Relapse prevention in alcoholics by cigarette smoking? Involvement of nicotinic-dopaminergic mechanisms

Because of a controversial view on the role of smoking in the recovery proc ess of alcoholism, outcome data obtained for alcoholics who had been includ ed in a long-term clinical trial with a putative anticraving drug were anal yzed. To avoid unknown interactions between the drug under study and smokin g behavior, only placebo-treated patients were evaluated in this investigat ion. 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 nonsmok ers (173 vs. 114 days; P = .092). This possible advantage might be related to nicotinic effects on central dopamine systems in smokers, as indicated b y higher growth hormone secretion after apomorphine stimulation obtained in smokers, compared with findings for nonsmokers (area under the curve durin g chronic intoxication: 2253 vs. 1247 mug/min/1; P = .019). Multivariate re gression 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 = .0 12) on stimulated growth hormone secretion. In contrast, the reported numbe r of smoked cigarettes per day had an increasing effect (P = .034), account ing for 6% of the variance of growth hormone secretion. However, difference s 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 ad mission (262 g vs. 192 g; P = .044), and met more criteria for the ICD-10 a lcohol dependence syndrome (6.6 vs. 6.0; P = .047). Therefore, it cannot be stringently inferred from our data that a possible advantage of smoking fo r alcoholism recovery is causally related to the effects of nicotine on cer ebral systems or human behavior, as our findings had not been based on a ra ndomized design. (C) 2001 Elsevier Science Inc. All rights reserved.