Effect of transdermal nicotine replacement on alcohol responses and alcohol self-administration

Psychopharmacology (Impact Factor: 3.88). 02/2008; 196(2):189-200. DOI: 10.1007/s00213-007-0952-3


Nicotine replacement is commonly used to treat tobacco use in heavy-drinking smokers. However, few studies have examined the effect of nicotine replacement on subjective and physiological responses to alcohol and alcohol drinking behavior.
The primary aim of this within-subject, double-blind study was to examine whether transdermal nicotine replacement (0 mg vs 21 mg/day) altered response to a low-dose priming drink and subsequent ad libitum drinking behavior.
Materials and methods
Subjects (n = 19) were non-treatment-seeking, non-dependent heavy drinkers who were daily smokers. Six hours after transdermal patch application, subjective and physiological responses to a priming drink [designed to raise blood alcohol levels (BALs) to 0.03 g/dl] were assessed. This was followed by a 2-h self-administration period where subjects could choose to consume up to eight additional drinks (each designed to raise BALs by 0.015 g/dl) or to receive monetary reinforcement for drinks not consumed.
We found that 6 h after patch application, tobacco craving associated with withdrawal relief was decreased, and systolic blood pressure and heart rate were increased in the active patch condition compared to the placebo patch condition. Subjective intoxication in response to the priming drink was attenuated in the active nicotine patch condition compared to 6 h of nicotine deprivation (i.e., placebo patch). During the self-administration period, subjects had longer latencies to start drinking and consequently appeared to consume fewer drinks when administered the active patch compared to the placebo patch.
In heavy drinkers, transdermal nicotine replacement compared to mild nicotine deprivation attenuated subjective and physiological alcohol responses and delayed the initiation of drinking.

