Short communicationCigarette smoking status in pathological gamblers: Association with impulsivity and cognitive flexibility
Introduction
Only recently has the comorbidity between cigarette smoking and pathological gambling been recognized, with as many as 60% of pathological gamblers (PG) also smoking (McGrath and Barrett, 2009). The reasons for this covariation are likely manifold. Nicotine causes increased expression of dopamine in brain reward centers, and may add to or even multiply the pleasurable effects of gambling. At the same time, gambling may enhance the enjoyment of cigarette smoking. Additionally, there are some 4000 chemical constituents in tobacco smoke, including inhibitors of the catabolic enzyme, monamine oxidaze (MAO) (Fowler et al., 2003, Hoffmann and Wynder, 1986). Inhibition of MAO, whose function is to decompose monoamine neurotransmitters (MN; e.g., dopamine), results in greater longevity and activity of MNs in the synapse. Blanco et al. (1996) found deficient MAO activity in individuals with pathological gambling. The possibility that PG use smoking to ameliorate MAO deficiencies remains to be confirmed.
Nicotine, the primary chemical responsible for smoking, has a diverse set of psychological effects, including on executive functioning. The role of nicotine as a cognitive enhancer has been controversial, but a recent review suggests that nicotine indeed yields improvements in mental functioning (e.g., attention and some forms of memory) that transcends mere withdrawal relief (Heishman et al., 2010). Yet the beneficial effects of nicotine are perhaps most apparent in those whose brains are not functioning optimally. For instance, nicotine has proven therapeutic in those with attention – deficit/hyperactivity disorder, schizophrenia, and Alzheimer's type dementia (Newhouse et al., 2004). Several studies have found that PG exhibit impaired performance on neurocognitive measures of response inhibition, including the domains of motor inhibition and delay discounting (van Holst et al., 2010). While a high proportion of PG currently smoke, a large percentage have either quit smoking or never smoked. In this report, we evaluate the association between cigarette smoking and two computerized tests of executive functioning; the Stop-Signal task (SST) and the Intradimensional/Extra-dimensional (ID/ED) set-shift task. Based on cognitive enhancing effects of nicotine, we hypothesized that PG who were current smokers would perform better than former- and non-smokers on tests of impulsivity and cognitive flexibility.
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Participants
Data for the current analyses were pooled from one pharmacological trial previously completed (n = 28) (Grant et al., 2010), and two ongoing clinical trials using cognitive behavioral therapy (n = 23) and pharmacotherapy (n = 4) for the treatment of PG. The institutional review board for the University of Minnesota approved procedures. After review of the study procedures and having had the opportunity to ask questions, all subjects provided voluntary written informed consent. All studies were
Sample characteristics
No differences in demographic variables were observed across smoking status. Of the 55 subjects (56.4% female), the mean age was 49.9 ± 11.5. The distribution of subjects in each group was NS (n = 11), FS (n = 10), and CS (n = 34). The majority of the sample was white (76.4%), unmarried (78.2%), and lacking at least a college education (61.8%). Current smokers smoked a mean 18.1 ± 7.8 cigarettes/day (56% smoked 1 pack/day or more). With respect to psychiatric history and symptoms, the sample was largely
Discussion
This is the first study to assess the association between smoking and cognitive function in PG. The key finding was that smoking was associated with greater inhibitory control and while smokers did not differ from non-smokers on a measure of cognitive flexibility, among smokers, greater tobacco consumption was associated with greater cognitive flexibility.
Stop-Signal performance is dependent on a right lateralized fronto-striatal neural network including the right inferior frontal and bilateral
Role of funding source
This research was funded in part by an American Recovery and Reinvestment Act (ARRA) Grant from the National Institute on Drug Abuse (1RC1DA028279-01) and through grant support from Forest Pharmaceuticals. The first author is supported by National Institute of Drug Abuse (NIDA) grant K01-DA-019446.
Contributors
Dr. Grant and Kim designed the study protocol. Dr. Mooney undertook the data analysis and drafted the initial manuscript. Mr. Odlaug compiled the data, performed some statistical analysis, and along with Drs. Grant and Kim, saw the subjects from which the data is compiled and contributed to the editing of the research manuscript. All authors have reviewed the manuscript, agree on author order, and consent to submission for review.
Conflict of interest
Dr. Grant has received research grants from NIMH, NIDA, National Center for Responsible Gaming and its affiliated Institute for Research on Gambling Disorders, Forest Pharmaceuticals and GlaxoSmithKline. Dr. Grant receives yearly compensation from Springer Publishing for acting as Editor-in-Chief of the Journal of Gambling Studies. Dr. Grant has performed grant reviews for NIH and the Ontario Gambling Association. Dr. Grant has received royalties from Oxford University Press, American
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