ArticlePDF Available
published: 13 February 2015
doi: 10.3389/fpsyt.2015.00020
Alternative models of addiction
Hanna Pickard1*, Serge H. Ahmed 2and Bennett Foddy 3
1University of Birmingham, Birmingham, UK
2University of Bordeaux: IMN CNRS UMR 5293, Bordeaux, France
3NewYork University, NewYork, NY, USA
Edited and reviewed by:
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 behav-
ior 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 phe-
nomena 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 addic-
tion 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 Fal-
lacy” 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 under-
stood as a choice. In “Intertemporal Bargaining in Addiction,
Ainslie (3) reprises his large body of work on the inherent weak-
nesses of the human capacity for choice, exploring its relevance
to questions of the nature of responsibility and our justifica-
tion in holding addicts accountable for addictive behavior and its
Other authors in this volume seek to understand the ways
in which these choices can be pathologically impaired by addic-
tion. 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 con-
sume, even when consumption is neither experienced nor judged
as desirable. Henden et al. (5) in Addiction: Choice or Compul-
sion?” 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
The importance of negative outcomes to understanding addic-
tion 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 neces-
sarily 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 demonstrat-
ing 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 con-
clusion 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 con-
sumption. To adapt, animals are likely to have evolved internal
protective mechanisms allowing them to use drugs in a controlled
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 distin-
guished 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
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 nat-
urally characterize as involving a need for control, as opposed to
involving a loss of control. February 2015 | Volume 6 | Article 20 | 1
Pickard et al. Alternative models of addiction
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.
1. Heyman G. Addiction and choice: theory and new data. Front Psychiatry (2013)
4:31. doi:10.3389/fpsyt.2013.00031
2. Satel S, Lilienfeld SO. Addiction and the brain-disease fallacy. Front Psychiatry
(2014) 4:141. doi:10.3389/fpsyt.2013.00141
3. Ainslie G. Intertemporal bargaining in addiction. Front Psychiatry (2013) 4:63.
4. Dill B, Holton R. The addict in us all. Front Psychiatry (2014) 5:139. doi:10.
5. Henden E, Melberg HO, Rogeberg O. Addiction: choice or compulsion? Front
Psychiatry (2013) 4:77. doi:10.3389/fpsyt.2013.00077
6. Levy N. Addiction is not a brain disease (and it matters). Front Psychiatry (2013)
4:24. doi:10.3389/fpsyt.2013.00024
7. Wakefield JC, Schmitz MF. How many people have alcohol use disorders? Using
the harmful dysfunction analysis to reconcile prevalence estimates in two com-
munity surveys. Front Psychiatry (2014) 5:10. doi:10.3389/fpsyt.2014.00010
8. Zernig G, Kummer KK, Prast JM. Dyadic social interaction as an alternative
reward to cocaine. Front Psychiatry (2013) 4:100. doi:10.3389/fpsyt.2013.00100
9. Hagen EH, Roulette CH, Sullivan RJ.Explaining human recreational use of ‘pes-
ticides’: the neurotoxin regulation model of substance use vs. the hijack model
and implications for age and sex differences in drug consumption. Front Psychi-
atry (2013) 4:142. doi:10.3389/fpsyt.2013.00142
10. Flanagan O. The shame of addiction. Front Psychiatry (2013) 4:120. doi:10.3389/
11. Heyman G, Dunn BJ, Mignone J. Disentangling the correlates of drug use in a
clinic and community sample: a regression analysis of the associations between
drug use, years-of-school, impulsivity, IQ, working memory, and psychiatric
symptoms. Front Psychiatry (2014) 5:70. doi:10.3389/fpsyt.2014.00070
Conflict of Interest Statement: The authors declare that the researchwas 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
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 distr ibuted
under the terms of the Creative Commons Attribution License (CC BY). The use, dis-
tribution 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.
Frontiers in Psychiatry | Addictive Disorders and Behavioral Dyscontrol February 2015 | Volume 6 | Article 20 | 2
... Present-day criticism directed at the conceptualization of addiction as a brain disease is of a very different nature. It originates from within the scientific community itself, and asserts that this conceptualization is neither supported by data, nor helpful for people with substance use problems [4][5][6][7][8]. Addressing these critiques requires a very different perspective, and is the objective of our paper. ...
... Driven by compulsion, or free to choose? A major criticism of the brain disease view of addiction, and one that is related to the issue of determinism vs indeterminism, centers around the term "compulsivity" [6,[87][88][89][90] and the different meanings it is given. Prominent addiction theories state that addiction is characterized by a transition from controlled to "compulsive" drug seeking and taking [91][92][93][94][95], but allocate somewhat different meanings to "compulsivity". ...
