Challenging the brain disease model of addiction: European launch of the addiction theory network

Introduction

In February 2014, the journal Nature published an editorial concerned primarily with the attempt by animal rights activists to close down addiction research labs that experimented on animals (Animal Farm 2014). The editorial also stated that drug addiction was ‘a chronic relapsing disease that changes the structure and function of the brain’ and that this was not ‘particularly controversial, at least among scientists’ (p. 5). Derek Heim wrote a letter to the journal protesting against these assertions and, with the assistance of Nick Heather, succeeded in obtaining the signatures of 94 addiction scholars and researchers from around the world. An abbreviated form of the letter was published in Nature (Heim 2014). It disagreed with the one-dimensional portrayal of addiction in the editorial and the claim that this was uncontroversial among scientists, further arguing that ‘substance abuse cannot be divorced from its social, psychological, cultural, political, legal and environmental contexts: it is not simply a consequence of brain malfunction’ (p. 40).

Then, following a vigorous defence of the brain disease model of addiction (BDMA) by its most prominent supporters (Volkow and Koob 2015; Volkow et al. 2016) against criticisms by Hall and colleagues (Hall et al. 2014, 2015), Heim and Heather contacted the letter signatories to ask whether they would be interested in joining a group, to be known as the Addiction Theory Network (ATN), with the aims of opposing the dominant influence of the BDMA and collaborating to develop alternative ways of understanding and responding to addiction. A high proportion agreed and others have subsequently joined. At the time of writing (27 June 2017), membership stands at 91. The network activity consists mainly of a google group https://groups.google.com/forum/#!forum/addictiontheorynetwork but there is also a ResearchGate project https://www.researchgate.net/project/Addiction-Theory-Network and a Twitter account (@AddictTheoryNet).

The exact organisational form and structure the ATN will take and the range of activities it will engage in is still developing and under discussion. However, occasional face-to-face meetings are considered essential. The first such meeting was the European launch of the network by means of a symposium held at the Annual Conference of the New Directions in the Study of Alcohol Group in Weston-super-Mare, Somerset, UK on 12 May 2017. The symposium was chaired by Professor Betsy Thom of Middlesex University and a panel discussion following the presentations was moderated by Derek Heim. There were six presentations, each of which is summarised by its author(s), in the order in which they were delivered at the conference, in the present editorial.

If obesity is also a brain disease, what are the implications for the brain disease model of addiction?

Matt Field

Nora Volkow, one of the most high-profile proponents of the BDMA (Volkow et al. 2016), has argued that obesity should be considered a brain disease that shares many features with the addiction brain disease (Volkow et al. 2008, 2013). The central tenets of the brain disease model of obesity are that, in vulnerable individuals, consumption of energy-dense food results in powerful momentary increases in dopamine activity in the reward system. This eventually overrides homeostatic control mechanisms that govern food intake and leads to a number of enduring changes in brain structure and function, resulting in loss of control over food intake. The brain disease model of obesity is supported by observations that obesity is characterised by structural and functional changes in regions of the brain that underlie reward sensitivity, incentive motivation, and self-control, and that these changes are largely indistinguishable from those seen in the ‘addicted brain’ (Volkow et al. 2008, 2013).

This is an interesting development. The most influential neurobiological models of addiction (i.e., ‘brain disease’ models) emphasise that the functional or structural changes in the brain that underlie the transition from recreational drug use to addiction occur after repeated consumption of addictive drugs (alcohol, nicotine, cocaine, opiates etc.), but are not an inevitable consequence of repeated consumption of all rewards, including natural rewards such as food, warmth and sex (Robinson and Berridge 1993; Koob and Le Moal 1997; Goldstein and Volkow 2002). Therefore, the suggestion that similar brain changes may, in fact, also arise after repeated exposure to food represents a quiet abandonment of those earlier claims that there is something special about addictive drugs that leads to brain disease if vulnerable people consume them in sufficient quantities.

