# ALTERNATIVE MODELS OF ADDICTION

EDITED BY: Hanna Pickard, Serge H. Ahmed and Bennett Foddy PUBLISHED IN: Frontiers in Psychiatry

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ISSN 1664-8714 ISBN 978-2-88919-713-2 DOI 10.3389/978-2-88919-713-2

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# **ALTERNATIVE MODELS OF ADDICTION**

Topic Editors: **Hanna Pickard,** University of Birmingham, UK **Serge H. Ahmed,** University of Bordeaux, France **Bennett Foddy,** New York University, USA

For much of the 20th century, theories of addictive behaviour and motivation were polarized between two models. The first model viewed addiction as a moral failure for which addicts are rightly held responsible and judged accordingly. The second model, in contrast, viewed addiction as a specific brain disease caused by neurobiological adaptations occurring in response to chronic drug or alcohol use, and over which addicts have no choice or control. As our capacity to observe neurobiological phenomena improved, the second model became scientific orthodoxy, increasingly dominating addiction research and informing public understandings of addiction. More recently, however, a dissenting view has emerged within addiction research, based partly on new scientific research and partly on progress in philosophical and psychological understandings of relevant mental phenomena. This view does not revert to treating addiction as a moral failure, but nonetheless holds that addictive behaviour is fundamentally motivated by choice and subject to at least a degree of voluntary control. On this alternative model of addiction, addictive behaviour is an instrumental means to ends that are desired by the individual, although much controversy exists with respect to the rationality or irrationality of these ends, the degree and nature of the voluntary control of addictive behaviour and motivation, the explanation of the difference between addictive and non-addictive behaviour and motivation, and, lastly, the extent to which addictive behaviour and motivation is correctly characterised as pathological or diseased. This research topic includes papers in the traditions of neuroscience, psychology, philosophy, law and social science that explore alternative understandings of addiction.

**Citation:** Pickard, H., Ahmed, S. H., Foddy, B., eds. (2015). Alternative Models of Addiction. Lausanne: Frontiers Media. doi: 10.3389/978-2-88919-713-2

# Table of Contents

Gene M. Heyman, Brian J. Dunn and Jason Mignone

# Alternative models of addiction

# **1 2 3 Hanna Pickard \*, Serge H. Ahmed and Bennett Foddy**

1 University of Birmingham, Birmingham, UK

3 New York University, New York, NY, USA

\*Correspondence<EMAIL_ADDRESS>
# **Edited and reviewed by:**

PSYCHIATRY

Giovanni Addolorato, Catholic University of Rome, Italy

**Keywords: drugs, addiction, disease, choice, compulsion, self-control, substance abuse, substance dependence**

For much of the twentieth century, theories of addictive behavior and motivation were polarized between two models. The first model viewed addiction as a moral failure for which addicts are rightly held responsible and judged accordingly. The second model, in contrast, viewed addiction as a specific brain disease caused by neurobiological adaptations occurring in response to chronic drug or alcohol use, and over which addicts have no choice or control. As our capacity to observe neurobiological phenomena improved, the second model became scientific orthodoxy, increasingly dominating addiction research and informing public understandings of addiction. The articles in this research topic aim to move beyond the polarization between the competing moral and disease models of addiction.

In the opening article of this e-book "Addiction and Choice: Theory and New Data," Heyman (1) examines new data on the ways that addicts recover, and argues that recovery from addiction is better predicted by a model in which addicts choose to use drugs, rather than one in which they are compelled to do so by a disease. This theme is echoed in other papers in this collection. Satel and Lilienfeld (2) in "Addiction and the Brain-Disease Fallacy" directly challenge the disease model, drawing on historical and clinical data to argue that addicts respond to incentives and use drugs for reasons, and so addictive behavior must be understood as a choice. In "Intertemporal Bargaining in Addiction," Ainslie (3) reprises his large body of work on the inherent weaknesses of the human capacity for choice, exploring its relevance to questions of the nature of responsibility and our justification in holding addicts accountable for addictive behavior and its consequences.

Other authors in this volume seek to understand the ways in which these choices can be pathologically impaired by addiction. For example, Dill and Holton's (4) article "The Addict In Us All" contrasts ordinary choices with what they call the "incentive salience" choices, which are typical in addictive consumption, and involve extreme cravings for drugs and strong motivation to consume, even when consumption is neither experienced nor judged as desirable. Henden et al. (5) in "Addiction: Choice or Compulsion?" chart a course between the moral and disease model by arguing that addictive behavior can be labeled both voluntary and compulsive, if this is understood as involving repeated decisions, which can lead to maladaptive and self-destructive behavioral outcomes.

The importance of negative outcomes to understanding addiction is emphasized by both Levy (6) and Wakefield and Schmitz (7). In "Addiction is Not a Brain Disease (And it Matters)," Levy argues that while addiction does produce neurological dysfunction, this is not enough to make it a disease. In Levy's eyes, disease necessarily involves impairment, and impairment must be understood relative to the social and practical context in which addicts live. In contrast, Wakefield and Shmitz's article "How Many People Have Alcohol Use Disorders?" points out that by focusing too heavily on the negative health correlates of chronic alcohol use, DSM-IV and DSM-V diagnostic criteria risk diagnosing non-addicts suffering the ill-effects of long-term use with an addictive "disease."

The social and practical context of addiction is also emphasized by other authors. It has long been known that cocaine-addicted rats will forego cocaine if offered alternative goods, such as sugar or saccharin. Zernig et al.'s (8) article "Dyadic Social Interaction as an Alternative Reward to Cocaine" presents data demonstrating that, in certain experimental conditions, rats will also forego cocaine for the opportunity of same-sex snuggling. Overall, these findings further show that drug choices are not determined by the ability of a drug to directly activate and/or sensitize the reinforcing and incentive salience neuronal pathways in the brain. This conclusion is consistent with the general evolutionary view of drug use advanced by Hagen et al. (9). Their article notes that the most currently widely used drugs, like cannabis, cocaine, and nicotine, are originally plant chemical defenses that evolved to deter consumption. To adapt, animals are likely to have evolved internal protective mechanisms allowing them to use drugs in a controlled manner.

In "The Shame of Addiction," Flanagan (10) argues that the first-personal experience of shame – typically a social and moral emotion – is central to understanding human addiction and the motivation addicts have to heal, but that shame can be distinguished from blame, allowing addiction to be conceived as an aspect of personal agency without returning to the moral model. In the final article of this e-book, Heyman et al. (11) present data suggesting that years spent in school is a key predictor of illicit drug use, after controlling for IQ and impulsivity, suggesting not only a potential social cause of addiction but also, equally, a social solution.

The e-book also contains articles exploring the classification of addiction and its potential status as a natural kind, the role and extent of pleasure in explanations of addiction, and various more unusual forms of addiction, such as workaholism, which we naturally characterize as involving a need for control, as opposed to involving a loss of control.

2 University of Bordeaux: IMN CNRS UMR 5293, Bordeaux, France

Considered as a whole, the articles in this volume demonstrate that we can conceptualize addiction as choice, while avoiding both the scylla of moralization and the charybda of brain disease. By doing so, they emphasize the need to give equal attention and weight to the historical, contextual, and biological factors that are significant in addiction, to move forward in understanding and responding to the problem. Addiction as choice may thus offer a unifying and integrative framework for future research in the field.

### **REFERENCES**

**Conflict of Interest Statement:** The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

*Received: 09 January 2015; accepted: 31 January 2015; published online: 13 February 2015.*

*Citation: Pickard H, Ahmed SH and Foddy B (2015) Alternative models of addiction. Front. Psychiatry 6:20. doi: 10.3389/fpsyt.2015.00020*

*This article was submitted to Addictive Disorders and Behavioral Dyscontrol, a section of the journal Frontiers in Psychiatry.*

*Copyright © 2015 Pickard, Ahmed and Foddy. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.*

# Addiction and choice: theory and new data

# **Gene M. Heyman\***

Department of Psychology, Boston College, Boston, MA, USA

### **Edited by:**

Hanna Pickard, University of Oxford, UK

### **Reviewed by:**

Serge H. Ahmed, CNRS, France Bennett Foddy, University of Oxford, UK

**\*Correspondence:**

Gene M. Heyman, Department of Psychology, McGuinn Hall, Boston College, Boston, MA 02467, USA. e-mail<EMAIL_ADDRESS><EMAIL_ADDRESS>
Addiction's biological basis has been the focus of much research. The findings have persuaded experts and the public that drug use in addicts is compulsive. But the word "compulsive" identifies patterns of behavior, and all behavior has a biological basis, including voluntary actions. Thus, the question is not whether addiction has a biology, which it must, but whether it is sensible to say that addicts use drugs compulsively. The relevant research shows most of those who meet the American Psychiatric Association's criteria for addiction quit using illegal drugs by about age 30, that they usually quit without professional help, and that the correlates of quitting include legal concerns, economic pressures, and the desire for respect, particularly from family members. That is, the correlates of quitting are the correlates of choice not compulsion. However, addiction is, by definition, a disorder, and thereby not beneficial in the long run. This is precisely the pattern of choices predicted by quantitative choice principles, such as the matching law, melioration, and hyperbolic discounting. Although the brain disease model of addiction is perceived by many as received knowledge it is not supported by research or logic. In contrast, well established, quantitative choice principles predict both the possibility and the details of addiction.

 In scientific journals and popular media outlets, these observations are cited as proof that "addiction is a chronic, relapsing brain disease, involving compulsive drug use" (e.g., Miller and Chappel, 1991; Leshner, 1999; Lubman et al., 2004; Quenqua, 2011). Yet, research shows that addiction has the highest remission rate of any psychiatric disorder, that most addicts quit drugs without professional help, and that the correlates of quitting are those that attend most decisions, such as financial and familial concerns (e.g., Biernacki, 1986; Robins, 1993; Stinson et al., 2005; Klingemann et al., 2010). However, addiction is "disease-like" in the sense that it persists even though on balance its costs outweigh the benefits (e.g., most addicts eventually quit). Thus, in order to explain addiction, we need an account of voluntary behavior that predicts the persistence of activities that from a global bookkeeping perspective (e.g., long-term) are irrational. That is, addiction is not compulsive drug use, but it also is not rational drug use. Several empirical choice principles predict the possibility of relatively stable yet suboptimal behavior. They include the matching law, melioration, and hyperbolic discounting (e.g., Herrnstein, 1990; Ainslie, 1992). These principles were discovered in the course of experiments conducted in laboratories and natural settings, and in experiments these same principles also distinguish addicted from non-addicted drug users (e.g., Kirby et al., 1999). For example, ex and current heavy drug users were more likely to suboptimally "meliorate" than were non-addicts in a choice procedure that invited both long-term maximizing and

melioration (Heyman and Dunn, 2002). Thus, we have on hand a research based, non-disease account of the defining features of addiction, which is to say its destructive and irrational aspects. As this essay is based on how those we call addicts behave, it would be most efficient to begin with a brief summary of key aspects of the natural history of addiction.

# **LIKELIHOOD OF REMISSION AND TIME COURSE OF ADDICTION**

**Figure 1** shows the cumulative frequency of remission as a function of the onset of dependence in a nation-wide representative sample of addicts (United States, Lopez-Quintero et al., 2011). The researchers first recruited a sample of more than 42,000 individuals whose demographic characteristics approximated those of the US population for individuals between the ages of 18 and 64 (Grant and Dawson, 2006). The participants were interviewed according to a questionnaire designed to produce an APA diagnosis when warranted. For those who currently or in the past met the criteria for "substance dependence" (the APA's term for addiction), there were additional questions aimed at documenting the time course of clinically significant levels of drug use. **Figure 1** summarizes the findings regarding remission and the duration of dependence.

On the *x-*axis is the amount of time since the onset of dependence. On the *y*-axis is the cumulative frequency of remission, which is the proportion of individuals who met the criteria for lifetime dependence but for the past year or more had been in remission. The fitted curves are negative exponentials, based on the assumption that each year the likelihood of remitting remained constant, independent of the onset of dependence (Heyman, 2013).

