WHAT’S WRONG WTH THE BDMA?
By Nick Heather PhD
On behalf of the Addiction Theory Network
The inadequacies of the brain disease model of addiction (BDMA) have been well described in many influential publications, some of which are given in the ATN Reading List available on this site. Criticisms of the model may also be found in the ATN book, Evaluating the Brain Disease Model of Addiction (Routledge, 2022), especially in Section II (Against the BDMA) but also in Section IV (Alternatives to the BDMA). Here I will attempt merely to summarize my own view of some of the leading criticisms of the BMDA. Although no citations are provided to the claims made here, all assertions of fact can be supported by references to published evidence. This evidence can be found in the works provided by the ATN Reading List and the ATN book.
What is the question?
In the critique of the BDMA, the key question is not whether addiction is or is not a brain disease but whether addiction is best regarded as a brain disease. This is because there is no universally accepted definition of ‘disease’; to debate whether or not addiction is a disease, including whether it is specifically a brain disease, risks becoming involved in an insoluble dispute.
The better question of whether or not addiction is best regarded as a brain disease breaks down into a consideration of the consequences of doing so. There are three types of consequences that come into play: a) for progress in the scientific understanding of addiction; b) for a more benign public understanding of and response to addiction; c) for the development of more effective treatment and prevention of addictive disorders. Evidence relevant to these three types of consequences must be taken into account in deciding whether or not addiction is best regarded as a brain disease.
What is not being denied
In criticising the brain disease model of addiction, it is important to be clear about what is not being denied, as this frequently leads to misunderstanding:
- In criticising the brain disease model, it is not being denied that addictive behavior has serious and often tragic consequences for the individual in question, for their loved-ones, and sometimes for society at large. Human behaviour can have very serious consequences without necessarily being seen as a disease;
- It is not being denied that the medical profession should be centrally involved in the response to addiction. This is because, although it may not be best seen as a disease in itself, addictive behavior causes diseases, so the medical profession must be closely involved in the response to the harm of addictive behaviour to the individual, i.e., in treatment. There is also no reason why medical practitioners should not engage in the attempt to modify addictive behaviour, as they currently do;
- In criticizing the brain disease model, it is not being denied that people with substance use problems should be treated with compassion and respect. It is frequently stated by supporters of the BDMA that the only alternative to their model is to revert to blaming and punishing addicts (i.e., the so-called ‘moral model’ of addiction) and that this will inevitably follow from abandoning the brain disease model. This is blatantly false. It is possible to have a coherent scientific account of addiction that avoids both the brain disease and the moral model, and that avoids stigmatizing individuals as being solely to blame for their problems.
Is addiction chronic and/or relapsing?
Before proceeding to the alleged deficiencies of the BDMA per se, it will be helpful to comment on two points of partial agreement - that addiction is a chronic condition and that it is a relapsing condition, as frequently asserted by NIDA and other authorities.
Chronic: addiction can be chronic but typically is not. There is now a very large amount of evidence, from nation-wide, population-based surveys that addictive disorders are time-limited and that most people with addiction recover without treatment. It is true that those who enter treatment take longer to recover but this may be because of high psychiatric comorbidity rather than severity of addiction per se, though this issue is urgently in need of research attention. It is obvious that some of those meeting criteria for addiction do not recover but it is an example of circular thinking to conclude that this is because it is impossible for them to recover in principle.
Relapsing: addiction is certainly relapsing and its relapsing nature is definitional. Addiction is defined by a difficulty in maintaining desired changes in behaviour. But this is still consistent with saying that addiction is not a chronic disorder. Histories of addiction careers typically show several, even many, unsuccessful attempts to quit or cut down before eventual success. In other cases recovery occurs after only a few attempts.
Two main criticisms of the BDMA
We come now to the main grounds for rejecting the BDMA as an adequate explanation of addiction. These are two in number:
1) Addictive behavior is voluntary and intentional.
The puzzle of addiction is that those we call addicted behave in ways they know to be harmful to themselves and others, and that they frequently wish to be rid of their addiction. In common with any kind of disease explanation of addiction, the BDMA assumes that addicts behave in this way because addictive behavior is compulsive, i.e., ‘against the will’ of the person concerned. In contrast to this fundamental assumption of the BDMA, there is now a very large amount of evidence that addictive behavior, rather than being compelled, is voluntary and intentional at the time it occurs (though running counter to previous commitments).