There have been challenges to the claim that obesity should be characterised as a brain disease, including observations that brain responses during anticipation and consumption of food, and differences in brain function between obese and normal weight individuals, are not consistent across studies and do not offer strong support for claims that energy-dense food is ‘addictive’ or that obesity should be characterised as a brain disease (Ziauddeen et al. 2012). However, I argue that these attempts to frame obesity as an addiction-like brain disease expose a more fundamental weakness in the BDMA. We could accept that both addiction and obesity are characterised by changes in the structure and function of the brain, and that these changes reflect a consequence of chronic exposure to rewarding, pleasurable stimuli that in turn increase the motivation to consume those rewards whilst reducing the ability to control behaviour. But if these brain changes are indeed an inevitable response to the repetition of pleasurable acts (rather than something specific to addictive drugs), then the more parsimonious explanation is that they are a completely ‘normal’ and predictable reorganisation of the structure of the brain and change in its function, rather than hallmarks of a ‘disease’. This is the argument favoured by Marc Lewis which can account for the brain changes that characterise addiction, overeating, and all manner of behavioural addictions such as problem gambling (Lewis 2017).

Challenging the brain disease model of addiction from a recovery perspective

David Best and Anna Kawalek

The American National Institute on Drug Abuse (2008) states that addiction is a chronic, relapsing brain disease characterised by compulsive drug seeking and use, despite harmful consequences. While this biology-based definition of addiction aims to ‘alleviate the moral judgement, discrimination and stigma associated with drug use’ (Seear 2017, p. 1), evidence suggests that the BDMA has only furthered the stigma associated with addiction, leaving addicts increasingly vulnerable to exclusion and marginalisation (Heather 2017b).

The emergence of a recovery paradigm has challenged the conceptualisation of addiction as a biologically-driven phenomenon rooted in human pathology. Evidence indicates that recovery is a social experience, occurring within social contexts which change recovery experiences at a subjective level, with the emphasis on the social and on strengths. There is a high prevalence of recovery; Sheedy and Whitter (2009) showed that, on average, over half (58%) of alcohol or other drug addicts recover (with variability), whilst in a recent survey of recovery in Canada 51% of participants reported achieving stable recovery at their first attempt in spite of entrenched addiction, challenging both the chronic and the relapsing components of the model (McQuaid et al. 2017).

There is also evidence that recovery is more than simply the reversal of addiction. Hibbert and Best (2011) demonstrated that those in long-term recovery were ‘better than well’ with higher life quality following recovery than ‘typical’ non-addict populations, challenging the idea that recovery is a return to a homeostatic zero (Lewis 2017). Similarly, the Life in Recovery Survey showed that, of those in stable recovery, 79.4% are engaged in meaningful activities; this made them twice as enmeshed within the wider community than individuals not in recovery (Best et al. 2015). Recovery is ultimately not about reversal of pathology but the growth of wellbeing as an intrinsically social process that is embedded in local communities.

It is not only the developmental pathway of recovery but the mechanisms of change that challenge 'brain disease' as a sufficient explanation for recovery (irrespective of the utility of the BDMA in explaining onset). Kelly (2017) has argued that, not only is Alcoholics Anonymous strongly associated with positive recovery outcomes, but that this peer-delivered mutual aid approach works primarily through its impact on social networks (for men) and changes in abstinence self-efficacy (for women). This is consistent with a social identity approach showing that recovery initiation and maintenance are most strongly explained by the transition from using to recovery groups. This is consistent with a re-analysis of Project MATCH data (Longabaugh et al. 2010) and is predicated on the transition in norms, values and beliefs associated with switching from using to recovery-oriented social groups.

