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 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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