title: The Longitudinal Relationship Between Cortisol Responses to Mental Stress and Leukocyte Telomere Attrition.
abstract: 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.
  
  
  
  To test the hypothesis that greater cortisol responsivity to acute stressors predicts more rapid telomere attrition.
  
  
  
  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.
  
  
  
  We studied 411 initially healthy men and women aged 54 to 76 years.
  
  
  
  Leukocyte telomere length.
  
  
  
  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.
  
  
  
  These findings suggest that cortisol responsivity may mediate, in part, the relationship between psychological stress and cellular aging.
authors.affiliation: Department of Epidemiology and Public Health, University College London, London WC1E 6BT, United Kingdom.
authors.forename: Andrew
authors.initials: A
authors.lastname: Steptoe
authors.affiliation: School of Sport, Exercise, and Health Sciences, Loughborough University, Loughborough LE11 3TU, United Kingdom.
authors.forename: Mark
authors.initials: M
authors.lastname: Hamer
authors.affiliation: Department of Biochemistry and Biophysics, University of California, San Francisco, California 94158; and.
authors.forename: Jue
authors.initials: J
authors.lastname: Lin
authors.affiliation: Department of Biochemistry and Biophysics, University of California, San Francisco, California 94158; and.
authors.forename: Elizabeth H
authors.initials: EH
authors.lastname: Blackburn
authors.affiliation: Cardiff School of Health Sciences, Cardiff Metropolitan University, Cardiff CF5 2YB, Wales, United Kingdom.
authors.forename: Jorge D
authors.initials: JD
authors.lastname: Erusalimsky
mesh_terms: D000368:Aged; D000375:Aging / Q000235:genetics* / Q000523:psychology; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism*; D007962:Leukocytes / Q000378:metabolism*; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D012463:Saliva / Q000737:chemistry; D012907:Smoking; D012923:Social Class; D013315:Stress, Psychological / Q000235:genetics* / Q000378:metabolism / Q000523:psychology; D016615:Telomere / Q000378:metabolism*; D059506:Telomere Shortening
chemical_list: D006854:Hydrocortisone