Promotions foster positive attitudes, beliefs, and expectations regarding tobacco use. This fosters intentions to use and increases the likelihood of initiation. Greater exposure to promotion leads to higher risk. This is seen in diverse cultures and persists when other risk factors, such as socioeconomic status or parental and peer smoking, are controlled. Causality is the only plausible scientific explanation for the observed data. The evidence satisfies the Hill criteria, indicating that exposure to tobacco promotion causes children to initiate tobacco use.

Recent reports suggest that nicotine withdrawal symptoms are common among adolescents after a few weeks of intermittent tobacco use. No current model of nicotine dependence had predicted the rapid development of symptoms of dependence and withdrawal before the development of tolerance. We present a model that integrates neuroscience with clinical observations regarding how nicotine dependence develops, progresses, and resolves in humans. The central tenet of this sensitization-homeostasis model is that nicotine's dependence liability derives from its ability to stimulate neural pathways responsible for the suppression of craving. As a result of sensitization, the craving suppression produced by nicotine is magnified to superphysiological levels. The overinhibition of neurons responsible for craving initiates compensatory homeostatic measures that stimulate the craving pathways and result in craving when nicotine is absent. Separate homeostatic mechanisms are responsible for craving, withdrawal, and tolerance. The sensitization-homeostasis model is unique in its attribution of dependence to craving suppression, its attention to the temporal relationships among clinical features of nicotine dependence, and its extensive integration of clinical observations and basic science. It provides a framework for theory-based research.

Once exposure to nicotine had occurred, remarkably few risk factors for smoking consistently contributed to individual differences in susceptibility to the development of dependence or loss of autonomy. An experience of relaxation in response to the first dose of nicotine was the strongest predictor of both dependence and lost autonomy. This association was not explained by trait anxiety or any of the other measured psychosocial factors. These results are discussed in relation to the theory that the process of dependence is initiated by the first dose of nicotine.

The most susceptible youths lose autonomy over tobacco within a day or 2 of first inhaling from a cigarette. The appearance of tobacco withdrawal symptoms and failed attempts at cessation can precede daily smoking; ICD-10-defined dependence can precede daily smoking and typically appears before consumption reaches 2 cigarettes per day.

Pro-tobacco marketing and media stimulate tobacco use among youth. A ban on all tobacco promotions is warranted to protect children.

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Predictors of smoking onset for which there is robust evidence should be considered in the design of interventions to prevent first puff in order to optimize their effectiveness. Future research should seek to define onset clearly as the transition from never use to first use (e.g., first few puffs).

Despite a rich neuroscience literature on sensitization, this phenomenon has been neglected in clinical nicotine research. This paper offers a primer on the neuroscience of nicotine sensitization for behavioral scientists, identifying key concepts, potential theoretical and clinical implications, and directions for future research. Sensitization to a drug occurs when repeated exposures to the same dose produce greater responses. In animals, sensitization to nicotine, morphine, alcohol, cocaine, amphetamine, and methamphetamine manifests as increased locomotor activity. In animals, sensitization to nicotine begins with the first dose and is maximal within 5-7 days. It involves multiple neurotransmitters, receptors, and brain structures and cannot be attributed to any single alteration. The processes involved in its induction and expression are not identical. The neurologic changes associated with sensitization are not consistent across drugs, suggesting that sensitization is not an accident of neurophysiology but perhaps an exaggerated adaptive response. Sensitization is incorporated into two theories of addiction: incentive-sensitization and sensitization-homeostasis. Whether sensitization occurs in humans and how it is expressed is unclear, as is its role in human addiction.