Concurrent Alcohol and Tobacco Dependence

Concurrent Alcohol and Tobacco Dependence Mechanisms and Treatment David J. Drobes, Ph.D. People who drink alcohol often also smoke and vice versa. Several mechanisms may contribute to concurrent alcohol and tobacco use. These mechanisms include genes that are involved in regulating certain brain chemical systems; neurobiological mechanisms, such as cross-tolerance and cross-sensitization to both drugs; conditioning mechanisms, in which cravings for alcohol or nicotine are elicited by certain environmental cues; and psychosocial factors (e.g., personality characteristics and coexisting psychiatric disorders). Treatment outcomes for patients addicted to both alcohol and nicotine are generally worse than for people addicted to only one drug, and many treatment providers do not promote smoking cessation during alcoholism treatment. Recent findings suggest, however, that concurrent treatment for both addictions may improve treatment outcomes. KEY WORDS: comorbidity; AODD (alcohol and other drug dependence); alcoholic beverage; tobacco in any form; nicotine; smoking; genetic linkage; cross-tolerance; AOD (alcohol and other drug) sensitivity; neurotransmitters; brain reward pathway; cue reactivity; social AODU (AOD use); cessation of AODU; treatment outcome; combined modality therapy; literature review lcohol consumption and tobacco ers who are dependent on nicotine Department of Health and Human use are closely linked behaviors. have a 2.7 times greater risk of becoming Services 1989). The concurrent use of A Thus, not only are people who alcohol dependent than nonsmokers both drugs by pregnant women can drink alcohol more likely to smoke (and (e.g., Breslau 1995). Finally, although also result in more severe prenatal dam- vice versa) but also people who drink the smoking rate in the general popula age and neurocognitive deficits in their larger amounts of alcohol tend to smoke tion has gradually declined over the offspring than use of either drug alone more cigarettes. Furthermore, patients past three decades, the smoking rate (e.g., Martin et al. 1997). Furthermore, diagnosed with dependence on one of among alcoholics has remained persis the combined use of alcohol and tobacco the drugs also are commonly diagnosed tently high (e.g., Hays et al. 1999). among adolescents is more predictive with dependence on the other drug Concerns about the concurrent use (e.g., Zacny 1990). In fact, smoking of alcohol and tobacco are particularly rates among alcoholics have been esti salient given the detrimental impact of DAVID J. DROBES, PH.D., is an associate mated to be as high as 90 percent, with this drug combination on the individ professor at the Moffitt Cancer Center & approximately 70 percent of alcoholics ual and on society. For instance, alcohol Research Institute, University of South smoking at least one pack of cigarettes and tobacco when used together increase Florida, Tampa, Florida. per day (National Institute on Alcohol the risk of various forms of cancer (e.g., Abuse and Alcoholism 1998). Similarly, mouth and esophageal cancer), as well Preparation of this article was supported smokers are far more likely to consume as cardiovascular disease, more than by National Institutes of Health grant alcohol than are nonsmokers, and smok use of either drug alone (e.g., U.S. AA–11157. 136 Alcohol Research & Health Concurrent Alcohol and Tobacco Dependence of illicit drug use and various personal between smoking and alcoholism— alcoholism and smoking will be the and social problems among this popu that is, genetic factors that increase the establishment of valid and reliable lation than use of either drug alone risk for smoking also increase the risk endophenotypes for these addictive (e.g., Hoffman et al. 2001). for alcoholism and vice versa (e.g., behaviors. An endophenotype is an Given the frequent occurrence and Koopmans et al. 1997; Prescott and objective and measurable characteristic broad implications of concurrent alco Kendler 1995). of a person that is thought to be more hol and tobacco use, research and clini The relative contributions of genetic directly related to the person’s genetic cal efforts clearly must focus on people and environmental risk factors may makeup (i.e., genotype) than are typical who abuse both drugs. Over the past depend on a person’s age and gender. diagnostic categorizations (e.g., alcohol decade, interactions between alcohol Thus, one study found that the com abuse or dependence). Perhaps the and tobacco have indeed received bined risk for alcohol use and smoking best-established example of such an growing attention from both basic and in adolescents was primarily attributable endophenotype in the drug addiction clinical researchers. Alcohol dependence to shared environmental features (e.g., field is the P300 component of the and smoking, individually and in com peer influences) whereas in young event-related brain potential (ERP). bination, are complex forms of addic adults, this risk was significantly influ ERPs are brain waves elicited by a sud tive behavior that may be influenced by enced by genetic factors (Koopmans et den stimulus (e.g., a light or sound). a variety of genetic, neurobiological, al. 1997). Laboratory findings suggest One component of an ERP typically conditioning, and psychosocial mecha that reduced subjective effects of alcohol can be measured approximately 300 nisms, as described in this article. In (e.g., euphoria or sedation) among milliseconds after the stimulus occurs addition to these mechanisms, the article smokers may underlie this genetic asso and is therefore called the P300 signal. discusses issues related to the treatment ciation (Madden et al. 1997), particu It is thought to represent cognitive, or of alcoholic smokers. This overview will larly among women. attentional, processing of novel infor necessarily be selective; for instance, Recent molecular genetic studies have mation. This P300 signal commonly there is little mention of sociocultural attempted to identify specific genetic is reduced in size in people at risk for (e.g., economic and demographic) fac factors that may underlie various forms alcoholism (e.g., Porjesz et al. 1998). tors that also may contribute to con- of addictive behavior. Perhaps the Recent work has also shown that smok current use of alcohol and tobacco (see strongest evidence for individual genes ers may exhibit ERPs with a reduced Bobo and Husten 2000). that may contribute to both smoking P300 signal (e.g., Anokhin et al. 2000). and alcoholism involves the dopamin By replicating these findings and identify ergic reward system. Dopamine is a ing additional valid endophenotypes Mechanisms Underlying brain chemical (i.e., neurotransmitter) for alcoholism and smoking, researchers Combined Alcohol and that mediates the communication among hope to detect stronger relationships Tobacco Use brain cells in certain brain regions. between these forms of addictive behav Some of these brain regions play a role ior and certain genes. In addition, these in the pleasant (i.e., rewarding) effects studies may lead to a fuller understand Genetic Factors of drugs such as alcohol and nicotine. ing of the mechanisms through which To exert its effects, dopamine released these genes influence behavior. The importance of genetic influences by one brain cell interacts with specific on both alcoholism and smoking has protein molecules (i.e., receptors) on Neurobiological Mechanisms gained widespread recognition over the the surface of neighboring cells, and past decade. Using behavioral genetic this interaction causes a biochemical Several neurobiological mechanisms methods, such as twin and adoption reaction in those cells. Some evidence may underlie the strong relationship studies, as well as genetic epidemiologi suggests that certain variants of genes between alcohol and tobacco use. Both cal approaches, researchers have estab that regulate the activity of dopamine the ability of one drug to reduce the lished that both alcoholism and smoking or its receptors may be related to the effects of the other drug (i.e., cross- have strong heritable components (e.g., risk of excessive alcohol consumption tolerance) and the ability of one drug Prescott and Kendler 1995). In general, or smoking (e.g., Lerman et al. 1999; to increase the effects of the other drug heritability, which estimates the propor Li 2000). The results at this stage are (i.e., cross-reinforcement) may play tion of variability within an observed merely suggestive, but the application important roles in mediating this characteristic that can be attributed to of molecular genetic research techniques relationship (Pomerleau 1995). Such genetic factors, appears to be slightly to studies of complex behaviors such as processes could act immediately when higher for smoking-related variables alcohol and nicotine addiction is pro alcohol and nicotine are taken together, (e.g., smoking initiation and smoking gressing rapidly and may yield impor or they could involve changes in nerve persistence) than for alcoholism (e.g., tant findings within the next decade. cell function that occur over time with Heath and Madden 1995). Moreover, One development that most likely repeated usage of either one or both several researchers have indicated that a will accelerate researchers’ understand drugs. It is also possible that the two substantial shared genetic risk exists ing of genetic factors contributing to drugs when taken together create a Vol. 26, No. 2, 2002 137 combined reward effect

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