Changes of Smoking Urge and Endogenous Opioids, Prolactin, ACTH, Cortisol Levels in Nicotine Dependents with Naltrexone Pretreatment .
- Author:
In Ki SOHN
1
;
Young Sik LEE
;
Chul NA
Author Information
1. Department of Psychiatry, College of Medicine, DongGuk University, Gyeongju, Korea. fiveway@shinbiro.com
- Publication Type:Randomized Controlled Trial ; Original Article
- Keywords:
Naltrexone;
Nicotine;
Prolactin;
ACTH;
Cortisol;
Smoking urge
- MeSH:
Adrenocorticotropic Hormone*;
Analgesics, Opioid*;
beta-Endorphin;
Carbon;
Cues;
Dynorphins;
Heart Rate;
Hydrocortisone*;
Naltrexone*;
Nicotine*;
Prolactin*;
Reinforcement (Psychology);
Smoke*;
Smoking*;
Substance Withdrawal Syndrome;
Tobacco Use Disorder
- From:Journal of Korean Neuropsychiatric Association
2003;42(4):476-484
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVES: There is a controversy on the mechanism of nicotine dependence. Some suggest that the negative reinforcement such as withdrawal symptoms plays an important role, but others suggest that the positive reinforcement through the opioid-dopamine system plays an important role. Under the assumptions that the positive reinforcement and the opioid-dopamine interaction to have an important role in nicotine dependence, this study examined the effects of chronic naltrexone treatment on smoking behaviors, smoking urges to smoking cues and neuroendocrine responses to smoking. METHODS: In a randomized, placebo-control, double-blind design, voluntarily admitted regular smokers who wanted to quit smoking received naltrexone (13 persons) or placebo (12 persons) treatment for 2 weeks. Each week, naltrexone side effects, discomforts after the reduction of cigarette smoking, smoking urges to smoking cues, daily cigarette smoking amount, and expiratory carbon monooxide levels were checked. Also blood beta-endorphin, dynorphin, prolactin, ACTH, and cortisol levels were measured before and after smoking. RESULTS: Naltrexone treatment group showed significantly reduced smoking urges to smoking cues (p=0.036 at 2nd week), daily cigarette smoking amount (p=0.027 at 1st week), and expiratory CO levels (p=0.002 at 1st week, p=0.039 at 2nd week). Naltrexone treatment group also showed significantly increase cortisol level after smoking during the 1st week (p=0.048), and ACTH and prolactin level during the 2nd week (respectively p=0.010, p=0.009). But, the levels of beta-endorphin and dynorphin A were not different between the two groups. Discomfort profiles after the reduction of cigarette smoking, systolic and diastolic BP, and pulse rates were not different between the two groups. CONCLUSION: Longterm naltrexone treatment could be an effective tool used for the cessdtion of smoking. It was suggested that naltrexone blocks the positive reinforcement effects of smoking rather than the negative reinforcement effects of nicotine withdrawal.
