scholarly journals Causes and Consequences of Chronic Sleep Deficiency and the Role of Orexin

2021 ◽  
pp. 128-138
Author(s):  
Janet M. Mullington ◽  
Tony J. Cunningham ◽  
Monika Haack ◽  
Huan Yang
Keyword(s):  
Sleep Deficiency ◽  
Chronic Sleep

scholarly journals Sleep Deprivation and Sleep-Onset Insomnia are Associated with Blunted Physiological Reactivity to Stressors

2021 ◽  
Vol 186 (Supplement_1) ◽  
pp. 246-252
Author(s):  
Devon A Hansen ◽  
Brieann C Satterfield ◽  
Matthew E Layton ◽  
Hans P A Van Dongen
Keyword(s):  
Sleep Deprivation ◽  
Laboratory Study ◽  
Salivary Cortisol ◽  
Sleep Onset ◽  
Deprivation Condition ◽  
Increased Risk ◽  
Significant Difference ◽  
Sleep Deficiency ◽  
The Impact ◽  
Chronic Sleep

ABSTRACT Introduction Military operations often involve intense exposure to stressors combined with acute sleep deprivation, while military personnel also experience high prevalence of chronic sleep deficiency from insomnia and other sleep disorders. However, the impact of acute and chronic sleep deficiency on physiologic stressor responses is poorly understood. In a controlled laboratory study with normal sleepers and individuals with chronic sleep-onset insomnia, we measured responses to an acute stressor administered in a sleep deprivation condition or a control condition. Methods Twenty-two adults (aged 22-40 years; 16 females)—11 healthy normal sleepers and 11 individuals with sleep-onset insomnia—completed a 5-day (4-night) in-laboratory study. After an adaptation day and a baseline day, subjects were assigned to a 38-hour total sleep deprivation (TSD) condition or a control condition; the study ended with a recovery day. At 8:00 PM after 36 hours awake in the sleep deprivation condition or 12 hours awake in the control condition, subjects underwent a Maastricht Acute Stress Test (MAST). Salivary cortisol was measured immediately before the MAST at 8:00 PM, every 15 minutes after the MAST from 8:15 PM until 9:15 PM, and 30 minutes later at 9:45 PM. Baseline salivary cortisol was collected in the evening of the baseline day. Additionally, before and immediately upon completion of the MAST, self-report ratings of affect and pain were collected. Results The MAST elicited a stressor response in both normal sleepers and individuals with sleep-onset insomnia, regardless of the condition, as evidenced by increases in negative affect and pain ratings. Relative to baseline, cortisol levels increased immediately following the MAST, peaked 30 minutes later, and then gradually returned to pre-MAST levels. At the cortisol peak, there was a significant difference across groups and conditions, reflecting a pronounced blunting of the cortisol response in the normal sleepers in the TSD condition and the sleep-onset insomnia group in both the TSD and control conditions. Conclusions Blunted stressor reactivity as a result of sleep deficiency, whether acute or chronic, may reflect reduced resiliency attributable to allostatic load and may put warfighters at increased risk in high-stakes, rapid response scenarios.

scholarly journals Young adults are more vulnerable to chronic sleep deficiency and recurrent circadian disruption than older adults

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Kirsi-Marja Zitting ◽  
Mirjam Y. Münch ◽  
Sean W. Cain ◽  
Wei Wang ◽  
Arick Wong ◽  
...  
Keyword(s):  
Older Adults ◽  
Young Adults ◽  
Circadian Disruption ◽  
Sleep Deficiency ◽  
Chronic Sleep

scholarly journals Sleep allostasis in chronic sleep restriction: The role of the norepinephrine system

2013 ◽  
Vol 1531 ◽  
pp. 9-16 ◽  
Author(s):  
Youngsoo Kim ◽  
Lichao Chen ◽  
Robert W. McCarley ◽  
Robert E. Strecker
Keyword(s):  
Sleep Restriction ◽  
Norepinephrine System ◽  
Chronic Sleep

scholarly journals Sleep modulates alcohol toxicity in Drosophila

2021 ◽  
Author(s):  
Eric J. Noakes ◽  
Aliza K. De Nobrega ◽  
Alana P. Mellers ◽  
Lisa C. Lyons
Keyword(s):  
Drosophila Melanogaster ◽  
Sleep Deprivation ◽  
Public Health Problem ◽  
Alcohol Exposure ◽  
Vulnerable Groups ◽  
Alcohol Tolerance ◽  
Alcohol Sensitivity ◽  
Chronic Sleep Deprivation ◽  
Chronic Sleep

