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dc.rights.licenseopenen_US
hal.structure.identifierSommeil, Addiction et Neuropsychiatrie [Bordeaux] [SANPSY]
dc.contributor.authorTAILLARD, Jacques
ORCID: 0000-0001-9067-8189
IDREF: 229930786
hal.structure.identifierSommeil, Addiction et Neuropsychiatrie [Bordeaux] [SANPSY]
dc.contributor.authorSAGASPE, Patricia
hal.structure.identifierSommeil, Addiction et Neuropsychiatrie [Bordeaux] [SANPSY]
dc.contributor.authorPHILIP, Pierre
hal.structure.identifierSommeil, Addiction et Neuropsychiatrie [Bordeaux] [SANPSY]
dc.contributor.authorBIOULAC, Stephanie
ORCID: 0000-0003-2618-4234
IDREF: 059280824
dc.date.accessioned2023-05-17T09:56:56Z
dc.date.available2023-05-17T09:56:56Z
dc.date.issued2021-09-01
dc.identifier.issn1873-2968en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/182195
dc.description.abstractEnSleep timing is controlled by the subtle interplay between circadian and homeostatic oscillators which, according to their endogenous properties, allow beings to feel spontaneously that it is time to go to bed or wake up in synchrony with the earth's light/dark cycle. In humans, however, social time and nocturnal artificial light modify sleep timing. Our modern lifestyle and artificial nocturnal light delay our bedtime, make us wake up, and lead to a greater intraindividual variability in sleep timing. Depending on the constraints that social time places on us, our sleep timing may be in or out of phase with the internal circadian timing determined by the circadian clock. When a person's social time is out of phase with their circadian time, they may be considered to suffer from circadian disruption or 'social jetlag'. There are interindividual differences in sleep timing that are known as morningness-eveningness preferences or chronotype, e.g. late chronotypes go to bed later. Chronotype may be assessed in terms of differences in kinetic homeostatic sleep pressure, intrinsic circadian period (ICP) and/or phase angle entrainment. In addition, chronotype depends on genetic and age-related factors, e.g. it gets earlier as people grow older. The social time of late chronotype individuals during week days is not adapted to their circadian time, unlike on free days. This results in social jetlag and circadian disruption, which in turn induces a chronic sleep debt due to a late bedtime and an early wake time, which is compensated on free days but only partially. Sleep and circadian clock disruption generally alter cognitive performance (alertness, attention, memory, higher-order executive functions such as response inhibition and decision-making) but their impact remains to be clarified. When subjects adopt their preferred sleep timing, a "synchrony effect" often appears with chronotypes performing better during daytime at optimal than at suboptimal timing (late chronotypes perform better in the evening, early chronotypes in the morning). Evening types appear to be cognitively more vulnerable to suboptimal times than morning types, probably because they have to deal with social jetlag and the "wake effort" period after awakening. Circadian disruption, but not chronotype, may impact attentional/inhibitory performance (more impulsivity and inattention). Strong associations have been found between mood disorders or attention deficit hyperactivity disorder (ADHD) and chronotype, with these psychiatric disorders typically being overrepresented in evening types. The association between social jetlag and these psychiatric disorders is less obvious. Social jetlag can be corrected by reducing exposure to evening light, although eveningness may be considered as a lifelong factor predisposing to depression or inattention.
dc.language.isoENen_US
dc.subject.enChronobiology Phenomena
dc.subject.enCircadian Rhythm
dc.subject.enCognition
dc.subject.enHumans
dc.subject.enJet Lag Syndrome
dc.subject.enMental Disorders
dc.subject.enSleep
dc.subject.enTime Factors
dc.subject.enWakefulness
dc.title.enSleep timing, chronotype and social jetlag: Impact on cognitive abilities and psychiatric disorders.
dc.title.alternativeBiochem Pharmacolen_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1016/j.bcp.2021.114438en_US
dc.subject.halSciences du Vivant [q-bio]/Médecine humaine et pathologie/Psychiatrie et santé mentaleen_US
dc.identifier.pubmed33545116en_US
bordeaux.journalBiochemical Pharmacologyen_US
bordeaux.page114438en_US
bordeaux.volume191en_US
bordeaux.hal.laboratoriesSANPSY (Sommeil, Addiction, Neuropsychiatrie) - UMR 6033en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionCNRSen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.import.sourcepubmed
hal.identifierhal-04099948
hal.version1
hal.date.transferred2023-05-17T09:56:58Z
hal.exporttrue
workflow.import.sourcepubmed
dc.rights.ccCC BY-NC-NDen_US
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