Not only does the success of mutual aid and peer-supported pathways challenge the idea of biological determinism in addiction, it also challenges the implicitly moral argument of partial determinism in which addicts are 'lesser' in their choices resulting from the draining of will and volition that addiction is perceived to cause. ‘Recovery’ also contributes to the challenge to the BDMA in the sense that, as well as characterising a personal experience, it summarises a pre-figurative political movement that resists medical labelling and the power of pharmaco-solutions in a latter-day version of anti-psychiatry. Recovery is a contested concept but one that shifts the timeline of addiction understanding, its locus and its mechanisms and that promotes self-determination and strength-based choices.

Bioethical implications of the brain disease model of addiction

Frederick Rotgers

Modern bioethics rests upon four basic principles of practice: respect for autonomy, nonmaleficence, beneficence, and justice (Beauchamp and Childress 1989; Childress 1997). Of these, respect for autonomy tends to trump the others when it comes to situations involving whether or not a person should receive treatment for addiction, and whether or not addicts are competent to make decisions about various aspects of their lives. The principle of respect for autonomy states that in any decision-making on the part or on behalf of an individual, specifically in clinician-patient relationships, the clinician’s duty is to respect the autonomous choice of the patient. Autonomous choice can be defined as ‘personal rule of the self by adequate understanding while remaining free from controlling interferences by others and from personal limitations that prevent choice’ (Faden and Beauchamp 1986, p. 6, emphasis added). This definition implies that clinicians should only withhold decisional power from individuals who suffer from either external control or personal limitations that prevent them from making adequate decisions that are consistent with personal values (Childress 1997).

The BDMA as proposed by Leshner (1997) and Volkow and colleagues (Volkow et al. 2016) has the basic tenet that repeated substance use leads to brain changes that render the individual incapable of making certain types of decisions and choices effectively. In essence, the BDMA suggests that addiction prevents addicts from making a variety of decisions about their lives, especially ones involving whether or not to use drugs at any given time. This view invites paternalism by treatment providers and others who view the addict as requiring treatment that he/she might not wish to undergo, but as incapable of effectively deciding to accept a treatment recommendation (Vandeveer 1986). This raises the question of the extent to which addicts are actually incapable of making decisions about their lives, the extent to which addiction actually prevents such decision-making, and how we are to ascertain when and whether addiction had rendered the individual incompetent in this way. It is clear from widely replicated research findings that most addicts clearly are not incompetent in this way—that is, most ultimately make effective decisions about their substance use in the context of personal values that emerge at some point in time and outweigh the value of drug-taking (see Heyman 2009). Heyman notes the experience of William Burroughs who, when his family declined to further support him financially, and unwilling to work at a traditional job, stopped taking drugs (Heyman 2009). The BDMA also raises questions about whether an addict has the capacity to effectively make decisions about other aspects of life that might intersect with decisions about drug-taking, e.g. finances, entry into contracts, etc., further inviting a paternalism that risks becoming coercive and disrespectful of individual autonomy.

Arguably, a fully-fledged acceptance of the BDMA could result in increased violation of addicts’ civil and human rights in the name of beneficence. Additionally, so doing may, given the toxicity of some treatments for some individuals, result in harm to the addict by virtue of creating a negative view of treatment that results in further reluctance to seek help for addiction. Such an outcome would clearly be in violation of the principle of nonmaleficence (Beauchamp and Childress 1989). Thus, in the author’s view, the BDMA raises significant bioethical questions that need to be addressed going forward.

Steering a path through addiction: lessons from tobogganing

Marc Lewis

As a developmental psychologist, I tend to see mental health issues and personality patterns as trajectories that continue to progress and modify their direction (as constrained by their own histories) from within, over the lifespan. Addiction can be viewed as a trajectory that emerges, becomes ingrained, and then in most cases evolves further (people quit or learn to control their use) over time (Lewis 2017).

Indeed, most people in addiction eventually quit, and a majority of those do so without treatment (Heyman and Mims 2017). When treatment is pursued, it is compromised by the dominant medical model of addiction, which tends to ignore the importance of personal empowerment for recovery. The help addicts need isn't medical; it's psychological. Certain cognitive, emotional and social skills are particularly useful for voluntarily steering one's path out of addiction.

