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PART I
What is addiction?
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SECTION A
Conceptions of addiction
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1
THE PUZZLE OF ADDICTION
Hanna Pickard
The orthodox conception of drug addiction1 within science and medicine is a neurobiological disease characterized by compulsive drug use despite negative consequences (cf. NIDA 2009; WHO 2004). This conception depends on three core ideas: disease, compulsion, and negative consequences. Yet the meaning of the ideas of disease and compulsion, and the significance of negative consequences, is rarely made explicit. I argue that it is only when the significance of negative consequences is appreciated that the puzzle of addiction comes clearly into view; and I suggest that there are both conceptual and empirical grounds for skepticism about the claim that addiction is a form of compulsion, and agnosticism about the claim that addiction is a neurobiological disease. Addiction is better characterized as involving choices which, while on the surface puzzling, can be explained by recognizing the multiple functions that drugs serve, and by contextualizing them in relation to a host of interacting factors, including psychiatric co-morbidity, limited socio-economic opportunities, temporally myopic decision-making, denial, and self-identity.2
The significance of negative consequences
As characterized by the orthodox conception, codified in diagnostic manuals, and of course widely known, drug addiction has severe negative consequences. These typically include the neglect of other pleasures and interests; the inability to fulfil important social and occupational roles and responsibilities; ruined relationships; the loss of social standing and community; cognitive impairment and mental health problems; physical disability and disease; and, lastly, death (cf. APA 2013; WHO 1992). In addition, addiction can be a source of terrible shame, self-hatred, and low self-worth (Flanagan 2013 and in this volume). From an ethical and public policy perspective, such pain and suffering matters straightforwardly, simply because it demands our help. However, from a theoretical perspective, negative consequences matter because they pinpoint what it is about addiction that demands explanation.
Common sense suggests that if a person knows that an action of theirs will bring about negative consequences and they are able to avoid doing it, then they do. We act, so far as we can, in our own best interests and the interests of others we care for. This is a basic folk psychological rule of thumb for explaining and predicting human action, ubiquitous in our ordinary interaction with and understanding of each other. But this is what addicts seem not to do. Although addiction has severe negative consequences, addicts continue to use drugs. This is the puzzle of addiction: why do addicts keep using drugs despite negative consequences?
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The orthodox conception of addiction offers a parsimonious and powerful solution to this puzzle. To use a common metaphor, the explanation is that addiction āhijacksā the brain, so that addicts lose all control and cannot help taking drugs, despite the consequences and against their best interests. Hence the puzzle of why addicts keep using drugs despite negative consequences can be straightforwardly explained. If addicts could avoid using drugs, they would ā but they canāt, so they donāt. The reason is simple: they suffer from a neurobiological disease that renders use compulsive.
No doubt there are many reasons why the orthodox conception of addiction has become so dominant. These include socio-historical, political, and economic forces (Heyman 2009; Satel and Lillienfeld 2013), arguably alongside a widespread belief that framing addiction as a disease is crucial for fighting blame and stigma and getting addicts the help they need (Volkow et al. 2016; but for critical discussion, see Hall et al. 2015 and Lewis 2015; Pickard 2017b articulates how choice models can combat blame and stigma). But, from a theoretical perspective, the orthodox conceptionās explanatory power is strong evidence in its support: it appears to solve the puzzle of addiction.
Compulsion
The orthodox conceptionās solution to the puzzle has two parts. The first appeals to compulsion to explain use in face of negative consequences. The second appeals to neurobiological disease to explain compulsion.
Consider first the idea of compulsion. There is no agreed definition. But it is standardly understood to mean an irresistible desire: a desire so strong that it is impossible for it not to lead to action. From a folk psychological perspective, we do not ordinarily conceive of our desires as irresistible. Desires may be strong and persistent. It may require sustained effort and concentration not to act on them. Meanwhile, the alternative actions genuinely available to us may be limited and the costs of not acting may be high. As a result, our desires may be hard to resist. In addition, in many circumstances, it may be justifiable not to resist, given the balance of costs for and against acting. But this is not the same as irresistibility. Desires that are hard to resist yet leave us some power to do other than what we desire should we choose: it is possible not to act on them. This possibility is what compulsion removes. Compulsion strips a person of all choice and power to do otherwise. If the desire for drugs is irresistible, then it is impossible for addicts not to use drugs. As Carl Elliott expresses this claim, an addict āmust go where the addiction leads her, because the addiction holds the leashā (Elliott 2002: 48).
The appeal to compulsion understood as irresistible desire is key to the orthodox conceptionās explanation of persistent use in the face of negative consequences. Suppose that, even if the desire to use is hard to resist, it is not irresistible. Then the question of why use persists in the face of negative consequences remains. For, given the severity of these consequences, the difficulty of resisting ā as opposed to the impossibility of resisting ā is not by itself explanatory. We need to know more. The point is not that this cannot be explained; indeed, my aim in what follows is to explain it. The point is rather that the parsimony and power of the orthodox conception to explain the puzzle of addiction depends on an appeal to compulsion understood as irresistible desire. Softening the meaning of compulsion costs the orthodox conception its explanatory force.
Are addictive desires irresistible? Cravings are of course a central component of addiction (Auriacombe et al. in this volume; Robinson et al. in this volume). When access to drugs is limited, the desire for them can be psychologically encompassing and distressing. When there is in addition a state of dependence, withdrawal can cause physical suffering. No one should deny that the desire to use drugs is extremely strong or minimize the very real struggle addicts face not using (for a discussion of self-control, see Henden in this volume). But there is increasing evidence that addicts are not compelled to use. They are responsive to incentives, suggesting that the desire to use is not irresistible.