... Critics question the existence of compulsivity in addiction altogether [5][6][7]89], typically using a literal interpretation, i.e., that a person who uses alcohol or drugs simply can not do otherwise. Were that the intended meaning in theories of addiction-which it is not-it would clearly be invalidated by observations of preserved sensitivity of behavior to contingencies in addiction. ...
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... Substance use disorders (SUDs) have the nature of being both a medical and a social issue contributing to a person's depressive and anxious mild to severe conditions, contributing to the dysfunctionality of both the person and his family (Salisbury-Afshar, 2017). One reason these substances are highly addictive is explained by Pickard, Ahmed, and Foddy (2015) in their theories of addictive behavior. The ideas are divided into two principal reasons: addictive behavior is considered a moral failure wherein the person using the substance is believed to have ethically failed and have become drug dependent. ...
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... Myths about the use of alcohol as a preventive measure for COVID-19 must be dispelled, particularly in developing countries with low literacy and health awareness levels. Healthy alternatives to alcohol use must be en1phasized through educational interventions (Pickard, Ahmed, & Foddy 2015). Policymakers, media, and health professionals should incorporate messages about reducing alcohol consumption along with COVID-19 messages (The Lancet Gastroenterology Hepatology, 2020). ...
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... One notable area in which externalism might perform this kind of integrative role is the classic dichotomy in the literature between the "Disease Model" and the "Choice Model" of addiction [40,41]. Caricaturing somewhat, we can say that theorists following the Disease Model tended to treat addiction as neurally-based, all-or-nothing (one is either an addict, or one is not), uncontrollable, progressive, and requiring treatment if it is not to result in eventual death (e.g. ...
In addiction, apparently causally significant phenomena occur at a huge number of levels; addiction is affected by biomedical, neurological, pharmacological, clinical, social, and politico-legal factors, among many others. In such a complex, multifaceted field of inquiry, it seems very unlikely that all the many layers of explanation will prove amenable to any simple or straightforward, reductive analysis; if we are to unify the many different sciences of addiction while respecting their causal autonomy, then, what we are likely to need is an integrative framework. In this paper, we propose the theory of "Externalist" or "4E"-for extended, embodied, embedded, and enactive-cognition, which focuses on the empirical and conceptual centrality of the wider extra-neural environment to cognitive and mental processes, as a candidate for such a framework,. We begin in Section 2 by outlining how such a perspective might apply to psychiatry more generally, before turning to some of the ways it can illuminate addiction in particular: Section 3 points to a way of dissolving the classic dichotomy between the "choice model" and "disease model" in the addiction literature; Section 4 shows how 4E concepts can clarify the interplay between the addict's brain and her environment; and Section 5 considers how these insights help to explain the success of some recovery strategies, and may help to inform the development of new ones.
... Clinicians and scholars began claiming in the late 1990s that excessive internet use was a growing problem that should be recognized as an addiction (Griffiths, 1998;Thompson, 1996;Young, 1998b). But there were then, and there continue to be, several controversies surrounding the concept of addiction (Du Plessis, 2012;Pickard, Ahmed, & Foddy, 2015;Shaffer, 1997;West & Brown, 2013) and its application to excessive use of the internet. To begin, there are multiple theories of addiction (West & Brown, 2013), including choice theories (which claim that addicts are not compelled to use an addictive substance but choose to do so because its perceived benefits are greater than its perceived costs; Ainslie, 2013;Becker & Murphy, 1988;Campbell, 2003;Heyman, 2009Heyman, , 2013Skog, 2003); disease theories (originating in the nineteenth century and officially endorsed by the American Medical Association in 1956, these claim addictive substances produce persistent pathological changes in vulnerable individuals that generate powerful craving and weakened self-control; Leshner, 1997;Levine, 1978;McLellan, Lewis, O'Brien, & Kleber, 2000;Volkow & Koob, 2015;Volkow, Koob, & McLellan, 2016); learning theories (which hold that addiction is a learned behavior acquired through a conditioning process of positive and negative reinforcement; Drummond, Cooper, & Glautier, 1990;Niaura, 2000); and, most recently, neurobiological theories (versions of disease theories developed in the 1990s, these propose specific molecular [e.g., the neurotransmitters dopamine and gamma-aminobutyric acid] and neurological [e.g., activity in the ventral tegmental area, the nucleus accumbens, and the prefrontal cortex] mechanisms of addiction; Fakhoury, 2014;Goldstein & Volkow, 2011;Koob & Simon, 2009). ...
