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The Brain Disease Model of Addiction: Is It Supported by the Evidence and Has It Delivered on Its Promises?



Since 1997 the US National Institute on Drug Abuse has advocated a brain disease model of addiction (BDMA). We assess the strength of evidence for the BDMA in animals, neuroimaging studies of people with addiction, and current research on the role of genetics in addiction. We critically assess claims about the medical and social benefits of use of the BDMA because the social implications are often implied as a reason to accept this model. Furthermore, we argue that the BDMA is not supported by animal and neuroimaging evidence to the extent its advocates suggest; it has not helped to deliver more effective treatments for addiction; and its effect on public policies toward drugs and people with addiction has been modest. The focus of the BDMA is on disordered neurobiology in a minority of severely addicted individuals, which undermines the implementation of effective and cost-effective policies at the population level to discourage people from smoking tobacco and drinking heavily. The pursuit of high technology direct brain interventions to cure addiction when most individuals with addiction do not have access to effective psychosocial and drug treatments is questionable.
Professor Wayne Hall PhD.,1,2,3,*, Adrian Carter PhD.3,4 and Cynthia Forlini PhD.3
1. The University of Queensland, Centre for Youth Substance Abuse Research,
Brisbane, Queensland, Australia
2. National Addiction Centre, King’s College London, London, UK
3. The University of Queensland Centre for Clinical Research, Brisbane,
Queensland, Australia
4. School of Psychological Sciences, Monash University, Melbourne, Victoria,
* Corresponding Author:
Professor Wayne Hall
Director, Centre for Youth Substance Abuse Research
Level K, Mental Health Buidling
The University of Queensland
Brisbane QLD 4029
Author Statement: The paper has not been submitted to another journal, and has not
been published in whole or in part elsewhere previously.
Word count: 3613 text; 5653 with abstract and references
Since 1997 a brain disease model of addiction (BDMA) has been promoted by the US
National Institute on Drug Abuse. We assess the strength of the evidence for the brain
disease model provided by animal studies, neuroimaging studies of addicted
individuals, and research on the role of genetics in addiction. We also critically
evaluate the claims made about the medical and social benefits of the brain disease
model because the latter are often presented as implicit reasons for accepting the
model. We argue: that the BDMA is not as well supported by animal and
neuroimaging evidence as its advocates argue; that it has not delivered more effective
treatments for addiction; and that its impact on public policies towards drugs and
addiction has been modest. We also argue that the BDMA’s focus on the disordered
neurobiology of a minority of severely addicted individuals risks undermining
effective and cost-effective population-based policies that discourage the whole
population from smoking tobacco and drinking heavily. We also question the pursuit
of high technology direct brain interventions to “cure” addiction when the majority of
addicted individuals do not have access to effective psychosocial and drug treatments
for addiction.
In 1997, Alan Leshner, then Director of the US National Institute on Drug Abuse
(NIDA), published a paper in Science in which he argued that addiction was best
conceptualised as a chronic, relapsing, brain disease.1 Drug use was initially
voluntarily, but he argued using animal studies that chronic drug use flicked a
neurochemical switch in the brain that made it very difficult for addicted persons to
stop using drugs and thereby explained the high relapse rates among persons treated
for addiction. Researchers at NIDA have since added a substantial number of
neuroimaging studies of addicted individuals which they argue explains how chronic
drug use “hijacks” the brain’s reward systems.2.
Proponents of the BDMA have been very influential in setting the funding priorities
of NIDA, and by extension the bulk of publically supported addictions research. In
1998, Leshner testified that NIDA “supports over 85 percent of the world’s research
on drug abuse and addiction”.3 The American Society of Addiction Medicine has
defined addiction as a “primary, chronic disease of brain reward, motivation, memory,
and related circuitry”.4 In July 2014, newly appointed acting US “drug czar” Michael
Botticelli launched a reformist national strategy with the claim that “decades of
research have demonstrated that addiction is a brain disorder – one that can be
prevented and treated”.5 The BMDA has also been widely promoted in leading
science journals 3, 6 and has recently been endorsed by the leading journal, Nature.7
In the US, advocates of the BDMA have also argued that it will deliver more effective
medical treatments for addiction that will be covered by health insurance and can
thereby be made more readily accessible to addicted persons.1, 2, 6 They have also
predicted that the greater acceptance of the BDMA will reduce stigma by replacing
the common view that addicted persons are weak or bad persons with a more science-
based view that depicts addicted individuals as persons with a brain disease requiring
medical treatment.
In this paper we briefly: (1) critically evaluate the scientific evidence used in
advocating for the BDMA in leading general scientific journals; and (2) assess the
extent to which the BDMA has produced, or is likely to produce, the social benefits
that its advocates claim will flow from its acceptance. The BDMA is not co-extensive
with neuroscience-based explanations of addiction, and our paper is not intended as a
critique of all neuroscience research on addiction. Rather we focus is on a popular
simplification of work in this field that has had a major influence on popular
discourse on addiction in scientific journals and mainstream media.
