TY - JOUR
T1 - The longitudinal relationship between cortisol responses to mental stress and leukocyte telomere attrition
AU - Steptoe, Andrew
AU - Hamer, Mark
AU - Lin, Jue
AU - Blackburn, Elizabeth H.
AU - Erusalimsky, Jorge D.
N1 - Publisher Copyright:
Copyright © 2017 by the Endocrine Society.
PY - 2016/12/14
Y1 - 2016/12/14
N2 - 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 protocolwere 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 (b = 20.061; standard error, 0.049). But cortisol responders had shorter telomeres andmore 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 (b =20.10; standard error, 0.046; P = 0.029). The association wasmaintained after additional control for cardiovascular risk factors (b = 20.11; 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.
AB - 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 protocolwere 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 (b = 20.061; standard error, 0.049). But cortisol responders had shorter telomeres andmore 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 (b =20.10; standard error, 0.046; P = 0.029). The association wasmaintained after additional control for cardiovascular risk factors (b = 20.11; 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.
UR - http://www.scopus.com/inward/record.url?scp=85015156393&partnerID=8YFLogxK
U2 - 10.1210/jc.2016-3035
DO - 10.1210/jc.2016-3035
M3 - Article
C2 - 27967317
AN - SCOPUS:85015156393
SN - 0021-972X
VL - 102
SP - 962
EP - 969
JO - Journal of Clinical Endocrinology and Metabolism
JF - Journal of Clinical Endocrinology and Metabolism
IS - 3
ER -