Stress has been cited as an important precipitator of smoking relapse. Dysregulation of neurobiological pathways related to stress might mediate effects of stress on smoking relapse. This study assessed the extent to which beta endorphin response to stress is associated with early smoking relapse. Forty-five smokers interested in smoking cessation were recruited and attended a laboratory session 24 h following the beginning of their abstinence period. During this session beta endorphin samples were collected before and after performing two acute stressors (public speaking and cognitive tasks). Participants also attended four weekly follow-up sessions to assess their smoking status. Results were compared between smokers who relapsed within the 4-week follow-up period and those who maintained abstinence over the same period. The acute stressors were associated with significant increases in measures of craving and withdrawal symptoms (ps < 0.01). While baseline measures of beta endorphin did not differ between relapsers and successful abstainers (F < 1), results demonstrated that smokers who relapsed exhibited attenuated beta endorphin response to the two stressors relative to those who maintained abstinence over the same period (ps < 05). These results support recent evidence indicating that a dysregulated stress response is a key component in predicting smoking relapse.
Bibliographical noteFunding Information:
This study was supported in part by National Institute of Health grants CA88272 and DA016351. We thank Clemens Kirschbaum, Ph.D., of Dresden University in Germany for help in assaying the hormonal samples and to Deanna Ellestad, Laurie Frank, and Angie Harju for help with the data collection and management of the study.
- Beta endorphin
- Endogenous opioid