Search Strategy and Selection Criteria
We searched PubMED, Web of Science and PsycINFO for peer-reviewed papers
describing the brain disease model of addiction by its leading advocates (e.g. Leshner,
Volkow, Koob, Li, O'Brien) and for authoritative reviews of the evidence on animal
models of addiction, neuroimaging studies of addicted persons, studies of the genetic
of addiction and the epidemiology of drug use and addiction. The following search
strategy was employed: “addiction” AND (“neuro*” OR “genetic*” OR “brain” OR
“epidemiolog*”). We also scanned the reference lists of these articles for any key
articles not retrieved by our search strategy. We limited our search to review articles
because it was not our intention to review the entire field of addiction neuroscience
but to identify consensus views in articles published in English between 1990 and the
Evidence for the BDMA
Animal models have played a central role in the BDMA by providing insights into the
effects that chronic drug administration has on brain processes.8, 9 These models have
shown that: rats and other animals will self-administer psychoactive drugs at high
frequencies (e.g. by pressing a lever);9, 10 the drugs that animals will self-administer
are those that are addictive in humans; and self-administration of drugs is reduced by
electrical stimulation of the brain’s “reward centres”.9 Animal models have also
enabled researchers to identify the neural circuitry on which the major drugs of
addiction act, namely the “mesolimbic brain reward system”, which includes the
ventral striatum, nucleus accumbens, amygdala, and frontal cortices. Dopamine plays
a key role in this system.11, 12
These animal models reproduce some key features of human addiction.13 Animals
free access to drugs often increase the frequency and amount of drugs that they self-
administer and work harder to obtain drugs, mimicking the development of tolerance
and dose escalation in humans. They continue to self-administer drugs in the face of
aversive stimuli (e.g. electrical foot shock). If self-administration has been
extinguished, animals will rapidly resume self-administration if they are given painful
stimuli, exposed to cues associated with the drug, or given a priming dose of the
drug.8, 12, 14
Findings from animal studies have been bolstered by neuroimaging studies of the role
of dopamine activation in the reward circuits in “normal” and “addicted” human
6, 15 16 These neuroimaging studies have also identified dopamine-mediated changes in
cortical areas that are correlated with impaired decision-making and poor impulse
control.17, 18 The persistence of many of these changes persist in addicted individuals
after long periods of abstinence is invoked to explain the high rates of relapse in
persons treated for addiction.19
Further support for a BDMA is provided by genetic research on addiction. Twin
studies indicate that genetic factors make a substantial contribution to the risk of
developing alcohol, nicotine and cannabis addiction.20, 21 Estimates of the heritability
of alcohol, nicotine and cannabis dependence range between 40 and 60%.21 Large
scale Genome Wide Association Studies have found correlations between genetic
markers and addiction risk. Risk alleles have been identified that influence drug
metabolism and the effects that drugs have on the mesolimbic reward system,
suggesting that addiction is the outcome of chronic drug use acting on the brains of
genetically vulnerable individuals.20, 21
A Critical Examination of the Evidence for a Brain Disease Model of Addiction
Is Addiction a Chronic Disorder?
Leading critics of the BDMA contest the claim that addiction is a chronic relapsing
disorder by citing epidemiological evidence that the majority of addicted persons
recover without treatment.22-24 Heyman, for example, points out that most persons
who meet diagnostic criteria for dependence in epidemiological surveys are not drug
dependent at the time of their interview, having ceased drug use years before, usually
in the absence of treatment.23 Similar evidence for high rates of recovery was
provided by high rates of recovery in follow up studies of heroin-addicted US
Vietnam veterans.25
Critics also argue that it is difficult to reconcile a strong form of the BDMA with
evidence that addictive drug use is responsive to small changes in consequences.22, 23
For example, receiving small financial rewards or avoiding 24 hours in gaol for
providing clean urine samples, substantially reduce drug use in addicted persons.23, 26
The responsiveness of addictive drug use to these small incentives is hard to reconcile
with the claim that such drug use is a compulsive behaviour over which addicted
persons have little or no control.22, 23
We can reconcile the BDMA with the high rates of recovery from addiction if we
allow that addictive disorders vary in severity and that less severe disorders are the
most common and those most likely to remit without treatment.27 On this account,
chronic addiction occurs in a minority of addicted persons, those who use drugs into
their early 30s despite an accumulation of adverse health and social consequences.
These drug users seem to better fit the picture of a chronic relapsing brain disease
because they are most likely to seek treatment after failing to control their drug use.
They are also most likely to show alterations in brain function that may play a role in
their continued drug use.24
This modified form of the BDMA applies to a minority of those who meet diagnostic
criteria for addiction in epidemiological studies. Advocates of the BDMA who accept
this weaker formulation cannot equate the lifetime prevalence of addictive disorders
with the prevalence of the severe and chronic addictive disorders that exemplify the
BDMA. A critical analysis of neurobiological research on addiction, however, also
raises doubts about how compelling an explanation the BDMA provides of the
minority of addicted persons with severe, chronic forms of addiction.
A Critique of Neurobiological Research on Addiction
Animal Models of Addiction
Addictive patterns of behaviour are not the invariable outcome of chronic drug self-
administration in animals. Popular accounts of these studies underplay the extent to
which their results depend upon specifically bred strains of rats and the conditions
under which the animals are housed.28 Rats taught to self-administer opiates under
standard conditions of addiction do not display this behaviour if housed in more
naturalistic conditions (e.g. with litter mates).29 Housing rats in ‘enriched
environments’ also affects patterns of drug self-administration and reinstatement.28
Rats that have been trained to self-administer drugs will abstain when given a choice
of other natural rewards.28
Animal models of addiction also have little to say about the high rates of recovery in
addiction in the absence of specific interventions.24 For example, Koob and
LeMoal’s12 analysis of analogies between animal models and “stages of human
addiction” does not include recovery. Their implicit assumption is that once addicted
an animal (or a person) will remain so unless treated, and if treated will be at high risk
of relapse. The epidemiological evidence reviewed above indicates that this is too
Genetics of Addiction
Addiction is not a disorder that is confined to individuals who carry a small number of
“addiction” genes. Very large numbers of alleles are involved in the genetic
susceptibility to addiction and individually these alleles very weakly predict addiction
risk.20, 21, 30 Genetic risk scores based on combinations of multiple risk alleles do
predict addiction risk but no better than simple family history information (e.g.
number of smoking parents).31 More generally, genetic prediction of disease risk
(even using whole genome sequencing information) is unlikely to be informative for
most people who are at “average risk”.30, 32
Human Neuroimaging Studies
Neuroimaging studies of addiction 33report more statistically significant differences
between addicted and non-addicted persons than they should, given the small samples
studied and the size of average differences between groups.33, 34 The excess number of
significant findings reflects capitalisation on chance when performing large numbers
of comparisons of activation between brain regions or structures, the selective
publication of positive findings, and delays in publishing failures to replicate the
positive findings.35 In studies that do find differences between cases and controls,
there are large overlaps in the size of brain structures and “hypo-” or “hyper-
functionality” of specific brain regions between addicted and control groups.36
Neuroimaging researchers in addiction clearly acknowledge these limitationse.g. 37
but more popular accounts often do not.