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Here is a brief review of the evidence. Anecdotal and first-person reports abound of addicts who are diagnosed as dependent (and so suffer withdrawal) going ācold turkeyā (cf. Heyman 2009, 2013a). Large-scale epidemiological studies suggest that the majority of addicts āmature outā without clinical intervention in their late twenties and early thirties, as the responsibilities and opportunities of adulthood, such as parenthood and employment, increase (for a review of these findings see Heyman 2009 and in this volume; but for criticism of this interpretation of the data, see Anthony in this volume). Rates of use are cost-sensitive: indeed, some addicts choose to undergo withdrawal in order to decrease tolerance, thereby reducing the cost of future use (Ainslie 2000). There is increasing evidence that contingency management treatment improves abstinence and treatment-compliance, compared with standard forms of treatment such as counselling and cognitive-behavioral therapy, by offering a reward structure of alternative goods, such as modest monetary incentives and small prizes, on condition that addicts produce drug-free urine samples (Zajac et al. in this volume). Experimental studies show that, when given a choice between small sums of money and taking drugs then and there in a laboratory setting, addicts will often choose money over drugs (Hart et al. 2000; Hart 2013). Finally, since Bruce Alexanderās classic āRat Parkā experiment (Alexander et al. 1978, 1985), animal research on addiction has convincingly demonstrated that, although the majority of cocaine-addicted rats will escalate self-administration if offered no alternative goods, they will forego cocaine and choose alternative goods, such as sugar, saccharin, or same-sex snuggling, if these are available (Ahmed 2010; Zernig et al. 2013).
This evidence is strong, but we need nonetheless to be careful in drawing conclusions. There is a basic, common-sense distinction between what a person can do but wonāt (because they are not motivated) and what a person wants to do but canāt (because they lack the ability) (Pickard 2012, 2017a). The evidence shows that the majority of addicts have the ability to refrain from use in many ordinary circumstances. But it does not demonstrate they have the ability in all possible circumstances. The attribution of an ability to refrain from use is consistent with there being occasions where, due to any variety of constraints, it cannot be exercised. Nor does the evidence demonstrate beyond doubt that the minority of addicts who do not respond to incentives have the ability to refrain but donāt exercise it, rather than not having the ability at all. In the absence of any clear marker between different sub-groups of addicts that would explain the difference between the majority who refrain and the minority who donāt, the evidence suggests the latter are like the former in having the ability and unlike them in not exercising it, but it does not conclusively establish this. Finally, there is the important question of how to understand conflicting self-reports from addicts, who often oscillate both intra- and inter-personally between using the language of compulsion and the language of choice (for discussion see Booth Davies 1992; Pickard 2012, 2017a). For all these reasons, caution is needed in interpreting the evidence. Nonetheless, our understanding of addiction should reflect what the evidence clearly does show, namely that, for many addicts, on many occasions, they are not compelled to use. For this reason, an appeal to compulsion understood as irresistible desire cannot be the fundamental explanation of the puzzle of persistent use despite negative consequences. It is simply not true, of too many addicts, too much of the time.
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Neurobiological disease
Consider now the idea of disease. What does this mean? Our ordinary concept of disease is complicated, as well as having important social and personal consequences in our culture, including a claim to care and a removal of responsibilities in virtue of occupying āthe sick roleā (Parsons 1951). But, in simple terms, it typically invokes the idea of underlying pathology as the cause of observable surface-level symptoms and suffering. For example, consider the way core symptoms of Parkinsonās Disease, like tremor and slow movement, are caused by brain degeneration. With respect to addiction, the surface-level symptom is drug use, and the suffering is the negative consequences thereby caused. In characterizing addiction as a neurobiological disease, the orthodox conception explains this symptom (and hence the consequent suffering) by appeal to underlying brain pathology. Addicts use drugs because something is wrong with their brains.
The ordinary concept of disease therefore invites an appeal to compulsion because prototypical symptoms of diseases are passive occurrences ā things that happen to us rather than things we do. But it is possible to reject the claim that drug use is compulsive while yet maintaining that addiction is nonetheless a neurobiological disease. Addiction could be a ādisease of choiceā if the neural changes and processes underlying drug choices that are found in addicts are pathological (Berridge 2017).
It is important to be clear that long-term heavy drug use has chronic effects on the brain (Zilverstand et al. in this volume). Drugs directly affect levels of synaptic dopamine as opposed to affecting them only indirectly via the neural states and processes sub-serving learning and reward. This can explain why cues associated with drugs trigger a desire that over-estimates their anticipated reward and hence is unusually strong in its motivational strength (Redish et al. 2008; see too Levy in this volume). Over time, wanting drugs may even come apart from liking them: cues may trigger cravings and strongly motivate drug-seeking and drug-taking, even though drug experience offers less pleasure than it initially did or than appears commensurate with the desire to use (Robinson et al. in this volume; cf. Holton and Berridge 2013). In line with what was argued above, these neural changes and processes do not establish that the desire for drugs is irresistible and use is compulsive. Rather, they explain (among other things) the intensity of the desire. But are they pathological?
The answer is that we do not yet know. Just as we cannot infer irresistibility and impossibility from descriptions of underlying neural states and processes, so too we cannot infer pathology. On the one hand, from a theoretical perspective, there is no agreed understanding in philosophy or in medicine of what makes a state or process pathological. However, this much is clear: deviation, however extreme, from the statistically average states and processes characteristic of any relevant level of explanation, whether that is personal-level, cognitive-psychological, or neurobiological, is not enough. Atypicality is neither necessary nor sufficient for pathology, as there is tremendous variation between individuals and some pathologies are near universal (cf. Boorse 1977). Rather, we need an account of the nat...
