Decision neuroscience and drug policy: Reframing the argument on addiction

“Don’t ask the barber if you need a haircut—and don’t ask an academic if what he does is relevant”7.

It is a primary aim of research to tackle questions that are of general relevance to society. In the case of neuroscience and psychology, this is often achieved by invoking medical relevance: for diagnosis or therapy of neurological and psychiatric disorders, or by informing the theory and practice of education: how best to teach children, how to implement cognitive training or how to promote rehabilitation in adults. We also often imply philosophical importance by questioning the essence of what makes us who we are. But, what of decision neuroscience? Could it have any political relevance?

The War on Drugs has been fiercely fought throughout the world. The term was first coined by United States President Richard Nixon in 1972, who declared drug abuse “public enemy number one” in a special message to Congress on Drug Abuse Prevention and Control. The Drug Policy Alliance, a New York City based advocacy group, estimates that the United States still spends $51 billion annually on the War on Drugs. Some of it is spent on military aid to other countries in order to combat guerrilla groups that are involved in illegal drug trade.

In most Western countries this War on Drugs has somewhat eased in the last decade: several states in the US, including Washington D.C., have legalised cannabis; much of Europe has decriminalised marijuana; heroin addicts in Western countries usually have access to clean needles, heroin-substitutes such as methadone and, in some European countries, heroin prescriptions. Indeed, many Western governments are starting to believe that managing drug use causes less harm than trying to battle it5.

However, in much of the rest of the world things look rather different. Many countries across Asia and the Middle East routinely execute drug offenders. Indonesia has recently executed eight drug traffickers in April 2015, despite lobbying by other governments and the United Nations. Saudi Arabia beheads smugglers of cannabis. China’s president, Xi Jinping recently promised “forceful measures to wipe out [drugs]”. In Iran drug offenders account for a majority of all those put to death2. Russia has banned methadone and is trying to convince other Eastern European countries to follow suit. Politicians take up such hard lines on drug offenders because they believe that cracking down on drugs will make addiction go away.

Is this belief realistic? Can cognitive neuroscience help us find an answer to whether addicts should be treated as patients or criminals? And more specifically, how can decision neuroscience – the branch of neuroscience that aims to understand how the brain values goods and generates choices – provide insights into drug-related behaviour in a way that could test current assumptions driving drug policies?

brain-chii-fenThe majority of the considerable body of research that investigates the neural correlates of drug addiction support the notion that drug addicts need treatment instead of prison. Elucidating some of the neural underpinnings of addiction suggest that addiction is a disease that must be treated, rather than a condition for which addicts can be blamed4. Neuroscientists have identified a range of neural mechanisms and neuroadaptations that are correlated with and are quite possibly causally involved in addiction. These include long-term depression of the reward circuitry – a group of neural structures critically involved in the response to positive reinforcement and driving behaviour towards items of hedonic value 1, as well as increased activity in the anti-reward circuitry – a system that has been argued to limit reward in response to excessive utilisation of the brain’s reward system. These neural systems are heavily involved in how we make decisions every day, from what cereal to buy to how much chocolate we eat.

Adaptations in these two systems have been suggested to explain the persistent changes in motivation that are associated with vulnerability to relapse in addicts3. The enhancement of the anti-reward circuitry during the addiction process is attributed to changes in the amygdala and the basal forebrain and linked to neurotransmitters such as norepinephrine, dynorphin, neuropeptide Y, and nociceptin. Depression of the reward-circuitry has been linked to changes in the dopamine system in the substantia nigra and ventral tegmental area and its projection zones in the striatum (particularly ventral striatum) and frontal cortex (particularly orbitofrontal cortex and anterior cingulate cortex). Together, findings suggest that repeated challenges to these neural systems as caused by recurrent consumption of a drug might lead to profound changes in brain structure and function.