Case-control studies do not tell us whether addiction is a cause or a consequence of
differences in brain structure and function or some combination of the two.38
Differences in patterns of activation in brain scans between addicted and non-addicted
persons also do not show whether the drug use of addicted persons is compulsive.39
the fact that reduced activity in frontal brain regions is modestly correlated with self-
reported craving does not demonstrate that drug use is driven by irresistible
The Increasing Complexity of Addiction Neurobiology
The neurobiology of the BDMA has become progressively more complicated since
1997, as revealed in Volkow’s papers. The hypothesis that chronic drug use “hijacks”
the brain’s pleasure centres has expanded to acknowledge that drug use also affects
brain structures involved in higher cognitive control of impulses.15, 40 Volkow also
acknowledges the neuropharmacological complexity of addiction in recognising that
multiple neurotransmitter systems are implicated in addiction (e.g. GABA, NMDMA,
opioid, serotonin).17, 41 She also emphasises the importance of epigenetics (changes in
gene expression in brain systems produced by chronic drug use), which she identifies
as a new target for drug treatments of addiction. Despite these acknowledgments of
the complex neurobiology of addiction, the simplest form of the BDMA continues to
dominate public education materials.42
The Promised Policy Pay-offs of the Brain Disease Model of Addiction
Improved Drug Treatments of Addiction
Leshner predicted that the BDMA would deliver more effective treatments of
addiction.1, 6 by developing medications and behavioural treatments that reversed or
compensated for the brain changes responsible for addiction.1, p.46 The new drug
treatments that have been investigated have included: drug vaccines and implantable
agonists and antagonists to reduce relapse; genomic tests to match patients to the most
effective treatment; drugs to modulate the stress response; drugs to modify memories
of drug-related cues; and most recently, drugs to reverse epigenetic changes produced
by chronic drug use.43-45
The treatment benefits of the BDMA remain uncashed promissory notes.46 Very few
new drug treatments have been approved for addiction over the past several decades.47
and the most widely used drug treatments for addiction (e.g. methadone and nicotine
replacement therapy (NRT)) preceded the BDMA by over 30 years. The few drugs
derived from neurobiological research (e.g. naltrexone, varenicline) only improve
modestly on older drugs, such as disulfiram and NRT.37, 48-50 NIDA’s investment in
research on vaccines for nicotine and cocaine dependence has also produced
disappointing results.51-53
Formidable obstacles remain to developing effective drug treatments for addiction.
Many of these are shared with drug development in biomedicine more generally.54
These include a very low success rate in replicating the findings of “promising drug
targets” identified in basic research55, 56 and the low replicability of the results of
small sample animal studies.57 Very few drugs show promise in animal models
progress to human clinical trials due to unacceptable human toxicity, while others fail
to show efficacy in phase II human trials.
There are also special challenges in developing new drug treatments for addiction.
Pharmaceutical company executives have been reluctant to invest because they doubt
that new drugs for addiction drugs will be profitable, given the limited capacity of
addicted individuals to pay for treatment, the lack of health insurance coverage for
addiction treatments in the USA, and the regulatory disincentives to the clinical use of
drugs that have similar effects to drugs of abuse.47 Drug companies may also fear that
the stigma of addiction will discourage other potentially more profitable uses of these
drugs (e.g. to treat chronic pain).47
Direct Brain Interventions for Addiction
Leshner’s argument that “attending to the brain needs to be a core part” of treating
addiction 46) has prompted proposals to directly intervene in the brains of addicted
individuals. In the early 2000s, Koob’s work was invoked to justify ablative
neurosurgery as a treatment for heroin addiction in China and Russia.58 Deep Brain
Stimulation (DBS) is now advocated as a more targeted and reversible alternative to
neurosurgical ablation.59, 60
Advocates of DBS for addiction cite animal studies in which lesions in the
dopaminergic reward pathway have reduced drug self-administration (e.g. 61). They
also cite case reports of patients who have been treated with DBS for indications other
than addiction and who have reported en passant that their addictive behaviour was
reduced.62 There are now also case reports of the apparently successful use of DBS to
treat alcohol and heroin dependence.62
Advocates of DBS for addiction have argued that it will be an effective and cost-
effective way to reduce the economic and social costs of addiction.60 They overstate
its likely population impact in order to justify the high costs of the procedure (over
US$50,000 to implant a stimulator and US$10,000 p.a. to maintain it).63 If DBS were
to prove effective, it would will most likely be used to treat the minority of addicted
patients wealthy enough to afford the treatment; it would be least likely to be offered
to the addicted persons who generate the social and economic costs that have been
used to justify DBS trials.60
Overinvestment in High Risk Strategies for Legal Drugs
A major risk is that the BDMA will lead to the neglect of public health policies in
favour of a search for biomedical treatments of severely addicted persons.64, 65 This
prioritization is reflected in NIDA’s allocation of its current $1065.24 million
research budge: 23.8% to epidemiology, health services and prevention; 41.4% to
basic and clinical neuroscience; and 16.5% to pharmacotherapies, with the rest spent
on intramural research and research support.66
Imposing high taxes on cigarettes, enacting advertising bans and restricting where
people can smoke, have halved cigarette smoking rates in Australia67 and the US68
over the past three decades. These strategies are much more efficient than high-risk
strategies aimed at smokers and persons at risk of smoking.64 It is much cheaper to
increase taxes, ban advertising, and restrict opportunities to smoke than to screen
whole populations and intervene with the minority who are at high genetic risk of
addiction if they smoke tobacco.69 Similar evidence supports the greater efficiency of
population-based strategies in reducing the societal harms of alcohol misuse.70 The
effectiveness of population level approaches is not an argument against providing
clinical treatment to addicted individuals. However, there is a real concern that an
overemphasis on the BDMA can undermine population level approaches when
misused by the alcohol and tobacco industries in opposing public health policies.71
Addiction Neurobiology and Illicit Drug Policy
There are striking transatlantic differences in the policy inferences drawn from
neurobiological research on addiction. In the USA, proponents of the BDMA have
largely been silent about its implications for US drug policy, arguably allowing the
BDMA to be in to support of an over-investment in law enforcement efforts to reduce
drug supply.72
NIDA has expended considerable resources in seeking to replace a moral view of
addiction with one that sees addiction as a treatable medical disorder.1, 2, 6 Until very
recently there have arguably been meagre returns on this investment. The most recent
positive development has been the inclusion of addiction treatment within the Patient
Protection and Affordable Care Act (PPACA), commonly referred to as ObamaCare.5
In the UK, by contrast, leading addiction neuroscientists have used their research to
question whether cannabis, MDMA and LSD should remain illegal. David Nutt has
argued that the harms caused by alcohol, cannabis, cocaine, heroin, MDMA and
tobacco do not justify the different legal status of these drugs.73
Neuroscience research on addiction cannot be, and ought not to be, the decisive factor
in setting drug policy. In democratic societies, drug policy should be the outcome of
societal trade-offs between competing goods and harms, such as the pleasurable
effects of drugs enjoyed by adults, the harms that drug use can cause, and the social
and economic costs and benefits of different ways of allowing or restricting their use
and sale. Ideally these trade-offs should be made by political representatives who are
well informed about epidemiological, sociological, economic and neurobiological
research on drug use and addiction.
