Surprisingly, few studies have addressed the association between smoking and drinking despite the fact that 80 to 95% of alcoholics smoke cigarettes. NIAAA estimates that alcoholism is 10 to 14 times more prevalent among smokers than non-smokers. Other studies estimate that roughly 70% of alcoholics are classified as "heavy smokers", smoking more than one pack a day.
A problem lies in the conventional wisdom regarding alcohol treatment, which argues that maintaining the alcoholic's sobriety is the central issue and any discussion regarding quitting smoking is secondary. The rationale behind this theory is that the patient would be more inclined to relapse back into alcoholism due to the added stress of abstaining from both alcohol and nicotine. Thus, historically, physicians were told not to recommend that a patient attempt to stop smoking while undergoing treatment for alcoholism.
Unfortunately, these guidelines may have fatal consequences for alcoholics. Many recovering alcoholics (including one of the founders of Alcoholics Anonymous) have managed to conquer their “primary addiction”, yet die from their “secondary addiction”. In fact, data shows that smoking actually kills more alcoholics than alcohol.
The prevalence of the dual dependence of alcohol and cigarette smoking suggests a strong correlation, although the precise mechanisms of the alcohol-nicotine connection are not completely understood. Traditionally, research funding has come from one agency for alcohol and another agency for tobacco, allowing joint studies on alcohol and smoking to fall through the cracks.
Despite the limited funding, there are still numerous theories to suggest a link between smoking and alcoholism. For instance, recent studies indicate that smoking may actually facilitate drinking by serving as a neurological cue. Researchers hypothesize that ethanol may foster the pleasurable, reinforcing effects associated with nicotine. Others suggest that those who abuse one substance are simply more inclined to abuse other substances (i.e. polysubstance abusers). Some studies suggest that the same set of genes that predispose an individual to alcoholism may also predispose them to smoking.
Another hypothesis is that since nicotine stimulates and alcohol sedates the body, the two may moderate each drug's effects. There may be truth to this theory since nicotine lowers blood alcohol concentration. Therefore, if a smoker starts drinking with the sole purpose of getting drunk, more alcohol would have to be consumed in order to reach intoxication.
Research by Le et al demonstrated that repeated exposure to nicotine enhanced alcohol consumption and that dose and duration of nicotine exposure might play a significant role in the stimulation of alcohol consumption. Animal studies may support this theory.
In laboratory animals, the joint administration of alcohol and nicotine altered the dosage ingested of each substance. For example, in at least one study an exposure to a low dose of nicotine resulted in an increase in alcohol consumption.
The role that smoking plays in alcohol relapse is very controversial. Some suggest that tobacco may stimulate neurological mechanisms, possibly increasing cravings and result in more frequent relapse. Two primary hypothesis regarding the interplay between nicotine and ethanol have surfaced, as explained below:
Coping Hypothesis: Tobacco may decrease the incidence of relapse by serving as a means of coping with alcohol urges.
Priming Hypothesis: Tobacco may increase the urge to drink since alcohol and tobacco spur the release of dopamine and endogenous opiods in mesolimbic pathways.