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... Debate continues about how addiction should be conceptualized, and what implications these definitions serve-whether, for instance, addiction is a choice or outside the locus of individual control, whether it is a disease of the brain or a moral failure, whether drug use is taken up hedonistically or in response to psychological trauma, and whether addiction only occurs among certain people under certain conditions or whether it can happen to anyone (J. B. Davies, 1997;Hammer et al., 2013;Keane, 2002;Pickard et al., 2015;Reinarman, 2005). Elsewhere, personal identity within addiction is queried, as in research on 12-step peer support programs, where members are encouraged to self-label as "addict," even in recovery; self-narrative is leveraged to explain past and negotiate present versions of the self (Frank, 2011;Rafalovich, 1999;Reinarman, 2005). ...
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Drugs of abuse are increasingly consumed worldwide. Such consumption could be back-calculated based on wastewater content. The West Indies, with its coca production and its thriving illicit drug market, is both a hub of world cocaine trafficking and a place where its consumption is prevalent particularly in the form of crack. The present study will firstly investigate Caribbean consumption by a daily 5 to 7 day sampling campaign of composite wastewater samples from the four wastewater treatment plants of the Martinique capital, including working and non-working periods. The local consumption of cocaine is ten to thirty times higher than OECD standards because of the prevalence of crack. The excretion coefficient for crack consumption and the impact of temperature on drug stability need further investigation. However, the low diversity of illicit drugs consumed and the crack prevalence suggest practices driven by the transiting of drugs for international trafficking.
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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 self-control 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.
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Years-of-school is negatively correlated with illicit drug use. However, educational attainment is positively correlated with IQ and negatively correlated with impulsivity, two traits that are also correlated with drug use. Thus, the negative correlation between education and drug use may reflect the correlates of schooling, not schooling itself. To help disentangle these relations we obtained measures of working memory, simple memory, IQ, disposition (impulsivity and psychiatric status), years-of-school and frequency of illicit and licit drug use in methadone clinic and community drug users. We found strong zero-order correlations between all measures, including IQ, impulsivity, years-of-school, psychiatric symptoms, and drug use. However, multiple regression analyses revealed a different picture. The significant predictors of illicit drug use were gender, involvement in a methadone clinic, and years-of-school. That is, psychiatric symptoms, impulsivity, cognition, and IQ no longer predicted illicit drug use in the multiple regression analyses. Moreover, high risk subjects (low IQ and/or high impulsivity) who spent 14 or more years in school used stimulants and opiates less than did low risk subjects who had spent <14 years in school. Smoking and drinking had a different correlational structure. IQ and years-of-school predicted whether someone ever became a smoker, whereas impulsivity predicted the frequency of drinking bouts, but years-of-school did not. Many subjects reported no use of one or more drugs, resulting in a large number of "zeroes" in the data sets. Cragg's Double-Hurdle regression method proved the best approach for dealing with this problem. To our knowledge, this is the first report to show that years-of-school predicts lower levels of illicit drug use after controlling for IQ and impulsivity. This paper also highlights the advantages of Double-Hurdle regression methods for analyzing the correlates of drug use in community samples.
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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. 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.”
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Community prevalence rates of alcohol use disorders (AUDs) provided by epidemiological studies using DSM-based diagnostic criteria pose several challenges: the rates appear implausibly high to many epidemiologists; they do not converge across similar studies; and, due to low service utilization by those diagnosed as disordered, they yield estimates of unmet need for services so high that credibility for planning purposes is jeopardized. For example, two early community studies using DSM diagnostic criteria, the Epidemiologic Catchment Area Study (ECA) and the National Comorbidity Survey (NCS), yielded lifetime AUD prevalence rates of 14 and 24%, respectively, with NCS unmet need for services 19% of the entire population. Attempts to address these challenges by adding clinical significance requirements to diagnostic criteria have proven unsuccessful. Hypothesizing that these challenges are due to high rates of false-positive diagnoses of problem drinking as AUDs, we test an alternative approach. We use the harmful dysfunction (HD) analysis of the concept of mental disorder as a guide to construct more valid criteria within the framework of the standard out-of-control model of AUD. The proposed HD criteria require harm and dysfunction, where harm can be any negative social, personal, or physical outcome, and dysfunction requires either withdrawal symptoms or inability to stop drinking. Using HD criteria, ECA and NCS lifetime prevalences converge to much-reduced rates of 6 and 6.8%, respectively. Due to higher service utilization rates, NCS lifetime unmet need is reduced to 3.4%. Service use and duration comparisons suggest that HD criteria possess increased diagnostic validity. Moreover, HD criteria eliminate 90% of transient teenage drinking from disorder status. The HD version of the out-of-control model thus potentially resolves the three classic prevalence challenges while offering a more rigorous approach to distinguishing AUDs from problematic drinking.