The cumulative frequency of remission increased each year for each drug. Indeed, the theoretical lines so closely approximated the observations that the simplest account is that each year a constant proportion of those who had not yet remitted did so regardless of how long they had been addicted. By year 4 (since the onset of dependence) half of those who were ever addicted to cocaine had stopped using cocaine at clinically significant levels; for marijuana the half-life of dependence was 6 years; and for alcohol, the halflife of dependence was considerably longer, 16 years. As the typical onset age for dependence on an illicit drug is about 20 (Kessler et al., 2005a), the results say that most people who become addicted to an illicit drug are "ex-addicts" by age 30. Of course, addicts may switch drugs rather than quit drugs, but other considerations indicate that this does not explain the trends displayed in **Figure 1**. For example, dependence on any illicit drug decreases markedly as a function of age, which would not be possible if addicts were switching from one drug to another (Heyman, 2013).

The graph also shows that there is much individual variation. Among cocaine users, about 5% continued to meet the criteria for addiction well into their 40s; among marijuana users, about 8% remained heavy users well into their 50s, and for alcoholics, more than 15% remained heavy drinkers well into their 60s. Thus, for both legal and illegal drugs some addicts conform to the expectations of the "chronic disease" label. However, as noted below, the correlates of quitting drugs are the correlates of decision making, not the correlates of the diseases addiction is said to be similar to.

### **CAN WE TRUST THE DATA?**

The results in **Figure 1** replicate the findings of previous nationwide surveys and targeted studies that selected participants so as to obtain representative samples (e.g., Robins and Murphy, 1967; Anthony and Helzer, 1991; Robins, 1993; Warner et al., 1995; Kessler et al., 2005a,b). For instance, in every national scientific survey of mental health in the United States, most of those who met the criteria for dependence on an illicit drug no longer did so by age 30, and addiction had the highest remission rate of any other psychiatric disorder. However, research on remission faces well-known methodological pitfalls. Those in remission may relapse at some post-interview date, and the subject rosters of the large epidemiological studies may be biased in favor of those addicts who do quit. For instance, addicts who remain heavy drug users may not cooperate with researchers or may be hard to contact because of their life style, illnesses, or have higher mortality rates. These issues have been discussed in some detail elsewhere (Heyman, 2013). The key results were that remission after age 30 was reasonably stable, and that it was unlikely that there were enough missing or dead addicts to alter significantly the trends displayed in **Figure 1**.

# **THE CORRELATES OF QUITTING AND THE ROLE OF TREATMENT**

The correlates of quitting include the absence of additional psychiatric and medical problems, marital status (singles stay addicted longer), economic pressures, fear of judicial sanctions, concern about respect from children and other family members, worries about the many problems that attend regular involvement in illegal activities, more years spent in school, and higher income (e.g., Waldorf, 1983; Biernacki, 1986; Waldorf et al., 1991; Warner et al., 1995). Put in more personal terms, addicts often say that they quit drugs because they wanted to be a better parent, make their own parents proud of them, and not further embarrass their families (e.g., Premack, 1970; Jorquez, 1983). In short, the correlates of quitting are the practical and moral concerns that affect all major decisions. They are not the correlates of recovery from the diseases addiction is said to be like, such as Alzheimer's, schizophrenia, diabetes, heart disease, cancer, and so on (e.g., Leshner, 1999; McLellan et al., 2000; Volkow and Li, 2004).

Much of what we know about quitting drugs has been provided by researchers who study addicts who are not in treatment (e.g., Klingemann et al., 2010). This is because most addicts do not seek treatment. For instance, in the survey that provided the data for **Figure 1**, only 16% of those who currently met the criteria for dependence were in treatment, and treatment was broadly defined so as to include self-help organizations as well as services by trained clinicians (Stinson et al., 2005). Since most addicts quit, the implication is that most addicts quit without professional help. Research supports this logic (e.g., Fiore et al., 1993).

# **A NON-DISEASE ETIOLOGY FOR PERSISTENT SELF-DESTRUCTIVE DRUG USE**

Although self-destructive, irrational behavior can be a sign of pathology,it need not be. The self-help industry is booming,which reflects the tendency of so many of us to procrastinate, overeat, skip exercising, and opt for whatever is most convenient. Why buy a book or go to a lecture on how to improve your life if you did not realize that (1) you were behaving imprudently, (2) knew you probably could change, but (3) so far have not taken the requisite steps. Similarly, human irrationality drives the story-line of most novels, memoirs, movies, and plays. Agamemnon sacrifices his

own daughter to advance his political and personal goals but then publicly embarrasses Achilles his most powerful and skillful warrior. Both actions are selfish, and the second undermines the goals of the first, which anyone could have foretold. However, Homer is portraying human nature not writing a psychiatric text. Thus, it seems fair to say that who cite selfishness and myopic choices as evidence of pathology (e.g., "she has to be sick because she bought drugs rather than groceries") naively misread human nature.

In support of the poet's as opposed to the brain disease account of human nature, behavioral psychologists and economists have discovered principles that predict self-defeating, selfish patterns of behavior. They include "hyperbolic discounting," "melioration," and the "matching law" (Herrnstein, 1970, 1990; Rachlin and Green, 1972; Ainslie, 1992; Rachlin, 2007). These are quantitative, empirical laws of choice that predict how different species, including humans, choose between different commodities and activities, such as food, water, and exercise. Their relevance to addiction and other self-defeating behaviors is that under some conditions they predict relatively stable yet suboptimal patterns of behavior. For example, Heyman and Herrnstein (1986) arranged an experiment in which the matching predicted the lowest possible rate of reinforcement. As predicted the subjects shifted to matching, lowering their overall reinforcement rate as they did so. This finding has been replicated numerous times (e.g., Herrnstein et al., 1997), and it is analogous as to what happens as drug use turns into addiction.

Or, put another way, general principles that apply to everyday choices, also predict compulsive-like consumption patterns that are consistent with the behavior of addicts.

These choice laws reflect a basic, but often overlooked property, of most choice situations. There is more than one "optimal" strategy (Heyman, 2009). One is optimal from the perspective of the most immediate circumstances, such as the current values of the options, taking into account just the most pressing needs and goals. The others are optimal in terms of wider time horizons and the perspectives of others. For example, in settings in which current choices affect the values of future options, it is possible for the current best choice to be the worst long-term choice (e.g., Herrnstein et al., 1993; Heyman and Dunn, 2002). This is relevant because a common feature of addictive drugs is that they provide immediate benefits but delayed costs. Thus, it is possible that the drug is the best choice when the frame of reference is restricted to the current values of the immediately available options but the worst choice when the frame of reference expands to include future costs and other people's needs. According to this account, persistent drug use reflects the workings of a local optimum, whereas controlled drug use or abstinence reflects the workings of a global optimum. Put somewhat differently, whether or not drug use persists depends on the factors that influence decision making, particularly values that emphasize global as opposed to a local frame of reference (e.g., values related to family, the future, one's reputation, and so on). Scores of studies support this analysis (e.g., Waldorf, 1983; Biernacki, 1986; Mariezcurrena, 1994; Klingemann et al., 2010).

# **OLD CLINICAL FOLLOW-UP STUDIES: EMPIRICAL SUPPORT FOR THE DISEASE ACCOUNT**

Imagine that what we knew about addiction was restricted to those individuals who make up the right-hand tails of the cumulative distribution curves in **Figure 1**. We would have good reason to believe that addiction is a chronic relapsing disease. This is precisely the situation for much of the history of addiction research. Until the mid 1970s virtually all empirical studies of addicts were based on individuals who had been in treatment, which was most often detoxification in American prison/hospitals or similar institutions (e.g.,Brecher, 1972;Vaillant, 1973; Maddux and Desmond, 1980; Hser et al., 1993). In some studies virtually all of the participants were males with extensive arrest records, poor work histories, lower than average marriage rates, and lower than average educational achievement (e.g.,Vaillant,1973). That is, the understanding of addiction as a chronic disorder was based on a population of drug users whose demographic characteristics – we now know – match those that predict not quitting (e.g., Klingemann et al., 2010). In the 1960s illicit drug use spread to college campuses and upscale neighborhoods. This new generation of addicts included individuals who were employed, married, and well-educated (e.g., Waldorf et al., 1991).With these demographic changes, the natural history of addiction changed. More often than not, the pressures of family, employment, and the hassles of an illegal life style eventually trumped getting high. **Figure 1**, which is representative of every major epidemiological study conducted over the past 30 years, reflects this reality; received opinion does not.

# **BUT DRUGS CHANGE THE BRAIN**

With the exception of alcohol, addictive drugs produce their biological and psychological changes by binding to specific receptor sites throughout the body. As self-administered drug doses greatly exceed the circulating levels of their natural analogs, persistent heavy drug use leads to structural and functional changes in the nervous system. It is widely – if not universally – assumed that these neural adaptations play a causal role in addiction. In support of this interpretation brain imaging studies often reveal differences between the brains of addicts and comparison groups (e.g., Volkow et al., 1997; Martin-Soelch et al., 2001) However, these studies are cross-sectional and the results are correlations. There are no published studies that establish a causal link between drug-induced neural adaptations and compulsive drug use or even a correlation between drug-induced neural changes and an increase in preference for an addictive drug. For example, in a frequently referred to animal study, Robinson et al. (2001) found dendritic changes in the striatum and the prefrontal cortex of rats who had self-administered cocaine. They concluded that this was a "recipe for addiction." However, they did not evaluate whether their findings with rodents applied to humans, nor did they even test if the dendritic modifications had anything to do with changes in preference for cocaine in their rats. In principle then it is possible that the drug-induced neural changes play little or no role in the persistence of drug use. This is a testable hypothesis.

First, most addicts quit. Thus, drug-induced neural plasticity does not prevent quitting. Second, in follow-up studies, which tested Robinson et al.'s claims, there were no increases in preference for cocaine. For instance in a preference test that provided both cocaine and saccharin, rats preferred saccharin (Lenoir et al., 2007) even after they had consumed about three to four times more cocaine than the rats in the Robinson et al study, and even

though the cocaine had induced motoric changes which have been interpreted as signs of the neural underpinnings of addiction (e.g., Robinson and Berridge, 2003). Third, **Figure 1** shows that the likelihood of remission was constant over time since the onset of dependence. Although this is a surprising result, it is not without precedent. In a longitudinal study of heroin addicts,Vaillant (1973) reports that the likelihood of going off drugs neither increased nor decreased over time (1973), and in a study with rats, Serge Ahmed and his colleagues (Cantin et al., 2010) report that the probability of switching from cocaine to saccharin (which was about 0.85) was independent of past cocaine consumption. Since drugs change the brain, these results suggest that the changes do not prevent quitting, and the slope of **Figure 1** implies that drug-induced neural changes do not even decrease the likelihood of quitting drugs once dependence is in place.

### **BUT THERE IS A GENETIC PREDISPOSITION FOR ADDICTION**

Twin and adoption studies have repeatedly demonstrated a genetic predisposition for alcoholism (e.g., Cloninger, 1987), and the limited amount of research on the genetics of illicit drug use suggests the same for drugs such as heroin, cocaine, and marijuana (Tsuang et al., 2001). However, all behavior has a genetic basis, including voluntary acts. The brain is the organ of voluntary action, and brain structure and development follow the blueprint set by DNA. Thus, there is no necessary connection between heritability and compulsion. In support of this point,monozygotic twins are much more likely to share similar religious and political beliefs than are dizygotic twins, even when they are separated before the age of 1 year old (e.g., Waller et al., 1990; McCourt et al., 1999). That is, learned, voluntary religious and political beliefs have substantial heritabilities just as do many involuntary human characteristics. The relevance to addiction is that a genetic predisposition is not a recipe for compulsion, just as brain adaptations are not a recipe for compulsion.

