Nicotine, caffeine, impulsivity, and arousal are all intercorrelated: both drugs increase arousal, and impulsivity is theoretically related to arousal. However, the independent and joint effects of nicotine and caffeine on impulsive behavior are unclear. In this study, male college students (N = 63) were administered either caffeine or lactose placebo (double-blind) and either nicotine or placebo cigarettes (double-blind). Participants engaged in three behavioral tasks: the Stop Signal Task (SST), the Stroop Color-Word Test (SCWT), and the Delay Discounting Task (DDT). Drug intake did not produce significant changes across conditions on any of the three tasks. The hypothesis that caffeine and nicotine have an interactive effect on impulsivity in men was not supported by the data. Potential reasons for the lack of significant findings include variability within the sample on consumption history.
Any substance that systematically affects arousal may well differentially affect those low and high on a personality dimension that is based on arousal differentials (i.e. impulsivity). Nicotine, a drug that produces physiological arousal, is one such substance. While the relationship of impulsivity to illegal arousal drugs has been studied, the relationship of impulsivity to smoking, a common and legal form of drug use, deserves examination (Acton, 2003). Nicotine is a powerful drug that reaches its maximum brain concentrations within one minute of smoke inhalation (United States Department of Health and Human Services [USDHHS], 1988) and smoking one to two cigarettes (with a typical nicotine yield of 0.6 to 1.4mg per cigarette) reduces subjective distress while increasing arousal of the nervous system (Gilbert, 1979; Parrott, 1998). At typical doses of one to two cigarettes in short succession, nicotine affects nicotinic acetylcholine receptors (nAChRs) to activate reward centers in the central nervous system (CNS), increasing dopamine (DA) and epinephrine release in the cerebral cortex of the brain (Mansvelder & McGehee, 2002; National Institute on Drug Abuse [NIDA], 2005; Nutt, 1997).
Additionally, nicotine increases regional cerebral blood flow (rCBF) in the left frontal region of the cortex, and decreases rCBF in the left amygdala and the right hemisphere of the cortex (Rose, et al., 2003). Laboratory studies of nicotine (e.g. Garrett & Griffiths, 2001) have shown a dose-dependent positive effect on mood, subjective “high,” and liking for drug, at a rate as high as 3.0 mg per 70 kg of body weight – roughly the equivalent of two cigarettes smoked in succession for an average weight male college student. Thus, nicotine may be considered a stimulant drug in terms of its effects on physiological arousal, although it has a calming effect on the orthogonal construct of mood (Parrott, 1998), Dose effects on activation have been found for nicotine, such that lower doses equivalent to those received from smoking one or two cigarettes, increase reticular activation, but doses higher than those obtained from normal smoking, when administered in the laboratory, decrease reticular activation.
For the present experiment, the following hypotheses were made:
1. Nicotine intake decreases impulsive behavior compared with placebo;
2. Caffeine intake increases impulsive behavior compared with placebo;
3. The combined intake of nicotine and caffeine decreases impulsive behavior compared with caffeine.
These hypotheses reflected several considerations. First, nicotine has been shown in previous research to decrease impulsive behavior in the absence of caffeine and thus, it was hypothesized that nicotine intake decreases impulsivity. Second, caffeine should, theoretically, increase impulsive behavior in the absence of nicotine, due to its well-established effect on cortical and sympathetic activation (e.g. Nehlig, Daval, & Debry, 1992), to which impulsivity is theoretically tied. Thus, it was hypothesized that caffeine intake increases impulsivity as a function of its increasing arousal. Third, it was hypothesized that nicotine intake blocks the increase in impulsivity from caffeine, such that individuals who receive both caffeine and nicotine together do not experience the increase in impulsivity associated with caffeine intake in the absence of nicotine. These hypotheses are consistent with prior research findings that suggest caffeine has an arousing effect on behavior (Smith, et al., 2004), nicotine has a paradoxical calming effect on behavior despite producing autonomic arousal (Parrott, 1998), and nicotine intake blocks the arousal effects of caffeine (Rose, 1986; Rose & Behm, 1991), presumably including its effects on impulsivity. Thus, according to these hypotheses, individuals who wish to increase their impulsivity use caffeine in the absence of nicotine, but those who wish to increase their arousal but not experience an increase in impulsivity use nicotine in conjunction with caffeine.
A power analysis (Cohen & Cohen, 2001) showed that for large effect sizes (f2 = 0.40), it is necessary to have 15 subjects in each cell. With four cells, an N of 60 was needed to have adequate power (1-β ≥. 8). Male smokers experience heightened sensitivity to the pharmacological effects of nicotine compared with female smokers (Benowitz & Hatsukami, 1998; Daurignac, Perez-Diaz, Grillon, & Jouvent, 2001; Ikard & Tomkins, 1973; Perkins, 1996; Perkins, Jacobs, Crow, & Blackburn, 2002). To avoid confounds based on gender differences, only male participants were recruited. Further, the subject pool from which participants were selected was comprised of students in introductory psychology courses at the University of Maryland. Because most students in these courses are between the ages of 18 and 25, the age of 30 was chosen as an upper cutoff to avoid a skewed distribution with a few outliers. Because smoking is illegal for those 17 years of age or younger, the age of 18 was chosen as a lower cutoff.
A number of adverse health effects are associated with acute caffeine intake and cigarette smoking. These include dry mouth, increased heart rate or blood pressure, irregular heartbeat, and dizziness. To minimize the potential for unforeseen adverse health effects, only participants who reported prior smoking of two cigarettes within a half-hour period, and prior caffeine intake of 300mg or more in a half-hour period, were allowed to participate in the study. Because the half-life of caffeine has been found to average five hours (James, 2000), and because nicotine withdrawal has not been associated with significant decrements in laboratory study performance at periods under 24 hours of abstinence (Hatsukami, Fletcher, Morgan, Keenan, & Amble, 1989), participants were asked to abstain from products containing either caffeine or nicotine for a period of six hours prior to participation. This six-hour abstinence period is consistent with previous studies conducted in our laboratory measuring the effects of caffeine (e.g. Davidson & Smith, 1989, 1991; Smith, Davidson, & Green, 1993), as well as a number of similar studies in the literature
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Seth, P., Cheeta, S., Tucci, S., & File, S. E. (2002). Nicotinic – serotonergic interactions in brain and behaviour. Pharmacology, Biochemistry & Behavior, 71, 795-805.
Dissertation Done by Thomas James White, University of Maryland