There is sometimes confusion here between the terms ‘voluntary’ and ‘intentional’. ‘Voluntary’ means under conscious control, while ‘intentional’ means goal-directed in the sense of being driven by the expected beneficial effects of the drug. The claim is that addictive behavior is both. It is important to clarify here that describing a behavior as voluntary (consciously controlled) and intentional (goal-directed) does not mean that the decision to engage in the behaviour was made ‘entirely freely’, i.e., without being caused by forces the individual may or may not be aware of. We are all constantly subject to a range of factors which influence our decisions; some decisions might satisfy short-term goals at the expense of achieving longer-term goals (e.g., drinking alcohol to alleviate withdrawal symptoms, despite a longer-term goal to abstain).
The main lines of evidence relevant to this question are as follows:
- Studies of operant behavior in persons labelled as addicts. There is an enormous body of experimental evidence to show that the addictive behavior of those regarded as addicted to alcohol or to cocaine is operant behavior, i.e., behavior that is determined by its environmental consequences. The particular reinforcement contingencies applying to the consumption behavior of chronic addicts obviously show differences from those applying to non-addicts – self-evident from the existence of markedly different consumption practices. But what these findings show is that, rather than being qualitatively different and compelled, addictive behavior is subject to the same general laws that govern goal-directed, voluntary behaviour of any kind.
- Addictive behavior is responsive to cost. For example, much evidence from economic surveys shows that raising the prices of cigarettes reduces consumption and, generally speaking, when smokers' incomes rise they smoke more. At the same time, compliance among nicotine addicts with smoking restrictions, like bans on indoor smoking, is generally high, which would not be the case if urges to smoke were truly irresistible and compulsive.
- Success of contingency management programs. As shown by a large number of randomised controlled trials, the most efficacious method of treatment for addictive behaviors is contingency management (CM), based on principles of operant conditioning. Studies of CM programmes with physicians, airline pilots and other professional groups have reported remarkably successful results, but high rates of recovery have been obtained too among much less privileged groups including those with psychiatric comorbidity. This evidence further supports the conclusion that addictive behavior is not impervious to its environmental consequences and is rather voluntary and goal-directed behavior.
- The flexibility of addictive behavior. The idea of compulsion implies that addictive behavior is inflexible, stereotyped and unreflective. However, qualitative studies of heroin addicts find that they are typically self-respecting and self-determining individuals who actively confront and purposefully respond to external constraints and life opportunities.
- The Vietnam Veterans follow-up study. This famous research study overturned preconceptions about the compulsive nature of addiction. Towards the end of the Vietnam war, the US government became alarmed about reports that a large proportion of American servicemen in Vietnam were addicted to heroin or other drugs. A team of researchers was commissioned to interview a large sample of men in Vietnam to determine the extent and characteristics of their drug use, and then to follow them up on their return to the US after discharge in 1971. Against all expectations, the great majority of those followed-up had simply ‘given up’ addiction. This did not occur because drugs were unavailable after return home; interviewees reported that they knew how to obtain heroin and some had occasionally, but not regularly, used. This evidence is simply incompatible with any notion of a biological disease characterized by compulsive drug use.
- Evidence on ways in which addicts recover. In research on reasons for recovery from addiction, it is reported time and again that the main determinants are environmental and personal changes, e.g., marriage, family, occupation, health, finance. There is also typically a ‘cognitive appraisal’ in which the initiation of change is preceded by a process of weighing up the advantages and disadvantages of changing substance use and thereby becoming committed to change. Again, this evidence is inconsistent with addiction being driven by an underlying compulsion.
In considering the evidence above, and although there is no universally-accepted definition of disease or brain disease, it might be asked whether there is any reasonable understanding of ‘brain disease’ that can accommodate this evidence. In other words, it may be helpful to ask whether the characteristics of addiction, as revealed by the evidence reviewed above, resemble the characteristics of established brain diseases - like Alzheimer’s disease or other types of dementia, Parkinson’s disease, and various forms of epilepsy - about which there would be wide agreement among scientists, health professionals and the general public that they were bona fide brain diseases. The answer to this question is self-evidently ‘no’. As a simple illustration of this point, one can ask when was the last time someone with Alzheimer’s disease (or Parkinsonism, or epilepsy, etc.) woke up one morning and decided to quit the disease, as undoubtedly happens occasionally with quitting addiction. To object to this example by arguing that, although the ‘symptoms’ of addiction in addictive behavior may disappear, there is an underlying disease process which continues to exist simply ignores the mountain of evidence showing that most people with addiction recover on their own without treatment.
2) The BDMA disguises the societal causes of addiction.
