The belief that having a couple of alcoholic drinks increases the desire for a cigarette has found experimental support in recent years. King and Epstein (2005) found that the administration of alcohol to occasional smoker-drinkers led to a dose-dependent increase in the desire to smoke.1 Subjects who ingested the equivalent of two to three drinks showed an increased desire for tobacco over those who received no alcohol, and subjects who received the equivalent of four to five drinks showed a stronger desire to smoke than the other two groups. Smoking urges increased as blood alcohol content increased, and persisted as blood alcohol content declined. Epstein et al. (2007) found similar results, noting that "this effect appears to be driven by heightened stimulation levels rather than as a means to offset alcohol's sedative effects."2

Overwhelming evidence exists that repeated and regular use of tobacco cigarettes can lead to robust dependency, driven by both the positive reinforcement associated with nicotine's stimulation of pleasure centers in the brain3 and negative reinforcement associated with aversion to unpleasant effects of withdrawal.4 However, recent animal studies provide evidence that nicotine also shows complex interactions with the brain's reinforcement systems.

Using a technique called intracranial self-stimulation, Kenny and Markou (2006) surgically connected electrodes to the posterior lateral hypothalamus in rats.5 Animals were periodically allowed to deliver a rewarding electrical stimulation to their brains by pressing a lever. A control group was compared against rats that were also allowed to self-administer nicotine. The "reward threshold", or minimum intensity of electrical stimulation that resulted in continued pressing of the lever, was then compared for the two groups.

The authors found that nicotine-ingesting rats showed lower reward thresholds compared to control rats that did not receive nicotine. In other words, the nicotine-ingesting rats required less intense electrical stimulation to cause them to continue self-administering that stimulation. This effect lasted for more than 36 days after nicotine was discontinued.

The lowered reward threshold effect was reversed by administration of dihydro-betaerythroidine, an antagonist that blocks nicotine's effects, suggesting that the lowered threshold is a direct effect of the nicotine. The authors conclude that "self-administered nicotine resets the sensitivity of reward systems to a new increased level, thereby imprinting an indelible 'memory' of its effects in reward systems, an action that so far appears unique to nicotine among drugs of abuse."5

It is not immediately clear to what degree these results may be generalized, but this experiment provides evidence that not only does nicotine cause pleasurable effects for people at low doses, but it makes other stimuli seem more pleasurable than they are without nicotine.