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PMID
38185236
TITLE
Evening chronotypes with depression report poorer outcomes of SSRIs: A survey-based study of self-ratings.
ABSTRACT
BACKGROUND NlmCategory: BACKGROUND
Preliminary evidence suggests evening chronotype relates to poorer efficacy of selective-serotonin reuptake inhibitors (SSRIs). It is unknown whether this is specific to particular medications, self-rated chronotype, or efficacy.
METHODS NlmCategory: METHODS
Preliminary evidence suggests evening chronotype relates to poorer efficacy of selective-serotonin reuptake inhibitors (SSRIs). It is unknown whether this is specific to particular medications, self-rated chronotype, or efficacy. In the Australian Genetics of Depression Study (N=15,108; 75% female; 18-90 years; 68% with ≥1 other lifetime diagnosis), a survey assessed experiences with 10 antidepressants and the reduced Morningness-Evening Questionnaire; a chronotype polygenic score (PGS) was calculated. Age- and sex-adjusted regression models (Bonferroni-corrected) estimated associations among antidepressants variables ("how well the antidepressant worked" [efficacy], duration of symptom improvement, side effects, discontinuation due to side effects) and self-rated and genetic chronotypes.
RESULTS NlmCategory: RESULTS
Preliminary evidence suggests evening chronotype relates to poorer efficacy of selective-serotonin reuptake inhibitors (SSRIs). It is unknown whether this is specific to particular medications, self-rated chronotype, or efficacy. In the Australian Genetics of Depression Study (N=15,108; 75% female; 18-90 years; 68% with ≥1 other lifetime diagnosis), a survey assessed experiences with 10 antidepressants and the reduced Morningness-Evening Questionnaire; a chronotype polygenic score (PGS) was calculated. Age- and sex-adjusted regression models (Bonferroni-corrected) estimated associations among antidepressants variables ("how well the antidepressant worked" [efficacy], duration of symptom improvement, side effects, discontinuation due to side effects) and self-rated and genetic chronotypes. The chronotype-PGS explained 4% of the variance in self-rated chronotype (r=0.21). Higher self-rated eveningness was associated with poorer efficacy of escitalopram (OR=1.04; 95% CI 1.02-1.06; p=0.000035), fluoxetine (OR=1.03; 95% CI 1.01-1.05; p=0.001), sertraline (OR=1.02; 95% CI 1.01-1.04; p=0.0008), and desvenlafaxine (OR=1.03; 95% CI 1.01-1.05; p=0.004), and a profile of increased side effects (80% of those recorded; ORs=0.93-0.98), with 'difficulty getting to sleep' most likely. Self-rated chronotype was not related to duration of improvement or discontinuation due to side effects. The chronotype-PGS was only associated with suicidal thoughts and attempted suicide (self-reported). While our measures are imperfect, and not of circadian phase under controlled conditions, the model coefficients suggest that dysregulation of phenotypic chronotype relative to its genetic proxy was driving relationships with antidepressant outcomes.