The other main criticism of the BDMA is that it obscures and mystifies the societal origins of addiction. ‘Societal’ here includes socio-environmental, socio-economic and socio-cultural. This charge is based on the following considerations:
- There is abundant evidence that addiction is strongly associated with socio-economic deprivation and/or socio-cultural dislocation;
- In the BDMA these associations are regarded merely as ‘social factors’ that affect the expression of an underlying brain disease, rather than part of a network of direct causes of addiction;
- Any attempt to reduce rates of addiction must therefore attempt to change the socio-economic or socio-cultural determinants of addiction;
- Thus, rates of addiction are a reflection of the kind of society we live in but the effect of the BDMA is to rule this out of consideration. There is no clearer demonstration of this point than the nature of the current ‘opioid crisis’ in the USA.
The immediate consequence of these observations is that the response to addiction, as well as being a medical, psychological and sociological issue, is essentially a political issue. If, for example, rates of addiction are caused by high rates of poverty and inequality in society, as the evidence seems to suggest they are, then the effort to reduce rates of addiction must involve the reduction of poverty and inequality.
There is another important point. The two main criticisms of the BDMA that have been listed here – that addictive behavior is voluntary and intentional rather than compelled and that the BDMA disguises the societal causes of addiction – are not inconsistent with each other. Indeed, it is only by regarding addictive behaviour as voluntary and intentional that socio-economic and cultural causation can come into play in our explanations of it. If it were an automatic, compulsive phenomenon, it is difficult to see how addictive behaviour could by influenced by economic, social and cultural factors; once it is seen as voluntarily chosen, it can immediately be seen as subject to influence by social norms, learned expectations, cultural traditions etc. This greatly extends the range of potential causative factors that have to be considered in a novel understanding of addiction beyond the disease tradition.
The usual rejoinder: evidence from neuroimaging proves that addiction is a brain disease
Having reviewed some of the evidence suggesting that addiction is not best seen as a brain disease, we must now consider the almost reflex response to this evidence by those who favour the BDMA. The argument is that addiction must be a brain disease because evidence from neuroimaging (fMRI or PET) shows that the brains of addicts are different from non-addicts, especially if they have consumed drugs for a long period of time. The evidence typically consists of colorful illustrations of the brains of drug takers compared with those who do not take drugs and the finding of differences in brain structure and/or activity level (inferred brain function) between the two groups. This ‘proof’ of the BDMA is frequently accepted by members of the general public and by many practitioners and scientists in the addiction field too. However, the assumption that the brain differences play a causal role in addictive behaviour is unfounded for the following reasons:
- Methodological problems. There are considerable methodological problems associated with the neuroimaging research in question. These include lack of replication of findings, small sample sizes and low statistical power, inappropriate selection of control groups, failure to control for pre-existing differences between experimental and control groups, questionable interpretation of results, and lack of demonstrated relationships between neurological and cognitive/behavioural measures. There is also a strong pressure to publish any result to justify the high cost of neuroimaging research to public or university finances.
- Illegitimate causal inference. Even accepting the validity of the evidence demonstrating differences between the brains of ‘addicts’ and ‘non-addicts’, the question arises whether these differences can be interpreted as causing addictive behaviour. For this causal inference to be made, it is obviously necessary that a relationship between brain changes and behaviour can be demonstrated to exist over time. However, nearly all the existing neuroimaging evidence refers only to a single point in time; the brains of addicts are compared with those of non-addicts on a single occasion but not thereafter. This kind of evidence can, at best, establish only correlation, not cause, and is unable to distinguish between whether drug use caused the brain changes, whether the brain changes cause addiction, or whether the brain changes are caused by some other variable that differs between drug users and non-users (for example, childhood nutrition, childhood trauma, psychiatric comorbidity etc.).
- The brain changes all the time. Once again, for the purposes of this argument, let us assume that some causal link between changes in the brains of addicts and observed addictive behaviour has been shown. Does this make addiction a brain disease? A clear demonstration that changes to the brain need not betoken brain disease comes from a study in which structural MRIs of the brains of licensed taxi drivers in London were compared to those of control subjects who did not drive taxis. The main finding was that the posterior hippocampi of taxi drivers were significantly larger than those of the controls. (The posterior hippocampus is known to be the area of the brain responsible for storing a spatial representation [maps] of the environment.) The conclusion is that changes to the structure of the brain are insufficient in themselves to warrant the attribution of brain disease, for no-one would presumably wish to claim that intimate knowledge of London streets was a symptom of a brain disease! With regard to addiction, the alleged brain changes in ‘addicts’ can be considered a normal brain adaptation to the effects of psychoactive drugs. The attribution of brain disease must be based on other grounds than the mere demonstration of differences in brain structure and function between drug users and non-users.
