Modeling the effect of alcohol on smoking lapse behavior

Abstract

The primary aim of this project was to examine the role of alcohol use in smoking lapse behavior, as alcohol consumption is a known risk factor for poor smoking cessation outcomes. We have developed a novel human laboratory model to examine two primary aspects of alcohol-mediated tobacco relapse: 1) Does alcohol facilitate the initiation of the first cigarette? 2) Once the first cigarette is initiated, does alcohol facilitate subsequent smoking? Using a within-subject design, 16 daily smokers who were also heavy social drinkers received a priming drink (0.03 g/dl or taste masked placebo) and then had the option of initiating a tobacco self-administration session or delaying initiation by five minute increments for up to 50 minutes in exchange for monetary reinforcement. Subsequently, the tobacco self-administration session consisted of a one-hour period, in which subjects could choose to smoke their preferred brand of cigarettes using a smoking topography system or receive monetary reinforcement for cigarettes not smoked. Alcohol craving, tobacco craving, subjective reactivity to alcohol, and nicotine withdrawal were assessed as secondary outcomes. Results demonstrated that after consuming the alcohol beverage, subjects were less able to resist the first cigarette and initiated their smoking sessions sooner, and smoked more cigarettes compared to the placebo beverage. These findings have implications for smoking cessation in alcohol drinkers and model development to assess smoking lapse behavior. Keywordssmoking; lapse behavior; alcohol; craving; human laboratory; monetary reinforcement It is well established that alcohol consumption and tobacco use are highly correlated in both clinical and non-clinical samples. Among alcoholics, 80% to 95% are smokers (DiFranza & Guerrera, 1990;Hughes, 1993;Kalman et al., 2005;Patten et al., 1996;Sobell et al., 1990), as compared to 23% in the general population (CDC, 2003 (DiFranza & Guerrera, 1990;Grant et al., 2004;Hurt et al., 1994) and the severity of alcohol and tobacco dependence is positively correlated (Ellingstad et al., 1999;Gulliver et al., 1995). Smoking is also highly correlated with drinking in nonalcoholic individuals (Carmody et al., 1985;Istvan & Matarazza, 1984), particularly among those who are heavy drinkers. Both laboratory studies and naturalistic observations have demonstrated that alcohol consumption is strongly associated with increased rates of smoking (Glautier et al., 1996;Mitchell et al., 1995;Shiffman et al., 1994). Additionally, there is evidence for cross-substance craving from both clinical and non-clinical samples (Drobes et al., 2000;Tiffany, 1995). Given the high co-occurrence of alcohol and tobacco use, it is not surprising that alcohol has been identified as a risk factor for poor smoking cessation outcomes (Baer & Lichenstein, 1988;Shiffman 1986;Zimmerman et al., 1990). For example, Shiffman (1986) found that 20% of all relapse episodes in smokers involved alcohol consumption. In a real-time examination of first lapse episodes, ...

Interactive effects of ethanol and nicotine on learning in C57BL/6J mice depend on both dose and duration of treatment

“…Nicotine withdrawal may lead to increased ethanol consumption in an attempt to reverse withdrawal-associated cognitive deficits, but increased consumption of ethanol also induces cognitive deficits, which could lead to smoking relapse in an attempt to ameliorate ethanol-associated deficits, producing a downward spiral into co-abuse. This hypothesis is supported by findings that nicotine withdrawal is associated with increases in both alcohol craving and consumption (Palfai et al 2000), that the impairments associated with ethanol are reversed by nicotine (Gould and Lommock 2003;Lyon et al 1975), and, finally, that ethanol decreases the ability to limit nicotine consumption (McKee et al 2006). Despite these findings, it is important to remember that the cognitive effects of these drugs comprise only one aspect of co-abuse; alcohol and nicotine also act on the brain's reward system, and interactive effects on this system could increase consumption as well.…”

Drinking Patterns of Older Adults with Chronic Medical Conditions

“…41 Among middle-aged men with COPD, a 20-year study in three European countries found more than double the risk of death among heavy drinkers compared with light to moderate drinkers. 42 Moreover, drinking has been found to negatively impact smoking cessation, 43 a critical recommendation in the management of COPD. 44 Finally, research on Alzheimer's disease and alcohol consumption has been suggestive of brain protection at lower levels of alcohol consumption but cognitive decline at higher levels.…”

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

“…In the Acheson et al (2006) study, the selfadministration phase commenced while the blood alcohol levels produced by the priming drink were ascending, while our self-administration phase began when the blood alcohol levels were descending. Alcohol-nicotine interactions have been shown to be sensitive to ascending and descending limb effects (King and Epstein 2005;McKee et al 2006;Mitchell et al 1995), and others have demonstrated that medication effects are sensitive to the interval between the priming drink and the self-administration phase (Anton et al 2004). Additional work is needed to delineate how nicotine replacement interacts with temporal effects of the priming drink on inhibiting or promoting further alcohol consumption.…”

“…Moreover, little is known about what effects standard smoking cessation treatments have on alcohol consumption in non-dependent heavy drinking smokers. Alcohol use has been shown to promote smoking relapse across studies using different methodologies (Baer and Lichenstein 1988;McKee et al 2006;Shiffman 1986;Shiffman et al 1996;Zimmerman et al 1990). One way in which smoking cessation medications could promote quitting behavior in this population is by reducing alcohol responses and consumption, thereby attenuating the ability of alcohol to prompt smoking relapse.…”