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Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us 2 Determinants and Consequences of Drug Use In this chapter, the committee provides a general overview of the extant research on the determinants and consequences of drug use, with special emphasis on methodology and integration among research traditions. In it we do not make recommendations; rather, this chapter provides relevant background material for analyses of illegal drug policy. DETERMINANTS OF DRUG USE A basic understanding of the determinants of drug use, especially of abuse and addiction, is a prerequisite to serious discussion of drug control policy. Different research disciplines, from neuroscience to economics to social psychology, offer distinct perspectives. These perspectives are not mutually exclusive, but, in practice, each discipline has investigated some determinants of drug use to the exclusion of others. Efforts to integrate the various disciplines will enhance understanding of drug use and help to inform drug policy. Advances in neuroscience suggest that the addiction process involves multiple factors that vary across drugs, individuals, and the environment (O’Brien, 1995). To focus only on one of these elements is to oversimplify, yet research on drug use has often isolated certain variables to the exclusion of others. For example, economic research tends to focus on the price of illegal drugs as a general measure of the incentives faced by consumers (Becker and Murphy, 1988; Orphanides and Zervos, 1995; Hung, 2000). Other nonpecuniary costs undoubtedly also influence drug use, but they
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Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us have been hard to quantify, so economic research into these areas has been scant. Little is known about the incentives provided by legal and social sanctions aiming to deter drug use (discussed in Chapter 6). Moreover, economists have generally not considered environmental, family, or peer influence on drug use. Conversely, social psychologists have studied individual, family, peer, neighborhood, and social risk factors for drug use but have generally neglected the economic costs of using drugs. The first section of this chapter summarizes what is known about the determinants of drug use and describes methodological and data-related problems in evaluating these determinants. It begins with a review of the neuroscience perspective, with an emphasis on how the effects of drug use vary across drugs, individuals, and their circumstances. It then examines economic research on the price sensitivity of drug use. Finally, it summarizes what is known about how individual and social factors may influence drug use. This survey is intentionally brief. The literature on the determinants of drug use is enormous in volume and scope. Researchers in criminology, economics, sociology, psychology, biochemistry, neurobiology, and epidemiology have sought to understand the determinants of illegal drug use. Since a comprehensive survey of this large literature is beyond the purview of this report, this section attempts to summarize key features of the knowledge base that may be important to evaluate the effectiveness of drug control policies. For a contemporary and more comprehensive review of what is known about the addictive process, see the recent Institute of Medicine reports, Pathways of Addiction (1996) and Dispelling the Myths About Addiction (1997). The Neuroscience Perspective on Addiction Many medical researchers view addiction as a disease similar to other chronic and relapsing conditions, such as asthma, diabetes, and hypertension (Institute of Medicine, 1995, 1996, 1997; O’Brien and McLellan, 1996; Leshner, 1997). According to this perspective, the physical dependence created by some drugs plays a relatively minor role. Treating the pain and suffering that starts when drug use stops is straightforward, while effective intervention to prevent relapse into drug-taking is quite complex. Long-term changes to the brain circuitry and the emotional cues that can trigger this circuitry may last a lifetime (Institute of Medicine, 1997). As with any chronic relapsing disease, understanding the dynamic processes of initiation, escalation, reduction, persistence, and relapse are especially important and difficult challenges. The processes that affect initiation of drug use are not identical to those that promote persistence of drug use or development of drug dependence (e.g., see Tsuang et al., 1999; Stallings et
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Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us al., 1999; Kendler et al., 1999; Bucholz et al., 2000). Similarly, the processes that influence relapse are not necessarily identical to either of these earlier processes (e.g., see Siegel, 1984; Childress et al., 1993; Brewer et al., 1998; Robbins et al., 2000). Advances in the neuroscience of addiction are beginning to provide a strong scientific basis for drug abuse treatment and prevention programs as well as other drug control policies (Institute of Medicine, 1996). Neuroscientists have long linked drug addiction with some disruption of the brain reward system (Olds and Milner, 1954; Wise, 1978; Cooper et al., 1996). Many drugs, including illegal drugs, can change feeling-states and may induce pleasurable feelings through actions within the central nervous system. This can happen in a number of different ways, depending on the drug, and often involves the neurotransmitter dopamine (Institute of Medicine, 1997). Normally, after release, a “transporter” returns dopamine back to the neuron that released it.1 Cocaine causes a buildup of dopamine by effectively blocking the transporter and preventing the neurotransmitter from deactivating. Amphetamine causes the neuron to release more dopamine by essentially putting the transporter into “reverse.” Heroin, alcohol, and other drugs also affect an array of reward and neurotransmitter pathways, some (but not all) linked to the dopamine transporter mechanisms (e.g., see Ritz et al., 1987, 1988; Maldonado et al., 1997; Self, 1998; Yoshimoto et al., 2000). An important feature of the addictive process is that the feeling-states induced by drug use can be affected by past consumption. The mechanisms are different for each category of drug: nicotine, opioids (heroin), sedatives (alcohol), and stimulants (cocaine, amphetamines). Some research on the stimulant drugs suggests a sensitization model. According to this model, repeated use of stimulants sensitizes certain aspects of the reward system so that a small amount of the drug or even an environmental cue previously associated with the drug can precipitate renewed drug use. Desensitization, or tolerance, involves a different model, in which exposure to a drug causes less response than was previously caused. This phenomenon is particularly prominent with opiates, such as heroin, and sedatives, such as alcohol. Tolerance can be explained in part by the response of the nervous system acting to maintain a constant balance of neural activity in spite of major changes in stimulation. The nervous system integrates attempts to keep the body in a state of equilibrium. These neuro-adaptive changes are critical for producing addiction. Taken with adequate dose and frequency, addictive drugs produce long- 1 Recent evidence points to other potential pathways of reinforcement-related neurotransmission (e.g., see Cornish et al., 1999; Cornish and Kalivas, 2000; Koob, 2000).