In this contribution I explore some of these skills through the use of a metaphor. These skills are similar to those needed to steer a toboggan racing down a hill. What are the parallels between steering one's drug use and one's toboggan run?

1. There is a strong force pulling the path in the present direction. For tobogganing it's gravity – the slope of the hill; for addiction it's habit strength – the recurrence of the addictive urge. The force of gravity translates to speed in tobogganing; the force of habit translates to intensity or duration in addiction. The better we understand these forces, the more easily we can help those whose momentum is propelled by them.

2. Techniques for steering have remarkable similarities. On a toboggan, you'd best use small, subtle movements, like leaning in one direction or sticking your elbow in the snow. If you try a sharp turn, say by leaning too forcefully or thrusting your foot out, you will surely topple. In addiction, it is also useful to apply subtle cognitive tricks, like choosing the street you take home from work to avoid the liquor store, or telling yourself you can get through a day at a time. Gentle self-directed nudges and self-talk work far better than ‘I must never do this again!’ (Snoek et al. 2016). For both tobogganing and addiction, precision and timing are more important than brute force.

3. For both tobogganing and addiction, the contribution of other people – especially those at hand – is critical. Toboggans can be more easily steered when all three or four passengers lean in the same direction at the same time (in sync). In addiction, interpersonal advice, emotional availability, and support work best when they are in sync with the addict's own plans, intentions, and timing. That's why we need to be ready to help when someone is ‘ready’ to quit.

4. Repetition is fundamental to tobogganing and recovery. In tobogganing it's simple – the more runs you make, the more skilled you become. But in addiction, repeated attempts are criticised, especially by those entrenched in legalistic or moralistic positions. Addiction experts remind us that ‘Relapse is part of recovery’ (Witkiewitz and Marlatt 2004). Each time you go through the process of failing, or almost succeeding, you are more likely to try more skilfully next time. Few addicts quit without several tries.

5. For both tobogganing and recovery, self-compassion, self-confidence, and respect and admiration from others help the person keep trying until they get it right. If we were to scorn and denigrate those whose toboggan flips over, they'd be less likely to take another run. So let's respect and encourage addicts who need a number of tries to finally quit.

Risks of being misunderstood when one denies that addiction is best viewed as a brain disease

Nick Heather

Portrayals of addiction rejecting the premise that it is a chronic, relapsing brain disease – for example, that it is better seen as a disorder of choice (Heyman 2009; Heather and Segal 2017) - are frequently misunderstood or misrepresented. Examples may be found in the comments of an anonymous reviewer of an article now published analysing the role of ‘compulsion’ in theories of addiction (Heather 2017a). Some of these misunderstandings and how they may be countered might be paraphrased as follows:

1. The view that addiction is a disorder of choice trivialises a tragic condition and does a huge disservice to the field. There are no logical grounds for concluding that seeing it as a disorder of choice trivialises addiction; no advocate of such a view is unaware of the tragic consequences of addiction.

2. Seeing addiction as a disorder of choice is dangerous because it is close to the moral argument that we in the addictions field have been trying to stamp out for 40 years - that individuals with addiction are bad people who should be punished. Advocates of addiction as a disorder of choice explicitly state that it is not a free choice for which addicts should be blamed and specifically reject the idea that it represents a moral failing (e.g, Heather 2017b). It is conceded that a theory couched in terms of ‘weakness of will’ and self-control may present special difficulties for communication with the general public. Misunderstandings would likely be fuelled by oversimplified, distorted or sensationalist portrayals in the media, including those prompted or taken advantage of by scientists and clinicians with vested interests in the BDMA.

3. The argument that cravings are only sometimes powerful and generally not difficult to resist is blatantly false. Such an argument would be blatantly false if it had been made but those who reject the BDMA repeatedly stress that addictive desires can be abnormally strong and extremely difficult to resist (e.g. Heather 2017a).