# **SUMMING UP**

Addiction involves an initial "honey moon" period, followed by alternating periods of remission and relapse, and then an eventual return to a more sober life. Most addicts quit using drugs at clinically significant levels, they typically quit without professional help, and in the case of illicit drugs, they typically quit before the age of 30. The correlates of quitting include many of the factors that influence voluntary acts, but not, according to **Figure 1**, drug exposure once drug use meets the criteria for dependence. Thus, we can say that addiction is ambivalent drug use, which eventually involves more costs than benefits (otherwise why quit?). Behavioral choice principles predict ambivalent preferences, semistable suboptimal behavior patterns, and the capacity to shift from one option to another. In contrast, the brain disease account of addiction fails to predict the high quit rates; it fails to predict the correlates of quitting; it fails to predict the temporal pattern of quitting; and it is tied to unsupportable assumptions, such as the claims that neural adaptations, heritability, and irrationality are *prima facie* evidence of disease. To be sure "compulsion" and "choice" can be seen as points on a continuum, but **Figure 1** and research on quitting make it clear that addiction is not a borderline case.

It is time to think about addiction in terms of what the research shows, particularly the more recent epidemiological studies, and it is time to abandon the medical model of addiction. It does not fit the facts. The matching law,melioration, and hyperbolic discounting predict that drugs and similar commodities will become the focus of destructive, suboptimal patterns of behavior. These same choice models also predict that individuals caught in a destructive pattern of behavior retain the capacity to improve their lot and that they will do so as a function of changes in their options and/or how they frame their choices. This viewpoint fits the facts of addiction and provides a practical guide to measures that will actually help addicts change for the better.

# **REFERENCES**

*Hallucinogens, and Marijuana– Including Caffeine, Nicotine, and Alcohol*, 1st Edn. Boston, MA: Little, Brown.

and related conditions. *Alcohol Res. Health* 29, 74–78.

Heyman, G. M., and Dunn, B. (2002). Decision biases and persistent illicit drug use: an experimental study of distributed choice in drug clinic patients. *Drug Alcohol Depend.* 67, 192–203.

literature review. *Scand. J. Behav. Ther.* 23, 131–154.

*Public Health Nations Health* 57, 1580–1596.

*Experience of Using and Quitting*. Philadelphia, PA: Temple University Press.

**Conflict of Interest Statement:** The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

*Received: 18 March 2013; accepted: 23 April 2013; published online: 06 May 2013.*

*Citation: Heyman GM (2013) Addiction and choice: theory and new data. Front. Psychiatry 4:31. doi: 10.3389/fpsyt.2013.00031*

*This article was submitted to Frontiers in Addictive Disorders and Behavioral Dyscontrol, a specialty of Frontiers in Psychiatry.*

*Copyright © 2013 Heyman. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.*

# Intertemporal bargaining in addiction

# **George Ainslie1,2\***

1 School of Economics, University of Cape Town, Cape Town, South Africa

2 Department of Veterans Affairs, Coatesville, PA, USA

### **Edited by:**

Hanna Pickard, University of Oxford, UK

### **Reviewed by:**

Serge H. Ahmed, CNRS, France Bennett Foddy, University of Oxford, UK

#### **\*Correspondence:**

George Ainslie, 151 Veterans Affairs Medical Center, Coatesville, PA 19320 USA

e-mail<EMAIL_ADDRESS>
The debate between disease models of addiction and moral or voluntarist models has been endless, and often echoes the equally endless debate between determinism and free will. I suggest here that part of the problem comes from how we picture the function of motivation in self-control. Quantitative experiments in both humans and non-humans have shown that delayed reward loses its effectiveness in proportion to its delay. The resulting instability of preference is best controlled by a recursive self-prediction process, intertemporal bargaining, which is the likely mechanism of both the strength and the experienced freedom of will. In this model determinism is consistent with more elements of free will than compatibilist philosophers have heretofore proposed, and personal responsibility is an inseparable, functional component of will. Judgments of social responsibility can be described as projections of personal responsibility, but normative responsibility in addiction is elusive.The cited publications that are under the author's control can be downloaded from www.picoeconomics.org.

**Keywords: addiction, hyperbolic discounting of reward, intertemporal choice, self-control, brain imaging of motivation**

Many factors promote the impulse for an addictive activity. In addition to social and informational differences between individuals, the differential attractiveness of such activity is associated with heritable differences in the highs people get from a given activity, differences in their inborn tendency to discount delayed rewards, and adaptation of their brain reward structures to repeated addictive activity (1). Prior factors that have increased the differential reward for addictive activities – even the self-inflicted adaptation factor – could be said to have created a disease, in that the person's current level of temptation is not subject to voluntary control. Eczema is called a disease, after all, even though the involuntary process is the itching, whereas voluntary scratching is what does the damage. However, discovery of the physical roots of temptation should not obscure the process of motivated choice that is never bypassed in addiction.

Addiction is sometimes identified with physiological patterns such as intoxication, tolerance, and withdrawal, regardless of how the person values them. However, the kind of addiction that a person complains of has two essential elements: temporary preference for inferior rewards, and failure to forestall the recurrent surrender to this preference. The first element arises from the universal over-valuation of imminent rewards, which will produce temporary preferences for them to the extent that the person does not compensate for it. It has been suggested that this over-valuation represents just the arousal of appetites or emotions (2), but a more fundamental pattern is now well documented (3–5). People have inherited a hyperbolic delay discount function from our non-human ancestors:

$$\text{Present value} = \text{Value}\_0 \Big/ \left[ 1 + \left( k \times \text{Delay} \right) \right]$$

where Value0 = value if immediate and *k* is degree of impatience.

This function makes the value of an event inversely proportional to its expected delay, which means that many objectively smaller sooner (SS) rewards will tend to be temporarily preferred to larger later (LL) alternatives when the SS rewards are imminent (**Figure 1**). The hyperbolic shape of the value/delay function probably survived natural selection because it is a basic psychophysical relation, the same as that for sensory perceptions such as brightness and heaviness (6). In species where instinct generates present reward for future-oriented tasks (hoarding, dam-building, migrating. . .) this shape is probably not maladaptive, but it gives humans a temptation problem.

Modern people are set up for addictions at birth. Since Isaac Marks' seminal article (7) many activities have been identified as addictive without the involvement of substances, or even external rewards. Analysis of hyperbolic discounting suggests how the great human ability to coin reward by imagination can be channeled into addictive temptations, by patterns of outcomes that serve as occasions for reward but that make no prediction at all of external rewarding events, as in video games (8). What differentiates the addict from her neighbor is not the strong temptation, when close up, to seek options that she would avoid from a distance. Rather it is the collapse of her resistance to this temptation. This is the other essential element of addiction. We normally reach compromises with our urges, and set boundaries to our bad habits. Understanding this failure – indeed understanding why "compromise"is the right word – will be key to understanding responsibility in addiction.

# **RECURSIVE SELF-PREDICTION**

Motivation for impulse control comes from the value described by the hyperbolic discount function at long delays, which is proportional to objective value when both alternatives are distant – and

much higher for each than is described by either conventional exponential or "quasi-hyperbolic" (cue-driven) functions (9). The need to adopt protections for long term plans is unique to humans, and the number of these that the new human species has been able to learn has been limited: to some extent a person can avoid paths that take her close to SS alternatives, or she can avoid revaluation of them when close, but these strategies will necessarily be hard to maintain for long periods. Alternatively she can set up incentives, especially social ones, that will add deterrence at crucial moments. However, I have argued that a great part of impulse control in an individualistic society is accomplished by the person's perception that large future benefits depend on regular choices of a particular kind – such as not to drink, spend, or play too much – and that each current choice is a test case for the choices she can expect future selves to make (4, 9). Such self-prediction creates a potentially strong but somewhat rigid mechanism of impulse control, willpower, without the need for a separate organ or faculty. The person can then afford to live closer to temptations, although her self-control will be at risk from her thinking of reasons that a future self should not count a present indulgence as a lapse – that is, from rationalizations.

The person will see a current abstinence as worth the effort if and only if this is necessary to maintain a credible pattern of abstinence, a perception that organizes her relevant choices into a repeated prisoner's dilemma – or self-enforcing contract – where a current defection jeopardizes future cooperation. The devil is in the word "relevant." If the person can see how a current consumption should not change her future expectation – "today is special" – then she may get to enjoy it without damaging her long term prospects. Auditioning rationales for their credibility and modifying them accordingly is a recursive, often rapid process. If successful, it maintains the compromise between urges and long term expectations. Rationalizations may not be especially risky when the stakes are low ("I resolve to clean my room today"), but the risk becomes demonstrable when large amounts of incentive hinge on the test, as when a recovering alcoholic decides to try drinking just once. This plan is apt to follow the same logic as the decision of a party to a self-enforcing contract to cheat her partner; defection by a current self often leads to the notorious abstinence violation effect (10; for dieters, see 11). Such a sudden loss of control after a single lapse has sometimes been blamed on a physical stimulation of appetite; however, when alcoholic volunteers are given either alcohol punch or an indistinguishable placebo, the belief that they have had alcohol leads to craving whereas the alcohol itself does not (12).

# **EVIDENCE OF RECURSIVE SELF-PREDICTION IN WILL**

Recursive (fed-back) processes are notoriously hard to experiment on, even in physical systems (e.g., 13, pp. 191–211), let alone motivational ones, a difficulty which may have concealed their prevalence. Recursive self-prediction is most evident in common intuitions about the motivational consequence of a single lapse in a diet or sobriety, as above, which are sharpened in thought problems such as Kavka's, Monterosso's, and Newcomb's (14). There have been some suggestive experiments: pointing out to subjects that their current choice in a series of SS/LL reward choices may be predictive of their future preferences raises their frequency of LL choices, although not as much as does obligatory commitment for the whole series with their first choice (15, 16). The intertemporal bargaining model fits the properties of will specified by the early psychologists who analyzed will (4, pp. 79–80, 117–120), and predicts the behavior of subjects in 2- and *N*-person prisoner's dilemma analogs (4, pp. 90–94; 17). However, given that intertemporal bargaining depends on intrapsychic contingencies, we might hope for better evidence from brain imaging.

Unfortunately, imaging experience is rudimentary. Using functional magnetic resonance imaging (fMRI), Luo et al., found that equal preference between a LL reward and a SS alternative cannot be predicted from the activity in brain reward centers when those alternatives are offered singly, outside of the choice situation (18). After establishing a behavioral indifference point, subjects were given chances to respond for each outcome separately. They showed less activity in their reward centers for what had been the LL rewards than for the erstwhile SS rewards, even though they had been indifferent when choosing between these rewards, and were still indifferent when the choice contingency was offered again. That is, the mere establishment of a choice contingency changes the relative value of SS and LL outcomes, in favor of the LL one. The implication is that when impulse control is relevant, motivation beyond what arises from the current rewards themselves must be active. In other studies the lateral frontal cortex has been found to be more active when a subject makes LL choices (e.g., 19), but a recent experiment raises a question of whether this activity is tracking motivation for those LL choices. Luo et al. observed individual subjects' stochasticity (variability) of SS/LL choice over time (20). By finding the ratio of SS to LL amount that produced equal preference, and then offering differing amounts in the same ratio at the same alternative delays, it was possible in effect to offer a subject the same choice repeatedly in a way that the subject would not recognize, and thus to observe small, spontaneous variations over trials of SS vs. LL preference. Lateral frontal cortical activity was indeed often greater with LL choice, but mostly in subjects who showed relatively great stochasticity – the ones who

wavered most. This somewhat counterintuitive finding suggests that activity in lateral frontal cortical "executive centers" may not reflect preference for LL alternatives *per se*, but perhaps represents a response by which subjects compensate for a perceived unreliability of such preference. These studies are far from definitive, but they suggest that self-control in SS/LL choices may be determined by processes on at least two levels above the spontaneous valuation of rewards that is seen in non-choice designs: mental effort, possibly reflected in lateral frontal cortical activity; and a non-effortful evaluative process in which the most stable long term preferences are established – possibly by intertemporal bargaining – which so far lacks fMRI correlates. It may be significant that subjects with relatively great ventromedial prefrontal cortical activity when imagining future selves also prefer LL rewards relatively more than do other subjects (21), but the role of such "prospection" centers in self-control has not been explored.

