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CHRONIC SLEEP DEPRIVATION AND ITS EFFECT ON THE LENGTH OF HUMAN TELOMERES: A REVIEW
Abstract
Chronic Sleep deprivation has developed into a routine in today's rapidly growing world. Variety of factors including shift works, medical conditions, sleep disorders, household stress, domestic duties, social and work pressures, etc. are responsible for increased prevalence of Sleep restriction over extended periods and subject body to stress. It produces associated observable physiological and psychological changes. The present analysis has provided certain evidences suggesting that the chronic sleep deprivation as prolonged partial sleep restriction and accelerated telomere attrition are closely linked. Telomeres are the crucial targets for the effects of myriad factors influencing ageing and age related disorders. Telomeres are 'Biomarkers of Ageing' and the chronological age advancement is closely associated with these molecular structures. Newly emerging research in telomere biology highlights variety of stress factors with all culminating into accelerated telomere shortening. The present review summarizes the studies that have investigated chronic sleep deprivation as a major stress factor with effects of prolonged sleep loss on telomeres. A brief review of methodologies used to assess sleep and quantify Telomere Length (TL) is done to aid in postulating their feasibility, sensitivity, specificity and reproducibility to help standardize future research directions in this field.
... Moreover, sleep deprivation connected with chronic diseases such as type II diabetes and cardiovascular disease. 2,3,[6][7][8][9][10][11] Academic performance in university is a significant predictor of products. For instance, cumulative grade point average (GPA) forecasts upcoming financial success and traces psychosocial well-being. ...
Purpose:
Explore the quality of sleep and investigate the relationship between sleep quality, using social media platforms, and academic performance among university students.
Design and methods:
A cross-sectional correlation design was used, 412 students completed an electronic questionnaire.
Findings:
The majority of university students suffer from poor quality of sleep. The most frequently used social media platforms were WhatsApp, Snapchat, and YouTube. The strongest predictor of having very poor sleep quality was addiction on twitter.
Practice implications:
An educational program about the importance of adequate sleep should be supported university students.
Actigraphy is generally compared to polysomnography (PSG), which has been considered the gold standard for sleep studies. The objective of the present study was to evaluate the concordance between PSG and two previously proposed algorithms (Cole et al, 1992; Sadeh et al, 1994) to analyze actigraphic recordings. The minute-by-minute agreement rate was evaluated through calculation of sensitivity, specificity, and accuracy. Regarding the sleep parameters, the concordance was performed through the Bland and Altman technique.
A night of adaptation to the sleep laboratory followed by simultaneous polysomnographic and actigraphic recordings throughout the night.
21 healthy volunteers.
A sleep laboratory
None.
Ninety-one percent of all PSG epochs were correctly identified by both algorithms, and this accuracy is reasonably satisfactory. The actigraphy was a sensitive method, with values of 99% and 97% for Cole's and Sadeh's algorithms, respectively. However, actigraphy had a low specificity: 34% and 44% for Cole's and Sadeh's algorithms, respectively. The Bland and Altman technique showed that actigraphy systematically overestimated Sleep Latency, Total Sleep Time and Sleep Efficiency while it underestimated Intermittent Awakenings.
The results of this study show the utility of actigraphy as a useful method for assessment of sleep, despite its limitations regarding identification of waking epochs during sleep. The Bland and Altman concordance technique was revealed to be a powerful tool to evaluate how well actigraphy agreed with polysomnography. This technique, combined with calculations of sensitivity and specificity, appears to be the most adequate procedure for the assessment of concordance.