There is considerable scientific value in neurobiological and genetic research on
addiction, but this research does not justify the simplified BDMA that dominates
discourse about addiction in the USA and increasingly elsewhere. Nature was
mistaken to assume that the BMDA represents the consensus view in the addictions
field.7, as shown by a letter signed by 94 addiction researchers and clinicians
(including one of the authors).74 Our understanding of addiction, and the policies we
adopt to treat and prevent problem drug use, should give biology its due, but no more
than its due. The effects of chronic drug use can act on brain systems in ways that
may make cessation more difficult for some. But evidence from economics,
epidemiology and social sciences shows that neurobiology is not the over-riding
factor when formulating policies towards drug use and addiction.
The BMDA has not delivered the more effective treatments for addiction that were
originally promised by Leshner and its impact on public policies towards problem
drug use has been modest. The BMDA has arguably led to over-investment by US
research agencies in research on biological interventions to cure addiction that will
have a limited impact on addiction as a public health issue. Increased access to more
effective addiction treatment is a worthy goal that we support but this should not be
pursued at the expense of simpler, cheaper and more efficient population-based
policies that discourage the whole population from smoking tobacco and drinking
heavily. Nor should the pursuit of high technology “cures” distract us from increasing
access to currently available psychosocial and drug treatments for addiction, which
the majority of addicted individual are still unable to access.
Our rejection of the BDMA is not intended as a defence of the moral model of
addiction.65 We share many of the aspirations of those who advocate for the BDMA,
especially the delivery of more effective treatment and less punitive responses to
addicted persons. Addiction is a complex biological, psychological and social
disorder that needs to be addressed by a variety of clinical and public health
approaches.65 Neuroscience research on addiction has provided useful insights into
the neurobiology of decision-making, motivation and behavioural control. These
insights help to understand how chronic use of addictive drugs can impair cognitive
and motivational processes and may partially explain why some persons are more
vulnerable than others to developing an addiction. The challenge for all addiction
researchers - including neurobiologists - is to incorporate the emerging insights of
neuroscience research into those provided by economics, epidemiology, sociology,
psychology, and political science so that we can better reduce the harms caused by
drug misuse and all forms of addiction.46
We would like to thank Sarah Yeates for comments on an earlier draft of this
manuscript and her assistance in doing literature searches for the paper. Wayne Hall
and Cynthia Forlini were funded by an NHMRC Australia Fellowship awarded to
Wayne Hall. Adrian Carter was supported by an NHMRC Post-Doctoral Fellowship.
Conflicts of Interest
The other authors declare no conflicts of interest.
The study and drafting of the paper was led by WH. WH and AC designed the study
and conducted an initial search of the literature. All authors were involved in devising
the final search strategy, retrieving and critically reviewing the articles. WH prepared
the initial draft of the paper. All authors were involved in the subsequent writing and
editing of the manuscript.
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... Despite decades of research and considerable progress in our understanding of the neurobiological processes mediating the transition to addiction, most of the promising pharmacotherapies developed in animals failed to prove effective in the treatment of addiction in humans [1]. Besides these unsuccessful efforts, sometimes characterized as a waste of time and resources, preclinical research significantly contributed to the predominance of the Brain Disease Model of Addiction (BDMA) [3], increasingly criticized in the scientific community [1,4,5]. In fact, it has even been suggested that viewing addiction as a brain disease could hinder recovery from addiction and promote social injustice [6][7][8]. ...
... Preclinical research may not have led to major breakthrough in the development of new pharmacotherapies, but it has generated neurobiological theories that have significantly shaped our conception of addiction with many clinical and societal implications (for better or for worse). My goal here is not to advocate for or against the BDMA, a topic already extensively covered in the literature [1,4,[9][10][11]. Instead, I am specifically interested in determining how preclinical research has influenced addiction medicine over past decades and reciprocally, what can preclinical researchers learn from addiction medicine to help develop more effective therapies. ...
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The debate surrounding the brain disease model and the associated questioning of the relevance of animal models is polarizing the field of addiction, and tends to widen the gap between preclinical research and addiction medicine. Here, we aimed at bridging this gap by establishing a dialog between a preclinical researcher and a clinician in addiction medicine. Our objective was to evaluate animal models and the neuroscientific conceptualization of addiction in light of alcohol or drug dependence and treatment in patients struggling with an addiction. We sought to determine how preclinical research influenced addiction medicine over past decades, and reciprocally, what can preclinical researchers learn from addiction medicine that could lead to more effective approaches. In this dialog, we talk about the co-evolution of addiction concepts and treatments from neuroscientific and medical perspectives. This dialog illustrates the reciprocal influences and mutual enrichment between the two disciplines and reveals that, although preclinical research might not produce new pharmacotherapies, it does shape the theoretical conceptualization of addiction and could thereby contribute to the implementation of therapeutic approaches.
... Priorities in research funding [5,6] as well as statements in publications [4,7] suggest that this approach might be widely accepted in the addiction research community. This, however, is disputed, as are the possible implications of this view [4,[8][9][10][11]. Especially a publication in the journal Nature, stating that neuroscientific explanations were not particularly controversial among scientists [7], provoked marked objection. ...
... In addiction research, the translation of (research-based) knowledge on the nature of the phenomenon also influences issues such as stigmatisation, treatment-seeking and self-efficacy expectation. It thus impacts public attitude as well as the behaviour and self-conception of affected individuals [1,8,[14][15][16]. Researchers, however, also act based on their personal convictions and values, as well as on the epistemological background of their disciplines, which shape their methodological approaches [27,28]. ...