# **FREEDOM OF WILL**

Assuming that recursive self-prediction is the basis of will, what are the implications for addicts' responsibility? Intertemporal bargaining increases the power of self-control but also its potential volatility. A recovering alcoholic may notice that she is procrastinating about an unrelated issue and interpret that as evidence of her will being weaker than she thought, which may in turn reduce her expectation of staying sober. That reduction may motivate increased rigidity to prove she is strong, or it may snowball into expectations that are too greatly lowered for their peril to deter a drinking episode. The potential for small or merely symbolic choices to shift much larger motives gives the will an element of chaos, in the technical sense (13). Whatever awareness of this process a person has acquired is apt to weigh on every choice that she notices to be evidence of her predilections. This extra motivation provides a rationale for strength of will – and also, arguably, for a mechanism that meets common definitions of freedom of will.

As characterized by Richard Holton, people's insistence on the freedom of will largely stems from two kinds of experience: the unpredictability of one's own behavior ("For all I know, I might have done otherwise") and the initiation of one's behavior ("Action is experienced as something that the agent instigates, rather than something that just happens to the agent as the result of the state that they were antecedently in" – 22). We do not feel as if we are passively responding to the incentives we detect. Chaotic systems such as weather have been proposed as models for the unpredictability of our choices (23), but critics have pointed out that being buffeted by the weather would not feel like being free, more like having seizures (24, p. 231). However, the feeding back of tentative choices to the process of choice itself makes the agent a participant in her motivational weather. In a simple linear choice I might decide how much food to take at a buffet lunch on the basis of how hungry I am or how long I expect to go without food in the afternoon. But if I am a restricted eater those considerations may be overshadowed by estimating whether the food I take looks like I am lapsing, and knowing that the prospect of lapsing may increase my hunger. [Recursive self-prediction as a cause of "conditioned" (cue-driven) appetite is discussed in 5, pp. 222–229]. The latter, recursive estimation is of the same cognitive kind as the linear, but the sensation that my making estimates is changing those estimates as I make them has an added quality. Choosing under the influence of the choice itself pulls attention back from the ostensible alternatives to an inward dialog, one that should produce a feeling of agency at the same time that it makes choice unpredictable from its original incentives. The outcome is still strictly determined, of course, but recursively rather than linearly, a distinction that keeps the self from being that old bugbear of determinism, a throughput – a mere conveyor of incentives (fuller discussion in 25).

# **RESPONSIBILITY FOR ADDICTIVE CHOICES**

Much of the effort that has gone into finding rationales for free will stems from its supposed necessity for holding people responsible for their choices (26). A theory that derives the functional properties of free will from recursive self-prediction is still deterministic, and thus does not seem at first to be a solution. However, the way that this theory relates strength to freedom of will suggests a functional framework for responsibility without indeterminacy – and thus a space in which the voluntarist model of addiction can be valid. Rather than testing this possibility by the truth or falsehood of determinism, it makes more sense for us to look at the practical roots of responsibility. Psychology has generally assumed that a personal sense of responsibility comes from internalization of pressure that is brought to bear by parents and other socializers, but with the logic of intertemporal bargaining their precepts cease to be needed to provide incentive, only to suggest compromises between internal interests. A serious lapse threatens such compromises, not because the person makes a decision to punish herself but because of the realistic fall in her expectation of future self-control. (This model is not contradicted by social psychology experiments in which subjects who read statements espousing determinism subsequently indulge in minor antisocial behaviors – see 22.)

Personal responsibility is thus an operational component of will. Its inseparability from volition raises the possibility that when people judge someone else to be guilty, they are projecting their own experience with lapses – feeling personal guilt empathically: "If I were in her shoes, I would feel guilty."That is, our understanding of other people's responsibility comes from our intuition of our own. Such a process would supply the element of deservingness that is missing from determinist models that explain social responsibility as a manipulation to create deterrence, which are intuitively unsatisfying (27). Thus for both personal and social responsibility, the truth of determinism is not relevant (discussed in 25). However, the question remains of how responsibility is affected by addiction.

An addict undeniably faces disease factors, but my argument is that they operate *through* motivation, not instead of it. Addiction becomes "hopeless" when the addict has no rationale by which abstention at crucial choice points would sufficiently increase the believability of her future sobriety. As described above, such belief is sensitively dependent on many self-generated signs and symbols, but at some point the addict has tried and spoiled all the ones she can think of. She is not sick in the sense of being beyond motivation, but her inability to propose any credible intertemporal deal constitutes a kind of bankruptcy, and she could be argued thus not to be responsible – except that, unlike a financial bankrupt, she sometimes has a sudden epiphany that re-orders her accounts (28). The advice of the Anonymous organizations that the addict is helpless against her addiction does not imply the irrelevance of intertemporal bargaining, but rather the danger of trying rationalizations where the bargaining is full of mistrust. Their injunction to resolve sobriety for only 1 day at a time aims at restarting the bargaining process with a low level of trust. To acknowledge helplessness against a temptation without attempting to renounce it forever sounds illogical, but it is often the only successful compromise after long histories of grand resolution and total collapse. These organizations have intuited most of the tactics that an intertemporal bargaining model would prescribe (which is not to argue for or against their clinical effectiveness).

# **CONCLUSION**

As is the case with so many ancient debates, both the disease theory and the moral theory of addiction have part of the truth on their side. The physical roots of addictive temptation are increasingly known, as is their unequal distribution among individuals and within the same individual at different points in her addictive history. In her current moment forces gathered by heredity, exposure, and even her own past behavior are givens, and could fairly be judged to constitute a disease.

# **REFERENCES**

However, their force is still one of temptation, even when giving in promises only a joyless oblivion instead of the pain of short-lived self-control. The error of policy-makers who rely on negative incentives is not their belief that addictive behavior is motivated, but their miscalculation of how much punishment can make up for the bankruptcy of a person's intertemporal bargaining process. Unless they have experienced such bankruptcy themselves, trying to put themselves in the addict's shoes leads them to conclude that she just needs an extra push, whereas in fact she needs to re-establish a relationship with her prospective future selves. Certainly cures for temptation itself can be a factor – for instance, buprenorphine for opiate craving – as can simply structuring modest incentives with a view toward immediacy and reliability (e.g., 29). And certainly, blanket forgiveness of bad deeds that have sprung from an addiction would create perverse incentives, "moral hazard." But beyond these straightforward contingencies, the difference between sobriety and ruin often lies with the turnings of intertemporal bargaining, which defy simplification.

# **ACKNOWLEDGMENTS**

This material is the result of work supported with resources and the use of facilities at the Department of Veterans Affairs Medical Center, Coatesville, PA, USA. The opinions expressed are not those of the Department of Veterans Affairs or of the US Government.

*Volition and Social Context*. Cambridge: MIT (2007). p. 169–96.

treatment programs. *Drug Alcohol Depend* (2007) **16**:175–82. doi:10.1016/j.drugalcdep.2006.08. 012

**Conflict of Interest Statement:** The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

*Received: 15 April 2013; accepted: 16 June 2013; published online: 14 August 2013. Citation: Ainslie G (2013) Intertemporal bargaining in addiction. Front. Psychiatry 4:63. doi: 10.3389/fpsyt.2013.00063 This article was submitted to Frontiers in Addictive Disorders and Behavioral Dyscontrol, a specialty of Frontiers in Psychiatry.*

*Copyright © 2013 Ainslie. This is an open-access article distributed under the* *terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.*

# Addiction and the brain-disease fallacy

# **Sally Satel 1 and Scott O. Lilienfeld2\***

1 Yale University School of Medicine, New Haven, CT, USA

2 Department of Psychology, Emory University, Atlanta, GA, USA

### **Edited by:**

Hanna Pickard, University of Oxford, UK

### **Reviewed by:**

Serge H. Ahmed, Centre National de la Recherche Scientifique, France Bennett Foddy, University of Oxford, UK

### **\*Correspondence:**

Scott O. Lilienfeld, Department of Psychology, Emory University, 473 Psychology Building, 36 Eagle Row, Atlanta, GA 30322, USA e-mail<EMAIL_ADDRESS>
The notion that addiction is a "brain disease" has become widespread and rarely challenged. The brain-disease model implies erroneously that the brain is necessarily the most important and useful level of analysis for understanding and treating addiction. This paper will explain the limits of over-medicalizing – while acknowledging a legitimate place for medication in the therapeutic repertoire – and why a broader perspective on the problems of the addicted person is essential to understanding addiction and to providing optimal care. In short, the brain-disease model obscures the dimension of choice in addiction, the capacity to respond to incentives, and also the essential fact people use drugs for reasons (as consistent with a self-medication hypothesis). The latter becomes obvious when patients become abstinent yet still struggle to assume rewarding lives in the realm of work and relationships. Thankfully, addicts can choose to recover and are not helpless victims of their own "hijacked brains."

**Keywords: brain-disease fallacy, addiction, fMRI, Project HOPE, brain-disease model**

**From Brainwashed: The Seductive Appeal of Mindless Neuroscience by Sally Satel and Scott Lilienfeld, copyright © 2013. Reprinted by permission of Basic Books, a member of The Perseus Books Group.**

# **INTRODUCTION**

In 1970, high-grade heroin and opium flooded Southeast Asia. Military physicians in Vietnam estimated that nearly half of all U.S. Army enlisted men serving there had tried opium or heroin [(1), p. 1046], and between 10 and 25% of them were addicted. Deaths from overdoses soared. In May 1971, the crisis reached the front page of the *New York Times*:"G.I. Heroin Addiction Epidemic in Vietnam" (2). Fearful that the newly discharged veterans would join the ranks of junkies already bedeviling inner cities, President Richard Nixon commanded the military to begin drug testing. No one could board a plane home until he had passed a urine test. Those who failed could attend an army-sponsored detoxification program (3).

Operation Golden Flow, as the military called it, succeeded. As word of the new directive spread, most GIs stopped using narcotics. Almost all the soldiers who were detained passed the test on their second try (4). Once they were home, heroin lost its appeal. Opiates may have helped them endure a war's alternating bouts of boredom and terror, but stateside, civilian life took precedence. The sordid drug culture, the high price of heroin, and fears of arrest discouraged use, veterans told Lee Robins, the Washington University sociologist who evaluated the testing program from 1972 to 1974 (5).

Robins' findings were startling. Only 5% of the men who became addicted in Vietnam relapsed within 10 months after return, and just 12% relapsed briefly within 3 years. "This surprising rate of recovery even when re-exposed to narcotic drugs," wrote Robins,"ran counter to the conventional wisdom that heroin is a drug which causes addicts to suffer intolerable craving that

rapidly leads to re-addiction if re-exposed to the drug"(1). Scholars hailed the results as "revolutionary" and "path-breaking" [(6), p. 215]. The fact that addicts could quit heroin and remain drug-free overturned the belief that "once an addict, always an addict."

Unfortunately, that lesson has faded into the past.  It was promoted tirelessly by psychologist Alan I. Leshner, then the director of the National Institute on Drug Abuse (NIDA), the nation's premier addiction research body and part of the National Institutes of Health, and is now the dominant view of addiction in the field (8). The brain-disease model is a staple of medical school education and drug counselor training and even appears in the antidrug lectures given to high-school students (9). Rehab patients learn that they have a chronic brain disease. And the American Society of Addiction Medicine, the largest professional group of physicians specializing in drug problems, calls addiction "a primary, chronic disease of brain reward, motivation, memory and related circuitry" (10). Drug czars under Presidents Bill Clinton, George W. Bush, and Barack Obama have all endorsed the brain-disease framework at one time or another (11). From being featured in a major documentary on HBO, on talk shows and *Law and Order*, and on the covers of *Time* and *Newsweek,*the brain-disease model has become dogma – and like all articles of faith, it is typically believed without question (12–15).

That may be good public relations, but it is bad public education. We also argue that it is fundamentally bad science. The brain-disease model of addiction is not a trivial rebranding of an age-old human problem. It plays to the assumption that if biological roots can be identified, then a person has a "disease."And being afflicted means that the person cannot choose, control his or her life, or be held accountable. Now introduce brain imaging, which seems to serve up visual proof that addiction is a brain disease. But neurobiology is not destiny: the disruptions in neural mechanisms associated with addiction do constrain a person's capacity for choice, but they do not destroy it. What's more, training the spotlight too intently on the workings of the addicted brain leaves the addicted person in the shadows, distracting clinicians, policy makers, and sometimes patients themselves from other powerful psychological and environmental forces that exert strong influence on them.

