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      Embodying addiction: A predictive processing account

      research-article
      a , * , b , e , b , c , d , e
      Brain and Cognition
      Academic Press

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          Highlights

          • New perspective on reward learning model of addiction based on predictive processing.

          • Reward learning systems track the agent’s confidence (precision) in its predictions.

          • Embodied feelings that track rate of error reduction weigh precision of predictions.

          • Substance addiction is the outcome of aberrant precision estimation.

          • Addiction is not a brain disease, but a breakdown in the agent-environment dynamics.

          Abstract

          In this paper we show how addiction can be thought of as the outcome of learning. We look to the increasingly influential predictive processing theory for an account of how learning can go wrong in addiction. Perhaps counter intuitively, it is a consequence of this predictive processing perspective on addiction that while the brain plays a deep and important role in leading a person into addiction, it cannot be the whole story. We’ll argue that predictive processing implies a view of addiction not as a brain disease, but rather as a breakdown in the dynamics of the wider agent-environment system. The environment becomes meaningfully organised around the agent’s drug-seeking and using behaviours. Our account of addiction offers a new perspective on what is harmful about addiction. Philosophers often characterise addiction as a mental illness because addicts irrationally shift in their judgement of how they should act based on cues that predict drug use. We argue that predictive processing leads to a different view of what can go wrong in addiction. We suggest that addiction can prove harmful to the person because as their addiction progressively takes hold, the addict comes to embody a predictive model of the environment that fails to adequately attune them to a volatile, dynamic environment. The use of an addictive substance produces illusory feedback of being well-attuned to the environment when the reality is the opposite. This can be comforting for a person inhabiting a hostile niche, but it can also prove to be harmful to the person as they become skilled at living the life of an addict, to the neglect of all other alternatives. The harm in addiction we’ll argue is not to be found in the brains of addicts, but in their way of life.

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          Most cited references49

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          Dysfunction of the prefrontal cortex in addiction: neuroimaging findings and clinical implications.

          The loss of control over drug intake that occurs in addiction was initially believed to result from disruption of subcortical reward circuits. However, imaging studies in addictive behaviours have identified a key involvement of the prefrontal cortex (PFC) both through its regulation of limbic reward regions and its involvement in higher-order executive function (for example, self-control, salience attribution and awareness). This Review focuses on functional neuroimaging studies conducted in the past decade that have expanded our understanding of the involvement of the PFC in drug addiction. Disruption of the PFC in addiction underlies not only compulsive drug taking but also accounts for the disadvantageous behaviours that are associated with addiction and the erosion of free will.
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            The debate over dopamine's role in reward: the case for incentive salience.

            Debate continues over the precise causal contribution made by mesolimbic dopamine systems to reward. There are three competing explanatory categories: 'liking', learning, and 'wanting'. Does dopamine mostly mediate the hedonic impact of reward ('liking')? Does it instead mediate learned predictions of future reward, prediction error teaching signals and stamp in associative links (learning)? Or does dopamine motivate the pursuit of rewards by attributing incentive salience to reward-related stimuli ('wanting')? Each hypothesis is evaluated here, and it is suggested that the incentive salience or 'wanting' hypothesis of dopamine function may be consistent with more evidence than either learning or 'liking'. In brief, recent evidence indicates that dopamine is neither necessary nor sufficient to mediate changes in hedonic 'liking' for sensory pleasures. Other recent evidence indicates that dopamine is not needed for new learning, and not sufficient to directly mediate learning by causing teaching or prediction signals. By contrast, growing evidence indicates that dopamine does contribute causally to incentive salience. Dopamine appears necessary for normal 'wanting', and dopamine activation can be sufficient to enhance cue-triggered incentive salience. Drugs of abuse that promote dopamine signals short circuit and sensitize dynamic mesolimbic mechanisms that evolved to attribute incentive salience to rewards. Such drugs interact with incentive salience integrations of Pavlovian associative information with physiological state signals. That interaction sets the stage to cause compulsive 'wanting' in addiction, but also provides opportunities for experiments to disentangle 'wanting', 'liking', and learning hypotheses. Results from studies that exploited those opportunities are described here. In short, dopamine's contribution appears to be chiefly to cause 'wanting' for hedonic rewards, more than 'liking' or learning for those rewards.
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              Neurobiologic Advances from the Brain Disease Model of Addiction.

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                Author and article information

                Contributors
                Journal
                Brain Cogn
                Brain Cogn
                Brain and Cognition
                Academic Press
                0278-2626
                1090-2147
                1 February 2020
                February 2020
                : 138
                : 105495
                Affiliations
                [a ]Department of Informatics, University of Sussex, Sussex House, Falmer, Brighton BN1 9RH, United Kingdom
                [b ]Amsterdam University Medical Center, Department of Psychiatry, University of Amsterdam, Amsterdam, the Netherlands
                [c ]Department of Philosophy, Institute for Logic, Language and Computation, University of Amsterdam, the Netherlands
                [d ]Department of Philosophy, University of Twente, Enschede, the Netherlands
                [e ]Amsterdam Brain and Cognition Centre, University of Amsterdam, Amsterdam, the Netherlands
                Author notes
                [* ]Corresponding author. m.d.miller@ 123456sussex.ac.uk
                Article
                S0278-2626(19)30406-3 105495
                10.1016/j.bandc.2019.105495
                6983939
                31877434
                5ac63ea1-a987-4083-aabb-422dff008f79
                © 2019 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 16 September 2019
                : 8 November 2019
                : 13 November 2019
                Categories
                Article

                Neurosciences
                Neurosciences

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