Introduction: Brain-based explanations of addiction have become a prominent explanatory model in recent decades. Although opposing views have been published, there is no large-scale study of researchers' opinions, unlike for treatment staff, the public and affected individuals. Therefore, this study aimed to examine international addiction researchers' perspectives on: (i) brain-based explanations of addiction; (ii) the perceived dominance of the concept in science, society, treatment and among those affected; and (iii) researchers' general conception of addiction in terms of ontologies and causes. Methods: A sample of 1440 international addiction researchers was compiled. Views were assessed online via LimeSurvey using a 'mixed methods light' approach (Likert-type scales, free-text fields). Qualitative content analyses of free-text comments complemented descriptive statistics. Results: One hundred and ninety researchers participated (13.19% response). The classification of substance use disorders as brain diseases/disorders was shared by about 60% of the respondents. Approximately 80% considered it the dominant view in science, but fewer in treatment, society and affected persons. Approximately 75% found it an oversimplification, but regarded it as helpful for understanding substance use disorders. Altogether, various biological, psychological and social factors were considered causal. Comments indicated that an over-simplistic nature of brain-based explanations of addiction was viewed as particularly problematic. Discussion and conclusions: A rejection of a simplistic view of addiction in favour of a multi-causal concept in which the brain plays a role seems to be the majority view of participating researchers. Therefore, the orientation of future research, treatment and support for addicted persons need to be reconsidered accordingly.
... However, it also points towards a reductionist conception of addiction, one which might clash with a subject's individual experience, especially if they feel they were never sick or have been cured (Lewis, 2017). Over the years, there have been heated arguments and counterarguments around the brain disease model (Heather et al., 2018;Field et al., 2019;Lewis, 2022;Alexander, 2022;Hall et al., 2015;Volkow & Koob, 2015). In this work, we focus on selected objections which tackle the features highlighted above, namely, brain changes, disease definition, and compulsivity. ...
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Substance addiction has been historically conceived and widely researched as a brain disease. There have been ample criticisms of brain-centred approaches to addiction, and this paper aims to align with one such criticism by applying insights from phenomenology of psychiatry. More precisely, this work will apply Merleau-Ponty’s insightful distinction between the biological and lived body. In this light, the disease model emerges as an incomplete account of substance addiction because it captures only its biological aspects. When considering addiction as a brain disorder, it will be shown that research fails to account for the contextual, functional, and emotional aspects inherent to subjective health. It is concluded that, while the disease model is fundamental to our understanding of what happens in the brain, its brain-centred approach is cure-oriented. Instead, we suggest a care-orientated approach, which understands and treats the psychological feel as bodily experience situated in an environment, allowing for a more encompassing therapeutic perspective.
... Identifying specific changes in neurocircuitry and neuroplasticity have helped the understanding of addiction as a neuropsychiatric brain disease of learning and memory as opposed to the traditional model of self-determination and personal responsibility (Volkow & Koob, 2015;Volkow et al., 2016). Nevertheless, the social and psychological aspects of this disease should not be overlooked and a balanced perspective in addiction treatment is needed (Hall et al., 2015;Lewis, 2018). ...
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Psychostimulant use disorder is a major health issue around the world with enormous individual, family-related and societal consequences, yet there are no effective pharmacological treatments available. In this review, a target-based overview of pharmacological treatments toward psychostimulant addiction will be presented. We will go through therapeutic approaches targeting different aspects of psychostimulant addiction with focus on three major areas; 1) drugs targeting signalling, and metabolism of the dopamine system, 2) drugs targeting either AMPA receptors or metabotropic glutamate receptors of the glutamate system and 3) drugs targeting the severe side-effects of quitting long-term psychostimulant use. For each of these major modes of intervention, findings from pre-clinical studies in rodents to clinical trials in humans will be listed, and future perspectives of the different treatment strategies as well as their potential side-effects will be discussed. Pharmaceuticals modulating the dopamine system, such as antipsychotics, DAT-inhibitors, and disulfiram, have shown some promising results. Cognitive enhancers have been found to increase aspects of behavioural control, and drugs targeting the glutamate system such as modulators of metabotropic glutamate receptors and AMPA receptors have provided interesting changes in relapse behaviour. Furthermore, CRF-antagonists directed toward alleviating the symptoms of the withdrawal stage have been examined with interesting resulting changes in behaviour. There are promising results investigating therapeutics for psychostimulant addiction, but further preclinical work and additional human studies with a more stratified patient selection are needed to prove sufficient evidence of efficacy and tolerability.
... Victims and their families were met with overwhelming contempt, rather than compassion [42]. Criticisms of the disease model of addiction notwithstanding, it was only when white populations became dependent on opioids that drug use started to be seen in the more sympathetic light of a biomedical disease, rather than a moral failing [28,43,44]. ...
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Background Increased opioid-related morbidity and mortality in racialized communities has highlighted the intersectional nature of the drug policy crisis. Given the racist evolution of the war on drugs and the harm reduction (HR) movement, the aim of this study is to explore racism within harm reduction services through the perspectives of our participants. Methods We conducted a qualitative descriptive study to explore the perspectives of racialized service users and providers on racism in the HR movement in the Greater Toronto and Hamilton Area (GTHA). Four racialized service users and four racialized service providers participated in semi-structured interviews that were audio-recorded, transcribed, and analysed thematically. Results Five themes related to racism in HR were generated: (1) whiteness of harm reduction as a barrier to accessing services, (2) diversifying HR workers as a step towards overcoming distrust, (3) drop-in spaces specific to Black, Indigenous, and people of colour are facilitators to accessing harm reduction, (4) lack of representation in HR-related promotional and educational campaigns, and (5) HR as a frontier for policing. Conclusions Our findings suggest that structural and institutional racism are prevalent in HR services within the GTHA, in the form of colour-blind policies and practices that fail to address the intersectional nature of the drug policy crisis. There is a need for local HR organizations to critically reflect and act on their practices and policies, working with communities to become more equitable, inclusive, and accessible spaces for all people who use drugs.
