Abstract

Work published in 1997 showed a link between the diagnosis of attention-deficit/hyperactivity disorder (ADHD) and early initiation of smoking (1). This association has been interpreted as evidence that smoking provides a form of self-medication for a pre-existing problem, particularly one involving attention. Arguing against this view are the results of animal studies, which have shown that nicotine exposure during adolescence induces changes in brain development, neurochemical markers, and various behavioral measures (2), including evidence for increased vulnerability to drug abuse. This evidence suggests that the direction of causality may be reversed and that smoking may be the cause, rather than the consequence, of attentional deficits in smokers. To distinguish between these two possibilities by minimizing cause-consequence confounding, Treur et al. (3) used a monozygotic discordant twin design, including longitudinal assessments to dissociate the influences of genetic factors and family environment from the effects of smoking on attentional performance. They found that among adult monozygotic twins discordant for smoking, twins who endorsed ever smoking exhibited greater attentional problems than their never-smoker co-twins. Among adolescent twin pairs discordant for smoking, greater attentional problems were observed at age 16 in twins who had initiated smoking compared with their nonsmoking co-twins. The differences were not seen in the same twin pairs at earlier ages, before the initiation of smoking. These findings support the conclusion that smoking in adolescence produces problems with attention that persist to adulthood. The results of studies that compared adolescent and adult smokers with age-matched nonsmokers are largely consistent with smokers having problems with attention, but there is evidence for more general differences in executive functions. For example, a population-based study including participants 18–65 years old demonstrated small but significant impairments in nondeprived smokers (n 5 1002) compared with never-smokers (n 5 1161) in visual attention and cognitive impulsivity (4). Assessments of adolescent smokers revealed impairments in accuracy of working memory performance after recent smoking (4) and in adaptive decision making (5). In the latter example, nonsmokers adaptively altered risk-taking behavior to approach an optimal strategy, whereas the smokers did not. Task-based functional magnetic resonance imaging studies of brain function also demonstrated differences between adolescent smokers and nonsmokers. For example, adolescent smokers exhibited a greater dorsolateral and ventrolateral prefrontal cortical sensitivity to risk during decision making than nonsmokers (6). Altered functional

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