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Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us lasting changes in brain functioning that continue after the last dose of the drug (Leshner, 1997; O’Brien, 1995).2 While all illegal drugs affect brain systems, they do so in different ways and thus have different behavioral effects. Table 2.1 displays nine general classes of drugs by functional or behavioral activity. In terms of behavioral responses, alcohol and marijuana are sedating, whereas cocaine and amphetamines are powerful stimulants. Opiates such as heroin have multiple effects, including stimulation, relaxation, and analgesic actions. Nicotine stimulates and relaxes different systems. All of these are associated with the development of dependence, and all can lead some users to report craving, obsession-like thinking about drug use, and compulsion to use drugs, even when the degree of stimulation or sedation is minimal. Other drug-related conditions and processes also come into play, including the purity and efficacy of one drug relative to another. Similarly, the route of administration appears to influence the addictive properties. Drugs that are smoked or injected reach the brain more rapidly than those that are ingested; these routes of administration are associated with more rapid onset and produce more powerful effects. The importance of purity and mode of administration can be demonstrated in considering the coca plant. Crack cocaine is far more addictive than chewed coca leaves, although both come from the same source. Crack cocaine is smoked, thereby producing volatized pure drug in the lungs’ surface area. This process is far more fast-acting and addictive than occurs when powder cocaine absorbed via the nasal passage (Institute of Medicine, 1997).3 The potency and form of administration may also play important roles in the initiation and intensification process. Smoking and injecting drugs cause discomforts that may discourage use and intensification. In contrast, ingesting drugs in either liquid or tablet form is not likely to cause similar physical discomfort. 2 There is a recent line of neuroscience research on the mechanisms that govern sensitization and tolerance, including research on postsynaptic signaling mechanisms. Through this research, it has been possible to discover pathways by which exposure to cocaine and other drugs can provoke neural and behavioral plasticity. It appears that the plasticity occurs in response to a cocaine-associated alteration in the expression of genes within the nucleus of the neuron postsynaptically. This cocaine-modulation of gene expression is linked to development of sensitivity to the drugs, possibly contributing to the drug dependence process (e.g., Kelz et al., 1999). 3 It would be unethical to expose cocaine-naïve human subjects to crack cocaine and to powder cocaine in order to determine which form of cocaine is more “addictive,” but the presently available evidence suggests most rapid and pronounced development of cocaine dependence symptoms when crack cocaine is smoked or when powder cocaine HCl is injected intravenously (e.g., see Gossop et al., 1994; Hastukami and Fischman, 1996).
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Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us TABLE 2.1 Classification of Abusive and Additive Drugs Class Description Caffeine Produces wakefulness, mild central nervous system (CNS) and cardiovascular stimulation, Mild tolerance, dependence following chronic use. Alcohol Produces dose-dependent relaxation, disinhibition, mild euphoria, inebriation, intoxication, CNS depression, liver damage. Significant tolerance and dependence-withdrawal following chronic use; intense craving, alcoholism. Nicotine Produces mild CNS and cardiovascular stimulation. Tolerance and dependence-withdrawal following chronic use; intense craving; nicotine addiction. Depressants (sedatives, hypnotics, anxiolytics): barbiturates, methadqualone, diazepam, and other benzodiazepines Produce dose-dependent relaxation, disinhibition, mild euphoria, inebriation, intoxication, CNS depression. Significant tolerance and dependence withdrawal following chronic use; craving; addiction. Cannabinoids (marijuana, hashish: tetrahydrocannabinol (THC) Produce dose-dependent relaxation, disinhibition; alterations of mood, emotion and behavior; inebriation, intoxication. Mild tolerance. Opiates (opioids) and related analgesics: heroin, codeine, morphine, synthetic opioids. Produce dose-dependent analgesia, euphoria, disinhibition, anesthesia, CNS depression. Significant tolerance and dependence-withdrawal following chronic use; intense craving; opioid addiction. Stimulant: cocaine, amphetamine, methamphetamine, methylphenidate Produce dose-dependent mild-strong CNS stimulation, behavioral hyperactivity, adverse cardiovascular effects, euphoria. Tolerance and dependence withdrawal following chronic use; intense craving; addiction. Hallucinogens: lysergic acid diethylamide (LSD), mescaline, psilocybin, dimethyltryptamine (DMT), dimethoxymethylamphetamine (DOM), MDA, MDMA (“ecstasy”), phensyclidine (PCP; “angel dust”) ketamine Symptoms vary depending on which drug: visual distortions, hallucinations, mood changes, arousal, euphoria, anxiety, agitation, emotional withdrawal, thought disturbances, aggressive behavior, panic, catatonia. Mild tolerance with chronic use; little or no withdrawal. Inhalants: solvents, aerosols, acetone, benzene, nitrous oxide, amyl nitrate Produce dose-dependent relaxation, mild euphoria, dizziness, disinhibition, inebriation, intoxication, anesthesia, CNS depression, liver damage, cardiovascular depression. Source: Institute of Medicine (1997: Table 1.1).
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Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us Why do some people who experiment with drugs become addicted, while others do not? The answer to this question is quite complicated. The ways in which a particular drug activates, reinforces, and desensitizes pleasure can vary with dose, frequency, and chronicity of use; drugs also vary in their effects across individuals and environments. Medical researchers often view the contraction of a disease as an interaction of an agent, a host, and the environment. Applying this framework to drug use, the agent is the drug taken. As described above, drugs differ in effect. The host refers to the characteristics of the individual drug user, including genetic makeup, family history, traits of temperament or personality (e.g., openness to experience, or to risk-taking behavior), affiliation with drug-using peers who provide models for drug-taking behavior, and expectations about the drug effects. Individuals respond to the same drug in the same dose in different ways. The last piece of this disease contraction sequence, the environment, refers to availability of the drug and the sociocultural context surrounding its use. Experience and social context exert powerful effects on the brain and thus on behavior. Environmental cues also alter the effects of use. Thus the addiction process involves multiple simultaneous factors that vary across drugs, individuals, and environments (O’Brien, 1995). Economic Research on Price Sensitivity Economic research on the determinants of drug use focuses on the relationship between quantity consumed and price. In particular, a demand function relates consumption of a commodity to its price. The price elasticity of demand is the percentage change in consumption that is caused by a 1 percent change in the price. For example, if a 1 percent increase in the price causes a 0.5 percent decrease in consumption, then the price elasticity of demand is –0.5. It may seem that demand for an addictive substance is likely to be insensitive to price, so that the price elasticity of demand is close to zero, but this is not necessarily the case. The demand for cigarettes provides an illustration. The many studies of the price elasticity of demand for cigarettes have found that the long-run price elasticity of demand is in the range –0.27 to –0.79 for the population as a whole and –0.9 to –1.3 for college students (Chaloupka, 1991; Becker et al., 1994; Chaloupka and Wechsler, 1997). Demand functions and price elasticities must be understood to formulate effective drug policies. In particular, many antidrug policies are aimed at increasing the price that consumers must pay for a drug. If demand does not change when the price increases, then such policies will have little effect on consumption but will increase drug sellers’ earnings. These policies may also increase property crimes by consumers who need
