Individual Differences in Adult Human Sleep and Wakefulness: Leitmotif for a Research Agenda

Dongen, Hans P A Van; Vitellaro, Kristen M.; Dinges, David F.

doi:10.1093/sleep/28.4.479

Cited by 306 publications

(245 citation statements)

References 207 publications

(269 reference statements)

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“…Together, these data indicate that, as a group, Amylase activity and mRNA levels are elevated by sustained waking in humans. Because individuals vary greatly in their response to sleep loss (12), it is important to present data from individual subjects. As shown in Fig.…”

Section: Resultsmentioning

confidence: 99%

“…This question is complicated by the growing awareness that individuals vary in their sensitivity to SD both in the extent to which they report being sleepy and in subsequent neurobehavioral deficits (12). These deficits are both task-specific and highly reproducible for a given subject, suggesting that they reflect trait characteristics.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to more focused basic research and increased educational campaigns to create public awareness, both regulatory and legislative initiatives have been implemented to address this problem. A general theme that has emerged from all of these efforts has been the importance of identifying a simple and quantifiable biomarker of sleepiness (11)(12)(13). A biomarker of sleepiness should be responsive to increasing levels of sleep debt and should only be activated by periods of waking that are followed by compensatory increases in sleep time (sleep homeostasis).…”

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confidence: 99%

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Identification of a biomarker for sleep drive in flies and humans

Seugnet

Boero

Gottschalk

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

106

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It is a common experience to sacrifice sleep to meet the demands of our 24-h society. Current estimates reveal that as a society, we sleep on average 2 h less than we did 40 years ago. This level of sleep restriction results in negative health outcomes and is sufficient to produce cognitive deficits and reduced attention and is associated with increased risk for traffic and occupational accidents. Unfortunately, there is no simple quantifiable marker that can detect an individual who is excessively sleepy before adverse outcomes become evident. To address this issue, we have developed a simple and effective strategy for identifying biomarkers of sleepiness by using genetic and pharmacological tools that dissociate sleep drive from wake time in the model organism Drosophila melanogaster. These studies have identified a biomarker, Amylase, that is highly correlated with sleep drive. More importantly, both salivary Amylase activity and mRNA levels are also responsive to extended waking in humans. These data indicate that the fly is relevant for human sleep research and represents a first step in developing an effective method for detecting sleepiness in vulnerable populations.Drosophila ͉ saliva ͉ sleep deprivation I t has been suggested that forced and self-inflicted sleep loss have reached epidemic proportions in Western industrialized populations (1, 2), costing billions of dollars in lost productivity and creating hazardous conditions on our roadways (3), in our skies (4), and in our hospitals (5). The National Highway Traffic Safety Administration estimates that 20% of motor vehicle crashes are attributed to sleepiness and fully 37% of adult drivers report falling asleep at the wheel at some point in their lives. Moreover, both regional and long-haul pilots accumulate sleep debt during trips, fall asleep in the cockpit, and experience levels of sleepiness that are associated with performance decrements (6, 7). In the hospital setting, training demands frequently disrupt the sleep of medical residents, which is then associated with increased attentional failures and medical errors (8). Indeed, after a heavy call rotation, the driving performance of medical residents was similar to those with a blood alcohol level of 0.05 g % (9) and is associated with increased risk of falling asleep while driving (10).Given the magnitude of this problem, it is not surprising that the sleep community, public health officials, and others have devoted considerable attention toward minimizing the negative impact of sleep loss on public health and safety (11). In addition to more focused basic research and increased educational campaigns to create public awareness, both regulatory and legislative initiatives have been implemented to address this problem. A general theme that has emerged from all of these efforts has been the importance of identifying a simple and quantifiable biomarker of sleepiness (11)(12)(13). A biomarker of sleepiness should be responsive to increasing levels of sleep debt and should only be activated by period...

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Identification of a biomarker for sleep drive in flies and humans

Seugnet

Boero

Gottschalk

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

106

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“…Similarly, the evolution of wakefulness-induced changes in EEG theta/alpha activity, subjective sleepiness, and neurobehavioral performance can widely dissociate [49,50,52]. Taken together, accumulating data suggest that the magnitude of performance impairment from sleep loss reflects trait-like individual vulnerability [53,54], yet the underlying neurobiological mechanisms are currently unknown.…”

Section: Homeostatic Sleep-wake Regulationmentioning

confidence: 99%

Genotype-Dependent Differences in Sleep, Vigilance, and Response to Stimulants

Landolt

2008

CPD

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Abstract:To better understand the neurobiology of sleep disorders, detailed understanding of circadian and homeostatic sleep-wake regulation in healthy volunteers is mandatory. Sleep physiology and the repercussions of experimentallyinduced sleep deprivation on sleep and waking electroencephalogram (EEG), vigilance and subjective state are highly variable, even in healthy individuals. Accumulating evidence suggests that many aspects of normal sleep-wake regulation are at least in part genetically controlled. Current heritability estimates of sleep phenotypes vary between approximately 20-40 % for habitual sleep duration, to over 90 % for the spectral characteristics of the EEG in nonREM sleep. The molecular mechanisms underlying the trait-like, inter-individual variation are virtually unknown, and the human genetics of normal sleep is only at the beginning of being explored. The first studies identified distinct polymorphisms in genes contributing to the endogenous circadian clock and neurochemical systems previously implicated in sleep-wake regulation, to modulate sleep architecture and sleep EEG, vulnerability to sleep loss, and subjective and objective effects of caffeine on sleep. These insights are reviewed here. They disclose molecular mechanisms contributing to normal sleep-wake regulation in humans, and have potentially important implications for the neurobiology of sleep-wake disorders and their pharmacological treatment.

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“…In adults, self-reported sleep duration has been described as a function of lifestyle choices (e.g., staying up late or getting up early to work; Van Dongen, Vitellaro, & Dinges, 2005). For older children and adolescent, lifestyle choices are often dictated by homework or activities, combined with early school start times.…”

Section: How Much Sleep Is Just Right?mentioning

confidence: 99%

Future Directions in Sleep and Developmental Psychopathology

Meltzer

2016

Journal of Clinical Child & Adolescent Psychology

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Individual Differences in Adult Human Sleep and Wakefulness: Leitmotif for a Research Agenda

Cited by 306 publications

References 207 publications

Identification of a biomarker for sleep drive in flies and humans

Identification of a biomarker for sleep drive in flies and humans

Genotype-Dependent Differences in Sleep, Vigilance, and Response to Stimulants

Future Directions in Sleep and Developmental Psychopathology

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