... Στο πεδίο των εξαρτήσεων τις τελευταίες δεκαετίες έχει ενταθεί η κριτική στο κυρίαρχο επιστημονικό παράδειγμα που διαμορφώνει τις εξελίξεις και τις πρακτικές αντιμετώπισης (Alexander, 2008, Hall, Carter & Forlini, 2015, Hart, 2013, Lewis, 2017, Peele, 1989, Ζαφειρίδης, 2018. Βασικά σημεία της κριτικής αποτελούν α) η αδυναμία επαρκούς ερμηνείας του φαινομένου λόγω της μονοδιάστατης έμφασης στη νοσολογική προσέγγιση, που αποπλαισιώνει το φαινόμενο από το ιστορικό, κοινωνικοπολιτικό και πολιτισμικό περιβάλλον στο οποίο αναπτύσσεται, β) η εντεινόμενη ιατρικοποίηση του που έχει ως αποτέλεσμα την αντίληψη ότι μόνο η ιατρική και παραϊατρική κοινότητα μπορούν να ασχοληθούν με την επίλυση του γ) η έλλειψη ουσιαστικής διεπιστημονικής προσέγγισης του φαινομένου με συμπερίληψη γνώσης από τις κοινωνικές επιστήμες και όχι μόνο από τις επιστήμες υγείας δ) η αδυναμία παραγωγής αποτελεσματικών πρακτικών αντιμετώπισης του προβλήματος ε) η μη ουσιαστική αξιοποίηση της βιωματικής γνώσης και των πρακτικών των άμεσα ενδιαφερομένων, οι οποίοι διαχρονικά προσφέρουν ελπιδοφόρες πρακτικές. ...
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Θεωρητικοί από διάφορα επιστημονικά πεδία συγκλίνουν στην άποψη ότι η πανδημία του COVID 19 αποτελεί ένα κομβικό σημείο στη νεότερη τουλάχιστον παγκόσμια ιστορία (Jones, 2020, Waitzkin, 2021). Ειδικότερα στο πεδίο της Ψυχολογίας και της Ψυχιατρικής έχει ήδη αναπτυχθεί έντονος προβληματισμός για την επιβάρυνση της ψυχικής υγείας του πληθυσμού λόγω της πανδημίας. Έντονη ανησυχία εκφράζεται επίσης για την πιθανή αύξηση διαφόρων ψυχοκοινωνικών προβλημάτων μετά το τέλος της πανδημίας, ως απότοκο των πολλαπλών οικονομικών και κοινωνικών προβλημάτων που θα δημιουργηθούν (Gruber et al., 2021) . Προεξάρχουσα θέση σε αυτή τη συζήτηση καταλαμβάνει το ζήτημα των εξαρτήσεων (είτε συμπεριφορικών, είτε από ψυχοτρόπες ουσίες), καθώς έχει ήδη παρατηρηθεί αύξηση της χρήσης ψυχοτρόπων ουσιών τον τελευταίο ενάμισι χρόνο στην Ελλάδα και διεθνώς. Ταυτόχρονα έχουν παρατηρηθεί σημαντικά ζητήματα στη διαχείρισή του φαινομένου εξαιτίας της πανδημίας (Farhoudian et al., 2020, 2021, Kouimtsidis et al., 2021). Καθώς πρόκειται για ένα εν εξελίξει φαινόμενο οφείλουμε να είμαστε προσεκτικοί, όσον αφορά στις παρατηρήσεις και τα συμπεράσματά μας. Στο παρόν κείμενο επιχειρείται να αναδειχθεί ένα πλαίσιο συζήτησης για την κατανόηση και την αντιμετώπιση των εξαρτήσεων, υπό το πρίσμα των αλλαγών που προκαλούνται ή επιταχύνονται λόγω της πανδημίας. Παρουσιάζονται τα βασικά προβλήματα που εμφανίστηκαν στο πεδίο και οι στρατηγικές που εφαρμόστηκαν για την υπέρβασή τους. Στη συνέχεια αναπτύσσεται ένας συνολικότερος προβληματισμός για την παρατηρούμενη (και προ της πανδημίας) κρίση του επιστημονικού παραδείγματος του πεδίου των εξαρτήσεων, η οποία γίνεται ολοένα και περισσότερο εμφανής. Σε αυτό το πλαίσιο, η πανδημία και οι συνέπειες της λειτουργούν καταλυτικά προς την κατεύθυνση «απομάγευσης» του κυρίαρχου επιστημονικού μοντέλου ερμηνείας της εξάρτησης, προκειμένου να προκύψουν περισσότερο ορθολογικές και αποτελεσματικές ερμηνείες και μεθοδολογίες αντιμετώπισης του φαινομένου.
... Research support for the BDMA indicates that brain changes associated with the process of addiction impair one's ability to discontinue substance use, regardless of intention or significant negative consequences secondary to use. Although there is considerable debate in the field regarding the implications of the neurobiological evidence in support of the BDMA (Hall et al. 2015;Lewis 2017Lewis , 2018, the purpose of the present study is not to question the neurobiology of the BDMA but to critically evaluate the efficacy of the model's use to increase public and sociopolitical support for alternatives to incarceration for those with SUDs. ...
The National Institute of Drug Addiction has promoted the Brain Disease Model of Addiction (BDMA) for several decades, believing it will have a positive impact on drug-related social policies. Per research, neither understanding nor accepting the BDMA positively influences social behavior and decision making related to decreased stigma or increased support for treatment and funding for substance use disorders. An alternative model, the Malleability Model, focuses on the changeability of psychopathology associated with psychiatric disorders, and is associated with decreased hopelessness and increased prognostic optimism. The Moral Weakness Model focuses on moral character as the reason for addiction and is associated with punitive responses to use disorders. The current study sought to identify whether Malleability values were more predictive of willingness to vote for harm reduction (HR) policies than BDMA and Moral values (H1); and if agreement with Malleability values were more predictive of willingness to fund such policies than agreement with BDMA and Moral values (H2). Contrary to hypotheses, results indicated the Malleability Model failed to predict votes and donations, while agreement with the Moral Weakness Model and conservative political affiliation was predictive of lower HR donations. Agreement with the BDMA did not reliably predict votes and donations to policies; the associations reflected were tenuous and should be interpreted with caution. Overall, results indicated the Malleability Model did not increase votes and donations to HR policies, while agreement with Moral Weakness Model and conservative affiliation consistently predicted votes and donations.