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Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us more money to buy higher-priced drugs. A policy that has such effects is counterproductive. In contrast, if demand is highly sensitive to price, then policies that increase drug prices will cause desirable decreases in consumption and sellers’ earnings. Recent estimates of price elasticities of demand for cocaine and heroin vary widely, although several studies report elasticities that are quite high (that is, the elasticities may have large negative values).4 Caulkins (1995) obtained price elasticity estimates of –2.5 and –1.5 for cocaine and heroin, respectively. Saffer and Chaloupka (1995) estimated the price elasticity of participation (that is, the fraction of individuals who use an illegal drug) to be in the range –0.8 to –0.9 for heroin and –0.4 to –0.6 for cocaine. Grossman et al. (1996) estimated the long-run price elasticity of participation in cocaine use to be in the range –1.3 to –1.6, and estimated the long-run price elasticity of frequency of use conditional on participation to be –0.5. Chaloupka et al. (1998) obtained estimates of cocaine participation elasticities by youths in the range –0.2 to –1.0. The elasticity of frequency of use conditional on participation was in the range –0.3 to –0.5, and the estimated elasticity of demand was in the range –0.6 to –1.5. In summary, recent estimates of the price elasticity of demand for cocaine span a range of –0.6 to –2.5. It is difficult to know how one should judge the various estimates of price elasticities of demand for cocaine and heroin. In addition to spanning a very wide range, they all suffer from a variety of severe conceptual and data-related difficulties, which are described below. The effects of these problems on estimation accuracy are unknown. Accordingly, existing estimates of demand functions and price elasticities should be treated as only suggestive. Certainly, none can be extrapolated to an environment in which prices for illegal drugs are much lower than they are now (due, for example, to a reduction in the penalties for possession, distribution, or sale). Why Estimating Demand Functions and Price Elasticities Is Difficult In the committee’s judgment, the severe, unsolved conceptual and data-related problems involved in the estimation of demand functions for illegal drugs mean that no persuasive demand function for cocaine or other illegal drugs has yet been estimated. The problems with existing estimates include: 4 Caulkins and Reuter (1998) and Saffer and Chaloupka (1995) review earlier elasticity estimates. These vary widely but tend to be closer to zero than are more recent estimates.
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Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us Lack of reliable price data. The development of a demand function consists of using statistical methods to relate observed price changes to changes in consumption. Price data that indicate what consumers really pay are needed to do this. The committee found that existing data on the prices of illegal drugs do not represent actual drug prices in cities. Price dispersion. The prices of illegal drugs vary greatly among transactions. The same dealer may charge different prices to different buyers, and prices may vary greatly over the distance of a few city blocks. In addition, the prices paid by different buyers may change in different ways over time. Moreover, a buyer may have some control over the price he pays. One way of controlling the price is by choosing the amount to purchase. There is substantial quantity discounting of cocaine and heroin, even within the range of quantities found in retail transactions. Thus, the price per unit purchased is likely to be lower if the quantity purchased is large than if it is small. A consumer may also be able to influence the price by his choice of seller. In particular, a consumer may choose to familiarize himself with several sellers and may choose not to buy from a high-priced seller if he knows that a lower-priced one is nearby. The committee knows of no model of demand for illegal drugs that takes account of potential price dispersion. All studies that have come to our attention use a price index as a proxy for sale prices. The price index typically is an estimate of the cost of one gram of pure cocaine or heroin in a city. The index is constant over all transactions in a given city and year (see Chapters 3 and 5 for a detailed discussion). Other costs. The sale price is only one of the costs that a consumer pays for an illegal drug. There are also search costs (the time spent looking for a seller), the costs associated with any legal penalty that may be incurred if the consumer is arrested, and, possibly, psychological costs associated with committing an illegal act. The committee found no source of data on search costs and no demand model that attempts to incorporate these costs.5 Data are available on legal penalties for possessing illegal drugs (see Chapter 6 for further discussion of this issue). The committee knows of three studies that have incorporated these into a model of de- 5 ADAM (Arrestee Drug Abused Monitoring) asks arrested drug users whether there was a time during the 30 days preceding the interview when they attempted to buy drugs and had the cash but were unsuccessful. ADAM also asks the reasons for lack of success. The answers to these questions provide crude indicators of the search costs experienced by ADAM respondents. It is not known whether the difficulties in buying drugs experienced by ADAM respondents are representative of difficulties experienced by consumers in general. No study that the committee knows of has used information from ADAM to construct an indicator of search costs for a demand model.
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Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us mand for an illegal drug (Saffer and Chaloupka, 1995; Chaloupka et al., 1998; DeSimone, 1998). Lack of quantity data. Data on the quantities of drugs that consumers buy do not exist. To be most useful, a dataset should give quantities purchased in individual transactions, but even city-level aggregate consumption data might be useful.6 Because quantity data are not available, existing demand models use proxies. One common proxy is participation; this is a binary indicator (or a yes/no measure) of whether an individual has used a specified drug in a specified time period such as the past 30 days. Another proxy is the frequency of use (the number of times that an individual has used a drug in a specified time period). Some studies use both proxies—for example, Grossman et al. (1996) and Chaloupka et al. (1998) —estimate models of participation and of frequency of use conditional on participation. The accuracy of participation and frequency of use as proxies for quantity consumed is unknown (see Chapter 3 for further discussion of quantity data). Addiction. The utility that a consumer obtains from current consumption of an addictive drug depends on his past consumption (Becker and Murphy, 1988). Therefore, in a demand model for an addictive drug, current consumption depends on past consumption in addition to the price. If the consumer is foresighted, then current consumption also depends on future consumption (Becker et al., 1994). The dependence of current consumption on past and (possibly) future consumption increases the difficulty of obtaining suitable consumption data. Specifically, longitudinal consumption data measuring the quantity consumed over time are needed.7 The Monitoring the Future (MTF) survey provides longitudinal data on participation and use frequency by youths. Grossman et al. (1996) used these data to estimate a demand function for cocaine that takes account of the effects of addiction. No other consumption study reviewed by the committee was longitudinal. Instead, studies employed a 6 Aggregate consumption in the U.S. as a whole has been estimated by combining estimates of numbers of consumers, expenditure estimates obtained from arrested consumers interviewed by DUF (the predecessor of ADAM), and price estimates obtained from STRIDE (Office of National Drug Control Policy, 1997). The resulting consumption estimates are not available for individual cities and, in any case, are probably too crude for use in estimating demand functions. 7 Becker et al. (1994) estimated a model of the demand for cigarettes by using state-level aggregate consumption data (a time-series of cross-sections) instead of panel data. They assumed that state-level aggregates can be treated as consumption by a representative consumer. Becker et al. (1994) did not discuss the accuracy of this assumption. The assumption is problematic for cocaine, because cocaine consumers are highly heterogeneous. The representative consumer assumption cannot account for differences between the consumption patterns of casual and heavy users of cocaine.
