RPAP and UMN-Duluth provide significant, complementary educational programs that lead more graduates to choose rural and primary care practices. Efforts across the nation to address the crisis in rural primary care should build on these successful efforts.
Objective
To examine the extent to which nicotine dependence alters endogenous opioid regulation of the hypothalamic-pituitary-adrenocortical (HPA) axis functions. Endogenous opiates play an important role in regulating mood, pain, and drug reward. They also regulate the HPA functions. Previous work has demonstrated an abnormal HPA response to psychological stress among dependent smokers.
Methods
Smokers and nonsmokers (total n = 48 participants) completed two sessions during which a placebo or 50 mg of naltrexone was administered, using a double-blind design. Blood and saliva samples, cardiovascular and mood measures were obtained during a resting absorption period, after exposure to two noxious stimuli, and during an extended recovery period. Thermal pain threshold and tolerance were assessed in both sessions. Participants also rated pain during a 90-second cold pressor test.
Results
Opioid blockade increased adrenocorticotropin, plasma cortisol, and salivary cortisol levels; these increases were enhanced by exposure to the noxious stimuli. These responses were blunted in smokers relative to nonsmokers. Smokers tended to report less pain than nonsmokers, and women reported more pain during both pain procedures, although sex differences in pain were significant only among nonsmokers.
Conclusions
We conclude that nicotine dependence is associated with attenuated opioid modulation of the HPA. This dysregulation may play a role in the previously observed blunted responses to stress among dependent smokers.
Rationale
We examined the hypothesis that stress-related blunting of cortisol in smokers is particularly pronounced in those with history of severe life adversity.
Objectives
The 2 aims of this study were first to examine hormonal, craving, and withdrawal symptoms during ad libitum smoking and after the first 24 hours of abstinence in smokers who experienced high or low levels of adversity. Secondly, we sought to examine the relationship between adversity and HPA hormones to predict relapse during the first month of a smoking cessation attempt.
Methods
Hormonal and self-report measures were collected from 103 smokers (49 women) during ad libitum smoking and after the first 24 hours of abstinence. Hypothalamic-pituitary-adrenal (HPA) hormones were measured during baseline rest and in response to acute stress in both conditions. All smokers were interested in smoking cessation, and we prospectively used stress response measures to predict relapse during the first four weeks of the smoking cessation attempt.
Results
The results showed that high adversity was associated with higher distress and smoking withdrawal symptoms. High level of early life adversity was associated with elevated HPA activity, which was found in both salivary and plasma cortisol. Enhanced adrenocorticotropic hormone (ACTH) stress response was evident in high adversity but not in low adversity relapsers.
Conclusions
This study demonstrated that early life adversity is associated with stress-related HPA responses. The study also demonstrated that, among smokers who experienced a high level of life adversity, heightened ACTH and cortisol responses were linked with increased risk for smoking relapse.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.