Publication

The low single nucleotide polymorphism heritability of plasma and saliva cortisol levels

Neumann, A., Direk, N., Crawford, A. A., Mirza, S., Adams, H., Bolton, J., Hayward, C., Strachan, D. P., Payne, E. K., Smith, J. A., Milaneschi, Y., Penninx, B., Hottenga, J. J., de Geus, E., Oldehinkel, A. J., van der Most, P. J., de Rijke, Y., Walker, B. R. & Tiemeier, H., Nov-2017, In : Psychoneuroendocrinology. 85, p. 88-95 8 p.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Neumann, A., Direk, N., Crawford, A. A., Mirza, S., Adams, H., Bolton, J., Hayward, C., Strachan, D. P., Payne, E. K., Smith, J. A., Milaneschi, Y., Penninx, B., Hottenga, J. J., de Geus, E., Oldehinkel, A. J., van der Most, P. J., de Rijke, Y., Walker, B. R., & Tiemeier, H. (2017). The low single nucleotide polymorphism heritability of plasma and saliva cortisol levels. Psychoneuroendocrinology, 85, 88-95. https://doi.org/10.1016/j.psyneuen.2017.08.011

Author

Neumann, Alexander ; Direk, Nese ; Crawford, Andrew A ; Mirza, Saira ; Adams, Hieab ; Bolton, Jennifer ; Hayward, Caroline ; Strachan, David P ; Payne, Erin K ; Smith, Jennifer A ; Milaneschi, Yuri ; Penninx, Brenda ; Hottenga, Jouke J ; de Geus, Eco ; Oldehinkel, Albertine J ; van der Most, Peter J ; de Rijke, Yolanda ; Walker, Brian R ; Tiemeier, Henning. / The low single nucleotide polymorphism heritability of plasma and saliva cortisol levels. In: Psychoneuroendocrinology. 2017 ; Vol. 85. pp. 88-95.

Harvard

Neumann, A, Direk, N, Crawford, AA, Mirza, S, Adams, H, Bolton, J, Hayward, C, Strachan, DP, Payne, EK, Smith, JA, Milaneschi, Y, Penninx, B, Hottenga, JJ, de Geus, E, Oldehinkel, AJ, van der Most, PJ, de Rijke, Y, Walker, BR & Tiemeier, H 2017, 'The low single nucleotide polymorphism heritability of plasma and saliva cortisol levels', Psychoneuroendocrinology, vol. 85, pp. 88-95. https://doi.org/10.1016/j.psyneuen.2017.08.011

Standard

The low single nucleotide polymorphism heritability of plasma and saliva cortisol levels. / Neumann, Alexander; Direk, Nese; Crawford, Andrew A; Mirza, Saira; Adams, Hieab; Bolton, Jennifer; Hayward, Caroline; Strachan, David P; Payne, Erin K; Smith, Jennifer A; Milaneschi, Yuri; Penninx, Brenda; Hottenga, Jouke J; de Geus, Eco; Oldehinkel, Albertine J; van der Most, Peter J; de Rijke, Yolanda; Walker, Brian R; Tiemeier, Henning.

In: Psychoneuroendocrinology, Vol. 85, 11.2017, p. 88-95.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Neumann A, Direk N, Crawford AA, Mirza S, Adams H, Bolton J et al. The low single nucleotide polymorphism heritability of plasma and saliva cortisol levels. Psychoneuroendocrinology. 2017 Nov;85:88-95. https://doi.org/10.1016/j.psyneuen.2017.08.011


BibTeX

@article{e641e96b0f5f411d9fdbe2c960f30188,
title = "The low single nucleotide polymorphism heritability of plasma and saliva cortisol levels",
abstract = "Cortisol is an important stress hormone affected by a variety of biological and environmental factors, such as the circadian rhythm, exercise and psychological stress. Cortisol is mostly measured using blood or saliva samples. A number of genetic variants have been found to contribute to cortisol levels with these methods. While the effects of several specific single genetic variants is known, the joint genome-wide contribution to cortisol levels is unclear. Our aim was to estimate the amount of cortisol variance explained by common single nucleotide polymorphisms, i.e. the SNP heritability, using a variety of cortisol measures, cohorts and analysis approaches. We analyzed morning plasma (n = 5705) and saliva levels (n = 1717), as well as diurnal saliva levels (n = 1541), in the Rotterdam Study using genomic restricted maximum likelihood estimation. Additionally, linkage disequilibrium score regression was fitted on the results of genome-wide association studies (GWAS) performed by the CORNET consortium on morning plasma cortisol (n = 12,597) and saliva cortisol (n = 7703). No significant SNP heritability was detected for any cortisol measure, sample or analysis approach. Point estimates ranged from 0% to 9%. Morning plasma cortisol in the CORNET cohorts, the sample with the most power, had a 6% [95%CI: 0-13%] SNP heritability. The results consistently suggest a low SNP heritability of these acute and short-term measures of cortisol. The low SNP heritability may reflect the substantial environmental and, in particular, situational component of these cortisol measures. Future GWAS will require very large sample sizes. Alternatively, more long-term cortisol measures such as hair cortisol samples are needed to discover further genetic pathways regulating cortisol concentrations.",
keywords = "Cortisol, Genetics, Heritability, GWAS, Single nucleotide polymorphism, DIURNAL CORTISOL, ASSOCIATIONS, PATTERNS, ATHEROSCLEROSIS, METAANALYSIS, ADOLESCENCE, OBJECTIVES, DISORDERS, CHILDHOOD, HEALTH",
author = "Alexander Neumann and Nese Direk and Crawford, {Andrew A} and Saira Mirza and Hieab Adams and Jennifer Bolton and Caroline Hayward and Strachan, {David P} and Payne, {Erin K} and Smith, {Jennifer A} and Yuri Milaneschi and Brenda Penninx and Hottenga, {Jouke J} and {de Geus}, Eco and Oldehinkel, {Albertine J} and {van der Most}, {Peter J} and {de Rijke}, Yolanda and Walker, {Brian R} and Henning Tiemeier",
note = "Copyright {\textcopyright} 2017 Elsevier Ltd. All rights reserved.",
year = "2017",
month = nov,
doi = "10.1016/j.psyneuen.2017.08.011",
language = "English",
volume = "85",
pages = "88--95",
journal = "Psychoneuroendocrinology",
issn = "0306-4530",
publisher = "PERGAMON-ELSEVIER SCIENCE LTD",