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Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us cross-sectional model, relating an indicator of current consumption to the current price, which does not take the effects of addiction into account. Heterogeneity of consumers. Cocaine consumers include casual and heavy users. These two groups face similar prices (or distributions of prices) but have very different consumption patterns. The levels of the demand functions of casual and heavy users are obviously different. It is possible that the slopes (the changes in consumption due to a unit change in price) are also different. For example, casual users may be more responsive to changes in prices than are heavy users. If so, the high elasticities of participation found in recent studies of demand may mainly reflect responses of casual users to price fluctuations. In addition, the finding that frequency of use (conditional on participation) is less responsive to price than the number of users may be strongly influenced by the behavior of heavy (high frequency) users who are relatively insensitive to price changes. No demand model that the committee has seen allows for the possibility that casual and heavy users have different price sensitivities. Cross-elasticities. Some illegal drugs may be substitutes or complements for others. If so, the demand for one drug may depend on the price of another. Most studies have ignored such cross-elasticity effects. Two exceptions are models of demand for heroin and cocaine by Caulkins (1995) and a model of marijuana participation by DeSimone (1998). Moreover, possible complementarities are the focus of research on what has been called the gateway effect (see Chapter 7 for further discussion). The dynamics of drug use. No existing empirical model of demand for drugs describes the process by which individuals initiate and make transitions among different levels of drug use (for example, from nonuse to casual use, from casual use to nonuse or heavy use). Everingham and Rydell (1994), Rydell and Everingham (1994) and Everingham et al. (1995) propose a conceptual framework for modeling such transitions. However, the data that are required for empirical study of drug use dynamics and their dependence on prices and other costs of drug use are not available to researchers. Implementation of such a study would require a longitudinal dataset that describes drug use by individuals over time. The Monitoring the Future survey gathers longitudinal data on participation and frequency of use by youth, but it rarely makes the data available to researchers. Heterogeneity of drugs. Cocaine is sold in several chemically distinct forms (mainly cocaine base and powder cocaine). These forms have different prices, and consumers consider them to be different products. It is therefore likely that different forms of cocaine have different demand functions and price elasticities. The committee is aware of no study that has estimated separate demand functions or price elasticities for different forms of cocaine.
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Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us The lack of suitable data is the most serious obstacle to developing better demand functions and estimates of price elasticities. It is unlikely that significantly better estimates can be developed without better data on retail prices, quantities transacted and consumed, and search costs. Improved data on quantities and search costs will be most useful if they are longitudinal. Without reliable price and consumption data, it is not possible to predict the outcomes of policy measures aimed at influencing the price or availability of illegal drugs, and it is not possible to evaluate the effects of these policies after they have been implemented. Individual and Social Risk Factors Some research explores the statistical association of drug use with risk factors, which characterize individuals or their environment. Risk factors are conditions and processes that, when present, signal an increased likelihood that individuals will develop a behavior or a health-related condition (Garmezy, 1983).8 A large literature provides a wealth of information on the risk factors associated with drug use: children growing up with addicted parents are more likely to use and abuse, deviant adolescents are more likely to use as adults, individuals residing in high-crime areas are more likely to use, etc. These and other risk factors are sometimes taken to be “candidate causes” of drug use—suspected causal influences for which there may not be enough evidence to make a firm claim of causation. Other risk factors, in contrast, signal a reduced likelihood of a behavior or condition, such as drug use or drug dependence. Some are thought to act by offering direct resistance to ill health or maladaptation. The gene-linked enzymes involved in alcohol and nicotine metabolism, which encourage drowsiness or another symptom that discourages further use, are of this type. Others are thought to act by canceling or modifying the negative effects of risk-increasing factors. For example, frequent participation in church-related activities may reduce the risks associated with living in neighborhoods with street-level drug markets (Crum et al., 1996). Some may directly reduce a dysfunction, lessen the effect of the risk-increasing factors, disrupt the process through which certain factors operate to cause a dysfunction, or prevent the initial occurrence of deleterious factors (Coie et al., 1993). 8 In the prevention field, no single theoretical model has been embraced, although most organized prevention activities rely on a risk and protective factor framework (Van Etten and Anthony, 1999; Institute of Medicine, 1994). Hansen and O’Malley (1996) identify eight different theoretical models that have dominated prevention activities.
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Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us dicted users engage in economically motivated violent crime (e.g., robbery) in order to support an expensive habit of drug use. Finally, systemic violence occurs as a consequence of the nature of illegal drug trafficking—territorial disputes among dealers, conflicts with disgruntled customers and angry neighbors, intimidation to promote debt collection, and so on. Goldstein and colleagues (1992) estimate that in New York City in 1988, 74 percent of all drug- and alcohol-related homicides fell into the systemic category; of those, 61 percent involved crack cocaine and 27 percent involved powder cocaine. Another 4 percent of all drug- and alcohol-related homicides were primarily economically compulsive. Only 14 percent were primarily psychopharmacological in nature, and 68 percent of those involved alcohol—a legal drug. Two open questions are whether the relative frequencies of each type of homicide have changed over time, and whether nonhomicide drug crimes fit a similar profile. But as several authors have argued in detail (Kleiman, 1992; MacCoun et al., 1996; MacCoun and Reuter, 2001), the premise that drug prohibition causes some drug-related harm does not necessarily imply that ending prohibition would, on net, reduce total drug-related harm. It is likely that many of the harmful consequences of drug use would be significantly reduced under a regulated policy of legal access to drugs—but not all harms. And even if average harm declined overall, there is no guarantee that net or total harm would decline as a result. Recall that total harm= average harm per incident of use×total use. If average harm declined under legalization, the effect on total harm would then depend on whether total use increased. If the average harmfulness of an incident of use (on any given dimension of harm) dropped but total use increased, the net effect on total harm is uncertain; it could fall, remain constant, or increase significantly (MacCoun and Reuter, 2001). Thus, legalization is an unproven and potentially risky strategy for reducing drug-related harms. For these reasons, the observation that drug illegality contributes to drug harmfulness is by no means tantamount to endorsing drug legalization. In discussing this point, we acknowledge concerns about the fear of sending the wrong message about the harms of drugs. However, inadequate analysis of the consequences of drug use gives a rhetorical advantage to advocates of legalization without allowing a serious examination of the merits and weaknesses of their arguments. Moreover, the failure to address the full consequences of drug prohibition results in lost opportunities for reducing drug-related harm under a policy of prohibition.