... Much of the model discussed above posits a dichotomous (casual drinking vs. AUD) 'shift' (sometimes characterized as a 'hijacking') of these three circuits in addiction (Koob and Volkow, 2010;Hall et al., 2015). In the healthy state, voluntary drinking engages intact circuits of reward, reinforcement and relief. ...
Aims The addiction neurocircuitry model describes the role of several brain circuits (drug reward, negative emotionality and craving/executive control) in alcohol use and subsequent development of alcohol use disorder (AUD). Human studies examining longitudinal change using resting-state functional magnetic resonance imaging (rs-fMRI) are needed to understand how functional changes to these circuits are caused by or contribute to continued AUD. Methods In order to characterize how intrinsic functional connectivity changes with sustained AUD, we analyzed rs-fMRI data from individuals with (n = 18; treatment seeking and non-treatment seeking) and without (n = 21) AUD collected on multiple visits as part of various research studies at the NIAAA intramural program from 2012 to 2020. Results Results of the seed correlation analysis showed that individuals with AUD had an increase in functional connectivity over time between emotionality and craving neurocircuits, and a decrease between executive control and reward networks. Post hoc investigations of AUD severity and alcohol consumption between scans revealed an additive effect of these AUD features in many of the circuits, such that more alcohol consumption or more severe AUD was associated with more pronounced changes to synchronicity. Conclusions These findings suggest an increased concordance of networks underlying emotionality and compulsions toward drinking while also a reduction in control network connectivity, consistent with the addiction neurocircuitry model. Further, they suggest a compounding effect of continued heavy drinking on these vulnerabilities in neurocircuitry. More longitudinal research is necessary to understand the trajectories of individuals with AUD not adequately represented in this study, as well as whether this can inform effective harm reduction strategies.
This paper examines the stories of transformative learning of two men reflecting on their recovery from addictions and trauma. We employ the Hero’s journey as a useful frame within which to understand their stories of becoming more and progressing towards a recovered self. The article challenges the dominant biomedical model of addiction, and of recovery as being primarily about abstinence. It also provides further evidence for understanding transformative learning as a process of (re)integration which is supported through archetypal storytelling.
Alcohol is not able to control the drinking habit due to both physical and emotional dependence on alcohol. Counseling aims to address the underlying causes of alcoholism. Alcohol is classified as a ‘brain disease’. Counseling services are therefore an important factor in recovering from addiction and promoting self-esteem. Self-esteemis a reflection of human understanding and a sense of human worth. Counseling is a method that helps to use a problem-solving process to promote self-esteem. This study aims to determine the effectiveness of counseling, promote self-esteem, and link self-esteem with demographic variability. Post-counseling study methodology after counseling, in the Study group, 8.33% of alcohol dependents had a low score, 50% alcohol dependence had a moderate level of the score and 41.67% was a high score. Among the control group, 41.67% of alcohol dependents had a low score, 58.33% received a moderate level and none of them achieved a high score. Therefore, counseling provides professional support, advice, and recommended addiction services.
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Background Deep-brain stimulation is the surgical procedure of choice for patients with advanced Parkinson's disease. The globus pallidus interna and the subthalamic nucleus are accepted targets for this procedure. We compared 24-month outcomes for patients who had undergone bilateral stimulation of the globus pallidus interna (pallidal stimulation) or subthalamic nucleus (subthalamic stimulation). Methods At seven Veterans Affairs and six university hospitals, we randomly assigned 299 patients with idiopathic Parkinson's disease to undergo either pallidal stimulation (152 patients) or subthalamic stimulation (147 patients). The primary outcome was the change in motor function, as blindly assessed on the Unified Parkinson's Disease Rating Scale, part III (UPDRS-III), while patients were receiving stimulation but not receiving antiparkinsonian medication. Secondary outcomes included self-reported function, quality of life, neurocognitive function, and adverse events. Results Mean changes in the primary outcome did not differ significantly between the two study groups (P=0.50). There was also no significant difference in self-reported function. Patients undergoing subthalamic stimulation required a lower dose of dopaminergic agents than did those undergoing pallidal stimulation (P=0.02). One component of processing speed (visuomotor) declined more after subthalamic stimulation than after pallidal stimulation (P=0.03). The level of depression worsened after subthalamic stimulation and improved after pallidal stimulation (P=0.02). Serious adverse events occurred in 51% of patients undergoing pallidal stimulation and in 56% of those undergoing subthalamic stimulation, with no significant between-group differences at 24 months. Conclusions Patients with Parkinson's disease had similar improvement in motor function after either pallidal or subthalamic stimulation. Nonmotor factors may reasonably be included in the selection of surgical target for deep-brain stimulation. ( numbers, NCT00056563 and NCT01076452.)
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BACKGROUND: Alcohol dependence is among the main leading health risk factors in most developed and developing countries. Therapeutic success of psychosocial programs for relapse prevention is moderate, but could potentially be increased by an adjuvant treatment with the glutamate antagonist acamprosate. OBJECTIVE: To determine the effectiveness and tolerability of acamprosate in comparison to placebo and other pharmacological agents. CRITERIA FOR CONSIDERING STUDIES FOR THIS REVIEW: We searched the Cochrane Drugs and Alcohol Group (CDAG) Specialized Register, PubMed, Embase and CINAHL in January 2009 and inquired manufacturers and researchers for unpublished trials. SELECTION CRITERIA: All double-blind randomised controlled trials (RCTs) which compare the effects of acamprosate with placebo or active control on drinking-related outcomes. DATA COLLECTION AND ANALYSIS: Two authors independently extracted data. Trial quality was assessed by one author and cross-checked by a second author. Individual patient data (IPD) meta-analyses were used to verify the primary effectiveness outcomes. MAIN RESULTS: 24 RCTs with 6915 participants fulfilled the criteria of inclusion and were included in the review. Compared to placebo, acamprosate was shown to significantly reduce the risk of any drinking RR 0.86 (95% CI 0.81 to 0.91); NNT 9.09 (95% CI 6.66 to 14.28) and to significantly increase the cumulative abstinence duration MD 10.94 (95% CI 5.08 to 16.81), while secondary outcomes (gamma-glutamyltransferase, heavy drinking) did not reach statistical significance. Diarrhea was the only side effect that was more frequently reported under acamprosate than placebo RD 0.11 (95% 0.09 to 0.13); NNTB 9.09 (95% CI 7.69 to 11.11). Effects of industry-sponsored trials RR 0.88 (95% 0.80 to 0.97) did not significantly differ from those of non-profit funded trials RR 0.88 (95% CI 0.81 to 0.96). In addition, the linear regression test did not indicate a significant risk of publication bias (P = 0.861). AUTHORS' CONCLUSIONS: Acamprosate appears to be an effective and safe treatment strategy for supporting continuous abstinence after detoxification in alcohol dependent patients. Even though the sizes of treatment effects appear to be rather moderate in their magnitude, they should be valued against the background of the relapsing nature of alcoholism and the limited therapeutic options currently available for its treatment
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Modern imaging techniques have allowed researchers to noninvasively peer into the human brain and investigate, among many other things, the acute effects and long-term consequences of drug abuse. Here, we review the most commonly used and some emerging imaging techniques in addiction research, explain how the various techniques generate their characteristic images, and describe the rational that researchers use to interpret them. In addition, examples of seminal imaging findings are highlighted that illustrate the contribution of each imaging modality to the expansion in our understanding of the neurobiological bases of drug abuse and addiction, and how they can be parlayed in the future into clinical and therapeutic applications.