# **DISEASE, MIND, AND BRAIN**

For over three centuries in the United States, physicians, legal scholars, politicians, and the public have debated the nature of addiction: is it a defect of the will or of the body? A moral or a medical problem? (16) Such polarization should by now have exhausted itself. After all, mountains of evidence attest to the fact that addiction entails both biological alterations in the brain and in personal agency. But given what is at stake in these debates – namely, our deep cultural beliefs about self-control and about deficits in personal responsibility paired with concerns about what society owes to addicts and what it can expect of them – we must be very careful not to ascribe too much influence to the addict's brain.

This is an opportune time to pause and clarify two potential sources of misunderstanding.

First, we do not address the question of whether addiction is a "disease." With the potential exception of certain organic brain syndromes, the field of psychiatry recognizes "disorders" or syndromes, rather than diseases because the etiologies of mental illness are not yet well understood. So, addiction fits the notion of disorder insofar as persistent craving and/or continued, excessive use leads to dysfunctional behavior. We are more concerned with the very different issue of whether addiction is best construed as a *brain* disease or *brain* disorder. Addiction is typically associated with brain changes, to be sure, but in contrast to conventional brain pathologies, such as Alzheimer's disease, those alterations rarely if ever preclude individuals' capacity to alter their behavior based on foreseeable consequences. The term "brain disease," which often implies a lack of control over behavior, obscures that crucial distinction. Moreover,although severe addictions are partly rooted in genetic predispositions that are themselves manifested in brain functioning, these conditions can be profitably understood at multiple levels of analysis (e.g., psychological, social, cultural) in addition to the neural level.

Second, our distinguishing between the addict's brain and his or her mind does not imply an endorsement of substance dualism. That is, we do not believe that the mind and the brain are independent of each other or composed of different physical substances with consciousness existing in a spiritual world separate from the body. Few scientifically literate persons do. But, speaking of literacy, there is indeed value in examining the language people use when talking about the relationship between the brain and the mind. To say that the brain and the mind are "different" does not necessarily mean that the two are *materially* separate domains. Every subjective experience, from the ache of nostalgia to the frisson of a Christmas morning, corresponds to physical events in the brain. The mind – the realm of feelings, desires, ideas, memories, intentions, and subjective experience – is

produced by the action of neurons and brain circuits. How else could it work?

Yet the mind is not identical with the matter that produces it; one cannot use the physical rules from the cellular level to completely predict activity at the psychological or behavioral level. Put somewhat differently, there is a fundamental difference between substance dualism and property dualism: the latter acknowledges that everything mental is ultimately produced by physical matter but allows for the fact that certain mental phenomena have different properties than neural phenomena (just as molecules themselves are not alive, but complex configurations of certain molecules can produce life).

At this time, one cannot rely on the brain alone to predict or understand everything important about human subjectivity or behavior. This is because many psychological phenomena are emergent properties of lower-order constituents such as neural circuits, neurons, proteins, and genes. "Constitutive" reductionism – reducing complex entities to the sum of their component parts to facilitate study – is not controversial in the scientific community; nor do we take issue with it. In his 2006 book,*An Argument for Mind*,Harvard University psychologist Jerome Kagan notes that the appreciation of an impressionistic painting requires far more than the sum of its parts (17). As the viewer slowly approaches Claude Monet's painting of the Seine at Dawn, Kagan notes, there comes a moment when the scene dissolves into tiny patches of color. When we adopt the eliminative reductionist position, he writes, "the coherent psychological component vanishes" [(17), p. 213]. Some philosophers of mind take a different view. They speculate that such properties (the painting in full) will ultimately prove reducible to more basic elements (the paint) (18). They may prove correct. But for the foreseeable future, valuable information is often lost when descending from higher explanatory levels, such as mental states, to lower levels, such as neuronal systems.

The distinctions between substance and property dualism and between constitutive and greedy reductionism may appear arcane, but overlooking them can lead us to overestimate the explanatory power of neuroscientific findings. Take addiction, for example. The dominant view among researchers is that it is a "brain disease," plain and simple. Without a doubt, chronic drug exposure often changes the brain, but knowledge of the neural mechanisms underlying addiction typically has less relevance to the treatment of drug addiction and alcoholism than the psychological and social causes. To be sure, intervening directly on the brain, say with medications such as methadone, can sometimes be of value too. But understanding the brain of addicts gives us only partial insight into why they become addicted and how they recover.

### **ADDICTION AS A "BRAIN DISEASE"**

So, what exactly makes addiction a brain disease? "That addiction is tied to changes in brain structure and function is what makes it, fundamentally, a brain disease," Leshner wrote in a now-landmark article in *Science* in 1997. But that can't be right. Every experience changes the brain – from learning a new language to navigating a new city. It is certainly true that not all brain changes are equal; learning French is not the same as acquiring a crack habit. In addiction, intense activation of certain systems in the brain makes

it difficult for users to quit. Genetic factors influence the intensity and quality of the subjective effect of the drug, as well as the potency of craving and the severity of withdrawal symptoms (19).

The process of addiction unfolds partly through the action of dopamine, one of the brain's primary neurotransmitters. Normally, dopamine surges in the so-called reward pathway, or circuit, in the presence of food, sex, and other stimuli central to survival. Dopamine enhancement serves as a "learning signal" that prompts us to repeat eating, mating, and other pleasures. Over time, drugs come to mimic these natural stimuli. With every puff of a Marlboro, injection of heroin, or swig of Jim Beam, the learning signal in the reward pathway is strengthened, and in vulnerable users, these substances assume incentive properties reminiscent of food and sex.

"Salience" is the term that neuroscientists often use to describe the pull of substances on the addicted – it's more of a sense of wanting, even needing, than liking. The development of salience has been traced to the nerve pathways that mediate the experience as they emerge from the underside of the brain, in an area called the ventral tegmentum, and sweep out to regions such as the nucleus accumbens, hippocampus, and prefrontal cortex, which are associated with reward, motivation, memory, judgment, inhibition, and planning.

Other nerve fibers travel from the prefrontal cortex, a region involved in judgment and inhibition, to parts of the brain that control behavior. As one psychiatrist put it memorably, "The war on drugs is a war between the hijacked reward pathways that push the person to want to use, and the frontal lobes, which try to keep the beast at bay" (20). Note the word "hijacked." As shorthand for the usurpation of brain circuitry during the addiction process, it is a reasonable metaphor [(21), p. 1715].In the hands of brain-disease purists, though, "hijacking" has come to denote an all-or-nothing process, likened to a"switch in the brain"that, once flipped, affords no retreat for the addict (22). "It may start with the voluntary act of taking drugs," Leshner said, "but once you've got (addiction), you can't just tell the addict, 'Stop,' any more than you can tell the smoker 'Don't have emphysema"' (23).

The reward circuit is also intimately involved in "cue-induced" craving. Such craving is a special species of desire that manifests itself in a sudden, intrusive urge to use brought on by "cues" associated with use. The mere clink of a whiskey bottle, a whiff of cigarette smoke, or a glimpse of an old drug buddy on the corner can set off an unbidden rush of yearning, fueled by dopamine surges. For the addict who is trying to quit, this is a tense feeling, not pleasurable at all. Because the rush of desire seems to come out of the blue, users may feel blindsided, helpless, and confused (24).

In a very impressive display of brain technology, scientists have used PET and fMRI scans to observe the neural correlates of craving. In a typical demonstration, addicts watch videos of people handling a crack pipe or needle, causing their prefrontal cortices, amygdala, and other structures to bloom with activity (25) (videos of neutral content, such as landscapes, induce no such response). Even in users who quit several months previously, neuronal alterations may persist, leaving them vulnerable to sudden, strong urges to use. The familiar "This is your brain on drugs" is still with us [this slogan was created in 1987 by an American drug-prevention charity. To illustrate how drugs affect the brain, an egg (representing the brain) was cracked on a sizzling frying pan (representing drugs). Result: fried brain]. Nowadays, however, the brain itself often substitutes for the fried egg.

# **THE ADDICTION PARADOX**

But that egg is not always sizzling. There is a surprising amount of lucid time in the daily life of addicts. In their classic 1969 study "Taking Care of Business: The Heroin User's Life on the Street," criminologists Preble and Casey (26) found that addicts spend only a small fraction of their days getting high. Most of their time is spent either working or hustling (27–29). The same is true for many cocaine addicts (30). We tend to think of them, at their worst, frantically gouging their skin with needles, jamming a new rock into a pipe every 15 min, or inhaling lines of powder. In the grip of such hunger, an addict cannot be expected blithely to get up and walk away.

These tumultuous states – with neuronal function severely disrupted – are the closest drug use comes to being beyond the user's restraint. But in the days between binges, cocaine users worry about a host of everyday matters: should I find a different job? Enroll my kid in a better school? Kick that freeloading cousin off the couch for good? Attend a Narcotics Anonymous meeting, enter treatment, or register at a public clinic? It is during these stretches of relative calm that many addicts could make the decision to get help or quit on their own – and many of them do. But the decision to quit can be long in coming, far too long for those who destroy their health, families, or careers in the meantime.

The paradox at the heart of addiction is this: How can the capacity for choice coexist with self-destructiveness? "I've never come across a single person that was addicted that wanted to be addicted," says neuroscientist Nora Volkow, who succeeded Leshner as director of NIDA in 2003 (31). Aristotle noted this paradox as well. He used the term Akrasia to denote an appetite or strong desire for pleasure that leads to actions that are harmful to our conscious wishes for our well-being (32). Hume spoke of "liberty" as being a "power of acting or not acting according to the determinations of the will" (33).

Indeed, how many of us have ever come across a heavy person who exercised his or her freedom expressly toward the goal of becoming fat? Many undesirable outcomes in life arrive incrementally. "We can imagine an addict choosing to get high each day, though not choosing to be an addict," says psychologist Gene Heyman. "Yet choosing to get high each day makes one an addict" (34).

Let's follow a typical trajectory to see how this dynamic plays out. In the early phase of addiction, drugs or alcohol become ever more appealing, while once-rewarding activities, such as relationships, work, or family, decline in value. The attraction of the drug starts to fade as consequences accrue – spending too much money, disappointing loved ones, attracting suspicion at work – but the drug still retains its allure because it blunts psychic pain, suppresses withdrawal symptoms, and douses intense craving [(35), p. 3]. Addicts find themselves torn between the reasons to use and reasons not to (36).

Sometimes a spasm of self-reproach or a flash of self-awareness tips the balance toward quitting. William S. Burroughs, an American novelist and heroin addict, calls this the "naked lunch" experience, "a frozen moment when everyone sees what is on the end of every fork" [(37), p. 199]. Lawford (38), himself in recovery from drugs and alcohol, edited a 2009 collection of essays called *Moments of Clarity* in which the actor Alec Baldwin, singer Judy Collins, and others recount the events that spurred their recoveries. Some quit on their own; others got professional help. A theme in each of their stories is a jolt to self-image: "This is not who I am, not who I want to be" (39). One recovered alcoholic describes the process: "You tear yourself apart, examine each individual piece, toss out the useless, rehabilitate the useful, and put your moral self back together again" (40). These are not the sentiments of people in helpless thrall to their diseased brains. Nor are these sentiments the luxury of memoirists. Patients have described similar experiences to us: "My God, I almost robbed someone!""What kind of mother am I?" or "I swore I would never switch to the needle."

 The Epidemiological Catchment Area Study, done in the early 1980s, surveyed 19,000 people. Among those who had become dependent on drugs by age 24, more than half later reported not a single drug-related symptom. By age 37, roughly 75% reported no drug symptom. The National Comorbidity Survey, conducted between 1990 and 1992 and again between 2001 and 2003 and the National Epidemiologic Survey on Alcohol and Related Conditions, done between 2001 and 2002 with more than 43,000 subjects, found that 77 and 86% of people who said they had once been addicted to drugs or alcohol reported no substance problems during the year before the survey (41).

