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J Clin Endocrinol Metab. 2017 Mar 1;102(3):962-969. doi: 10.1210/jc.2016-3035.

The Longitudinal Relationship Between Cortisol Responses to Mental Stress and Leukocyte Telomere Attrition.

Author information

1
Department of Epidemiology and Public Health, University College London, London WC1E 6BT, United Kingdom.
2
School of Sport, Exercise, and Health Sciences, Loughborough University, Loughborough LE11 3TU, United Kingdom.
3
Department of Biochemistry and Biophysics, University of California, San Francisco, California 94158; and.
4
Cardiff School of Health Sciences, Cardiff Metropolitan University, Cardiff CF5 2YB, Wales, United Kingdom.

Abstract

Context:

Chronic psychological stress has been associated with shorter telomeres, but the underlying mechanisms are poorly understood. One possibility is that the neuroendocrine responses to stress exposure are involved.

Objective:

To test the hypothesis that greater cortisol responsivity to acute stressors predicts more rapid telomere attrition.

Design:

We measured salivary cortisol responses to 2 challenging behavioral tasks. Leukocyte telomere length was measured at the time of mental stress testing and 3 years later.

Participants:

We studied 411 initially healthy men and women aged 54 to 76 years.

Main outcome measure:

Leukocyte telomere length.

Results:

Cortisol responses to this protocol were small; we divided participants into cortisol responders (n = 156) and nonresponders (n = 255) using a criterion (≥20% increase in cortisol concentration) previously shown to predict increases in cardiovascular disease risk. There was no significant association between cortisol responsivity and baseline telomere length, although cortisol responders tended to have somewhat shorter telomeres (β = -0.061; standard error, 0.049). But cortisol responders had shorter telomeres and more rapid telomere attrition than nonresponders on follow-up, after controlling statistically for age, sex, socioeconomic status, smoking, time of day of stress , and baseline telomere length (β = -0.10; standard error, 0.046; P = 0.029). The association was maintained after additional control for cardiovascular risk factors (β = -0.11; P = 0.031). The difference between cortisol responders and nonresponders was equivalent to approximately 2 years in aging.

Conclusions:

These findings suggest that cortisol responsivity may mediate, in part, the relationship between psychological stress and cellular aging.

PMID:
27967317
PMCID:
PMC5460695
[Available on 2018-03-01]
DOI:
10.1210/jc.2016-3035
[Indexed for MEDLINE]
Free PMC Article

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