I thank the Brains Blog for the opportunity to discuss further some of the issues raised in a special issue of Neuroethics that addressed Marc Lewis’s provocative claim that addiction is not a disorder because the addicted individual’s brain is normal and simply engaged in deep learning of an intense pleasure. Based on my “harmful dysfunction” (HD) analysis of the concept of disorder, I argued to the contrary that addiction is a disorder because the brain was not biologically designed to be reinforced by the kinds of substances and activities that create addiction, and that constitutes a kind of dysfunction. In my comments that follow, I address my fellow bloggers. I apologize ahead of time for any misunderstandings on my part of their claims or arguments. Finally, note that I address the phenomenon of addiction and not the category of people who fall under the supposed “addiction” category of DSM-5 (labeled “substance use disorder” or “behavioral addiction”), which I believe is too broad and mistakenly classifies many non-addicted individuals as addictively disordered (see “Missteps”).

KENT BERRIDGE: Addiction as Incentive Salience

Against all odds, Kent Berridge has found a scholarly sweet spot in the addiction debate. His work is so lucid, thoughtful, and persuasive that all the bloggers found his view to be congenial to their own! In addressing the supposed tension between “disorder” and “choice” models of addiction, Kent hits the nail on the head when he rejects the false dichotomy and says: “Addiction is a brain disease of temptation and of choice itself. Addiction doesn’t replace choice, it distorts choice.” Kent also explains, consistent with my view, that addiction is a disorder because the extreme incentive salience (i.e., salience of cues triggering wanting of drugs) that occurs in addiction is not an expression of any biologically designed function of our mental machinery, so is a harmful evolutionary dysfunction.

Not that Kent steers clear of all trouble. Being a brain scientist, he tries to establish the pathological bona fides of addiction by identifying a mark of pathology of the brain process underlying addiction. Addiction’s “’software pathology’ in craving and behavior” is rooted in “underlying extreme-parameter brain changes that are the ‘hardware pathology’,” consisting of abnormally large dopamine spikes in reaction to drug cues. Such spikes “occur as extreme values of some normal neuronal parameter. It is the extremity of those changes in neural-psychological parameter values that causes problems. Those changes are pathological partly in the sense that hardly anyone else has parameters that extreme.” Thus, addiction incentive-sensitization “pushes a normal brain mechanism to rare and extreme limits – operating outside the normal range” and “amplifies temptation for addicts to a level more intense than most people ever face.” Indeed, “the essence of [addiction] lies in the hyper-reactive response of brain and mind.”

The problem is that the claim that addiction is categorically distinguished by the magnitude of dopamine reactions to cues appears to be in conflict with Kent’s own assertion that the starving individual experiences wanting as intense as the addicted individual’s desire for drugs: “Starve us enough, and we’ll all become food addicts: food would be more tempting than ever before, difficult not to think about when absent and difficult to resist if available. Intense ‘wants’ are a normal feature of human psychology.” Hunger is neither a disorder nor true addiction, so Kent’s example seems to demonstrates that it is NOT hyper-reactivity that defines addictive pathology. Marc Lewis turns this sort of point against the “disorder” model by citing the intensity and cognitive distortions of love to show that addiction cannot be considered a disorder on any of the usual bases (see my response to Marc below).

Hanna also challenges Kent’s “size matters” claim on two grounds. First, in the spirit of the hunger and love counterexamples but based on what little empirical evidence we have that bears on the matter, she suggests that the size of dopamine spikes in addiction are not all that much greater than the spikes during normal-range cravings for food or sex. Second, at a more conceptual level, she argues that even if the spikes are larger and the wanting more intense, a quantitative difference along a dimension doesn’t translate into a qualitative disorder/nondisorder distinction because atypicality is not the same as pathology.