By comparison, people who were addicted within the year before the survey were more likely to have concurrent psychiatric disorders. Additionally, NIDA estimates that relapse rates of treated drug-addicted patients run from 40 to 60% (42). In other words, they are not representative of the universe of addicts. They are the hard cases – the chronic and relapsing patients. Yet these patients often make the biggest impressions on clinicians and shape their views of addiction, if only because clinicians are especially likely to encounter them.

Researchers and medical professionals err in generalizing from the sickest subset of people to the overall population of patients. This caveat applies across the medical spectrum. Just as the clinician wrongly assumes that all addicts must be like the recalcitrant ones who keep stumbling through the clinic doors, psychiatrists sometimes view people with schizophrenia as doomed to a life of dysfunction on the basis of their frequent encounters with those whose delusions and hallucinations don't improve with treatment. The error of extrapolating liberally from these subsets of difficult patients is so common that statisticians Patricia and Jacob Cohen gave it a name: the "clinician's illusion" (43).

# **INTENDED BENEFITS OF THE BRAIN-DISEASE MODEL**

Advocates of the brain-disease paradigm have good intentions. By placing addiction on an equal medical footing with more conventional brain disorders, such as Alzheimer's and Parkinson's, they want to create an image of addicts as victims of their own wayward neurochemistry. They hope that this portrayal will inspire insurance companies to expand coverage for addiction and politicians to allocate more funding for treatment [(44), p. 33]. And in the hands of Alan Leshner, the model has had real political utility (45). Before he was NIDA director, Leshner served as acting director of the National Institute of Mental Health. There, he saw how brain-disease "branding" could prompt Congress to act. "Mental health advocates started referring to schizophrenia as a 'brain disease' and showing brain scans to members of congress to get them to increase funding for research. It really worked," he said (46).

Many experts credit the brain-disease narrative with enhancing the profile of their field. The late Bob Schuster, head of NIDA from 1986 to 1991, admitted that although he did not think of addiction as a disease, he was "happy for it to be conceptualized that way for pragmatic reasons. . . for selling it to Congress"(47). For decades, addiction research had been a low-status field, disparaged by other researchers as a soft science that studied drunks and junkies. Now the field of neuroscience was taking greater notice. "People recognize that certain decision makers and others are very impressed with molecular biology," said Robert L. Balster, director of the Institute for Drug and Alcohol Studies at Virginia Commonwealth University (48).

Psychiatrist Jerome Jaffe, an eminent figure in the field and the first White House adviser on drugs (the precursor of the "drug czar"), sees the adoption of the brain-disease model as a tactical triumph and a scientific setback. "It was a useful way for particular agencies to convince Congress to raise the budgets (and) it has been very successful," he said. Indeed, neuroimaging, neurobiological research, and medication development consume over half of the NIDA research budget. In light of the agency's reach – it funds almost all substance-abuse research in the United States – it sets the national agenda regarding which research gets funded and therefore the nature of the data produced and the kinds of topics that investigators propose. But Jaffe argues that the braindisease paradigm presents "a Faustian bargain – the price that one pays is that you don't see all the other factors that interact (in addiction)" (3).

Many proponents of the brain-disease concept were deeply committed to dispelling the stigma surrounding addiction. Medicalizing the condition was a powerful way, they hoped, to rehabilitate addicts' poor public image from the perception of undisciplined deadbeats to people struggling with an ailment. This approach had its roots in the world of mental health advocacy. Until the early 1980s, plenty of people blamed parents for their children's serious mental problems. Then advocates began to publicize neuroscientific discoveries, demonstrating, for example, that schizophrenia is associated with abnormalities of brain structure and function. In this effort, brain imaging has served sufferers well, helping legitimize their symptoms by representing visually the illness in their brains (49–53). The idea, of course, was that these benefits would extend to addicts. But it turns out that it's harder to destigmatize addiction.

# **SHORTCOMINGS OF THE NEUROCENTRIC VIEW OF ADDICTION**

For all its benign aspirations, there are numerous problems with the brain-disease model. On its face, it implies that the brain is the most important and useful level of analysis for understanding and treating addiction. Sometimes the model even equates addiction with a neurological illness, plain, and simple (10). Such neurocentrism has clinical consequences, downplaying the underlying psychological and social reasons that drive drug use.

Recovery is a project of the heart and mind. The person, not his or her autonomous brain, is the agent of recovery. Notably, Alcoholics Anonymous, the institution perhaps most responsible for popularizing the idea that addiction is a disease, employs the term as a metaphor for loss of control. Its founders in the 1930s were leery of using the word "disease" because they thought that it discounted the profound importance of personal growth and the cultivation of honesty and humility in achieving sobriety (54).

The brain-disease narrative misappropriates language better used to describe such conditions as multiple sclerosis or schizophrenia – afflictions of the brain that are neither brought on by the sufferer nor modifiable by the desire to be well. It offers false hope that an addict's condition is completely amenable to a medical cure (much as pneumonia is to antibiotics). Finally, as we'll see, it threatens to obscure the vast role of personal agency in perpetuating the cycle of use and relapse.

Addicts embarking on recovery often need to find new clean and sober friends, travel new routes home from work to avoid passing near their dealer's street, or deposit their paycheck directly into a spouse's account to keep from squandering money on drugs. A teacher trying to quit cocaine switched from using a chalkboard – the powdery chalk was too similar to cocaine – and had a whiteboard installed instead. An investment banker who loved injecting speedballs – a cocktail of cocaine and heroin in the same syringe – made himself wear long-sleeved shirts to prevent glimpses of his bare and inviting arms. Former smokers who want to quit need to make many fine adjustments, from not lingering at the table after meals to ridding their homes of the ever-present smell of smoke, removing car lighters, and so on.

Thomas Schelling, a 2005 Nobel laureate in economics, refers to these purposeful practices as self-binding (55). The great selfbinder of myth was Odysseus. To keep himself from heeding the overpowering song of the sea sirens – the half-woman, half-bird creatures whose beautiful voices lured sailors to their deaths – Odysseus instructed his men to tie him to the mast of his ship (56). The famous Romantic English poet Samuel Taylor Coleridge, an opium addict, is said to have hired men to prevent him from entering a pharmacy to purchase opium (57). Today, one can hire a firm that will provide binding services. It imposes surprise urine tests on the client, collects evidence of attendance at AA meetings or treatment sessions, and sends a monthly status report (with the good or bad news) to another person, such as a parent, spouse, or boss (58).

Some addicts devise their own self-binding strategies. Others need the help of therapists, who teach them to identify and anticipate cues that trigger craving. Beyond the classic triad of people, places, and things, they come to realize that internal states, such as stress, bad moods, and boredom, can prompt drug urges (59).

Managing craving matters mightily in recovery, but it usually is not enough. Another very important truth is that an addict uses drugs or alcohol because they serve a purpose. Caroline Knapp, in her powerful 1996 memoir *Drinking: A Love Story*, recounted why she spent two decades of her life as an alcoholic: "You drank to drown out fear, to dilute anxiety and doubt and self-loathing and painful memories" (60). Knapp doesn't describe an urge to drink so much as a need to drink. She was not manipulated by an alien desire but by something woven into her being. To say that Knapp's problem was merely the effect of heavy drinking on her brain is to miss the true threat to her well-being: the brilliant but tormented Knapp herself.

Heroin and speed helped screenwriter Jerry Stahl, author of *Permanent Midnight*, attain "the soothing hiss of oblivion." But when the drugs wore off, his vulnerabilities throbbed like a fresh surgical incision. In surveying his life, Stahl wrote, "Everything, bad or good, boil(ed) back to the decade on the needle, and the years before that imbibing everything from cocaine to Romilar, pot to percs, LSD to liquid meth and a pharmacy in between: a lifetime spent altering the single niggling fact that to be alive means being conscious" [(61), p. 3–6]. The negative states to which we refer are typically underlying problems with emotional distress, especially mood or anxiety. To be sure, repeated use of drugs such as alcohol and cocaine can exacerbate primary depressive and anxiety disorders in the long term (62), but in the short term, the user almost always feels relief. Given the common problem of "steep discounting" in addicts, it is not surprising that addicts will attend to the experiencing self at the expense of the future self.

Or take Lisa, a 37-year-old woman featured in an HBO documentary on addiction. When we meet her, Lisa is living in a rundown hotel room in Toronto and working as a prostitute. She sits on the bed and talks with the filmmaker behind the camera. Flipping her shiny brown hair and inspecting her well-kept nails, Lisa is animated as she boasts about how much she makes selling sex, how much she spends on cocaine, and the longed-for "oblivion" that drugs help her attain. When Lisa was filmed, she was healthy and engaging; she looked and talked like someone who had recently been abstinent but was back in the early stages of her next downward spiral. She had no interest in stopping things at this point. "Right now, I am in no position to go into recovery (this way of life) is working for me . . .I have money, drugs, business. I'm O.K."To say that Lisa's problem is the effect of cocaine on her brain is to miss the true threat to her well-being: Lisa herself. "I always use for a reason. It's repressing what needs to be repressed," she says (63). To be certain, not all drug use in the service of improving mood is dysfunctional. But Lisa, who had been in treatment several times, is representative of individuals whose drug use starts out as a controlled and effective attempt at self-soothing but eventually becomes all-consuming and interferes with her life.

These stories highlight one of the shortcomings of the neurocentric view of addiction. This perspective ignores the fact that many people are drawn to drugs because the substances temporarily quell their pain: persistent self-loathing, anxiety, alienation, deep-seated intolerance of stress or boredom, and pervasive loneliness. The brain-disease model is of little use here because it does not accommodate the emotional logic that triggers and sustains addiction (35, 64, 65).

# **THE POWER OF INCENTIVES AND ADDICTS AS CHOOSING BEINGS**

In December 1966, Leroy Powell of Austin, TX, USA, was convicted of public intoxication and fined \$20 in a municipal court. Powell appealed the conviction to county court, where his lawyer argued that he suffered from "the disease of chronic alcoholism." Powell's public display of inebriation therefore was"not of his own volition," and the fine constituted cruel and unusual punishment. A psychiatrist concurred, testifying that Powell was "powerless not to drink" (66).

Then Powell took the stand. On the morning of his trial, he had a drink at 8 a.m. that his lawyer gave to him, presumably to stave off morning tremors. Here is an excerpt from the cross-examination:

Q: You took that one [drink] at eight o'clock [a.m.] because you wanted to drink?

A: Yes, sir.

Q: And you knew that if you drank it, you could keep on drinking and get drunk?

A: Well, I was supposed to be here on trial, and I didn't take but that one drink.

Q:You knew you had to be here this afternoon, but this morning you took one drink and then you knew that you couldn't afford to drink anymore and come to court; is that right?

A: Yes, sir, that's right.

Q: Because you knew what you would do if you kept drinking that you would finally pass out or be picked up?

A: Yes, sir.

Q: And you didn't want that to happen to you today? A: No, sir.

Q: Not today?

A: No, sir.

Q: So you only had one drink today?

A: Yes, sir (66).

The judge let stand Powell's conviction for public intoxication. A second appeal followed, this time to the U.S. Supreme Court. It, too, affirmed the constitutionality of punishment for public intoxication. "We are unable to conclude," said the court, "that chronic alcoholics in general, and Leroy Powell in particular, suffer from such an irresistible compulsion to drink and to get drunk in public that they are utterly unable to control their performance" (66).

For people like Powell who are not otherwise motivated to quit, consequences can play a powerful role in modifying behavior. Powell took only a single drink the morning of his trial because of foreseeable and meaningful consequences. Far from being unusual, his ability to curtail his drinking accords with a wealth of studies showing that people addicted to all kinds of drugs – nicotine, alcohol, cocaine, heroin, methamphetamines – can change in response to rewards or sanctions (67–69). Powell had surely experienced many alcohol-induced brain changes, but they did not keep him from making a choice that morning.