CONCLUSIONS NlmCategory: CONCLUSIONS
Preliminary evidence suggests evening chronotype relates to poorer efficacy of selective-serotonin reuptake inhibitors (SSRIs). It is unknown whether this is specific to particular medications, self-rated chronotype, or efficacy. In the Australian Genetics of Depression Study (N=15,108; 75% female; 18-90 years; 68% with ≥1 other lifetime diagnosis), a survey assessed experiences with 10 antidepressants and the reduced Morningness-Evening Questionnaire; a chronotype polygenic score (PGS) was calculated. Age- and sex-adjusted regression models (Bonferroni-corrected) estimated associations among antidepressants variables ("how well the antidepressant worked" [efficacy], duration of symptom improvement, side effects, discontinuation due to side effects) and self-rated and genetic chronotypes. The chronotype-PGS explained 4% of the variance in self-rated chronotype (r=0.21). Higher self-rated eveningness was associated with poorer efficacy of escitalopram (OR=1.04; 95% CI 1.02-1.06; p=0.000035), fluoxetine (OR=1.03; 95% CI 1.01-1.05; p=0.001), sertraline (OR=1.02; 95% CI 1.01-1.04; p=0.0008), and desvenlafaxine (OR=1.03; 95% CI 1.01-1.05; p=0.004), and a profile of increased side effects (80% of those recorded; ORs=0.93-0.98), with 'difficulty getting to sleep' most likely. Self-rated chronotype was not related to duration of improvement or discontinuation due to side effects. The chronotype-PGS was only associated with suicidal thoughts and attempted suicide (self-reported). While our measures are imperfect, and not of circadian phase under controlled conditions, the model coefficients suggest that dysregulation of phenotypic chronotype relative to its genetic proxy was driving relationships with antidepressant outcomes. The idea that variation in circadian factors influences antidepressant responses was supported and encourages exploration of circadian mechanisms of depressive disorders and antidepressant treatments.
Copyright © 2024. Published by Elsevier Inc.
DATE PUBLISHED
2024 Jan 05
HISTORY
PUBSTATUS PUBSTATUSDATE
received 2023/07/13
revised 2023/12/20
accepted 2023/12/28
medline 2024/01/08 00:42
pubmed 2024/01/08 00:42
entrez 2024/01/07 19:15
AUTHORS
NAME COLLECTIVENAME LASTNAME FORENAME INITIALS AFFILIATION AFFILIATIONINFO
Crouse JJ Crouse Jacob J JJ Brain and Mind Centre, The University of Sydney, NSW, Australia. Electronic address: jacob.crouse@sydney.edu.au.
Park SH Park Shin Ho SH Brain and Mind Centre, The University of Sydney, NSW, Australia.
Byrne EM Byrne Enda M EM Institute for Molecular Bioscience, The University of Queensland, Brisbane, QLD, Australia; Child Health Research Centre, The University of Queensland, Brisbane, QLD, Australia.
Mitchell BL Mitchell Brittany L BL Department of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
Chan K Chan Karina K Brain and Mind Centre, The University of Sydney, NSW, Australia.
Scott J Scott Jan J Brain and Mind Centre, The University of Sydney, Australia; Institute of Neuroscience, Newcastle University, United Kingdom.
Medland SE Medland Sarah E SE Mental Health and Neuroscience Program, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia.
Martin NG Martin Nicholas G NG Department of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
Wray NR Wray Naomi R NR Department of Psychiatry, University of Oxford, Oxford, United Kingdom; Oxford Big Data Institute, Li Ka Shing Centre for Health Information and Discovery, University of Oxford, Oxford, UK Institute for Molecular Bioscience, The University of Queensland, Brisbane, QLD, Australia.
Hickie IB Hickie Ian B IB Brain and Mind Centre, The University of Sydney, NSW, Australia.
INVESTIGATORS
JOURNAL
VOLUME:
ISSUE:
TITLE: Biological psychiatry
ISOABBREVIATION: Biol Psychiatry
YEAR: 2024
MONTH: Jan
DAY: 05
MEDLINEDATE:
SEASON:
CITEDMEDIUM: Internet
ISSN: 1873-2402
ISSNTYPE: Electronic
MEDLINE JOURNAL
MEDLINETA: Biol Psychiatry
COUNTRY: United States
ISSNLINKING: 0006-3223
NLMUNIQUEID: 0213264
PUBLICATION TYPE
PUBLICATIONTYPE TEXT
Journal Article
COMMENTS AND CORRECTIONS
GRANTS
GENERAL NOTE
KEYWORDS
KEYWORD
antidepressants
circadian
depressive disorders
diurnal
pharmacotherapy
treatment
MESH HEADINGS
SUPPLEMENTARY MESH
GENE SYMBOLS
CHEMICALS
OTHER ID's