Attenuated adrenocorticotropic responses to psychological stress are associated with early smoking relapse

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162 Scopus citations


Rationale: Research has demonstrated that psychosocial stressors increase smoking and risk for smoking relapse. Alterations in biological systems involved in the stress response caused by chronic smoking may contribute to early relapse. Objectives: We examined the extent to which pituitary-adrenocortical and cardiovascular responses to stress following the first 24 h of a quit attempt predict early relapse. Methods: Seventy-two smokers interested in cessation attended a laboratory stress session 24 h after the beginning of their cessation attempt. Adrenocorticotropin (ACTH), plasma and salivary cortisol concentrations, systolic and diastolic blood pressure (BP), and heart rate (HR) responses to acute psychological stressors (public speaking and cognitive challenges) were used to predict relapse over a 4-week follow-up period. Results: Those who relapsed within 4 weeks showed attenuated hormonal and cardiovascular responses to stress and exaggerated withdrawal symptoms. Cox proportional hazards survival analysis showed that attenuated ACTH, plasma cortisol, systolic and diastolic BP, positive affect, and exaggerated withdrawal symptoms and smoking urges during acute stress predicted early relapse. Stepwise model showed that ACTH, diastolic BP, and exaggerated withdrawal symptoms remain as significant predictors. When baseline smoking and psychological measures were included in the model, changes in ACTH, diastolic BP, and both factors of smoking urges remained significant predictors of relapse. Conclusions: These results demonstrate that altered stress response predicts increased vulnerability for smoking relapse.

Original languageEnglish (US)
Pages (from-to)107-117
Number of pages11
Issue number1
StatePublished - Aug 2005

Bibliographical note

Funding Information:
Acknowledgements We thank Deanna Ellestad, Angie Harju, Laurie Franks, Huong Tim, and Jonathan Erickson for assistance with data collection and management. We thank Clemens Kirschbaum of the University of Dresden, Germany, for assistance with the hormonal and cotinine assays. We thank Ron Regal for assistance with data analysis. This research was supported by a grant to the first author from the National Cancer Institute (CA 88272). The first author was also supported by grants from the National Institute on Drug Abuse (DA013435 and DA016351).


  • Adrenocorticotropic hormone
  • Cardiovascular responses
  • Cortisol
  • Relapse
  • Smoking
  • Stress
  • Withdrawal symptoms


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