AbstractStudy ObjectivesAlcohol abuse is a significant public health problem, particularly in populations in which sleep deprivation is common as such as shift workers and aged individuals. Although research demonstrates the effect of alcohol on sleep, little is known about the role of sleep in alcohol sensitivity and toxicity. We investigated sleep as a factor modulating alcohol toxicity using Drosophila melanogaster, a model system ideal for studies of sleep, alcohol and aging.MethodsFollowing 24 hours of sleep deprivation using mechanical stimulation, Drosophila were exposed to binge-like alcohol exposures. Behavioral sensitivity, tolerance, and mortality were assessed. The effects of chronic sleep deprivation on alcohol toxicity were investigated using a short sleep mutant insomniac. Pharmacological induction of sleep for prior to alcohol exposure was accomplished using a GABAA-receptor agonist, 4,5,6,7-tetrahydroisoxazolo(5,4-c)pyridin-3-ol (THIP) to determine if increased sleep mitigated the effects of alcohol toxicity on middle-aged flies and flies with environmentally disrupted circadian clocks mimicking groups more vulnerable to the effects of alcohol.ResultsAcute sleep deprivation increased alcohol-induced mortality following alcohol exposure. However, sleep deprivation had no effect on alcohol absorbance or clearance. Sleep deprivation also abolished functional tolerance measured 24 hours after the initial alcohol exposure, although tolerance at 4 h was observed. Pharmacologically increasing sleep prior to alcohol exposure decreased alcohol-induced mortality.ConclusionsSleep quantity prior to alcohol exposure affects alcohol toxicity with decreased sleep increasing alcohol toxicity and dampened 24-hour alcohol tolerance. In contrast, increased sleep mitigated alcohol-induced mortality even in vulnerable groups such as aging flies and those with circadian dysfunction.Statement of significanceWith the growing incidence of sleep deprivation and sleep disorders across adolescents and adults, it is important to understand the role of sleep in alcohol toxicity to develop future therapies for prevention and treatment of alcohol-induced pathologies. Using Drosophila melanogaster, an established model for both sleep and alcohol research, we found that acute and chronic sleep deprivation increased alcohol toxicity and eliminated long-term functional alcohol tolerance. In contrast, increased sleep prior to binge-like alcohol exposure mitigated alcohol-induced mortality even in vulnerable groups with higher susceptibility to alcohol toxicity.

scholarly journals Later School Start Time: The Impact of Sleep on Academic Performance and Health in the Adolescent Population

2020 ◽  
Vol 17 (7) ◽  
pp. 2574 ◽  
Author(s):  
Valentina Alfonsi ◽  
Serena Scarpelli ◽  
Aurora D’Atri ◽  
Giacomo Stella ◽  
Luigi De Gennaro
Keyword(s):  
Learning Ability ◽  
Treatment Programs ◽  
Physical And Mental Health ◽  
Sleep Patterns ◽  
Start Time ◽  
Impaired Sleep ◽  
The Impact ◽  
The Relationship ◽  
Chronic Sleep

The crucial role of sleep in physical and mental health is well known, especially during the developmental period. In recent years, there has been a growing interest in examining the relationship between sleep patterns and school performance in adolescents. At this stage of life, several environmental and biological factors may affect both circadian and homeostatic regulation of sleep. A large part of this population does not experience adequate sleep, leading to chronic sleep restriction and/or disrupted sleep–wake cycles. Studies investigating the effects of different sleep–wake schedules on academic achievement showed that impaired sleep quality and quantity are associated with decreased learning ability and compromised daytime functioning. This review focuses on the most recent studies that evaluated the effects of modified school start time on sleep patterns and related outcomes. Moreover, based on the available empirical evidence, we intend to propose a direction for future studies targeted to implement prevention or treatment programs by modifying sleep timing.

scholarly journals The role of sleep deficiency in the trajectory of postconcussive symptoms in adolescents

Brain Injury ◽  
2019 ◽  
Vol 33 (11) ◽  
pp. 1413-1419 ◽  
Author(s):  
See Wan Tham ◽  
Rachel V. Aaron ◽  
Tonya M. Palermo
Keyword(s):  
Postconcussive Symptoms ◽  
Sleep Deficiency

scholarly journals Decoupling of Sleepiness from Sleep Time and Intensity during Chronic Sleep Restriction: Evidence for a Role of the Adenosine System

SLEEP ◽  
2012 ◽  
Vol 35 (6) ◽  
pp. 861-869 ◽  
Author(s):  
Youngsoo Kim ◽  
Yunren Bolortuya ◽  
Lichao Chen ◽  
Radhika Basheer ◽  
Robert W. McCarley ◽  
...  
Keyword(s):  
Sleep Time ◽  
Sleep Restriction ◽  
Chronic Sleep

scholarly journals Modeling Neurocognitive Decline and Recovery During Repeated Cycles of Extended Sleep and Chronic Sleep Deficiency

SLEEP ◽  
2016 ◽  
Vol 40 (1) ◽  
Author(s):  
Melissa A. St. Hilaire ◽  
Melanie Rüger ◽  
Federico Fratelli ◽  
Joseph T. Hull ◽  
Andrew J. K. Phillips ◽  
...  
Keyword(s):  
Sleep Deficiency ◽  
Neurocognitive Decline ◽  
Chronic Sleep

scholarly journals Metabolic Disturbances Induced by Sleep Restriction as Potential Triggers for Alzheimer’s Disease

2021 ◽  
Vol 15 ◽  
Author(s):  
Jesús Enrique García-Aviles ◽  
Rebeca Méndez-Hernández ◽  
Mara A. Guzmán-Ruiz ◽  
Miguel Cruz ◽  
Natalí N. Guerrero-Vargas ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Deficit ◽  
Amyloid Β ◽  
Sleep Restriction ◽  
Amyloid Β Peptide ◽  
Metabolic Disturbances ◽  
The Brain ◽  
Chronic Sleep

Sleep has a major role in learning, memory consolidation, and metabolic function. Although it is known that sleep restriction increases the accumulation of amyloid β peptide (Aβ) and the risk to develop Alzheimer’s disease (AD), the mechanism behind these effects remains unknown. In this review, we discuss how chronic sleep restriction induces metabolic and cognitive impairments that could result in the development of AD in late life. Here, we integrate evidence regarding mechanisms whereby metabolic signaling becomes disturbed after short or chronic sleep restriction in the context of cognitive impairment, particularly in the accumulation of Aβ in the brain. We also discuss the role of the blood-brain barrier in sleep restriction with an emphasis on the transport of metabolic signals into the brain and Aβ clearance. This review presents the unexplored possibility that the alteration of peripheral metabolic signals induced by sleep restriction, especially insulin resistance, is responsible for cognitive deficit and, subsequently, implicated in AD development.

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