On the basic question of whether pathology must be more intense in circuit firing or phenomenological arousal than normality, the answer is clearly “no.” For example, pathological depression out of the blue may not be more intense than the throes of normal acute grief, and a pathological panic attack while standing in line at the grocery store need not be more intense than the normal anxiety you would feel dangling from a cliff. Beyond Kent’s illuminating empirical observations of dopamine response sizes, there is clearly a piece of the conceptual puzzle of the disorder status of addiction still missing. In my paper, I argued – and Kent also asserted — that it is the inappropriateness relative to the biologically designed triggering and functioning of these responses that makes certain reactions pathology.

Hanna is also, of course, right that atypicality is not itself disorder. However, atypicality can sometimes play an important evidential role in deciding whether a condition is a disorder. This is because certain forms of atypicality can reveal or at least suggest a failure of underlying mechanisms to function as they were biologically designed to function, thus the presence of underlying dysfunction, as in the above depression and panic examples in which emotional responses occur without the triggers that are biologically designed to cause such emotions. In such instances, the magnitude of a reaction is so disproportionate to appropriate contextual triggers that it suggests that something has gone wrong with underlying mechanisms designed to generate proportional emotional reactions.

Kent surely would not disagree upon reflection. Suppose that Marc is correct that passionate sexual love involves dopamine spikes as high and cognitive distortions as dramatic as any that occur in addiction, or Hanna turns out to be right that food and sex yield spikes and distortions comparable to addiction’s, or Kent himself is right that hunger can create addiction-size incentive sensitizations. Even if so, surely Kent would still hold that, say, opioid addiction is a disorder. He implicitly recognizes that there is an evolutionary component to addiction’s disorder status, and I would add that it is the ultimate grounds overriding even the issue of the magnitude of cue reactivity.

Kent (consistent with my own position) points out that addiction works by distorting choice. I think one might suggest two different approaches – I’ll call them the “force” and “field” approaches — to how such distortion works. A force view mimics the dopamine spike idea at the psychological level. It construes the addict’s problem as one of an extremely strong desire (or “want”) intruding on the overall psychological system of relatively stable beliefs and desires. No doubt this is part of the equation. This sort of force metaphor goes back to Plato and of course endured through to Freudian conflictual dynamics.

A “field” view refers to a global transformation of the psychological field’s phenomenology via a transformation of the relative saliences of a great variety of beliefs and desires as well as alterations in the inferential and associational linkages among psychological states. For example, consider Marc’s description of the global alterations in psychological functioning in both love and addiction: “Psychologically, both are characterized by narrowed attention and intense desire, overvaluation of the object of desire, entrapment in the ‘now’ which occludes rational, long-term decision making, impulsive and compulsive phases, and a preoccupation with goals that promote and maintain contact.” Much more than this happens, of course; associative pathways change so that many different things remind one of the beloved, and many cues trigger desire for the beloved. This sort of global alteration of the psychological system occurs transiently in all intense emotions and moods; when you are feeling enraged or terrified or joyously exuberant, some aspects of the world are more salient than usual and you are likely to make markedly different decisions than you usually do. Typical desires also work this way; Kent reminds us that severe hunger causes one to be unable to think of anything other than food, and the world is transformed into a set of potentials for finding food and associations to food. If wanting works by a global transformation of salience and causal links among psychological states, the sheer intensity of specific motives is not the full explanation for what is happening. The difference between these normal emotions and desires versus addiction is that emotions and desires are biologically designed alterations in global cognitive function, whereas addiction interferes with biologically designed functioning.

