Why do young women smoke? III. Attention and impulsivity as neurocognitive predisposing factors☆
Introduction
Although global trends indicate an overall decline in cigarette smoking, rates in high income countries appear to be declining less among young women than among men of the same age group (World Health Organization and Regional Office for Europe, 2005). In Israel, the most recent survey conducted by the Israel Ministry of Health showed that 20% of all Jewish women were smoking in 2004–2005 (Israel Ministry of Health, 2005), Among women in the 21–24 year age group the rate of smoking was 26.3% in the 2004–2005 survey, reflecting an increase of 2.6% from 2002–2003 (Israel Ministry of Health, 2003). The rate of smoking among men in the 21–24 age group was 39.1% in 2004–2005, a decrease of 4.7% from 2002–2003. Other age groups manifested trends that were similar between the genders over the equivalent period. Thus, in the context of overall public health concern about cigarette smoking, young women occupy a central position.
Cigarette smoking is a complex behavior that is influenced by genetic (Li, 2003), demographic (Meijer et al., 2001, Bergen and Caporaso, 1999), psychological (Pomerleau et al., 1992) and environmental (Beal et al., 2001, Den Exter Blokland et al., 2004) factors. Nicotine is the core addictive component of cigarette smoke and its reinforcing properties are well established (Jarvis, 2004). The factors that influence whether or not an individual initiates smoking are not necessarily the same as those that influence severity of nicotine dependence (ND) (Kendler et al., 1999). The effects of nicotine on neurocognitive function have long been held to play a role in ND. Previous studies hypothesized that smoking may be used as a form of self-medication due to beneficial acute effects of nicotine on cognitive functioning, mainly in the attention domain (Rezvani and Levin, 2001, Levin, 1992, Newhouse et al., 2004, Dinn et al., 2004). According to this view, nicotine serves as a positive reinforcer by facilitating attention capabilities. In support of this view are epidemiological reports that show a high prevalence of smoking among adolescents and adults diagnosed with attention deficit/hyperactivity disorder (ADHD) (Rezvani and Levin, 2001, Newhouse et al., 2004, Kollins et al., 2005).
Assessment of the acute effect of nicotine on cognition has employed two principal research strategies: (1) comparison of performance between non-abstinent smokers and non-smokers; and, (2) comparison of performance between non-abstinent and abstinent smokers. These two strategies yield different results (reviewed by Heishman et al., 1994). Studies conducted according to the first strategy have shown that nicotine improvement of cognitive functioning is rather minor and confined to pure motor speed tests (e.g. finger tapping) and motor responses in brief tests of attention. Heishman et al. (1994) conclude that “these enhancing effects do not appear to be of sufficient generality or magnitude to explain why people find cigarette smoking highly reinforcing during the initiation phase of tobacco dependence”. However, a recent review suggests that these effects are stronger among several neuropsychiatric populations including ADHD (Sacco et al., 2004), where ∼ 40% prevalence of smoking has been reported compared to ∼ 26% in non-ADHD samples (Pomerleau et al., 1995, Lambert and Hartsough, 1998).
Comparison of performance between non-abstinent and abstinent smokers has shown that abstinent smokers report greater improvement by nicotine of a wider range of cognitive functions including sensory abilities, finger tapping, and selective and sustained attention. Down-regulation of nicotine receptors may account for reduced effects in chronic smokers who are not abstinent. A widely accepted view is that nicotine serves as a negative reinforcer, abolishing the aversive withdrawal symptoms that an abstinent smoker experiences and thereby contributes to smoking maintenance (Heishman et al., 1994). This effect of nicotine on abstinent smokers may account for the findings of studies that report nicotine facilitation of many psychomotor functions (reviewed by Sherwood, 1993) including sensory processing, attention, information manipulation, memory, motor response and tasks involving complex performance (e.g. driving simulation). This facilitation varies among tasks and appears to have the strongest effect on tasks involving vigilance and attention.
In contrast to the findings reporting beneficial acute effects of nicotine, long term use of nicotine has been associated with poorer performance on a variety of neurocognitive tests (independent of confounding factors that include gender, alcohol consumption, baseline cognitive function, age, occupational class and education (Hill et al., 2003, Crevilla et al., 2000, Mitchell, 2004). Some studies have concluded that the cognitive impairment is more strongly associated with heavy smoking (Razani et al., 2004, Richards et al., 2003). On the other hand, epidemiological studies have found a lower than expected incidence of serious, cognition-impairing conditions such as Alzheimer's and Parkinson's diseases among smokers (Newhouse et al., 2004), raising the possibility that smoking may have a protective effect against some neurodegenerative processes involved in these conditions.
Overall, the principal focus of studies in this field has been on documenting the direct neurocognitive effects of nicotine and less on a-priori neurocognitive characteristics that might influence initiation and maintenance of smoking and severity of ND. We suggest that some individuals who initiate smoking and progress to dependence manifest a specific neurocognitive profile that will be evident mainly in tests that measure sustained attention and control of impulsivity (inhibition of pre-potent response) and will not be attributable to nicotine withdrawal or to the deleterious effects of long term nicotine consumption. In the context of the present project, we hypothesized that: (1) current smokers would perform worse than non-smokers on tests that mainly involve attention and control of impulsivity; (2) No difference in performance would be found between current and past smokers on these tests; (3) These differences would not be related to nicotine withdrawal or duration and intensity of smoking. These hypotheses were tested in subjects drawn from a large sample of female students that formed the basis for previous reports on the role of nicotinic cholinergic receptor genes, psychological features and life experience in smoking initiation and nicotine dependence (Greenbaum et al., 2006) and the direct and interactive contribution of serotonergic genes and traumatic life experience (Lerer et al., 2006).
Section snippets
Subjects
The subjects for this study were drawn from 501 female undergraduate students, who were recruited by advertisement for a comprehensive research project on smoking initiation and nicotine dependence among young Israeli women, between September 2002 and May 2004 and who were the focus of two previous publications (Greenbaum et al., 2006, Lerer et al., 2006). Inclusion criteria were age (20–30 years), enrollment in an institute of higher learning (secular or religious) in the Jerusalem area,
Background variables
CS and PS were slightly (∼ 1 year) but significantly older than NS (overall: F(3,324) = 7.7, p < 0.001, Scheffe post-hoc test: p = 0.005, p = 0.002, respectively) (Table 1). CS had slightly fewer years of schooling than PS (overall: F(3,323) = 3.0, p = 0.03, Scheffe post-hoc test: p = 0.04). This difference can be attributed to the fact that PS was the oldest group among the four. CS and PS groups were less likely to be religious (χ2(3) = 37.75, p < 0.001). The age factor was taken into account during the
Discussion
The main finding of this study is that smokers, both current and past, manifested a different neurocognitive performance than non-smokers on tests that assess sustained attention (CPT, TOL), control of impulsivity (MFFT, TOL) and planning (TOL) (Lezak, 1995, p. 657). Smokers made more errors of commission and omission such as responding to a black rectangle when they should not do so or missing a red rectangle when they should not (CPT), choosing a pattern that is not similar to the target
Acknowledgements
Supported in part by an unrestricted grant from Philip Morris Inc. and Philip Morris, USA. The project was initiated by the investigators and the sponsor had no role in its design, in the analysis and interpretation of the data or in the preparation of the paper.
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Presented at the 10th Annual Meeting of the Israel Society of Biological Psychiatry, Hagoshrim, Israel; March 2006. The two previous papers in this series (Greenbaum et al., 2006, Lerer et al., 2006 — see reference list) were published in a different journal.
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Conflict of Interest: Semion Kertzman MD is an employee of Anima Scan Ltd.