4. The Heyman (2009) argument is that addiction self-cures and therefore is not compulsive-like. Yet it is also argued that relapse can occur at any time. So how can one ever be self-cured? The discrepancy between the established fact of high rates of natural recovery from addiction in the general population and its characterisation as a relapsing condition is more apparent than real. Rates of natural recovery are high even though there is evidence that addicts may make many attempts to recover before they eventually succeed.

5. The National Institutes of Health, the American Society of Addiction Medicine and a recent Surgeon General's report make the identical case based on scientific evidence of addiction as a brain disorder. Proponents of the BDMA often defend the model by referring to respected organisations that endorse it but this merely illustrates how influential advocates of the BDMA have been and that it has been unquestioningly accepted in many quarters. But this is not a good reason for dismissing criticisms or alternative approaches. The pronouncements of these august bodies are precisely the views of addiction that should be challenged in the interests of a proper scientific understanding.

It should go without saying that the debate about whether or not addiction is best seen as a chronic, relapsing brain disease should eventually be decided, or at least strongly influenced, by evidence and reasoned debate. Tactics used by supporters of the BDMA are sometimes inimical to this aspiration. It does no good to avoid proper scientific debate by claiming that the issue has already been decided or by implying that raising doubts about the validity of the BDMA is always irresponsible and inevitably dangerous to the health and welfare of persons labelled as addicts.

Testing the brain disease model of addiction

Reinout W. Wiers

The BDMA has been proposed as a summary of the current scientific state of affairs (Leshner 1997; Koob and Volkow 2010; Volkow et al. 2016). This has been disputed by others, emphasising spontaneous recovery even after severe addiction (e.g. Heyman 2009; Lewis 2015). I argue that the BDMA is a testable hypothesis that remains to be (dis)proved.

The BDMA states that addictive behaviours change the brain in various ways, which makes repeated relapse more likely, including changes in reward sensitivity (stronger sensitivity to the rewarding effects of the addictive substance or behaviour, desensitisation of other rewards), stress reactivity and negative affect, and reduced cognitive control and self-regulation. There is strong evidence backing up these hypothesised changes, both from animal and human literatures (Koob and Volkow 2010); the question is whether this proves that addiction is a brain disease. Importantly, it has been claimed that addiction is not just a passing disease like the flu, but a chronic disease like diabetes and chronic hypertension (Leshner 1997). Hence, the BDMA not only states that there are brain changes which occur as one gets addicted (true), but also that these brain changes are chronic and cause relapse. In its strong form this statement is obviously untrue, as pointed out both with epidemiological and historical data (Heyman 2009) and with case-histories of severely addicted people who successfully quit (Lewis 2015). However, this falsifies the strong BDMA (one black swan is enough to falsify the statement that all swans are white), but does not mean a lighter form of the BDMA is not true: addiction severity is a continuum and for severe cases the BDMA may hold true (Berridge 2017; Fenton and Wiers 2017). However, it would then have to be shown that:

1. There are neural changes specifically related to severity of addiction;

2. These changes do not reverse with prolonged abstinence;

3. These changes increase the risk of relapse after a period of abstinence.

At present, none of these claims has been proven beyond dispute. First, many studies have compared brains of addicted people with controls, but any difference could be a risk-marker rather than a consequence; there are no convincing longitudinal studies yet available (Schulte et al. 2014), but this could change in the future with large prospective neuroimaging studies on the way (Imagen, ABCD)¹. The second claim also remains to be proven and, while there are indications of lack of recovery in some functions, there is evidence of recovery in others (Lewis 2017; Schulte et al. 2014). The third claim is likely to be true: a sensitised reward response, strong stress-reactivity, combined with lack of control are likely to contribute to relapse, as do other neurocognitive correlates of addiction such as lack of insight (Goldstein et al. 2009), and reduced ability of voluntary choice (Fenton and Wiers 2017; Wiers et al. 2016). In addition, there can be ‘collateral damage’ strongly related to the addiction (e.g. Korsakoff’s syndrome) which may contribute to relapse (Fenton and Wiers 2016). However, the causal role of these changes with respect to relapse remains to be established beyond doubt. (There is some evidence for a predictive value of cue reactivity (Schacht et al. 2012), but certainly not strong enough at this moment to support BDMA rather than alternative accounts.) In conclusion, the BDMA consists of a number of hypotheses that could be tested for different addictions. It appears premature at best to describe it as the current state of knowledge.