Allow me a final digression. Kent elsewhere distinguishes liking from wanting, arguing that due to sheer incentive salience one can want something without there being any “liking” driven by expectation of pleasure or reduction of pain. This idea is striking and a little frightening. For example, I incessantly check my iphone during the day, but I don’t feel any distress pushing me to do so and I don’t feel any pleasure or reduction of tension once I do it, it just arises in my mind saliently to do so and I want to do it (i.e., there is a pull to do it), and once I do it I experience a cessation of wanting to do it. In a related vein, I once suggested in a Merleau-Pontian phenomenological spirit (see “Phenomenology”) that action could occur without any motive at all, in some optimizing way in which body related to environment analogous to the formation of a bubble, where a perfect shape emerges without any guiding representation of the final shape just by virtue of the local dynamic interactions of the bits of bubble yielding a complex global result. I imagine pure wanting-based action in response to incentive saliences to be a little like that. An association I have to this is that maybe the wanting versus liking distinction can solve the “paradox of altruism,” that if you act to help another it is always for your own motive and therefore you are gaining some satisfaction out of it and therefore it cannot be fully and genuinely altruistic (see “Altruism”). One way out of this paradox may be to insist that altruism is pure wanting-to-help rather than liking-to-help and thus offers no selfish rewards at all, just action based on altruistic incentive saliences.

HANNA PICKARD: Responsibility Without blame

In my paper, I escaped Hanna’s false dichotomy by describing addictive disorder as a disorder that systematically distorts but does not fully derail the workings of the desire-deliberation-choice system. I think that Kent gets the reply to Hanna closest to exactly right.

Hanna Pickard usefully elaborates her appealing “responsibility without blame” framework for therapeutic intervention and for our attitudes towards addicted individuals more generally. Hanna’s approach was inspired by her experiences in a therapeutic community. It has been standard wisdom in the psychotherapy field since its inception that therapists must treat their patients without blaming them. Yet, the patient is seeking help to change something seen as negative that under usual circumstances might warrant blame or at least disapproval. How a therapist negotiates this dilemma is at the heart of many theoretical developments. Use of theoretical notions like “transference” help. Freud in his papers on technique asserted that psychoanalysis is the invention of a new form of human relationship, and by this I think he had in mind the shifting back and forth between what Strawson (see “Strawson”) called reactive and objective attitudes towards the patient evident in the therapeutic encounter. It is, I suppose, a new kind of human relationship to respond to the patient’s heartfelt declaration of love by neither embracing nor rejecting it (or, like Breuer, fleeing the relationship) but rather by analyzing its meaning as a specimen to fuel the therapy process.

Carl Rogers famously insisted on unconditional positive regard for the client, thus precluding blame. Albert Ellis insisted on evaluating only specific behaviors and never blaming a person (he seems to have embraced a Humean argument that over and above specific actions there is no self to blame, thus “self”-esteem is a conceptual error). I tend to resolve this issue by embracing what I call “Socratic interpretation,” accepting Socrates’s view that all human beings are pursuing their vision of the good. Thus, once one understands an individual’s belief system and desires from the inside, one understands why what they do appears to be good from their perspective. This makes it possible to evaluate a person’s beliefs and desires but not to blame them for their actions given their intentional system. (This view gives rise to vigorous dinner-party conversation about Hitler, etc.) Hanna takes on this hornet’s nest of issues in a deeper and more sustained way than others have before her, and her perspective should find application within psychotherapy training.

To sustain the responsibility-without-blame approach, Hanna rejects the pathology view of addiction because she believes that the pathology view entails that addicted individuals are acting involuntarily and cannot make choices. This would paralyze therapeutic efforts that all the bloggers agree often depend above all on the addicted individual making painful choices. Thus, Hanna sees a pathology versus choice dichotomy in understanding addiction. She argues that in a disorder “the underlying pathology is supposedly the cause of the surface-level symptoms” so “symptoms… are therefore involuntary” because they are “not caused by you but by the underlying pathology.” She concludes that “we can say with certainty that [the category of disorder] doesn’t apply to addiction” because “addicts retain choice and control over drug use in a great many circumstances” and are “responsive to incentives” so addiction “does not override agency.”