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Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us REFERENCES Adams, L.D., W.Gong, S.D.Vechia, R.G.Hunter, and M.J.Kuhar 1999 CART: From gene to function. Brain Research 848(1–2):137–40. Anthony, J.C., and J.E.Helzer 1995 Epidemiology of drug dependence. In Ming T.Tsuang, Mauricio Tohen, and G. E.P.Zahner, eds., Textbook in Psychiatric Epidemiology. New York. John Wiley and Sons. Argawal, D.P., and H.W.Goedde 1990 Alcohol Metabolism, Alcohol Intolerance, and Alcoholism. Berlin: Springer-Verlag. Bachman, J.G., L.D.Johnston, and P.M.O’Malley 1998 Explaining recent increases in students’ marijuana use: Impacts of perceived risks and disapproval, 1976 through 1996. American Journal of Public Health 88:887–892. Becker, G.S., M.Grossman, and K.M.Murphy 1994 An empirical analysis of cigarette addiction. American Economic Review 84:396– 418. Becker, G.S., and K.M.Murphy 1988 A theory of rational addiction. Journal of Political Economy 96:675–700. Brewer, D.D., R.F.Catalano, K.Haggerty, R.R.Gainey, and C.B.Fleming 1998 A meta-analysis of predictors of continued drug use during and after treatment for opiate addiction. Addiction 93(1):73–92. Brook, J.S., M.Whiteman, S.Finch, and P.Cohen 2000 Longitudinally foretelling drug use in the late twenties: Adolescent personality and social-environmental antecedents. Journal of Genetic Psychology 161(1):37–51. Bucholz, K.K., A.C.Heath, and P.A.Madden 2000 Transitions in drinking in adolescent females: Evidence from the Missouri adolescent female twin study. Alcoholism—Clinical and Experimental Research 24(6):914– 23. Buck, A.A., T.T.Sasaki, J.J.Hewitt, and A.A.Macrae 1968 Coca chewing and health. An epidemiologic study among residents of a Peruvian village. American Journal of Epidemiology 88(2):159–77. Caulkins, J.P. 1995 Estimating Elasticities of Demand for Cocaine and Heroin with Data from the Drug Use Forecasting System. H.John Heinz III School of Public Policy and Management, Carnegie Mellon University. 1994 Developing Price Series for Cocaine. Drug Policy Research Center. Santa Monica, CA: RAND. Caulkins, J.P., and P.Reuter 1998 What price data tell us about drug markets. Journal of Drug Issues 28:593–612. 1997 Setting goals for drug policy: Harm reduction or use reduction? Addiction 92:1143– 1150 . Chaloupka, F.J. 1991 Rational addictive behavior and cigarette smoking, Journal of Political Economy 99:722–742. Chaloupka, F.J., M.Grossman, and J.A.Tauras 1998 The Demand for Cocaine and Marijuana by Youth. Working paper 6411. Cambridge, MA: National Bureau of Economic Research.
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Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us Chaloupka, F.J., and H.Wechsler 1997 Price, tobacco control policies and smoking among young adults. Journal of Health Economics 16:359–373. Chilcoat, H.D., and J.C.Anthony 1996 Impact of parent monitoring on initiation of drug use through late childhood. Journal of the American Academy of Child and Adolescent Psychiatry 35(1):91–100. Chilcoat, H.D., N.Breslau, and J.C.Anthony 1996 Potential barriers to parent monitoring: Social disadvantage, marital status, and maternal psychiatric disorder. Journal of the American Academy of Child and Adolescent Psychiatry 35(12):1673–82. Childress, A.R., A.V.Hole, R.N.Ehrman, S.J.Robbins, A.T.McLellan, and C.P.O’Brien 1993 Cue reactivity and cue reactivity interventions in drug dependence. NIDA Research Monographs 137:73–95. Cohen, M.A. 1999 Alcohol, drugs and crime: Is “crime” really one-third of the problem? Addiction 94:644–647. Coie, J.D., N.F.Watt, S.G.West, J.D.Hawkins, J.R.Asarnow, H.J.Markman, S.L.Ramey, M.B.Shure, and B.Long. 1993 The science of prevention: A conceptual framework and some directions for a national research program. American Psychologist 48:1013–1022. Collins, W.A., E.E.Maccoby, L.Steinberg, E.M.Hetherington, and M.H.Bornstein 2000 Contemporary research on parenting: The case for nature and nurture. American Psychology 55(2):218–32. Cooper, J.R., F.E.Bloom, and R.H.Roth 1996 Cellular foundation of neuropharmacology. Pp. 9–48 in The Biochemical Basis of Neuropharmacology, 7th Edition. New York: Oxford University Press. Cornish, J.L., P.Duffy, and P.W.Kalivas 1999 A role for nucleus accumbens glutamate transmission in the relapse to cocaine-seeking behavior. Neuroscience 93(4):1359–1367. Cornish, J.L., and P.W.Kalivas 2000 Glutamate transmission in the nucleus accumbens mediates relapse in cocaine addiction. Journal of Neuroscience (Online). 20(15):RC89. Corrao, G., V.Bagnardi, A.Zambon, and S.Arico 1999 Exploring the dose-response relationship between alcohol consumption and the risk of several alcohol-related conditions: A meta-analysis. Addiction 94:1551–1573. Crane, B.D., A.R.Rivolo, and G.C.Comfort 1997 An Empirical Examination of Counterdrug Interdiction Program Effectiveness. IDA paper, p. 3219. Alexandria, VA: Institute for Defense Analyses. Crum, R.M., M.Lillie-Blanton, and J.C.Anthony 1996 Neighborhood environment and opportunity to use cocaine and other drugs in late childhood and early adolescence. Drug and Alcohol Dependence 43(3):155–61. Curtis, R., and T.Wendel 2000 Lockin’ Niggas Up Like It’s Goin’ Out of Style: The Differing Consequences of Police Interventions in Three Brooklyn, New York, Drug Markets. Conference on Drug Markets and Law Enforcement Strategies. Arlington, VA: National Institute of Justice. 1999 Toward the Development of a Typology of Illegal Drug Markets. Unpublished paper prepared for Committee on Data and Research for Policy on Illegal Drugs.
