Publication

Glucocorticoid receptor exon 1(F) methylation and the cortisol stress response in health and disease

Schur, R. R., van Leeuwen, J. M. C., Houtepen, L. C., Joels, M., Kahn, R. S., Boks, M. P. & Vinkers, C. H., Nov-2018, In : Psychoneuroendocrinology. 97, p. 182-189 8 p.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Schur, R. R., van Leeuwen, J. M. C., Houtepen, L. C., Joels, M., Kahn, R. S., Boks, M. P., & Vinkers, C. H. (2018). Glucocorticoid receptor exon 1(F) methylation and the cortisol stress response in health and disease. Psychoneuroendocrinology, 97, 182-189. https://doi.org/10.1016/j.psyneuen.2018.07.018

Author

Schur, Remmelt R. ; van Leeuwen, Judith M. C. ; Houtepen, Lotte C. ; Joels, Marian ; Kahn, Rene S. ; Boks, Marco P. ; Vinkers, Christiaan H. / Glucocorticoid receptor exon 1(F) methylation and the cortisol stress response in health and disease. In: Psychoneuroendocrinology. 2018 ; Vol. 97. pp. 182-189.

Harvard

Schur, RR, van Leeuwen, JMC, Houtepen, LC, Joels, M, Kahn, RS, Boks, MP & Vinkers, CH 2018, 'Glucocorticoid receptor exon 1(F) methylation and the cortisol stress response in health and disease', Psychoneuroendocrinology, vol. 97, pp. 182-189. https://doi.org/10.1016/j.psyneuen.2018.07.018

Standard

Glucocorticoid receptor exon 1(F) methylation and the cortisol stress response in health and disease. / Schur, Remmelt R.; van Leeuwen, Judith M. C.; Houtepen, Lotte C.; Joels, Marian; Kahn, Rene S.; Boks, Marco P.; Vinkers, Christiaan H.

In: Psychoneuroendocrinology, Vol. 97, 11.2018, p. 182-189.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Schur RR, van Leeuwen JMC, Houtepen LC, Joels M, Kahn RS, Boks MP et al. Glucocorticoid receptor exon 1(F) methylation and the cortisol stress response in health and disease. Psychoneuroendocrinology. 2018 Nov;97:182-189. https://doi.org/10.1016/j.psyneuen.2018.07.018


BibTeX

@article{d4c67416b8634e29bc9f2d711c90417b,
title = "Glucocorticoid receptor exon 1(F) methylation and the cortisol stress response in health and disease",
abstract = "Childhood trauma has been proposed to increase vulnerability to develop psychopathology in part through an altered cortisol stress response. Research in rats has suggested that this effect is mediated by methylation in the glucocorticoid receptor 1(7) region (GR-1(7) or GR-1(F) in humans), with higher methylation after poor maternal care leading to an increased cortisol stress response in adulthood. In humans, the associations between childhood trauma and GR-1(F) methylation or the cortisol stress response are equivocal. Remarkably, evidence for the relation between GR-1(F) methylation and the cortisol stress response has been conflicting as well. To further explore this, we investigated the associations of peripheral GR-1(F) methylation (52 CpGs) with the cortisol stress response (Trier Social Stress Test) and with childhood trauma in three independent studies (total N = 241) including healthy controls, patients with schizophrenia and bipolar disorder and unaffected siblings of patients with one of these disorders. We did not find any significant association between GR-1(F) methylation and the cortisol stress response (areas under the curve) or childhood trauma, nor did we observe any group differences between patients, siblings and healthy controls. Our findings do not support GR-1(F) methylation as a proxy for the cortisol stress response, nor its link with childhood trauma or psychopathology. These results suggest that multifactorial models for stress-related psychopathology are needed. Alternatively, future longitudinal studies may reveal GR-1(F) methylation to be a useful parameter at an individual level.",
keywords = "NR3C1, TSST, Psychopathology, Trauma, Methylation, CHILDHOOD TRAUMA, GENE METHYLATION, HPA-AXIS, DISORDER, REACTIVITY, MALTREATMENT, ASSOCIATION, VALIDATION, DEPRESSION, PATTERNS",
author = "Schur, {Remmelt R.} and {van Leeuwen}, {Judith M. C.} and Houtepen, {Lotte C.} and Marian Joels and Kahn, {Rene S.} and Boks, {Marco P.} and Vinkers, {Christiaan H.}",
year = "2018",
month = "11",
doi = "10.1016/j.psyneuen.2018.07.018",
language = "English",
volume = "97",
pages = "182--189",
journal = "Psychoneuroendocrinology",
issn = "0306-4530",
publisher = "PERGAMON-ELSEVIER SCIENCE LTD",

}

RIS

TY - JOUR

T1 - Glucocorticoid receptor exon 1(F) methylation and the cortisol stress response in health and disease

AU - Schur, Remmelt R.