- Even if brain changes among ‘addicts’ play a causal role in addictive behavior, they are likely to be part of a complex network of causal determinants. A point related to the previous one is that, even if it is accepted that repeated ingestion of psychoactive drugs causes brain changes that increase desire for drug effects, these causal influences are likely to be one component in a complex system of interacting causal factors that include psychological, interpersonal, social, environmental, and cultural variables. On this more complex account, intervention should not necessarily be directed at the brain changes, as BDMA theorists often insist, but rather at the earlier social risk factors that initiated the cascade of harms that culminated in addiction.
- The question is not whether drugs change the brain but whether they change the brain so that drug use is no longer voluntary and intentional. Finally, the crucial question here is whether evidence on brain changes in addiction from neuroimaging research solves the puzzle of addiction by demonstrating that those brain changes remove the possibility of choice and make drug seeking and use compulsive. To date, there is no evidence whatever that they do.
The BDMA does not reduce stigma and may actually increase it
Turning now to consequences of the BDMA for a more benign public understanding of and response to addiction, it should be acknowledged that the disease concept has been responsible over the years for diverting addicts from prison to treatment and that this is unequivocally a good thing. However, it is frequently claimed by enthusiasts for the BDMA that it reduces the stigma of addiction among the general public and professional workers, and that this is one of its major benefits. Is this true?
- There is good evidence that expressed endorsement of the disease model of addiction is only ‘lip-service’, i.e., that it has few or no implications for a humane and compassionate response to addicts;
- Other evidence indicates that biogenetic and neuroscientific explanations of addiction result in the attribution of less blame to addicts but, at the same time, lead people to regard addicts as being dangerous, to desire for social distance from them, and to have less faith in their potential to recover. That someone has a disease of the brain is surely one of the most frightening and stigmatizing beliefs;
- The claim that the BDMA removes stigma among professional workers, and is therefore of benefit in the treatment of addiction, is simply not supported by evidence.
The BDMA reduces self-efficacy for changing behaviour and is unhelpful in treatment/self-change
In considering the practical consequences of the BDMA for the treatment of addiction, it should first be noted that addiction is probably ‘a human kind’ rather than ‘a natural kind’, i.e., it is an example of the way in which official classifications of problematic behavior (e.g., the diagnosis of brain disease) feed back through society to further influence the behavior of those so classified. Certainly, there is now an enormous body of evidence to indicate the pervasive effects of ‘expectancies’ on human behavior. In support of these generalizations:
- There is good evidence that addicts’ belief in the disease concept of addiction is associated with increased risk of relapse;
- People's belief in their capacity to change is the single greatest factor in psychological and behavioural change (self-efficacy) and is one of the underlying principles of the modern cognitive behavioural therapy, repeatedly shown to be the most empirically well supported model of therapy. The effect of telling people that they have a brain disease is to reduce their self-efficacy for changing addictive behavior.
- It follows from this that what is needed is a radical transformation in communications to the general public about addiction, one in which they are persuaded to believe that breaking free from addiction is possible and told what we know about how this can be successfully accomplished.
Consequences for policies on treatment and prevention of addictive disorders
In terms of the wider consequences of the BDMA for national or local policies on the treatment and prevention of addiction, the following considerations are relevant:
- Since the BDMA began to be promoted in the 1990s, it has simply failed to deliver on its promises for improvements in treatments for addiction;
- The focus of the BDMA on disordered neurobiology in a minority of severely addicted individuals has undermined the implementation of policies which have established effectiveness and cost-effectiveness at the population level, e.g., those aimed at discouraging people from smoking tobacco and drinking heavily;
- Similarly, the pursuit of high technology brain interventions has distracted attention and funding from treatment methods that are cheap and effective but to which most people with addiction do not have access;
- With regard to primary prevention, the focus on the BDMA has distracted attention and funding from how rates of addiction can be lowered by changing the societal conditions giving rise to addiction, e.g., poverty, inequality, lack of life opportunities, etc..
Summary: main limitations of the BDMA
To return to the three types of consequences that must be taken into account in deciding whether or not addiction is best regarded as a brain disease, the following conclusions seem justified:
Limitations for scientific understanding of addictive behaviour
The BDMA cannot accommodate the enormous body of evidence showing that addictive behaviour is intentional and voluntary;
Notwithstanding the possible role of brain changes in the network of causes giving rise to addiction, the BDMA obscures the societal causes of addiction which would otherwise attract more attention as targets for intervention;
Limitations for public understanding of addiction
The BDMA does not reduce stigma towards addicts and may actually increase it.
Limitations for the treatment and prevention of addiction
The BDMA reduces self-efficacy for change among self-changers and clients of addiction treatment;
It also directs attention away from existing methods of treatment and prevention that are effective and cheap;
It obscures the more effective (political) interventions by which rates of addiction may be reduced, i.e., by changing the societal conditions that gives rise to addiction in the first place.