Evidence map›Paper›PMID 36516465›Full record

ArticleSleep2023

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

Ross J Purple, Jan Cosgrave, Iona Alexander, Benita Middleton, Russell G Foster, Kate Porcheret, Katharina Wulff

Open access · hybridAbstract read
In one paragraph

Article in Sleep, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.6field-weighted citation impact, top 29% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed, 3 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 5 institutions in 3 countries.

Ross J PurpleSchool of Physiology Pharmacology and Neuroscience, University of Bristol, Bristol, UK.ORCID 0000-0003-1061-8106
Jan CosgraveSleep and Circadian Neuroscience Institute, Nuffield Department of Clinical Neurosciences, Sir William Dunn School of Pathology, University of Oxford, Oxford, UK.
Iona AlexanderSleep and Circadian Neuroscience Institute, Nuffield Department of Clinical Neurosciences, Sir William Dunn School of Pathology, University of Oxford, Oxford, UK.
Benita MiddletonDepartment of Chronobiology, Faculty of Health and Medical Sciences, University of Surrey, Guildford, UK.
Russell G FosterSleep and Circadian Neuroscience Institute, Nuffield Department of Clinical Neurosciences, Sir William Dunn School of Pathology, University of Oxford, Oxford, UK.
Kate PorcheretNorwegian Centre for Violence and Traumatic Stress Studies, University of Oslo, Oslo, Norway.
Katharina WulffDepartment of Radiation Sciences and Department of Molecular Biology, Umeå University, Umeå, Sweden.ORCID 0000-0003-2480-3329
University of Oxford · GBUmeå University · SEUniversity of Bristol · GBUniversity of Oslo · NOUniversity of Surrey · GB

Funding

Department of HealthWellcome TrustWellcome Trust 098461/Z/12/Z
6 · The paper itself

Abstract

STUDY

objectivesEnvironmental 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.

methodsUsing 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).

resultsPsychiatric 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.

conclusionDistinguishing 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.

Indexed as

MelatoninPsychotic DisordersCircadian RhythmHumansPhenotypeSleepMelatoninactigraphyenvironmental risk factorsmelatoninpsychosissleep EEG

Identifiers

PMID36516465
PMCPMC9995776
OpenAlexW4311448146

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.