Lower cortisol levels and attenuated cortisol reactivity to daily-life stressors in adults with 22q11.2 deletion syndrome.


Journal

Psychoneuroendocrinology
ISSN: 1873-3360
Titre abrégé: Psychoneuroendocrinology
Pays: England
ID NLM: 7612148

Informations de publication

Date de publication:
08 2019
Historique:
received: 09 10 2018
revised: 25 01 2019
accepted: 21 03 2019
pubmed: 9 4 2019
medline: 1 4 2020
entrez: 9 4 2019
Statut: ppublish

Résumé

22q11.2 deletion syndrome (22q11DS) is a genetic disorder associated with neurodevelopmental, anxiety and mood disorders, as well as an increased risk for developing psychosis. Cortisol levels and stress reactivity reflect hypothalamic-pituitary-adrenal (HPA)-axis activity, and are believed to be altered in individuals that often experience daily-life stress, depression, and psychotic symptoms. However, it is unknown whether individuals with 22q11DS display an altered stress reactivity. We included 27 adults with 22q11DS (mean age: 34.1 years, 67% female) and 24 age and sex-matched healthy controls (HC; mean age: 39.9 years, 71% female) into an experience sampling study. Throughout 6 consecutive days, we measured participants' subjective stress related to current activity and at the same time collected salivary cortisol samples. Multilevel regression models were used to analyze cortisol reactivity to activity-related stress. Diurnal cortisol levels were significantly lower in the 22q11DS group compared to HCs (B=-1.03, p < 0.001). 22q11DS adults displayed significantly attenuated cortisol reactivity to activity-related stress compared to HCs (B = -0.04, p = 0.026). Post-hoc exploratory analysis revealed that these results were independent from 22q11DS psychiatric diagnosis or medication use. These results indicate that adults with 22q11DS have lower cortisol levels and attenuated cortisol response to daily stress, possibly resulting from an increased sensitization of the HPA-axis. This suggests that alterations in HPA-axis functioning, previously reported in several psychiatric disorders including post-traumatic stress disorder (PTSD), psychotic disorder, and mood disorder, also appear to be present in adults with 22q11DS.

Sections du résumé

BACKGROUND
22q11.2 deletion syndrome (22q11DS) is a genetic disorder associated with neurodevelopmental, anxiety and mood disorders, as well as an increased risk for developing psychosis. Cortisol levels and stress reactivity reflect hypothalamic-pituitary-adrenal (HPA)-axis activity, and are believed to be altered in individuals that often experience daily-life stress, depression, and psychotic symptoms. However, it is unknown whether individuals with 22q11DS display an altered stress reactivity.
METHODS
We included 27 adults with 22q11DS (mean age: 34.1 years, 67% female) and 24 age and sex-matched healthy controls (HC; mean age: 39.9 years, 71% female) into an experience sampling study. Throughout 6 consecutive days, we measured participants' subjective stress related to current activity and at the same time collected salivary cortisol samples. Multilevel regression models were used to analyze cortisol reactivity to activity-related stress.
RESULTS
Diurnal cortisol levels were significantly lower in the 22q11DS group compared to HCs (B=-1.03, p < 0.001). 22q11DS adults displayed significantly attenuated cortisol reactivity to activity-related stress compared to HCs (B = -0.04, p = 0.026). Post-hoc exploratory analysis revealed that these results were independent from 22q11DS psychiatric diagnosis or medication use.
CONCLUSION
These results indicate that adults with 22q11DS have lower cortisol levels and attenuated cortisol response to daily stress, possibly resulting from an increased sensitization of the HPA-axis. This suggests that alterations in HPA-axis functioning, previously reported in several psychiatric disorders including post-traumatic stress disorder (PTSD), psychotic disorder, and mood disorder, also appear to be present in adults with 22q11DS.

Identifiants

pubmed: 30959234
pii: S0306-4530(18)30991-0
doi: 10.1016/j.psyneuen.2019.03.023
pii:
doi:

Substances chimiques

Hydrocortisone WI4X0X7BPJ

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

85-94

Subventions

Organisme : NIMH NIH HHS
ID : U01 MH101722
Pays : United States

Informations de copyright

Copyright © 2019 Elsevier Ltd. All rights reserved.

Auteurs

Esther D A van Duin (EDA)

Department of Psychiatry & Neuropsychology, Maastricht University, Maastricht, the Netherlands; Department of Radiology and Nuclear Medicine, Amsterdam University Medical Centers, location Academic Medical Center, Amsterdam, the Netherlands.

Thomas Vaessen (T)

Center for Contextual Psychiatry, Department of Neurosciences, KU Leuven, Leuven, Belgium. Electronic address: thomas.vaessen@kuleuven.be.

Zuzana Kasanova (Z)

Center for Contextual Psychiatry, Department of Neurosciences, KU Leuven, Leuven, Belgium.

Wolfgang Viechtbauer (W)

Department of Psychiatry & Neuropsychology, Maastricht University, Maastricht, the Netherlands.

Ulrich Reininghaus (U)

Department of Psychiatry & Neuropsychology, Maastricht University, Maastricht, the Netherlands; Centre for Epidemiology and Public Health, Health Service and Population Research Department, Institute of Psychiatry, Psychology & Neuroscience, King's College London, London, UK.

Peter Saalbrink (P)

Department of Psychiatry & Neuropsychology, Maastricht University, Maastricht, the Netherlands.

Claudia Vingerhoets (C)

Department of Psychiatry & Neuropsychology, Maastricht University, Maastricht, the Netherlands; Department of Radiology and Nuclear Medicine, Amsterdam University Medical Centers, location Academic Medical Center, Amsterdam, the Netherlands.

Dennis Hernaus (D)

Department of Psychiatry & Neuropsychology, Maastricht University, Maastricht, the Netherlands.

Jan Booij (J)

Department of Radiology and Nuclear Medicine, Amsterdam University Medical Centers, location Academic Medical Center, Amsterdam, the Netherlands.

Ann Swillen (A)

Department of Human Genetics, KU Leuven - Leuven University, Leuven, Belgium; Center for Human Genetics, Hospital Gasthuisberg, Leuven, Belgium.

Jacob Vorstman (J)

Department of Psychiatry, The Hospital for Sick Children and University of Toronto, Toronto, ON, Canada; Program in Genetics and Genome Biology, Research Institute, The Hospital for Sick Children, Toronto, ON, Canada.

Thérèse van Amelsvoort (T)

Department of Psychiatry & Neuropsychology, Maastricht University, Maastricht, the Netherlands.

Inez Myin-Germeys (I)

Center for Contextual Psychiatry, Department of Neurosciences, KU Leuven, Leuven, Belgium.

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