OCR for page 67
Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us Daniels, D., J.Dunn, F.F.Furstenberg, Jr., and R.Plomin 1985 Environmental differences within the family and adjustment differences within pairs of adolescent siblings. Child Development 56(3):764–74. DeSimone, J. 1998 Is marijuana a gateway drug? Eastern Economic Journal 24:149–164. Doyle, J.K. 1997 Judging cumulative risk. Journal of Applied Social Psychology 27:500–524. Duncan, T.E., S.C.Duncan, H.Hops, and A.Alpert 1997 Multi-level covariance structure analysis of intra-familial substance use. Drug and Alcohol Dependence 46(3):167–80. Eaves, L., A.Heath, N.Martin, H.Maes, M.Neale, K.Kendler, K.Kirk, and L.Corey 1999 Comparing the biological and cultural inheritance of personality and social attitudes in the Virginia 30,000 study of twins and their relatives. Twin Research 2(2):62–80. Edwards, G., P.Anderson, T.F.Babor, S.Casswell, R.Ferrence, N.Giesbrecht, C.Godfrey, H.D.Holder, P.Lemmens, K.Mäkelä, L.T.Midanik, T.Norström, E.Österberg, A.Romesljö, R.Room, J.Simpura, and O.Skog 1994 Alcohol Policy and the Public Good. Oxford, England: Oxford University Press. Everingham, S.S., and C.P.Rydell 1994 Modeling the Demand for Cocaine. Prepared for the Office of National Drug Control Policy and the U.S. Army. Santa Monica, CA: RAND. Everingham, S.M.S., C.P.Rydell, and J.P.Caulkins 1995 Cocaine consumption in the United States: Estimating past trends and future scenarios. Socio-Economic Planning Sciences 29:305–314. Fagan, J. 1992 Drug selling and licit income in distressed neighborhoods: The economic lives of street-level drug users and dealers. In A.V.Harrell and G.E.Peterson, eds., Drugs, Crime, and Social Isolation. Washington, DC: Urban Institute Press. Fazio, R.H., M.P.Zanna, and J.Cooper 1978 Direct experience and attitude-behavior consistency: An information processing analysis. Personality and Social Psychology Bulletin 4:48–51. Feldman, H. 1968 Ideological supports to becoming and remaining a heroin addict. Journal of Health and Social Behavior 9(14):31–155. Foroud, T., and T.K.Li 1999 Genetics of alcoholism: a review of recent studies in human and animal models. American Journal of Addictions 8(4):261–278. Gable, R.S. 1993 Toward a comparative overview of dependence potential and acute toxicity of psychoactive substances used nonmedically. American Journal of Drug and Alcohol Abuse 19:263–281. Garmezy, N. 1983 Stressors of childhood. In N.Garmezy and N.Rutter, eds., Stress, Coping and Development in Children. New York: McGraw-Hill. Goldstein, P. 1985 The drug/violence nexus: A tripartite conceptual framework. Journal of Drug Issues 14:493–506.
OCR for page 68
Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us Goldstein, P., H.H.Brownstein, and P.J.Ryan 1992 Drug-related homicide in New York: 1984 and 1988. Crime and Delinquency 38:459– 476. Gossop, M., P.Griffiths, B.Powis, and J.Strang 1994 Cocaine: Patterns of use, route of administration, and severity of dependence. British Journal of Psychiatry 164(5):660–664. Gottfredson, D.C. 2000 Delinquency Prevention in Schools. New York: Cambridge University Press. Gottfredson, D.C., M.A.Harmon, G.D.Gottfredson, E.M.Jones, and J.A.Celestin 1996 Compendium of Prevention Program Outcomes and Instrument Locator. Ellicott City, MD: Gottfredson Associates, Inc. Groenewegen, P.P., H.G.Leufkens, P.Spreeuwenberg, and W.Worm 1999 Neighbourhood characteristics and use of benzodiazepines. Netherlands Social Science Medicine 48(12):1701–1711. Grossman, M., F.J.Chaloupka, and C.C.Brown 1996 The Demand for Cocaine by Young Adults: A Rational Addiction Approach. Working paper 5713. Cambridge, MA: National Bureau of Economic Research. Hansen, W.B., and P.M.O’Malley 1996 Drug use. In R.J.DiClemente, W.B.Hansen, and L.E.Ponton, eds. Handbook of Adolescent Health Risk Behavior. New York: Plenum Press. Harwood, H.J., D.Fountain, and G.Livermore 1998 The Economic Costs of Alcohol and Drug Abuse in the United States, 1992. Rockville, MD: National Institute on Drug Abuse. Hatsukami, D.K., and M.W.Fischman. 1996 Crack cocaine and cocaine hydrochloride. Are the differences myth or reality? Journal of the American Medical Association 276(19):1580–1588. Hawkins, J.D., M.W.Arthur, and R.F.Catalano 1995 Building a Safer Society: Strategic Approaches to Crime Prevention: Preventing Substance Abuse. Chicago: University of Chicago Press. Hawkins, J.D., R.F.Catalano, and J.Y.Miller 1992 Risk and protective factors for alcohol and other drug problems in adolescence and early adulthood: Implications for substance abuse prevention. Psychological Bulletin 112(1):64–105. Hirschi, T. 1969 Causes of Delinquency. Berkeley: University of California Press. Hung, A. 2000 A Behavioral Theory of Addiction. Working Paper, The Heinz School, Carnegie Mellon University. Institute of Medicine 1997 Dispelling the Myths About Addiction: Strategies to Increase Understanding and Strengthen Research. Washington, DC: National Academy Press. 1996 Pathways of Addiction: Opportunities in Drug Abuse Research. Washington, DC: National Academy Press. 1995 The Development of Medications for the Treatment of Opiate and Cocaine Addictions: Issues for the Government and Private Sector. Washington, DC: National Academy Press . 1994 Reducing Risks For Mental Disorders: Frontiers for Preventive Intervention Research. Washington, DC: National Academy Press.
