Personal ViewThe brain disease model of addiction: is it supported by the evidence and has it delivered on its promises?
Introduction
In 1997, Alan Leshner, then Director of the US National Institute on Drug Abuse (NIDA), published a report1 in Science in which he argued that addiction was best conceptualised as a chronic, relapsing, brain disease. Although Leshner acknowledged that drug use was initially voluntary, he argued on the basis of animal models that chronic drug use flicked a neurochemical switch in the brain, making it very difficult for people addicted to drugs to stop using them, which would explain the high incidence of relapse in people treated for addiction. Researchers at NIDA have since done a substantial number of neuroimaging studies on people with drug addiction and they argue that the results explain how chronic drug use hijacks the brain's reward systems.2
Proponents of the brain disease model of addiction (BDMA) have been very influential in setting the funding priorities of NIDA, and by extension the bulk of publically supported research on addiction. In 1998, Leshner testified that NIDA supports more than 85% 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 Director of US National Drug Control Policy, Michael Botticelli, launched a reformist strategy nationally, claiming decades of research have demonstrated that addiction is a brain disorder—one that can be prevented and treated.5 The BDMA has also been widely discussed in leading scientific research journals3, 6 and most recently in a positive editorial in Nature.7
In the USA, proponents of the BDMA have argued that it will help to deliver more effective medical treatments for addiction with the cost covered by health insurance, making treatment more accessible for people with addictions.1, 2, 6 An increased acceptance of the BDMA is also predicted to reduce the stigma associated with drug addiction by replacing the commonly held notion that people with drug addiction are weak or bad with a more scientific viewpoint that depicts them as having a brain disease that needs medical treatment.
In this Personal View, we critically assess the scientific evidence for the BDMA reported in leading general scientific journals and the extent of the social benefits that advocates of the BDMA claim it has produced, or is likely to produce, with its widespread acceptance among clinicians, policy makers, and the public. The BDMA is not co-extensive with neuroscience-based explanations of addiction. This review is not intended as a critique of all neuroscience research on addiction. We focus instead on the popular simplification of work in this specialty that has had a major influence on popular discourse on addiction in scientific journals and mainstream media.
Section snippets
Evidence for the BDMA
Studies of animal models have had a central role in the development of the BDMA by providing insights into the effects that chronic drug administration has on brain processes.8, 9 These studies show that rats and other animals will self-administer psychoactive drugs at high frequencies (eg, by pressing a lever);9, 10 the drugs that animals self-administer are similarly addictive in humans; and self-administration of drugs is decreased by electrical stimulation of the so-called reward centres in
Is addiction a chronic disorder?
Critics of BDMA contest claims by its proponents that addiction is a chronic relapsing disorder and cite epidemiological evidence that most people with addiction recover without treatment.22, 23, 24 Heyman23 points out that most people with diagnosed drug dependence in epidemiological surveys are not drug dependent at the time of their interview, and have ceased recreational drug use years previously, usually in the absence of treatment. Similarly, a high incidence of recovery was shown in
Improved drugs to treat addiction
Leshner predicted the BDMA would help to develop drugs and behavioural treatments to reverse or compensate for the brain changes underlying addiction,1 thereby delivering more effective treatment for addiction. New drugs to treat addiction include vaccines and implantable agonists and antagonists against neurotransmitters to decrease the risk of relapse; DNA tests to match patients to the most effective treatment; drugs to modulate the stress response; drugs to modify memories of drug-related
Illicit drug policy
Striking differences exist in policies based on research into the neurobiology of addiction. In the USA, proponents of the BDMA have been mostly silent about its implications for US drug policy, arguably allowing the BDMA to become part of an overinvestment in law enforcement efforts to decrease drug supply.72
NIDA has expended substantial resources to replace the view of addiction as morally wrong with one of addiction as a treatable medical disorder.1, 2, 6 Until now there have arguably been
Conclusions
Considerable scientific value exists in the research into the neurobiology and genetics of addiction, but this research does not justify the simplified BDMA that dominates discourse about addiction in the USA and, increasingly, elsewhere. Editors of Nature were mistaken in their assumption that the BDMA represents the consensus view in the addictions specialty,7 as shown by a letter signed by 94 addiction researchers and clinicians (including one of the authors of this Personal View).74
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