The enhanced reinforcing effect of drugs is a result of their ability to trigger dopaminergic firing, exceeding in magnitude and duration the dopamine increases that occur with natural reinforcers, such as food and sex. Dopamine is a neurotransmitter that has long been known to play a key part in our so-called “reward prediction system”. It allows us to learn the value of a reward and the relationship between stimuli and rewards. Dopamine neurons in the ventral tegmental area fire strongly if an outcome is better than expected and are inhibited when outcomes “disappoint” our expectations. Crucially, when reward can be expected based on predictive stimuli, dopamine neurons do not fire when the reward is finally obtained. Cocaine, amphetamine, methamphetamine and ecstasy increase dopamine by inhibiting dopamine reuptake or promoting dopamine release through their effects on dopamine transporters. Other drugs, such as nicotine, alcohol, opiates and marijuana, work indirectly by stimulating neurons that modulate dopamine cell firing. The manner in which drugs “hijack” the mesolimbic dopamine system in order to increase the dopamine signal is widely thought to be central to the explanation of how addiction develops and why it is a chronic, relapsing condition.

Notably some hypotheses of addiction do not even claim that it is a “brain disease” in the narrow sense. A dopamine system, operating in exactly the manner it should, would attenuate dopamine activation in response to expected reward. Eating a surprisingly delicious chocolate bar for the first time would trigger bigger dopamine responses compared to eating it for the fourth or fifth time. The dopamine-reward prediction error hypothesis holds that if the world is exactly as expected, there ought to be no dopamine response. If drugs worked like chocolate bars, we could expect them to trigger an initial dopamine response to consumption, but an attenuation of this response as consumption is repeated. In this case, the dopamine response would be moved to predictors of drug consumption rather than consumption itself. However, research suggests that there are two dopamine responses in sequence: the first response to signals of drug availability and a second response following consumption of the drug whereby the chemical action directly triggers the release of dopamine. “Pathological learning” leads to the drug being of ever-increasing value. This account does not need to assume brain pathology in a narrow sense, but would suggest that addiction arises from a brain living in a world to which it had not adapted to (chemical substances that are able to directly release dopamine did not play a role in the evolution of the dopamine system).

This last hypothesis might be promising on a more general level. We might consider understanding some psychiatric disorders, such as addiction or impulsivity, to be emerging from an “ecologically valid“ adaptation of a person (and their brain) to their specific environment. That means rather than being the result of a dysfunctional and mis-wired brain, psychiatric disorders might result from a functional brain which has adapted to a (potentially extreme) environment which then in turn causes dysfunctional behaviour. Such a framework goes beyond the resilience–vulnerability dichotomy and suggests that maladaptive behaviour emerges as the result of a functional brain living in an environment that is largely different from the average one for which it was adapted.

It remains to be clarified whether addiction should be viewed as a brain disease in the narrow neurological sense or whether it should be viewed as a functional disorder arising from mis-adaptation. In any case, we can be hopeful that decision neuroscience will be able to contribute to the understanding of the condition of addiction and, by doing so, affect political decisions and society. After all, this would not be the first time: psychiatric patients used to be imprisoned together with criminals until, at the end of the 18th century, (neuro-)scientific insight led to the removal of chains from patients with mental illness and the introduction of the “moral treatment” 6.

1          Barry J Everitt, and Trevor W Robbins, ‘Neural Systems of Reinforcement for Drug Addiction: From Actions to Habits to Compulsion’, Nature neuroscience, 8 (2005), 1481-89.

2          Patrick Gallahue, Ricky Gunawan, Fifa Rahman, Karim El Mufti, Najam U Din, and Rita Felten, ‘The Death Penalty for Drug Offences Global Overview 2011’, International Harm Reduction Association (2011).

3          G. F. Koob, and M. Le Moal, ‘Addiction and the Brain Antireward System’, Annu Rev Psychol, 59 (2008), 29-53.

4          A. I. Leshner, ‘Addiction Is a Brain Disease, and It Matters’, Science, 278 (1997), 45-7.

5          Arthur J Lurigio, ‘A Century of Losing Battles: The Costly and Ill-Advised War on Drugs in the United States’, (2014).

6          Philippe Pinel, ‘A Treatise on Insanity’, (1806).

7          Nassim Nicholas Taleb, The Black Swan : The Impact of the Highly Improbable (London: Allen Lane, 2007), pp. xxviii, 366 p.

Edited by Chii Fen Hiu.

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