The problem with this argument, as Kent also points out, is that it is a fallacy to say that because there is choice and agency, therefore there is no underlying pathology or dysfunction. The dysfunction is in the brain processes that distort the preference function on the basis of which agency and choice are exercised. Choice is pathologically biased or restricted in certain ways but not eliminated, so “choice versus pathology” is a false dichotomy. Hanna seems to be thinking of the symptom as choosing to take a drug or engage in a behaviour, whereas in fact the symptom is the set of background perceptions that shape the likelihood of that choice – which is still nonetheless a choice. All the bloggers agree with Hanna that understanding that the addicted individual has the capacity for choice is critical for a sensible approach to treatment that exploits the addicted individual’s ability to make choices. The difference is that Kent and I see no conlict between choice and pathology.

Is there a paradox in holding both that addiction is a pathological impairment of choice and that making difficult choices is an integral part of escaping addiction? Marc and Hanna go to great lengths to evade this supposed paradox. Perhaps a vivid (to me) analogy would help explain why there is no such paradox in using choice in treating a pathological impairment of choice. At the moment, I am suffering from an excruciatingly painful malady called frozen shoulder, in which the range of motion of my shoulder is severely impaired due to inflammation-caused pain whenever I attempt to move my left arm too much in any direction. The orthopedist’s prescription for physical therapy specified the treatment in one elegant but terrifying phrase: “aggressive stretching.” Now, a medical sophist might argue that there is a tension here: how can I treat my condition by undergoing “aggressive stretching” when the stretching movement involved in the treatment is precisely the function that is impaired and exquisitely painful? Common sense answers that, with courage, one can push the shoulder at the threshold where the pain and movement inhibition occurs to gradually increase the range of motion; one can treat motion impairment by systematically using motion to push back the impairment’s boundaries. Analogously, one can think of addiction treatment as painful “aggressive stretching” of an impaired choice function, where, with courage, a choice disorder is treated by systematic and gradual “stretching” of the individual’s choices in ways that have hitherto seemed impossible. Although choice is malfunctioning, its healthy aspects can be exploited for treatment progress.

Hanna’s statement to the contrary notwithstanding, addiction as it standardly occurs fits well the usual requirement of the classic “sick role” that the condition happens to you and is not a voluntary action. Taking drugs or engaging in gambling are voluntary actions, but having your choice function altered and thus becoming addicted is not a voluntary action or even a series of actions. Becoming addicted in its ontological status is analogous to falling asleep; you can place yourself in the circumstances where it is likely to happen and you can even intend to bring it about as a result of placing yourself in those circumstances, but it is still not in itself an action but rather something that happens to you. You cannot will yourself to be addicted any more than you can will yourself not to be addicted, although of course you can will yourself to engage in actions that bring about your being addicted or non-addicted.

As to the fact, emphasized by Hanna, that circumstances (such as poverty) can influence an addicted individual’s choice, that is not in tension with a disorder attribution. Many disorders are context-sensitive with symptoms that emerge only under certain circumstances. (E.g., my brother had terrible asthma in New York and moved to Arizona where his pathology was no longer triggered to yield symptoms.) Circumstances such as poverty do explain drug use, but they do not explain the development of addiction per se. Like Hanna, Marc also tended to put emphasis on social factors like poverty in the genesis of addiction, but — as I discussed in my paper — when he was challenged by someone who cited the opioid epidemic in the U.S., he retreated from that position. This is because the opioid epidemic, an iatrogenic scourge generated by the decision to widely prescribe opioids for noncancer pain, is destroying middle class intact families and communities that have traditionally not had social problems of the sort appealed to by Hanna. The problem followed not an increase in poverty or other such factors but simply the increased availability of opioid pain medicines to the general population of people with chronic noncancer pain (which includes about a third of the U.S. population).