If Powell came before a judge today, his lawyer might well introduce a scan of his brain "craving" alcohol as evidence of his helplessness. If so, the judge would be wise to reject the scan as proof. After all, a judge, or anyone, can ponder scans of "addicted" brains all day, but he or she would never consider someone an

addict unless that person behaves like one (70–73). As legal scholar Stephen Morse puts it, "actions speak louder than images" (74).

Consider the following fMRI experiment by researchers at Yale and Columbia. They found that the brains of smokers reporting a strong desire to smoke displayed enhanced activation of reward circuitry, as would be expected (75). But they also showed that subjects could reduce craving by considering the long-term consequences of smoking, such as cancer or emphysema, while observing videos depicting people smoking. When subjects did so, their brains displayed enhanced activity in areas of the prefrontal cortex associated with focusing, shifting attention, and controlling emotions. Simultaneously, activity in regions associated with reward, such as the ventral striatum, decreased (76).

Investigators at NIDA observed the same pattern when they asked cocaine users to inhibit their craving in response to cues. Subjects underwent PET scanning as they watched a video of people preparing drug paraphernalia and smoking crack cocaine. When researchers instructed the addicts to control their responses to the video, they observed inhibition of brain regions normally implicated in drug craving. When not deliberately suppressing their cravings, the addicts reported feeling their typical desire to use, and the PET scans revealed enhanced activation in brain regions that mediate craving (77).

These powerful findings illuminate the capacity for self-control in addicts. They also underscore the idea that addicts persist not because of an inability to control the desire to use but from a failure of motivation. Granted, summoning sustained motivation can be a great challenge: it takes a lot of energy and vigilance to resist craving, especially urges that ambush the addict unexpectedly. Studies on the regulation of craving also help distinguish behavior that people do not control from behavior that they cannot control. Imagine, by way of contrast, promising a reward to people with Alzheimer's if they can keep their dementia from worsening. That would be both pointless and cruel because the kinds of brain changes intrinsic to dementia leave the sufferer resistant to rewards or penalties.

What Powell's case showed was that even though he sustained brain changes, those changes did not prevent his behavior from being shaped by consequences. Contingency management – the technical term for the practice of adjusting consequences, including incentives – often succeeds with people who face serious losses, such as their livelihood, professional identity, or reputation. When addicted physicians come under the surveillance of their state medical boards and are subject to random urine testing, unannounced workplace visits, and frequent employer evaluations, they fare well: 70–90% are employed with their licenses intact 5 years later [(78), p. 165]. Likewise, scores of clinical trials show that addicts who know they will receive a reward, such as cash, gift certificates, or services, are nearly two to three times as likely to submit drug-free urine samples as addicts not offered rewards (79, 80).

Unfortunately, treatment programs are rarely in a position to offer cash or costly rewards. But the criminal justice system has an ample supply of incentives at its disposal and has been using such leverage for years. One of the most promising demonstrations of contingency management comes from Honolulu in the form of Project HOPE, Hawaii's Opportunity Probation with Enforcement.

Project HOPE includes frequent random drug testing of offenders on probation. Those who test positive are subject to immediate and brief incarceration. Sanctions are fair and transparent: all offenders are treated equally, and everyone knows what will happen in case of an infraction. The judges express a heartfelt faith in offenders' ability to succeed. These basic elements of HOPE's contingency administration – swiftness, sureness, transparency, and fairness combined with expectation for achievement – are a potent prescription for behavior change in just about anyone.

Indeed, after 1 year of enrollment in Project HOPE, participants fared considerably better than probationers in a group who served as a comparison. They were 55% less likely to be arrested for a new crime and 53% less likely to have had their probation revoked. These results are even more impressive in light of the participants' criminal histories and their heavy, chronic exposure to methamphetamine, which can impair aspects of cognitive function [on project HOPE, see (81); on the effects of methamphetamines, see (82–86)].

These findings join a vast body of experimental data attesting to the power of incentives to override the lure of drugs. Yet because the facts contradict the idea that addiction is analogous to Alzheimer's disease, some HOPE personnel objected to incentives, arguing that addicts couldn't be accountable for their behavior. Likewise, when researchers asked NIDA to consider reviewing HOPE in its formative years, the agency declined on the grounds that methamphetamine addicts are not capable of responding to incentives alone (87–91).

# **CAN MEDICINE "CURE" ADDICTION?**

The brain-disease model leads us down a narrow clinical path. Because it states that addiction is a "chronic and relapsing" condition, it diverts attention from promising behavioral therapies that challenge the inevitability of relapse by holding patients accountable for their choices. At the same time, because the model implies that addicts cannot stop using drugs until their brain chemistry returns to normal, it overemphasizes the value of brain-level solutions, such as pharmaceutical intervention. In 1997, Leshner ranked the search for a medication to treat methamphetamine addiction as a "top priority (23). A decade later, Volkow predicted, "We will be treating addiction as a disease (by 2018), and that means with medicine" (15).

The search for a magic bullet is folly – and even NIDA has given up hope of finding a wonder drug – but the brain-disease narrative continues to inspire unrealistic goals. When British pop star Amy Winehouse succumbed to her high-profile alcoholism in the summer of 2011, a *Psychology Today* columnist asked, "Could neuroscience have helped Amy Winehouse?"(92). The author answered in the affirmative, suggesting a dopamine-altering medication of the future because addiction "may be a brain problem that science can eventually solve." Neuroscientist David Eagleman goes even further, asserting that "addiction can be reasonably viewed as a neurological problem that allows for medical solutions, just as pneumonia can be viewed as a lung problem" (93). But the analogy doesn't hold up. Changing a behavior like addiction requires addicts to work hard to change their patterns of thought and behavior. In contrast, antibiotic cures for pneumonia work even if the patient is in a coma.

The hope of a medical treatment is the logical outgrowth of placing the brain at the center of the addictive process. Overall, success to date has been genuine but modest. When motivated patients take medications – especially patients already armed with relapseprevention strategies and the support of family and friends – they can sometimes vault into sustained recovery. Methadone, a longacting synthetic opiate taken once a day to prevent opiate withdrawal, has played a major role in treating addiction to heroin and painkillers since the 1960s (94). Still, to their counselors' chagrin, up to half the patients in methadone clinics also fortify themselves with heroin, cocaine, or Valium-like tranquilizers called benzodiazepines, sold on the street (95). Despite three decades of effort, there is still no medication therapy for cocaine. Cocaine immunotherapy (popularly called a cocaine "vaccine") to prevent cocaine molecules from entering the brain is now in development, but previews do not look promising for wide-scale use (96). Other types of medications include blocking agents, such as naltrexone for opiate addiction, which occupy neuronal receptors and blunt a drug's effect (97). Aversive agents, such as Antabuse (disulfiram), cause people to feel nauseated and vomit when they ingest alcohol (98). They can be effective in some cases, although many individuals elect to stop taking them.

These medications are not the product of modern neuroscience; they were developed decades ago. Even a vaccine was sought in the 1970s, although today's techniques are vastly more sophisticated. More recently, neuroscientists have collaborated with pharmacologists to develop medications to reverse or compensate for the pathological effects of drugs on the brain. The premise is that different components of addiction can be targeted by different medications. These components are the "reward" circuit (which mediates a strong desire to use and preoccupation with imminent use) and the craving mechanism associated with conditioned cues. Thus far, success has been elusive. Anticraving agents have shown some promise for alcoholics, but treatments for cocaine addiction have been disappointing (99–102).

Traditionally, pharmacologists have approached the treatment of alcoholics and addicts in the same way they address most psychiatric diseases: as a matter of reversing or compensating for neuropathology – in this case, the neural alteration resulting from repeated use. This is a logical approach, but instead of focusing almost exclusively on what is wrong in the brain, perhaps they should also investigate the ways in which addicts recover. Addicts find non-drug sources of interests and gratification that generate their own outpourings of dopamine; they practice self-binding and mindfulness exercises that make the prefrontal cortex better at controlling impulses. Relinquishing drugs and alcohol is accompanied by a shift in the brain's valuation systems. How, and even whether, these dynamics will translate into pharmacotherapy is a complicated question, but perhaps the answer will spur discovery of more effective medications – not panaceas but helpful aids to hasten the process of recovery. Some proponents of the brain-disease model would say that emphasizing the role of choice in addiction is just another way to stigmatize addicts and justify penal responses over therapeutic ones. To this way of thinking, if we see the addict as a "chronic illness sufferer," we will no longer view him or her as a "bad person" (23, 103). This sentiment echoes throughout the addiction community. "We can continue playing the blame game," said Volkow in 2008 "Or we can parlay the transformative power of scientific discovery into a brighter future for addicted individuals" (104).

# **FALSE CHOICES: SICK OR BAD**

Sick brain versus flawed character? Biological determinism versus bad choices? Why must these be our only options?  The bind, of course, is that it is impossible to understand addiction if one glosses over the reality that addicts do possess the capacity for choice and an understanding of consequences. Forcing a choice between "sick or bad" adds confusion, not clarity, to the long-standing debate over just how much to hold addicts responsible in ways that are beneficial to them and to the rest of society.

Although it makes no sense to incarcerate people for minor drug crimes, exempting addicts from social norms does not ensure them a brighter future. Stigmatization is a normal part of social interaction – a potent force in shaping behavior. Author Susan Cheever, a former alcoholic, coined a new word, "drunkenfreude," to denote how the embarrassing antics of intoxicated friends and strangers keep her sober."[Watching] other people get drunk helps me remember," Cheever writes. "I learn from seeing what I don't want and avoiding it" (105).

Too often, well-meaning family members and friends try to insulate individuals from the consequences of their behavior and thereby miss an important opportunity to help the addict quit. There is nothing unethical – and everything natural and socially adaptive – about condemning reckless and harmful acts. At the same time, because addicts are people who suffer, we must also provide effective care and support progressive approaches, such as Project HOPE. If we want to garner social and political support for addicts' plight, the best way to do that is to develop the most effective modes of rehabilitation possible – not to advance a reductive and one-dimensional version of addiction.

And what of the efforts to destigmatize addiction through medicalization? Results are mixed. In some surveys of the public, well over half of respondents saw addiction as a "moral weakness" or "character flaw." In others, over half to two-thirds classified it as a "disease." An Indiana University study asked over 600 people whether they viewed alcoholism as the result of a genetic problem or chemical imbalance (i.e., a "neurobiological conception") or as an outgrowth of "bad character" or "the way he or she was raised." Those endorsing a neurobiological explanation rose from 38% in 1996 to 47% in 2006; the proportion endorsing psychiatric treatment increased from 61 to 79% (106–112).

Another study revealed an unexpected pattern over the past few decades.  Biological explanations also appear to foster pessimism about the likelihood of recovery and the effectiveness of treatment (113–121). This finding may seem counterintuitive. One might think that a biological explanation would be good news to a patient – and to be sure, some people with mental illness do indeed find it a relief. But when the patient's affliction is addiction and there are no medical cures to restore an addict's disrupted brain, emphasizing the biological dimension seems misguided.

The authors of the chronic-brain-disease narrative were inspired by discoveries about the effects of drugs on the brain. The promise of finding powerful antiaddiction medications seemed great. The maturing science of addiction biology would mean that once and for all, the condition would be taken seriously as an illness – a condition that began with the explicit, voluntary decision to try drugs but transitioned into an involuntary and uncontrollable state. This knowledge, they hoped, would sensitize policy makers and the public to the needs of addicts, including access to public treatment and better private insurance coverage. A softening of puritanical attitudes and an easing of punitive law enforcement were also on the agenda.

The mission was worthy, but the outcome has been less salutary. The neurocentric perspective encourages unwarranted optimism regarding pharmaceutical cures and oversells the need for professional help. It labels as "chronic" a condition that typically remits in early adulthood. The brain-disease story gives short shrift to the reality that substances serve a purpose in addicts' lives and that neurobiological changes induced by alcohol and drugs can be overridden.

