@article{98abeea83c404b34b66ab665673826ea,
title = "Cortisol Levels in Childhood Associated with Emergence of Attenuated Psychotic Symptoms in Early Adulthood",
abstract = "Background: In individuals at clinical high-risk for psychosis, elevated cortisol levels predict subsequent onset of psychotic disorder. However, it is unclear whether cortisol alterations are evident at an earlier clinical stage and promote progression of psychosis expression. This study aimed to address this issue by investigating whether cortisol levels in childhood were associated with the emergence of attenuated psychotic symptoms in early adulthood. In exploratory analyses, we examined whether cortisol and psychosocial stress measures interacted in predicting attenuated psychotic symptoms. Methods: A sample of children (N = 109) enriched for psychosis risk factors were recruited at age 9–12 years and assessed at age 11–14 years (T1) and 17–21 years (T2). Measures of psychopathology, psychosocial stressors, and salivary cortisol were obtained at T1. Attenuated psychotic symptoms were assessed at T2 using the Prodromal Questionnaire. Results: Diurnal cortisol (β = 0.915, 95% confidence interval: 0.062–1.769) and daily stressors (β = 0.379, 95% confidence interval: 0.034–0.723) at T1 were independently associated with total Prodromal Questionnaire scores at T2 after accounting for demographic factors and T1 psychopathology. Exploratory analyses indicated a significant interaction between T1 diurnal cortisol and daily stressors (β = 0.743, 95% confidence interval: 0.081–1.405), with the highest predicted T2 total Prodromal Questionnaire scores occurring when both diurnal cortisol and daily stressors were increased. Conclusions: Our findings suggest that daily stressors and elevations in diurnal cortisol in late childhood/early adolescence increases risk for developing attenuated psychotic symptoms. These findings emphasize the importance of assessing environmental and biological risk factors for psychosis during neurodevelopmentally vulnerable time periods.",
keywords = "schizophrenia, psychosis, HPA axis, stress, salivary cortisol, adversity",
author = "Alexis Cullen and Helen Fisher and Nancy Gullett and Elizabeth Fraser and Roberts, {Ruth E.} and Uzma Zahid and Melody To and Natalie Yap and Patricia Zunszain and Carmine Pariante and Stephen Wood and Philip McGuire and Robin Murray and Valeria Mondelli and Laurens, {Kristin R.}",
note = "Funding Information: This research was supported by grants from a Sir Henry Wellcome Postdoctoral Fellowship (Grant No. 107395/Z/15/Z [to AEC]), a British Medical Association Margaret Temple Award 2012 (to HLF), a National Institute for Health Research Career Development Fellowship (Grant No. CDF/08/01/015 [to KRL]), a Brain & Behavior Research Foundation Young Investigator Award (to KRL), a British Medical Association Margaret Temple Award 2006 (to KRL), and BIAL Foundation research grants (Grant Nos. 35/06 [to KRL and RMM] and 192/12 [to KRL and RER]), a Young Investigator Grant awarded by the Brain & Behavior Research Foundation (Grant No. 28336 [to AEC]), the Evelyn Toll Family Foundation (to AEC), the Economic and Social Research Council Centre for Society and Mental Health at King's College London (Grant No. ES/S012567/1 [to HLF]), a Ph.D. scholarship supported by Lord Leverhulme's Charitable Trust (to UZ), National Institute for Health Research Senior Investigator Awards (CMP and PM), and an Australian Research Council Future Fellowship (Grant No. FT170100294 [KRL]). All authors are affiliated with the National Institute for Health Research Biomedical Research Centre at South London and Maudsley National Health Service Foundation Trust and King's College London. The views expressed are those of the authors and not necessarily those of the NHS, the National Institute for Health Research, the Department of Health and Social Care, the Economic and Social Research Council, or King's College London. We thank the children and caregivers who participated in the study and the research staff and students who contributed to data collection. RMM has received honoraria giving lectures/seminars at meetings supported by Janssen, Lundbeck, Recordati, Otsuka, and Sunovian. All other authors report no biomedical financial interests or potential conflicts of interest. Funding Information: This research was supported by grants from a Sir Henry Wellcome Postdoctoral Fellowship (Grant No. 107395/Z/15/Z [to AEC]), a British Medical Association Margaret Temple Award 2012 (to HLF), a National Institute for Health Research Career Development Fellowship (Grant No. CDF/08/01/015 [to KRL]), a Brain & Behavior Research Foundation Young Investigator Award (to KRL), a British Medical Association Margaret Temple Award 2006 (to KRL), and BIAL Foundation research grants (Grant Nos. 35/06 [to KRL and RMM] and 192/12 [to KRL and RER]), a Young Investigator Grant awarded by the Brain & Behavior Research Foundation (Grant No. 28336 [to AEC]), the Evelyn Toll Family Foundation (to AEC), the Economic and Social Research Council Centre for Society and Mental Health at King{\textquoteright}s College London (Grant No. ES/S012567/1 [to HLF]), a Ph.D. scholarship supported by Lord Leverhulme{\textquoteright}s Charitable Trust (to UZ), National Institute for Health Research Senior Investigator Awards (CMP and PM), and an Australian Research Council Future Fellowship (Grant No. FT170100294 [KRL]). Publisher Copyright: {\textcopyright} 2021 Society of Biological Psychiatry",
year = "2022",
month = jan,
day = "15",
doi = "10.1016/j.biopsych.2021.08.009",
language = "English",
volume = "91",
pages = "226--235",
journal = "Biological psychiatry",
issn = "0006-3223",
publisher = "Elsevier",
number = "2",
}