Concluding remarks

It is clear from the six summaries presented above that there are a range of views on what is wrong with the BDMA, both from a strictly scientific perspective and from a consideration of its consequences for the avoidance and reduction of harm due to addiction. Some find that some forms of what is known as addiction are not usefully thought of as brain disease, some that addiction is not just brain disease in the absence of other kinds of determinant, and some that it is not best seen as brain disease of any kind or in any way. At the same time, criticisms come from various vantage points that may seem to have little in common with each other – from philosophy, psychology and behavioural science, social science and even from neuroscience. This is not the place to attempt to identify all the objections to the BDMA that currently exist or might conceivably exist, but the question can be asked, in the midst of this diversity, what is the point of forming a network dedicated to challenging the brain disease model.

Perhaps the best answer to this question is that all adherents of the ATN share an objection to what they perceive as the dogma of the BDMA – the repeated, public pronouncements that science has already clearly established that addiction is a chronic, relapsing brain disease and that it is surprising anyone should continue to doubt the truth of this assertion (Volkow et al. 2016). At the same time, anyone who does voice such doubts is often castigated as reckless and irresponsible, ignorant of the realities of addiction and as potentially placing the lives of addicts at risk. In other circumstances such dogma might be harmless and could be justifiably ignored but the problem is that it is a dogma that has come to dominate public discourse and national policy on addiction, at least in the USA and increasingly, we fear, in other countries of the world. Research linked to the BDMA has also come to swallow up almost all the funding for research on addiction on the planet, resulting in a demise in funding for research on the prevention of addiction and approaches other than pharmacotherapy to its treatment. This self-perpetuating research agenda has also tended to appropriate all available data on neurobiological change in addiction, thus side-lining interpretations that stress neuropsychological development and neuroplasticity in contrast to pathology (Lewis 2017). And the dominance of the BDMA has limited the dissemination of approaches to addiction that are known to be cheap and effective in reducing harm (Hall et al. 2014, 2015).

We therefore see the future tasks of the ATN as the clarification and articulation of the main grounds for criticising the BDMA, and their dissemination both to the scientific and addiction professional communities and to the general public and decision-makers. The network will hopefully provide the opportunity for colleagues in different geographical areas and/or from different scientific disciplines to form collaborations to work towards these ends. While network members may differ in their specific objections to the BDMA, there may also be disagreement on what models of addiction should replace it. Nevertheless, the ATN will hopefully foster collaborations on developing new ways of understanding addiction and their consequences for the prevention and reduction of harm. Lastly, as a counterpoint to the dogma of the BDMA, we will make strenuous efforts to avoid slipping into dogma ourselves. In disputes of this kind, involving fundamental assumptions about human nature and society, it is all too easy to descend into ideological rancour. As scientists, we need to keep in mind Popper’s (1992) admonitions concerning the need for falsifiability in scientific propositions; we must always be willing to say, as clearly as we can, what it would take to change our minds and admit that addiction was, after all, best seen as a disease of the brain. We trust that advocates of the BDMA will do the same from their point of view.

Acknowledgements

Thanks are due to Anthony Moss for useful comments on parts of a previous version of this editorial. We also thank Wulf Livingstone, Betsy Thom and all others who contributed to the success of the symposium held at the NDSAG Annual Conference. The symposium was supported by a Network Grant from Alcohol Research UK.

Disclosure statement

The authors have no conflicts of interest to declare.

Notes

1 See the homepages of these two studies: https://imagen-europe.com/ & https://abcdstudy.org/