OCR for page 69
Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us Johanson, C.E., F.F.Duffy, and J.C.Anthony 1996 Associations between drug use and behavioral repertoire in urban youths. Addiction 91(4):523–534. Johnston, L.D. 1991 Toward a theory of drug epidemics. In L.Donohew and H.E.Sypher, eds., Persuasive Communication and Drug Abuse Prevention. Hillsdale, NJ: Lawrence Erlbaum Associates. Julien, R.M. 1998 A Primer of Drug Action, 8th ed. New York: W.H.Freeman. Kelz, M.B., J.Chen, W.A.Carlezon, Jr, K.Whisler, L.Gilden, A.M.Beckmann, C.Steffen, Y.J.Zhang, L.Marotti, D.W.Self, T.Tkatch, G.Baranauskas, D.J.Surmeier, R.L.Neve, R.S. Duman, M.R.Picciotto, and E.J.Nestler 1999 Expression of the transcription factor deltaFosB in the brain controls sensitivity to cocaine. Nature 16:401(6750):272–276. Kendler, K.S., and C.O.Gardner, Jr. 1998 Twin studies of adult psychiatric and substance dependence disorders: Are they biased by differences in the environmental experiences of monozygotic and dizygotic twins in childhood and adolescence? Psychological Medicine 28(3):625–633. Kendler, K.S., L.Karkowski, and C.A.Prescott 1999 Hallucinogen, opiate, sedative and stimulant use and abuse in a population-based sample of female twins. Acta Psychiatrica Scandinavica 99(5):368–376. Kendler, K.S., J.Myers, and C.A.Prescott 2000 Parenting and adult mood, anxiety and substance use disorders in female twins: An epidemiological, multi-informant, retrospective study. Psychological Medicine 30(2):281–294. Kendler, K.S., and C.A.Prescott 1998a Cocaine use, abuse and dependence in a population-based sample of female twins. British Journal of Psychiatry 173:345–350. 1998b Cannabis use, abuse, and dependence in a population-based sample of female twins. American Journal of Psychiatry 155(8):1016–1022. Kendler, K.S., P.C.Sham, and C.J.MacLean 1997 The determinants of parenting: An epidemiological, multi-informant, retrospective study. Psychological Medicine 27(3):549–563. Kendler, K.S., L.M.Karkowski, L.A.Corey, C.A.Prescott, and M.C.Neale 1999 Genetic and environmental risk factors in the aetiology of illicit drug initiation and subsequent misuse in women. British Journal of Psychiatry 175:351–356. Kessler, R.C., and R.H.Price 1993 Primary prevention of secondary disorders: A proposal and agenda. American Journal of Community Psychology 21(5):607–633. Kleiman, M.A.R. 1999 “Economic cost” measurements, damage minimization and drug abuse control policy. Addiction 94:638–641. 1992 Against Excess: Drug Policies for Results. New York: Basic Books. Koob, G.F. 2000 Neurobiology of addiction. Toward the development of new therapies. Annals of the New York Academy of Science 909:170–185. Kosten, T.A., S.A.Ball, and B.J.Rounsaville 1994 A sibling study of sensation seeking and opiate addiction. Journal of Nervour and Mental Disease 182(5):284–289.
OCR for page 70
Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us Ledermann, S. 1956 Alcool, Alcoolisme, Alcoolisation, Volume 1. Paris: Presses Universitaires de France. Leshner, A. 1997 Addiction is brain disease, and it matters. Science 278. Levitt, S.D., and S.A.Venkatesh 1998 An Economic Analysis of a Drug-Selling Gang’s Finances. Working paper 6592. Cambridge, MA: National Bureau of Economic Research. Lilienfeld, D.E., and P.D.Stolley 1994 Foundations of Epidemiology, 3rd ed. New York: Oxford University Press. Luthar, S.S., and G.Cushing 1999 Neighborhood influences and child development: A prospective study of substance abusers’ offspring. Development and Psychopathology 11(4):763–784. MacCoun, R. 1993 Drugs and the law: A psychological analysis of drug prohibition. Psychological Bulletin 113:497–512. 1998 Toward a psychology of harm reduction. American Psychologist 53:1199–1208. MacCoun, R., and P.Reuter 2001 Drug War Heresies: Learning from Other Vices, Times, and Places. New York: Cambridge University Press. MacCoun, R., P.Reuter, and T.Schelling 1996 Assessing alternative drug control regimes. Journal of Policy Analysis and Management 15:1–23. Maldonado, R., A.Saiardi, O.Valverde, T.A.Samad, B.P.Roques, and E.Borrelli 1997 Absence of opiate rewarding effects in mice lacking dopamine D2 receptors. Nature 388(6642):586–589. Manski, C.F. 2000 Economic analysis of social interactions. Journal of Economic Perspectives 14:115– 136. 1995 Identification Problems in the Social Sciences. Cambridge, MA: Harvard University Press. Merikangas, K.R., R.L.Mehta, B.E.Molnar, E.E.Walters, J.D.Swendsen, S.Aguilar Gaziola, R.Bijl, G.Borges, J.J.Caraveo-Anduaga, D.J.DeWit, B.Kolody, W.A.Vega, H.U.Wittchen, and R.C.Kessler 1998a Comorbidity of substance use disorders with mood and anxiety disorders: Results of the International Consortium in Psychiatric Epidemiology. Addictive Behavior 23(6):893–907. Merikangas, K.R., M.Stolar, D.E.Stevens, J.Goulet, M.A.Preisig, B.Fenton, H.Zhang, S.S. O’Malley, and B.J.Rounsaville 1998b Familial transmission of substance use disorders. Archives of General Psychiatry 55(11):973–979. Moffitt, T.E. 1993 Adolescent-limited and life-course-persistent antisocial behavior: A developmental taxonomy. Psychological Review 100:674–701. Morgan, M.G. 1981 Probing the question of technology-induced risk. IEEE Spectrum 18:58–64. Musto, D.F. 1995 Perception and regulation of drug use: The rise and fall of the tide. Annals of Internal Medicine 15:123(6):468–469.
OCR for page 71
Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us 1971/1987 The American Disease: Origins of Narcotic Control New York: Oxford University Press. National Development and Research Institutes 1997 Natural History of Crack Distribution/Abuse. Rockville, MD: National Institute on Drug Abuse. Negrete, J.C. 1992 Cocaine problems in the coca-growing countries of South America. CIBA Foundation Symposium 166:40–50. Neiderhiser, J.M., D.Reiss, E.M.Hetherington, and R.Plomin 1999 Relationships between parenting and adolescent adjustment over time: Genetic and environmental contributions. Developmental Psychology 35(3):680–692. O’Brien, C.P. 1995 Drug addiction and drug abuse. In The Pharmacological Basis of Therapeutics, 9th Edition, J.G.Hardman and L.E.Limbard, eds. New York: McGraw Hill. O’Brien, C.P., and A.T.McLellan 1996 Myths about the treatment of addiction. Lancet 347:237–240. Office of National Drug Control Policy 1999 The Price of Illicit Drugs: 1981 through the Second Quarter of 1998. Washington, DC: Abt Associates. 1997 What America’s Users Spend on Illegal Drugs: 1988–1995. Washington, DC: Abt Associates. Olds, M.E., and P.Milner 1954 Positive reinforcement produced by electrical stimulation of septal area and other regions of the rat brain. Journal of Comparative and Physiological Psychology 47:419– 427. Orphanides, A., and D.Zervos 1995 Rational addiction with learning and regret. Journal of Political Economy 103(4):739– 758. Petronis, K.R., and J.C.Anthony 2000 Perceived risk of cocaine use and experience with cocaine: Do they cluster within U.S. neighborhoods and cities? Drug and Alcohol Dependence 57(3):183–192. Petraitis, J., B.R.Flay, T.Q.Miller, E.J.Torpy, and B.Greiner 1998 Illicit substance use among adolescents: A matrix of prospective predictors. Substance Use and Misuse 33(13):2561–2604. Reuter, P., R.MacCoun, and P.Murphy 1990 Money from Crime: A Study of the Economics of Drug Dealing in Washington, D.C. Report R-3894-RF. Santa Monica, CA: RAND. Reuter, P. 1999 Are calculations of the economic costs of drug abuse either possible or useful? Addiction 94:635–638. Reuter, P., and J.Caulkins 1995 Redefining the goals of national drug policy: Recommendations from a working group. American Journal of Public Health 85:1059–1064. Rice, D.P. 1999 Economic costs of substance abuse, 1995. Proceedings of the Association of American Physicians 111:119–125.