Like many misleading metaphors, the brain-disease model contains some truth. There is a genetic influence on alcoholism and other addictions, and prolonged substance-abuse often damages brain structures that mediate self-governance. Yet the problem with the brain-disease model is its misplaced emphasis on biology as the star feature of addiction and its relegation of psychological and behavioral elements to at best supporting roles. "If the brain is the core of the problem, attending to the brain needs to be a core part of the solution," as Leshner once put it (7). The clinical reality is just the opposite: The most effective interventions aim not at the brain but at the person. It's the *minds* of addicts that contain the stories of how addiction happens, why people continue to use drugs, and, if they decide to stop, how they manage to do so. This deeply personal history can't be understood exclusively by inspecting neural circuitry.

### **BEYOND THE BRAIN**

In the end, the most useful definition of addiction is a descriptive one, such as this: Addiction is a behavior marked by repeated use despite destructive consequences and by difficulty quitting not withstanding the user's resolution to do so. This "definition" isn't theoretical; it explains nothing about why one "gets" addiction – and how could it offer a satisfying causal account when there are multiple levels at which the process can be understood? Our proposed definition merely states an observable fact about the behavior generally recognized as addiction. That's a good thing because a blank explanatory slate (unbiased by biological orientation or any other theoretical model) inspires broad-minded thinking about research, treatment, and policy. Is there room for neuroscience in this tableau? Of course. Brain research is yielding valuable information about the neural mechanisms associated with desire, compulsion, and self-control – discoveries that may one day be better harnessed for clinical use. But the daily work of recovery, whether or not it is abetted by medication, is a human process that is most effectively pursued in the idiom of purposeful action, meaning, choice, and consequence.

# **REFERENCES**

http://www.nytimes.com/2000/06/ 24/arts/seeing-drugs-as-a-choiceor-as-a-brain-anomaly.html? pagewanted=all&src=pm

*J Bioethic Inq* (2011) **1**:15–25. doi: 10.1007/s11673-010-9271-1

of substance use disorders: a meta-analysis. *Addiction* (2006) **11**:1546–60. doi:10.1111/j.1360- 0443.2006.01581.x

(2011) **3**:132–9. doi:10.1073/pnas.<PHONE_NUMBER>

functioning impaired in methamphetamine users? A critical review. *Neuropsychopharmacology* (2012) **37**:586–608. doi:10.1038/npp.2011.276

causal explanations on anxious and depressed patients' perception of a person with panic disorder. *Behav Res Ther* (2006) **45**: 405–11. doi:10.1016/j.brat.2006. 03.005

*Epidemiol* (2005) **40**:391–5. doi:10.1007/s00127-005-0903-4

121. Haslam N. Genetic essentialism, neuroessentialism, and stigma: commentary on dar-nimrod and heine. *Psychol Bull* (2011) **137**:819–24. doi:10.1037/a0022386

**Conflict of Interest Statement:** The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

*Received: 26 June 2013; accepted: 08 October 2013; published online: 03 March 2014.*

*Citation: Satel S and Lilienfeld SO (2014) Addiction and the brain-disease fallacy. Front. Psychiatry 4:141. doi: 10.3389/fpsyt.2013.00141*

*This article was submitted to Addictive Disorders and Behavioral Dyscontrol, a section of the journal Frontiers in Psychiatry.*

*Copyright © 2014 Satel and Lilienfeld. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.*

# The addict in us all

# **Brendan Dill 1\* and Richard Holton2**

1 Department of Linguistics and Philosophy, Massachusetts Institute of Technology, Cambridge, MA, USA

2 Department of Philosophy, University of Cambridge, Cambridge, UK

### **Edited by:**

Hanna Pickard, University of Oxford, UK

### **Reviewed by:**

Serge H. Ahmed, CNRS, France Bennett Foddy, University of Oxford, UK

### **\*Correspondence:**

Brendan Dill, 77 Massachusetts Avenue, 32-D808, Cambridge, MA 02139-4307, USA e-mail<EMAIL_ADDRESS>
In this paper, we contend that the psychology of addiction is similar to the psychology of ordinary, non-addictive temptation in important respects, and explore the ways in which these parallels can illuminate both addiction and ordinary action. The incentive salience account of addiction proposed by Robinson and Berridge (1–3) entails that addictive desires are not in their nature different from many of the desires had by non-addicts; what is different is rather the way that addictive desires are acquired, which in turn affects their strength. We examine these "incentive salience" desires, both in addicts and non-addicts, contrasting them with more cognitive desires. On this account, the self-control challenge faced by addicted agents is not different in kind from that faced by non-addicted agents – though the two may, of course, differ greatly in degree of difficulty. We explore a general model of selfcontrol for both the addict and the non-addict, stressing that self-control may be employed at three different stages, and examining the ways in which it might be strengthened. This helps elucidate a general model of intentional action.

**Keywords: addiction, self-control, desire, incentive salience, ego depletion, mindfulness meditation, mental contrasting, implementation intentions**

# **INTRODUCTION**

On a common conception, addicts and non-addicts are very different. Addicts' compulsions drive them to act in ways that are quite foreign to the non-addicted. They consume drugs in the full knowledge that they are harmful, and in the face of a desire to stop, something that the normal agent does not do.

We argue here that this picture is quite misleading. Non-addicts, like addicts, have to contend with desires that are quite insensitive to their reflective judgments about what is good. And addicts, like non-addicts, have at their disposal a capacity for self-control that can enable them to resist and overcome these desires.

The situation faced by the addicted agent is thus parallel to that faced by the non-addicted agent. It is an extreme example of the same kind of thing. Both will have desires that persist even in the belief that their objects are worthless, or even actively harmful. And so both will be faced with the self-control problem of resisting these troublesome desires in the light of these beliefs. This self-control challenge, faced by both addicted and non-addicted agents, is the focus of this paper.

We begin by briefly outlining the empirical support for our first claim, that addictive desires are instances of a kind of desire common to all agents (see Desire). They result from a system – the "incentive salience" system – that has evolved to create desires, for foods and other things, that are independent from the agent's evaluations of the worth of those things. What is different in the addict is not the intrinsic nature of these desires, but their origin. Addictive drugs cause the desire-formation process to malfunction, with the result that they come to be desired with an intensity and permanence that is quite out of proportion to any pleasure they have given. However, the same problematic features of addictive desires arise even when the incentive salience system does not malfunction. We see this in more mundane desires such as

the craving for chocolate. We characterize the common features of these "incentive salience" desires, and contrast them with the more reasons-sensitive desires, which we call "cognitive desires," on the basis of which agents reflectively deliberate about what to do. The competition between these two kinds of desire for control over behavior poses the problem with which we are concerned throughout the remainder of the paper: the problem of self-control.

We begin our discussion of self-control by arguing that an agent's course of action is not solely determined by the relative strengths of her desires; it also matters whether, and how, she exerts *self-control* on behalf of some desires over others. Our argument centers on two subject populations whose behaviors are, we think, best explained as resulting from selective deficits in self-control capacity: subjects with lesions in the ventromedial prefrontal cortex (vmPFC), and subjects experiencing *ego depletion* (see The Existence of Self-Control).

The picture that emerges from these first two sections portrays intentional action as the result of a competition between two systems: the incentive salience system, which automatically guides behavior on the basis of appetitive desires, and the self-control system, by means of which an agent can, with effort, bring her actions in accordance with her more reflective desires. Though the conflict between these systems is typically more dramatic in addicts, it pervades ordinary action as well.

Though we offer some new arguments in its support, this two-system picture is far from novel. The basic outlines of the approach date back to Plato [(4), *Republic* Book IV] and the more contemporary version of this picture we present here has been defended before (5–8). What we hope to add to this literature is a more detailed picture of how these two systems interact to produce behavior (see Three Stages of Self-Control). We propose that there are three distinct loci of self-control conflict – at the point of deliberation, of formation of intention, and of execution of action – which we call the *deliberative, volitional,* and *implemental* stages of self-control. Distinguishing between these stages brings into focus the nature of the self-control challenge faced by addicts and non-addicted agents alike. Drawing on a large body of empirical work, we articulate the nature of the conflict between the self-control and incentive salience systems at each stage, and suggest ways in which each kind of self-control might be improved. What emerges is a single model of human motivational psychology that captures the predicaments of addiction and ordinary temptation with equal aptitude.1

### **DESIRE**

Let us start with the question of how we form desires. One might think – many have thought – that we are hedonists at heart. On such a view all of our desires stem from a fundamental intrinsic desire for pleasure. When we desire things other than pleasure we desire them *instrumentally*: that is, we desire them derivatively, because we believe that they will give us pleasure.

Many have objected that such an account makes us seem far too selfish: sometimes we want things because of the benefits that they will bring other people, independently of any benefits they may bring to us. We think that this point is probably right,2 but it is not our primary concern here. Our argument is rather that such a picture is wrong even when we consider such simple self-regarding desires as those we have for different foods. Suppose that an agent were to sample many different foods. Some they would like, others not, and they would then go on to regulate their future desires for them accordingly. We might expect these to be instrumental desires, formed in the service of the desire for pleasure. But the empirical evidence suggests not. It suggests instead that pleasure typically causes us to have intrinsic desires for the foods themselves, which then motivate independently of any beliefs about the pleasure that such foods will bring.

The crucial evidence for this is that our desires for different foods are not always directly responsive to our explicit beliefs about how pleasurable they are to eat. The desires do not need such beliefs to bring them into existence; and they can persist in their absence. We sometimes get a sense of this in our direct experience – many of us experience a desire to eat more of a thing (chocolates? over-rich desserts? peanuts? potato chips?) even when we know that we won't enjoy it and that it may leave us feeling somewhat nauseated. However, the best evidence for this phenomenon comes from studies, not of normal foods, but of addictive drugs, and moreover, of how they work on rats. So let us start there, and then return to the case of how more normal foods work on us. Our account will follow the "incentive salience" theory developed by Robinson and Berridge (1–3).3

Addictive drugs artificially increase the levels of the neurotransmitter dopamine in the brain. Different drugs do this in different ways: nicotine stimulates the production of dopamine directly, opiates decrease the production of substances that inhibit the production of dopamine, cocaine reduces the activity of the system that reabsorbs dopamine after it has been released, and so on [(9), pp. 245–246]. What is remarkable is that these various substances with otherwise disparate biological and neurological effects have this single common feature: they all boost the effect of dopamine.

It is reasonable to infer that this shared neurobiological quirk must play a role in explaining these substances' more obvious common feature: that they all cause addiction. Although there remains controversy here, this idea is borne out by the evidence. By boosting dopamine levels, addictive drugs artificially stimulate the mesolimbic dopamine system, which has long been known to play an important role in motivation. That is, they stimulate it directly, and not in the normal way via an experience that also gives rise to pleasure. (Compare getting someone to see stars by banging them on the head, rather than by showing them stars.) So to understand how drug addiction works, we need to understand what role dopamine plays in motivation.

For many years dopamine was thought to be a pleasure signal. But it is not. Whilst it is typically accompanied by pleasure, that is not what it is causing or registering [for a detailed defense of this claim, see Ref. (10)]. Separate the indicators of a rat's pleasure (its facial movements) from the indicators of its desire (the effort it will expend to attain the thing), and you find that dopamine is linked to desire and not to pleasure. Artificially increase a rat's dopamine levels by giving it amphetamines, and it will work much harder to get something even if that thing gives it no pleasure, and it knows it (11). Reduce the rat's dopamine levels via genetic modification and it will fail to work for a thing even if that thing will give it great pleasure, and it knows it (12). Moreover – and this is crucial given the implications for addiction – if you increase the dopamine levels when a rat is sampling a foodstuff, what you bring about is not just an immediate desire for that foodstuff, but also a long-term dispositional desire for it (13). Show the rat the foodstuff again later, and it will still want it strongly.

What is happening here? Rats are opportunistic creatures, who need to be able to accommodate their tastes to a new environment. It makes sense for them to be able to regulate their desires in proportion to the pleasure that they get from various foodstuffs. Dopamine is clearly involved in this process. But it looks as though dopamine works directly on desires, without the need for the involvement of pleasure or beliefs about pleasure. It may be that dopamine release is typically *caused* by pleasure: in the case of most non-addictive foodstuffs, the most pleasurable ones will give the greatest dopamine release. But if dopamine is artificially increased,