Neurobiology of Addiction is conceived as a current survey and synthesis of the most important findings in our understanding of the neurobiological mechanisms of addiction over the past 50 years. The book includes a scholarly introduction, thorough descriptions of animal models of addiction, and separate chapters on the neurobiological mechanisms of addiction for psychostimulants, opioids, alcohol, nicotine and cannabinoids. Key information is provided about the history, sources, and pharmacokinetics and psychopathology of addiction of each drug class, as well as the behavioral and neurobiological mechanism of action for each drug class at the molecular, cellular and neurocircuitry level of analysis. A chapter on neuroimaging and drug addiction provides a synthesis of exciting new data from neuroimaging in human addicts a unique perspective unavailable from animal studies. The final chapters explore theories of addiction at the neurobiological and neuroadaptational level both from a historical and integrative perspective. The book incorporates diverse finding with an emphasis on integration and synthesis rather than discrepancies or differences in the literature. Presents a unique perspective on addiction that emphasizes molecular, cellular and neurocircuitry changes in the transition to addiction Synthesizes diverse findings on the neurobiology of addiction to provide a heuristic framework for future work Features extensive documentation through numerous original figures and tables that that will be useful for understanding and teaching.
Since the crime explosion of the 1960s, the prison population in the United States has multiplied fivefold, to one prisoner for every hundred adults--a rate unprecedented in American history and unmatched anywhere in the world. Even as the prisoner head count continues to rise, crime has stopped falling, and poor people and minorities still bear the brunt of both crime and punishment. When Brute Force Fails explains how we got into the current trap and how we can get out of it: to cut both crime and the prison population in half within a decade. Mark Kleiman demonstrates that simply locking up more people for lengthier terms is no longer a workable crime-control strategy. But, says Kleiman, there has been a revolution--largely unnoticed by the press--in controlling crime by means other than brute-force incarceration: substituting swiftness and certainty of punishment for randomized severity, concentrating enforcement resources rather than dispersing them, communicating specific threats of punishment to specific offenders, and enforcing probation and parole conditions to make community corrections a genuine alternative to incarceration. As Kleiman shows, "zero tolerance" is nonsense: there are always more offenses than there is punishment capacity. But, it is possible--and essential--to create focused zero tolerance, by clearly specifying the rules and then delivering the promised sanctions every time the rules are broken. Brute-force crime control has been a costly mistake, both socially and financially. Now that we know how to do better, it would be immoral not to put that knowledge to work.
Addiction is a significant health and social problem and one of the largest preventable causes of disease globally. Neuroscience promises to revolutionise our ability to treat addiction, lead to recognition of addiction as a ‘real’ disorder in need of medical treatment and thereby reduce stigma and discrimination. However, neuroscience raises numerous social and ethical challenges: • If addicted individuals are suffering from a brain disease that drives them to drug use, should we mandate treatment? • Does addiction impair an individual's ability to consent to research or treatment? • How will neuroscience affect social policies towards drug use? Addiction Neuroethics addresses these challenges by examining ethical implications of emerging neurobiological treatments, including: novel psychopharmacology, neurosurgery, drug vaccines to prevent relapse, and genetic screening to identify individuals who are vulnerable to addiction. Essential reading for academics, clinicians, researchers and policy-makers in the fields of addiction, mental health and public policy.
Neuropsychology and neuroimaging provide valuable insights into the neurophysiological basis of drug addiction. This knowledge needs to be integrated into current models on drug use to achieve neuroscientists' and clinicians' goals to improve both early detection and the therapeutic process by developing more effective intervention tools. Identifying neuropsychological and new biological markers of susceptibility to drug addiction or drug relapse raise important ethical concerns. This article outlines the current status of drug addiction research as it relates to the susceptibility to drug addiction. The specific emphasis is put on the neuropsychological and neurofunctional characteristics of drug use and their relation to personality and other modulating variables. Recent imaging findings on relevant neuropsychological constructs such as decision-making and inhibition are discussed in light of their implications for the understanding of the underlying processing dysfunction. The article proposes that the degree of dysfunction in substance users can be more comprehensively assessed using neuroimaging.
This chapter examines technical, ethical, and social issues in the bioprediction of addiction liability and treatment response. Genetic information could also be used to select the most effective treatment for people who are alcohol or nicotine dependent. Effective use of pharmacogenetics to personalize treatment of alcohol dependence also requires highly prevalent genes that are strongly predictive of treatment response. Genetic information on addiction risk may potentially be used by insurance companies, employers and educators, and the courts. This information may affect not only individuals being tested but also their close relatives. Genes expressed in the central nervous system and associated with complex behavioral phenotypes are likely to influence multiple phenotypes. Therefore, genes associated with addiction may also carry information about the risk of developing other mental disorders. The pharmacogenetic test for naltrexone response does have the potential to provide actionable information, assuming the consumer can correctly interpret the test result. Public health professionals are also concerned about the potential misuse of genetic risk information by industries that wish to promote harmful forms of consumption.