OCR for page 72
Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us Riley, K.J. 1997 Crack, Powder Cocaine, and Heroin: Drug Purchase and Use Patterns in Six U.S. Cities . Office of National Drug Control Policy and the National Institute of Justice. Ritz, M.C., R.J.Lamb, S.R.Goldberg, and M.J.Kuhar 1988 Cocaine self-administration appears to be mediated by dopamine uptake inhibition. Progress In Neuro-Psychopharmacology and Biological Psychiatry 12(2–3):233–9.6. 1987 Cocaine receptors on dopamine transporters are related to self-administration of cocaine. Science 237(4819):1219–1223. Robbins, S.J., R.N.Ehrman, A.R.Childress, J.W.Cornish, and C.P.O’Brien 2000 Mood state and recent cocaine use are not associated with levels of cocaine cue reactivity. Drug and Alcohol Dependence 1:59(1):33–42. Rose, G. 1992 The Strategy of Preventive Medicine. New York: Oxford University Press. Rose, R.J., M.Koskenvuo, J.Kaprio, S.Sarna, and H.Langinvainio. 1988 Shared genes, shared experiences, and similarity of personality: Data from 14,288 adult Finnish co-twins. Journal of Perspectives in Social Psychology 54(1):161–171. Rydell, C.P., and S.S.Everingham 1994 Controlling Cocaine. Report prepared for the Office of National Drug Control Policy and the U.S. Army. Santa Monica, CA: RAND. Saffer, H., and F.Chaloupka 1995 The Demand for Illicit Drugs. Working paper 5238. Cambridge, MA: National Bureau of Economic Research. Self, D.W. 1998 Neural substrates of drug craving and relapse in drug addiction. Annals of Medicine 30(4):379–389. Sellers, E.M., and R.F.Tyndale 2000 Mimicking gene defects to treat drug dependence. Annuals of the New York Academy of Science 909:233–246. Siegel, R.K. 1984 Cocaine aroma in the treatment of cocaine dependency. Journal of Clinical Psychopharmacology 4(1):61–62. Simon, D., and E.Burns 1997 The Corner: A Year in the Life of an Inner City Neighborhood. New York: Broadway Books. Skog, O.J. 1993 The tail of the alcohol consumption distribution. Addiction 88:601–610. Stallings, M.C., J.K.Hewitt, T.Beresford, A.C.Heath, and L.J.Eaves 1999 A twin study of drinking and smoking onset and latencies from first use to regular use. Behavioral Genetics 29(6):409–421. Tourangeau, R., L.J.Rips, and K.Rasinski 2000 The Psychology of Survey Response. New York: Cambridge University Press. True, W.R., A.C.Heath, J.F.Scherrer, H.Xian, N.Lin, S.A.Eisen, M.J.Lyons, J.Goldberg, and M.T.Tsuang 1999 Interrelationship of genetic and environmental influences on conduct disorder and alcohol and marijuana dependence symptoms. American Journal of Educational Genetics 88(4):391–397.
OCR for page 73
Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us Tsuang, M.T., M.J.Lyons, R.M.Harley, H.Xian, S.Eisen, J.Goldberg, W.R.True, and S.V. Farina 1999 Genetic and environmental influences on transitions in drug use. Behavioral Genetics 29(6):473–479. Tsuang, M.T., M.J.Lyons, J.M.Meyer, T.Doyle, S.A.Eisen, J.Goldberg, W.True, N.Lin, R. Toomey, and L.Eaves 1998 Co-occurrence of abuse of different drugs in men: the role of drug-specific and shared vulnerabilities. Archives of General Psychiatry 55(11):967–972. Uhl, G.R. 1999 Molecular genetics of substance abuse vulnerability: A current approach. Neuropsychopharmacology 20(1):3–9. Uhl, G.R., G.I.Elmer, M.C.LaBuda, R.W.Pickens. F.E.Bloom, and D.J.Kupfer, eds. 1995 Genetic influences in drug abuse. In Psychopharmacology: The Fourth Generation of Progress. New York: Raven Press. Van Etten, M.L., and J.C.Anthony. 1999 Comparative epidemiology of initial drug opportunities and transitions to first use: Marijuana, cocaine, hallucinogens and heroin. Drug and Alcohol Dependence 54(2):117–125. Van Etten, M.L., Y.D.Neumark, and J.C.Anthony. 1997 Initial opportunity to use marijuana and the transition to first use: United States, 1979–1994. Drug and Alcohol Dependence 49(1):1–7. Wise, R.A. 1978 Catecholamine theories of reward: A critical review. Brain Research 152:215–247. Yoshida, A., L.Hsu, and M.Yasunami 1991 Genetic of human alcohol metabolizing enzymes. Progress in Nucleic Acid Research and Molecular Biology 40:235–287. Yoshimoto, K., S.Ueda, M.Nishi, Y.Yang, H.Matsushita, Y.Takeuchi, B.Kato, Y.Kawai, K.Noritake, S.Kaneda, Y.Sorimachi, and M.Yasuhara 2000 Changes in dopamine transporter and c-Fos expression in the nucleus accumbens of alcohol-tolerant rats. Alcohol—Clinical and Experimental Research 24(3):361–365. Zuckerman, M. 1994 Behavioral Expressions and Biosocial Bases of Sensation Seeking. New York: Cambridge University Press.
OCR for page 74
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