AU - van Leeuwen, Judith M. C.

AU - Houtepen, Lotte C.

AU - Joels, Marian

AU - Kahn, Rene S.

AU - Boks, Marco P.

AU - Vinkers, Christiaan H.

PY - 2018/11

Y1 - 2018/11

N2 - Childhood trauma has been proposed to increase vulnerability to develop psychopathology in part through an altered cortisol stress response. Research in rats has suggested that this effect is mediated by methylation in the glucocorticoid receptor 1(7) region (GR-1(7) or GR-1(F) in humans), with higher methylation after poor maternal care leading to an increased cortisol stress response in adulthood. In humans, the associations between childhood trauma and GR-1(F) methylation or the cortisol stress response are equivocal. Remarkably, evidence for the relation between GR-1(F) methylation and the cortisol stress response has been conflicting as well. To further explore this, we investigated the associations of peripheral GR-1(F) methylation (52 CpGs) with the cortisol stress response (Trier Social Stress Test) and with childhood trauma in three independent studies (total N = 241) including healthy controls, patients with schizophrenia and bipolar disorder and unaffected siblings of patients with one of these disorders. We did not find any significant association between GR-1(F) methylation and the cortisol stress response (areas under the curve) or childhood trauma, nor did we observe any group differences between patients, siblings and healthy controls. Our findings do not support GR-1(F) methylation as a proxy for the cortisol stress response, nor its link with childhood trauma or psychopathology. These results suggest that multifactorial models for stress-related psychopathology are needed. Alternatively, future longitudinal studies may reveal GR-1(F) methylation to be a useful parameter at an individual level.

AB - Childhood trauma has been proposed to increase vulnerability to develop psychopathology in part through an altered cortisol stress response. Research in rats has suggested that this effect is mediated by methylation in the glucocorticoid receptor 1(7) region (GR-1(7) or GR-1(F) in humans), with higher methylation after poor maternal care leading to an increased cortisol stress response in adulthood. In humans, the associations between childhood trauma and GR-1(F) methylation or the cortisol stress response are equivocal. Remarkably, evidence for the relation between GR-1(F) methylation and the cortisol stress response has been conflicting as well. To further explore this, we investigated the associations of peripheral GR-1(F) methylation (52 CpGs) with the cortisol stress response (Trier Social Stress Test) and with childhood trauma in three independent studies (total N = 241) including healthy controls, patients with schizophrenia and bipolar disorder and unaffected siblings of patients with one of these disorders. We did not find any significant association between GR-1(F) methylation and the cortisol stress response (areas under the curve) or childhood trauma, nor did we observe any group differences between patients, siblings and healthy controls. Our findings do not support GR-1(F) methylation as a proxy for the cortisol stress response, nor its link with childhood trauma or psychopathology. These results suggest that multifactorial models for stress-related psychopathology are needed. Alternatively, future longitudinal studies may reveal GR-1(F) methylation to be a useful parameter at an individual level.

KW - NR3C1

KW - TSST

KW - Psychopathology

KW - Trauma

KW - Methylation

KW - CHILDHOOD TRAUMA

KW - GENE METHYLATION

KW - HPA-AXIS

KW - DISORDER

KW - REACTIVITY

KW - MALTREATMENT

KW - ASSOCIATION

KW - VALIDATION

KW - DEPRESSION

KW - PATTERNS

U2 - 10.1016/j.psyneuen.2018.07.018

DO - 10.1016/j.psyneuen.2018.07.018

M3 - Article

VL - 97

SP - 182

EP - 189

JO - Psychoneuroendocrinology

JF - Psychoneuroendocrinology

SN - 0306-4530

ER -

ID: 66295588