Tobacco use, including smoking and chewing, is highly addictive due to the effects of the nicotine present in tobacco. Smoking increases the risk of small-cell lung carcinoma and is responsible for millions of deaths each year due to cancer, heart disease, and stroke. Unlike the opioids involved in analgesia and addiction, nicotine does not directly target any of the opioid receptors. The primary targets for nicotine are instead the nicotinic acetylcholine receptors, a family of ligand-gated ion channels. Despite the differences in target receptors, however, nicotine still causes many downstream effects that are similar to those of opioid use and result in the onset of addiction. These effects, such as activation of reward pathways and increased dopamine release, are mediated by the release of endogenous opioids following nicotine use. With this important connection between the opioid system and nicotine, genetic variation in OPRM1 may affect susceptibility to nicotine dependence and the efficacy of smoking cessation treatments.