}

RIS

TY - JOUR

T1 - The low single nucleotide polymorphism heritability of plasma and saliva cortisol levels

AU - Neumann, Alexander

AU - Direk, Nese

AU - Crawford, Andrew A

AU - Mirza, Saira

AU - Adams, Hieab

AU - Bolton, Jennifer

AU - Hayward, Caroline

AU - Strachan, David P

AU - Payne, Erin K

AU - Smith, Jennifer A

AU - Milaneschi, Yuri

AU - Penninx, Brenda

AU - Hottenga, Jouke J

AU - de Geus, Eco

AU - Oldehinkel, Albertine J

AU - van der Most, Peter J

AU - de Rijke, Yolanda

AU - Walker, Brian R

AU - Tiemeier, Henning

N1 - Copyright © 2017 Elsevier Ltd. All rights reserved.

PY - 2017/11

Y1 - 2017/11

N2 - Cortisol is an important stress hormone affected by a variety of biological and environmental factors, such as the circadian rhythm, exercise and psychological stress. Cortisol is mostly measured using blood or saliva samples. A number of genetic variants have been found to contribute to cortisol levels with these methods. While the effects of several specific single genetic variants is known, the joint genome-wide contribution to cortisol levels is unclear. Our aim was to estimate the amount of cortisol variance explained by common single nucleotide polymorphisms, i.e. the SNP heritability, using a variety of cortisol measures, cohorts and analysis approaches. We analyzed morning plasma (n = 5705) and saliva levels (n = 1717), as well as diurnal saliva levels (n = 1541), in the Rotterdam Study using genomic restricted maximum likelihood estimation. Additionally, linkage disequilibrium score regression was fitted on the results of genome-wide association studies (GWAS) performed by the CORNET consortium on morning plasma cortisol (n = 12,597) and saliva cortisol (n = 7703). No significant SNP heritability was detected for any cortisol measure, sample or analysis approach. Point estimates ranged from 0% to 9%. Morning plasma cortisol in the CORNET cohorts, the sample with the most power, had a 6% [95%CI: 0-13%] SNP heritability. The results consistently suggest a low SNP heritability of these acute and short-term measures of cortisol. The low SNP heritability may reflect the substantial environmental and, in particular, situational component of these cortisol measures. Future GWAS will require very large sample sizes. Alternatively, more long-term cortisol measures such as hair cortisol samples are needed to discover further genetic pathways regulating cortisol concentrations.

AB - Cortisol is an important stress hormone affected by a variety of biological and environmental factors, such as the circadian rhythm, exercise and psychological stress. Cortisol is mostly measured using blood or saliva samples. A number of genetic variants have been found to contribute to cortisol levels with these methods. While the effects of several specific single genetic variants is known, the joint genome-wide contribution to cortisol levels is unclear. Our aim was to estimate the amount of cortisol variance explained by common single nucleotide polymorphisms, i.e. the SNP heritability, using a variety of cortisol measures, cohorts and analysis approaches. We analyzed morning plasma (n = 5705) and saliva levels (n = 1717), as well as diurnal saliva levels (n = 1541), in the Rotterdam Study using genomic restricted maximum likelihood estimation. Additionally, linkage disequilibrium score regression was fitted on the results of genome-wide association studies (GWAS) performed by the CORNET consortium on morning plasma cortisol (n = 12,597) and saliva cortisol (n = 7703). No significant SNP heritability was detected for any cortisol measure, sample or analysis approach. Point estimates ranged from 0% to 9%. Morning plasma cortisol in the CORNET cohorts, the sample with the most power, had a 6% [95%CI: 0-13%] SNP heritability. The results consistently suggest a low SNP heritability of these acute and short-term measures of cortisol. The low SNP heritability may reflect the substantial environmental and, in particular, situational component of these cortisol measures. Future GWAS will require very large sample sizes. Alternatively, more long-term cortisol measures such as hair cortisol samples are needed to discover further genetic pathways regulating cortisol concentrations.

KW - Cortisol

KW - Genetics

KW - Heritability

KW - GWAS

KW - Single nucleotide polymorphism

KW - DIURNAL CORTISOL

KW - ASSOCIATIONS

KW - PATTERNS

KW - ATHEROSCLEROSIS

KW - METAANALYSIS

KW - ADOLESCENCE

KW - OBJECTIVES

KW - DISORDERS

KW - CHILDHOOD

KW - HEALTH

U2 - 10.1016/j.psyneuen.2017.08.011

DO - 10.1016/j.psyneuen.2017.08.011

M3 - Article

C2 - 28843169

VL - 85

SP - 88

EP - 95

JO - Psychoneuroendocrinology

JF - Psychoneuroendocrinology

SN - 0306-4530

ER -

ID: 47425018