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Most globally popular drugs are plant neurotoxins or their close chemical analogs. These compounds evolved to deter, not reward or reinforce, consumption. Moreover, they reliably activate virtually all toxin defense mechanisms, and are thus correctly identified by human neurophysiology as toxins. Acute drug toxicity must therefore play a more central role in drug use theory. We accordingly challenge the popular idea that the rewarding and reinforcing properties of drugs "hijack" the brain, and propose instead that the brain evolved to carefully regulate neurotoxin consumption to minimize fitness costs and maximize fitness benefits. This perspective provides a compelling explanation for the dramatic changes in substance use that occur during the transition from childhood to adulthood, and for pervasive sex differences in substance use: because nicotine and many other plant neurotoxins are teratogenic, children, and to a lesser extent women of childbearing age, evolved to avoid ingesting them. However, during the course of human evolution many adolescents and adults reaped net benefits from regulated intake of plant neurotoxins.
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Addiction is a person-level phenomenon that involves twin normative failures. A failure of normal rational effective agency or self-control with respect to the substance; and shame at both this failure, and the failure to live up to the standards for a good life that the addict himself acknowledges and aspires to. Feeling shame for addiction is not a mistake. It is part of the shape of addiction, part of the normal phenomenology of addiction, and often a source of motivation for the addict to heal. Like other recent attempts in the addiction literature to return normative concepts such as "choice" and "responsibility" to their rightful place in understanding and treating addiction, the twin normative failure model is fully compatible with investigation of genetic and neuroscientific causes of addiction. Furthermore, the model does not re-moralize addiction. There can be shame without blame.
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Individuals suffering from substance use disorders often show severely impaired social interaction, preferring drugs of abuse to the contact with others. Their impaired social interaction is doubly harmful for them as (1) therapy itself is based and dependent on social interaction and as (2) social interaction is not available to them as an "alternative", i.e., non-drug reward, decreasing their motivation to stop drug use. We therefore developed an animal experimental model to investigate the neurobiology of dyadic social interaction- vs. cocaine reward. We took care to avoid: (a) engaging sexual attraction-related aspects of such a social interaction and (b) hierarchical difference as confounding stimuli. The cocaine- or social interaction stimulus was offered - in a mutually exclusive setting - within the confines of a conditioned place preference (CPP) apparatus. In our paradigm, only four 15-min episodes of social interaction proved sufficient to (i) switch the rats' preference from cocaine-associated contextual stimuli to social interaction CPP and (ii) inhibit the subsequent reacquisition/reexpression of cocaine CPP. This behavioral effect was paralleled by a reversal of brain activation (i.e., EGR1 expression) in the nucleus accumbens, the central and basolateral amygdala, and the ventral tegmental area. Of relevance for the psychotherapy of addictive disorders, the most rewarding sensory component of the composite stimulus "social interaction" was touch. To test our hypothesis that motivation is encoded in neuron ensembles dedicated to specific reward scenarios, we are currently (1) mapping the neural circuits involved in cocaine- vs. social-interaction reward and (2) adapting our paradigm for C57BL/6 mice to make use of the plethora of transgenic models available in this species.
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Normative thinking about addiction has traditionally been divided between, on the one hand, a medical model which sees addiction as a disease characterized by compulsive and relapsing drug use over which the addict has little or no control and, on the other, a moral model which sees addiction as a choice characterized by voluntary behavior under the control of the addict. Proponents of the former appeal to evidence showing that regular consumption of drugs causes persistent changes in the brain structures and functions known to be involved in the motivation of behavior. On this evidence, it is often concluded that becoming addicted involves a transition from voluntary, chosen drug use to non-voluntary compulsive drug use. Against this view, proponents of the moral model provide ample evidence that addictive drug use involves voluntary chosen behavior. In this article we argue that although they are right about something, both views are mistaken. We present a third model that neither rules out the view of addictive drug use as compulsive, nor that it involves voluntary chosen behavior.
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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
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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.