Hanna in her blog comment, in arguing against an evolutionary pathology approach, mentions work by evolutionary psychologists that argues that perhaps some human ingestion of some addictive substances that evolved in plants as defensive neurotoxins is not entirely an evolutionary novelty for humans and that perhaps we used these naturally occurring substances during our evolution, so our brains are actually evolved to cope with them to some extent. This approach might offer an explanation of the pleasure experienced from certain substances that is different from the standard “hijack” account that it is just an accident that these substances stimulate and take over our reward systems. However, even if this speculative theory turns out to be true, the amounts and purity of currently available substances certainly remains an evolutionary novelty that goes way beyond anything our forebears could generally access to an extent that might have led to selection pressures. So, there is no reason to think that this hypothesis would explain modern addiction-related phenomena as a naturally selected response. The theorists Hanna cites themselves make clear that their approach does not address addiction (e.g., “A caveat: neurobiological theory of drug use usually contrasts initial seeking and use with longer-term phenomena such as drug tolerance and addiction. We focus on initial drug seeking” [Hagen et al.]). Thus, this theory of some level of brain adaptation to certain substances remains consistent with conceptualizing addiction as a disorder, even if the “hijack” notion would require some revising.

Both Hanna and I tend to place considerable responsibility on society at large for the problem of addiction, but with different emphases. Hanna sees unfortunate social circumstances such as poverty and lack of life options as largely explanatory of addiction. I agree that such factors enter into the explanation of behaviors that lead to and maintain addiction, but the primary social factor in addiction is the social creation of evolutionarily novel addictive substances and activities and their active promotion, often for profit. The interaction of these novel stimuli with normal genetic and psychological variation creates vulnerability to specific addictions in subsets of the population. An analogy is to the misguided “blaming” of many individuals who are obese for their overeating. There are a few true genetic obesity syndromes that account for a small percentage of cases of obesity. However, most cases of obesity appear to be due to normal variations in genes regulating fat storage that were adaptive during our evolutionary past interacting with the unprecedented amount of high-calorie food not only easily available to people in a contemporary advanced society but marketed to them in ways aimed at maximizing temptation. In many cases, individuals with the same so-called obesity genes would be fine in an evolutionarily expectable environment of relative food scarcity. Similarly, evolutionarily novel addictive substances and activities are made available by our society and interact with normal-range genetic variation to produce addiction in individuals who would be fine in an evolutionarily expectable environment. Thus, society has a heavy responsibility – and perhaps blame! – for much of the problem of addiction. Offering treatment is not just a matter of compassion but also a matter of justice. This principle seems to be recognized, for example, when localities that allow gambling accept the inevitability of some percentage of the population developing gambling addiction as a result and factor support for treatment into the cost of allowing such activities.

References

Hagen, E. H., Roulette, C. J., & Sullivan, R. J.(2013). Explaining human recreational use of ‘pesticides’: The neurotoxin regulation model of substance use vs. the hijack model and implications for age and sex differences in drug consumption. Frontiers of Psychiatry, 4:142. doi: 10.3389/fpsyt.2013.00142.

Mayberg, H. S., et al. (1999). Reciprocal limbic-cortical function and negative mood: Converging PET findings in depression and normal sadness. American Journal of Psychiatry, 156, 675–682.

Spitzer, R. L. (1981). The diagnostic status of homosexuality in DSM-III: A reformulation of the issues. American Journal of Psychiatry 138, 210–15.

Strawson, P.F. (1962). Freedom and resentment. Proceedings of the British Academy, 48, 1–25.

Wakefield, J. C. (1993). Is altruism part of human nature? Toward a theoretical foundation for the helping professions. Social Service Review, 67, 406-458.

Wakefield, J. C. (2014). The biostatistical theory versus the harmful dysfunction analysis, part 1: Is part-dysfunction sufficient for medical disorder? Journal of Medicine and Philosophy, 39(6), 648-682.

Wakefield, Jerome C. (2015). DSM-5 substance use disorder: How conceptual missteps weakened the foundations of the addictive disorders field. Acta Psychiatrica Scandinavica, 132, 327–334.

Wakefield, J. C., & Dreyfus, H. L. (1991). Phenomenology and the intentionality of action. In E. LePore & R. V. Gulick (Eds.), John Searle and his critics (pp. 259-270). Oxford: Basil Blackwell.