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Available from: Stephanie S. O’Malley, Jan 02, 2015
    • "Similar inconsistencies have been observed with regard to the effects of nicotine on SR. Some studies have found that nicotine (administered via smoking, intranasally, or by transdermal patch) reduces craving for alcohol (Cooney et al., 2001) and attenuates the experience of intoxication and/or reduces ad libitum drinking (McKee et al., 2008), whereas others suggest that nicotine use increases subjective intoxication and craving (Kouri et al., 2004) and, for men, results in increased self-administration (Acheson et al., 2006). "
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    ABSTRACT: Subjective response to alcohol (SR) has been shown to differ by gender, family history of alcoholism, drinking status, and cigarette smoking status. However, the requisite statistical basis for making mean-level comparisons (scalar measurement invariance; MI) has not been established for any SR measure, making it impossible to determine whether observed differences reflect true differences or measurement bias. Secondary data analyses were conducted to evaluate (a) MI of the Subjective Effects of Alcohol Scale (SEAS) by gender, family history, heavy drinking status, and cigarette smoking status using multigroup confirmatory factor analysis; and (b) the impact of these group-level variables on SR using multivariate general linear modeling. A central strength, the SEAS assesses novel high arousal negative (HIGH-; e.g., aggressive) and low arousal positive effects (LOW+; e.g., relaxed) in addition to commonly assessed high arousal positive [HIGH+; e.g., sociable] and low arousal negative effects [LOW-; e.g., woozy]). A total of 215 young adults reported on SR during a placebo-controlled alcohol administration study in a simulated bar setting (target blood alcohol concentration = .08%). Scalar MI was achieved for each group. After consuming alcohol, family history-positive individuals reported stronger HIGH- effects and female smokers reported weaker LOW+ effects than their counterparts. Heavy episodic drinkers and family history-positive females reported weaker LOW- effects than their counterparts. The SEAS permits meaningful SR comparisons within several important groups. SR differences largely were observed on the novel SEAS subscales, highlighting the importance of assessing a full range of SR. (J. Stud. Alcohol Drugs, 76, 287-295, 2015).
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    • "For example , 2 recent double-blind clinical studies demonstrated that transdermal nicotine or nicotine delivered by tobacco smoke can increase alcohol consumption in men (Acheson et al., 2006; Barrett et al., 2006). In contrast, transdermal nicotine has been shown to decrease alcohol intake in women (Acheson et al., 2006) and delay alcohol drinking in heavy drinkers (McKee et al., 2008). Preclinical findings have provided further evidence that nicotine can increase ethanol (EtOH) intake (Blomqvist et al., 1996; Clark et al., 2001; Ericson et al., 2000; Lallemand et al., 2007; Le et al., 2003; Olausson et al., 2001; Potthoff et al., 1983; Smith et al., 1999), as well as decrease it (Dyr et al., 1999; Nadal et al., 1998; Sharpe and Samson, 2002) in rodents. "
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    ABSTRACT: Alcohol is frequently co-abused with smoking. In humans, nicotine use can increase alcohol craving and consumption. The objectives of the current study were to assess the acute effects of nicotine on alcohol seeking and relapse at 2 different time points. Adult female alcohol-preferring (P) rats were trained in 2-lever operant chambers to self-administer 15% ethanol (EtOH) (v/v) and water on a concurrent fixed-ratio 5-fixed-ratio 1 (FR5-FR1) schedule of reinforcement in daily 1-hour sessions. Following 10 weeks of daily 1-hour sessions, rats underwent 7 extinction sessions, followed by 2 weeks in their home cages. Rats were then returned to the operant chambers without EtOH or water being present for 4 sessions (Pavlovian Spontaneous Recovery [PSR]). Rats were then given a week in their home cage before being returned to the operant chambers with access to EtOH and water (relapse). Nicotine (0, 0.1, 0.3, or 1.0 mg/kg) was injected subcutaneously immediately or 4 hours prior to PSR or relapse testing. Injections of nicotine immediately prior to testing reduced (5 to 10 responses PSR; 50 to 60 responses relapse), whereas injections of nicotine 4 hours prior to testing increased (up to 150 responses for PSR; up to 400 responses for relapse with 1.0 mg/kg dose) responses on the EtOH lever during PSR and relapse tests. The results of this study demonstrate that acute effects of nicotine on EtOH-seeking and relapse behaviors may be time dependent, with the immediate effects being a result of nicotine possibly acting as a substitute for EtOH, whereas with a delay of 4 hours, priming effects of nicotine alterations in nicotinic receptors, and/or the effects of nicotine's metabolites (i.e., cotinine and nornicotine) may enhance the expression of EtOH-seeking and relapse behaviors.
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    • "There is recent preclinical (Steensland et al., 2007) and clinical (McKee et al., 2009) evidence to support the use of varenicline, a partial ß 2 -nAChR agonist, for reducing alcohol consumption. Additionally, the nicotine patch reduced alcohol self-administration in a human laboratory paradigm in heavy drinking daily smokers (McKee et al., 2008). Although studies examining the direct effects of ethanol on ß 2 -nAChRs are mixed (Gorbounova et al., 1998; Ribeiro-Carvalho et al., 2009; Robles and Sabria, 2008), prolonged abstinence from chronic alcohol consumption was recently associated with decreased ß 2 -nAChR availability compared to baseline in nonhuman primates (Cosgrove et al., 2010). "
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    ABSTRACT: This paper reviews evidence suggesting that nicotine and tobacco smoke profoundly modulate the effects of alcohol on γ-aminobutyric acid (GABA) neuronal function, specifically at the GABA(A)-benzodiazepine receptor (GABA(A)-BZR). The focus of this paper is on recent neuroimaging evidence in preclinical models as well as clinical experiments. First, we review findings implicating the role of alcohol at the GABA(A)-BZR and discuss the changes in GABA(A)-BZR availability during acute and prolonged alcohol withdrawal. Second, we discuss preclinical evidence that suggests nicotine affects GABA neuronal function indirectly by a primary action at neuronal nicotinic acetylcholine receptors. Third, we show how this evidence converges in studies that examine GABA levels and GABA(A)-BZRs in alcohol-dependent smokers and nonsmokers, suggesting that tobacco smoking attenuates the chemical changes that occur during alcohol withdrawal. Based on a comprehensive review of literature, we hypothesize that tobacco smoking minimizes the changes in GABA levels that typically occur during the acute cycles of drinking in alcohol-dependent individuals. Thus, during alcohol withdrawal, the continued tobacco smoking decreases the severity of the withdrawal-related changes in GABA chemistry. This article is part of a Special Issue entitled 'Trends in neuropharmacology: in memory of Erminio Costa'.
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