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Phenotypic divergence in sleep and circadian cycles linked by affective state and environmental risk related to psychosis

Purple, Ross J. (författare)
School of Physiology Pharmacology and Neuroscience, University of Bristol, Bristol, United Kingdom
Cosgrave, Jan (författare)
Sleep and Circadian Neuroscience Institute, Nuffield Department of Clinical Neurosciences, Sir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom
Iona, Alexander (författare)
Sleep and Circadian Neuroscience Institute, Nuffield Department of Clinical Neurosciences, Sir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom
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Middleton, Benita (författare)
Department of Chronobiology, Faculty of Health and Medical Sciences, University of Surrey, Guildford, United Kingdom
Foster, Russell G. (författare)
Sleep and Circadian Neuroscience Institute, Nuffield Department of Clinical Neurosciences, Sir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom
Porcheret, Kate (författare)
Norwegian Centre for Violence and Traumatic Stress Studies, University of Oslo, Oslo, Norway; Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway
Wulff, Katharina (författare)
Umeå universitet,Institutionen för strålningsvetenskaper,Wallenberg centrum för molekylär medicin vid Umeå universitet (WCMM),Institutionen för molekylärbiologi (Medicinska fakulteten),Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet)
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 (creator_code:org_t)
2022-12-14
2023
Engelska.
Ingår i: Sleep. - : Oxford University Press. - 0161-8105 .- 1550-9109. ; 46:3
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • Study Objectives: Environmental cues influence circadian rhythm timing and neurochemicals involved in the regulation of affective behavior. How this interplay makes them a probable nonspecific risk factor for psychosis is unclear. We aimed to identify the relationship between environmental risk for psychosis and circadian timing phenotypes sampled from the general population.Methods: Using an online survey, we devised a cumulative risk exposure score for each of the 1898 survey respondents based on 23 empirically verified transdiagnostic risks for psychosis, three dimensions of affect severity, psychotic-like experiences, and help-seeking behavior. Quantitative phenotyping of sleep and circadian rhythms was undertaken using at-home polysomnography, melatonin and cortisol profiles, and 3-week rest-activity behavior in individuals with a high-risk exposure load (top 15% of survey respondents, n = 22) and low-risk exposure load (bottom 15% of respondents, n = 22).Results: Psychiatric symptoms were present in 100% of the high-load participants and 14% of the low-load participants. Compared to those with a low-load, high-load participants showed a later melatonin phase which was reflected by a greater degree of dispersion in circadian timing. Phase relationships between later circadian melatonin phase and later actigraphic sleep onsets were maintained and these were strongly correlated with self-reported sleep mid-points. No differences were identified from polysomnography during sleep between groups.Conclusion: Distinguishing circadian timing from other sleep phenotypes will allow adaptation for dosage of time-directed intervention, useful in stabilizing circadian timekeeping physiology and potentially reducing the multisystemic disruption in mental health disorders.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Neurovetenskaper (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Neurosciences (hsv//eng)

Nyckelord

actigraphy
environmental risk factors
melatonin
psychosis
sleep EEG

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