Deficits in daytime performance due to sleep loss are experienced universally and associated with a significant social, financial, and human cost. Microsleeps, sleep attacks, and lapses in cognition increase with sleep loss as a function of state instability. Sleep deprivation studies repeatedly show a variable (negative) impact on mood, cognitive performance, and motor function due to an increasing sleep propensity and destabilization of the wake state. Specific neurocognitive domains including executive attention, working memory, and divergent higher cognitive functions are particularly vulnerable to sleep loss. In humans, functional metabolic and neurophysiological studies demonstrate that neural systems involved in executive function (i.e., prefrontal cortex) are more susceptible to sleep deprivation in some individuals than others. Recent chronic partial sleep deprivation experiments, which more closely replicate sleep loss in society, demonstrate that profound neurocognitive deficits accumulate over time in the face of subjective adaptation to the sensation of sleepiness. Sleep deprivation associated with disease-related sleep fragmentation (i.e., sleep apnea and restless legs syndrome) also results in neurocognitive performance decrements similar to those seen in sleep restriction studies. Performance deficits associated with sleep disorders are often viewed as a simple function of disease severity; however, recent experiments suggest that individual vulnerability to sleep loss may play a more critical role than previously thought.
To inform the debate over whether human sleep can be chronically reduced without consequences, we conducted a dose-response chronic sleep restriction experiment in which waking neurobehavioral and sleep physiological functions were monitored and compared to those for total sleep deprivation.
The chronic sleep restriction experiment involved randomization to one of three sleep doses (4 h, 6 h, or 8 h time in bed per night), which were maintained for 14 consecutive days. The total sleep deprivation experiment involved 3 nights without sleep (0 h time in bed). Each study also involved 3 baseline (pre-deprivation) days and 3 recovery days.
Both experiments were conducted under standardized laboratory conditions with continuous behavioral, physiological and medical monitoring.
A total of n = 48 healthy adults (ages 21-38) participated in the experiments.
Noctumal sleep periods were restricted to 8 h, 6 h or 4 h per day for 14 days, or to 0 h for 3 days. All other sleep was prohibited.
Chronic restriction of sleep periods to 4 h or 6 h per night over 14 consecutive days resulted in significant cumulative, dose-dependent deficits in cognitive performance on all tasks. Subjective sleepiness ratings showed an acute response to sleep restriction but only small further increases on subsequent days, and did not significantly differentiate the 6 h and 4 h conditions. Polysomnographic variables and delta power in the non-REM sleep EEG-a putative marker of sleep homeostasis--displayed an acute response to sleep restriction with negligible further changes across the 14 restricted nights. Comparison of chronic sleep restriction to total sleep deprivation showed that the latter resulted in disproportionately large waking neurobehavioral and sleep delta power responses relative to how much sleep was lost. A statistical model revealed that, regardless of the mode of sleep deprivation, lapses in behavioral alertness were near-linearly related to the cumulative duration of wakefulness in excess of 15.84 h (s.e. 0.73 h).
Since chronic restriction of sleep to 6 h or less per night produced cognitive performance deficits equivalent to up to 2 nights of total sleep deprivation, it appears that even relatively moderate sleep restriction can seriously impair waking neurobehavioral functions in healthy adults. Sleepiness ratings suggest that subjects were largely unaware of these increasing cognitive deficits, which may explain why the impact of chronic sleep restriction on waking cognitive functions is often assumed to be benign. Physiological sleep responses to chronic restriction did not mirror waking neurobehavioral responses, but cumulative wakefulness in excess of a 15.84 h predicted performance lapses across all four experimental conditions. This suggests that sleep debt is perhaps best understood as resulting in additional wakefulness that has a neurobiological "cost" which accumulates over time.
The molecular features of telomeres and telomerase are conserved among most eukaryotes. How telomerase and telomeres function and how they interact to promote the chromosome-stabilizing properties of telomeres are discussed here.
Telomeres provide an essential 'capping' function, which prevents the natural end of a chromosome from being recognised as a simple dsDNA break. The biology of human telomeres is inextricably linked with both cancer and ageing. As such there is considerable interest in determining the length of these essential and dynamic structures. Here I review, from the standpoint of ageing research in humans, the current situation with regards to technologies available to determine telomere length in human cells and tissues.
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