title: Relapse prevention in alcoholics by cigarette smoking? Involvement of nicotinic-dopaminergic mechanisms.
abstract: Because of a controversial view on the role of smoking in the recovery process of alcoholism, outcome data obtained for alcoholics who had been included in a long-term clinical trial with a putative anticraving drug were analyzed. To avoid unknown interactions between the drug under study and smoking behavior, only placebo-treated patients were evaluated in this investigation. After 12 months of rehabilitation, there was no significant difference regarding abstinence rate between 48 smoking alcoholics (who reported that they smoked 32 cigarettes on average per day) and 15 nonsmoking alcoholics (33% vs. 20%). However, smokers tended to be abstinent longer than nonsmokers (173 vs. 114 days; P= .092). This possible advantage might be related to nicotinic effects on central dopamine systems in smokers, as indicated by higher growth hormone secretion after apomorphine stimulation obtained in smokers, compared with findings for nonsmokers (area under the curve during chronic intoxication: 2253 vs. 1247 microg/min/l; P= .019). Multivariate regression analysis revealed a decreasing effect of ethanol blood level (P= .006) and the number of fullfilled International Classification of Diseases, 10th edition (ICD-10) criteria of the alcohol dependence syndrome (P= .012) on stimulated growth hormone secretion. In contrast, the reported number of smoked cigarettes per day had an increasing effect (P= .034), accounting for 6% of the variance of growth hormone secretion. However, differences in outcome could also be explained by other clinical features as smokers, compared with nonsmokers, were more frequently males (78.3% vs. 60.7%) and younger when studied at index episode (mean age 44.45 vs. 48.21 years; P= .054), reported higher ethanol consumption in the month before hospital admission (262 g vs. 192 g; P= .044), and met more criteria for the ICD-10 alcohol dependence syndrome (6.6 vs. 6.0; P= .047). Therefore, it cannot be stringently inferred from our data that a possible advantage of smoking for alcoholism recovery is causally related to the effects of nicotine on cerebral systems or human behavior, as our findings had not been based on a randomized design.
authors.affiliation: Department of Psychiatry, University of Mainz, Untere Zahlbacher Strasse 8, 55131 Mainz, Germany. schmidt@psychiatrie.klinik.uni-mainz.de
authors.forename: L G
authors.initials: LG
authors.lastname: Schmidt
authors.forename: M
authors.initials: M
authors.lastname: Smolka
mesh_terms: D000368:Aged; D000437:Alcoholism / Q000503:physiopathology / Q000517:prevention & control* / Q000534:rehabilitation; D001058:Apomorphine / Q000494:pharmacology; D004298:Dopamine / Q000378:metabolism / Q000502:physiology; D018491:Dopamine Agonists / Q000494:pharmacology; D000431:Ethanol / Q000097:blood; D005260:Female; D019382:Human Growth Hormone / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D009538:Nicotine / Q000494:pharmacology; D016032:Randomized Controlled Trials as Topic; D055502:Secondary Prevention; D012907:Smoking; D014029:Tobacco Use Disorder / Q000503:physiopathology
chemical_list: D018491:Dopamine Agonists; D019382:Human Growth Hormone; D000431:Ethanol; D009538:Nicotine; D001058:Apomorphine; D004298:Dopamine