. Conclusions: These data suggested that sleep's impact on emotional memory and affective responses is time-dependent: sleep preserved memories and affective tones in the short term, while ameliorating affective tones in the long term. Univariate and multivariate EEG analyses revealed different neurocognitive processing of remote, emotional memories between sleep and sleep deprivation groups. Key words: emotional memory; sleep deprivation; memory consolidation; ERP; short- vs. long-term effects
Effect of sleep deprivation on the human metabolome Davies, Sarah K.; Ang, Joo Ern; Revell, Victoria L. ...
Proceedings of the National Academy of Sciences,
07/2014, Letnik:
111, Številka:
29
Journal Article
Recenzirano
Odprti dostop
Sleep restriction and circadian clock disruption are associated with metabolic disorders such as obesity, insulin resistance, and diabetes. The metabolic pathways involved in human sleep, however, ...have yet to be investigated with the use of a metabolomics approach. Here we have used untargeted and targeted liquid chromatography (LC)/MS metabolomics to examine the effect of acute sleep deprivation on plasma metabolite rhythms. Twelve healthy young male subjects remained in controlled laboratory conditions with respect to environmental light, sleep, meals, and posture during a 24-h wake/sleep cycle, followed by 24 h of wakefulness. Two-hourly plasma samples collected over the 48 h period were analyzed by LC/MS. Principal component analysis revealed a clear time of day variation with a significant cosine fit during the wake/sleep cycle and during 24 h of wakefulness in untargeted and targeted analysis. Of 171 metabolites quantified, daily rhythms were observed in the majority (n = 109), with 78 of these maintaining their rhythmicity during 24 h of wakefulness, most with reduced amplitude (n = 66). During sleep deprivation, 27 metabolites (tryptophan, serotonin, taurine, 8 acylcarnitines, 13 glycerophospholipids, and 3 sphingolipids) exhibited significantly increased levels compared with during sleep. The increased levels of serotonin, tryptophan, and taurine may explain the antidepressive effect of acute sleep deprivation and deserve further study. This report, to our knowledge the first of metabolic profiling during sleep and sleep deprivation and characterization of 24 h rhythms under these conditions, offers a novel view of human sleep/wake regulation.
Chronic sleep loss and associated sleepiness and daytime impairments in adolescence are a serious threat to the academic success, health, and safety of our nation's youth and an important public ...health issue. Understanding the extent and potential short- and long-term repercussions of sleep restriction, as well as the unhealthy sleep practices and environmental factors that contribute to sleep loss in adolescents, is key in setting public policies to mitigate these effects and in counseling patients and families in the clinical setting. This report reviews the current literature on sleep patterns in adolescents, factors contributing to chronic sleep loss (ie, electronic media use, caffeine consumption), and health-related consequences, such as depression, increased obesity risk, and higher rates of drowsy driving accidents. The report also discusses the potential role of later school start times as a means of reducing adolescent sleepiness.
Chronic sleep fragmentation (SF) commonly occurs in human populations, and although it does not involve circadian shifts or sleep deprivation, it markedly alters feeding behaviors ultimately ...promoting obesity and insulin resistance. These symptoms are known to be related to the host gut microbiota. Mice were exposed to SF for 4 weeks and then allowed to recover for 2 weeks. Taxonomic profiles of fecal microbiota were obtained prospectively, and conventionalization experiments were performed in germ-free mice. Adipose tissue insulin sensitivity and inflammation, as well as circulating measures of inflammation, were assayed. Effect of fecal water on colonic epithelial permeability was also examined. Chronic SF-induced increased food intake and reversible gut microbiota changes characterized by the preferential growth of highly fermentative members of Lachnospiraceae and Ruminococcaceae and a decrease of Lactobacillaceae families. These lead to systemic and visceral white adipose tissue inflammation in addition to altered insulin sensitivity in mice, most likely via enhanced colonic epithelium barrier disruption. Conventionalization of germ-free mice with SF-derived microbiota confirmed these findings. Thus, SF-induced metabolic alterations may be mediated, in part, by concurrent changes in gut microbiota, thereby opening the way for gut microbiome-targeted therapeutics aimed at reducing the major end-organ morbidities of chronic SF.
Sleep loss and inflammation Mullington, Janet M., Ph.D; Simpson, Norah S., Ph.D; Meier-Ewert, Hans K., M.D ...
Best Practice & Research Clinical Endocrinology & Metabolism,
10/2010, Letnik:
24, Številka:
5
Journal Article
Recenzirano
Odprti dostop
Controlled, experimental studies on the effects of acute sleep loss in humans have shown that mediators of inflammation are altered by sleep loss. Elevations in these mediators have been found to ...occur in healthy, rigorously screened individuals undergoing experimental vigils of more than 24 h, and have also been seen in response to various durations of sleep restricted to between 25 and 50% of a normal 8 h sleep amount. While these altered profiles represent small changes, such sub-clinical shifts in basal inflammatory cytokines are known to be associated with the future development of metabolic syndrome disease in healthy, asymptomatic individuals. Although the mechanism of this altered inflammatory status in humans undergoing experimental sleep loss is unknown, it is likely that autonomic activation and metabolic changes play key roles.
Abstract
Introduction
Effective memory often requires recall of both specific information and the context in which the information was encountered. Total sleep deprivation (TSD) is known to impair ...memory for information items (e.g., words on a studied list), but the impact of TSD on binding, or associative linking, between items and context is not clear.
Methods
N=68 healthy adults (ages 22–40; 35 females) completed a 4-day (3-night) in-laboratory study. After a baseline night with 10h nighttime sleep opportunity, participants were randomly assigned to either 38h TSD (n=38) or a well-rested control (WRC) condition with 10h nighttime sleep opportunity (n=30). Both study arms concluded with a 10h nighttime recovery sleep opportunity. Participants completed a standardized recognition memory task at 14:50 on day 2 (baseline, session 1) and again 24h later (session 2). The memory task consisted of a study phase in which words with negative, positive, and neutral affective valence were spoken by a female or male speaker (50% each); followed immediately by a test phase, in which subjects made recognition judgments for the items (words) and their source (speaker).
Results
Mixed-effects ANOVA revealed significant interactions of session by condition for both word and speaker recognition (p<0.001). When sleep-deprived, TSD participants recognized fewer words and, for words that were correctly recognized, they were worse at recognizing the speaker, compared to baseline and to the WRC group. Negatively valenced words were associated with poorer word recognition (p<0.001), and in session 1 poorer source recognition (p = 0.032), but these valence effects did not interact with sleep deprivation.
Conclusion
TSD impaired memory for items, but more importantly, also impaired memory for the context in which items were presented, even if the items were themselves correctly recognized, and regardless of their affective valence. These results indicate that TSD may disrupt binding of information to its context, which could explain TSD deficits in decision-making tasks that require novel associative linking. Furthermore, our findings are important in real-world situations such as eyewitness accounts and perseveration of the influence of misinformation.
Support (if any)
NIH grant R21 CA167691 and CDMRP award W81XWH-20-1-0442
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