Several decision-making vulnerabilities have been identified as underlying causes for addictive behaviours, or the repeated execution of stereotyped actions despite their adverse consequences. These vulnerabilities are mostly associated with brain alterations caused by the consumption of substances of abuse. However, addiction can also happen in the absence of a pharmacological component, such as seen in pathological gambling and videogaming. We use a new reinforcement learning model to highlight a previously neglected vulnerability that we suggest interacts with those already identified, whilst playing a prominent role in non-pharmacological forms of addiction. Specifically, we show that a dual-learning system (i.e. combining model-based and model-free) can be vulnerable to highly rewarding, but suboptimal actions, that are followed by a complex ramification of stochastic adverse effects. This phenomenon is caused by the overload of the capabilities of an agent, as time and cognitive resources required for exploration, deliberation, situation recognition, and habit formation, all increase as a function of the depth and richness of detail of an environment. Furthermore, the cognitive overload can be aggravated due to alterations (e.g. caused by stress) in the bounded rationality, i.e. the limited amount of resources available for the model-based component, in turn increasing the agent’s chances to develop or maintain addictive behaviours. Our study demonstrates that, independent of drug consumption, addictive behaviours can arise in the interaction between the environmental complexity and the biologically finite resources available to explore and represent it.

Ognibene, D., Vincenzo Guido, F., Xiaosi, G. (2019). Addiction beyond pharmacological effects: the role of environment complexity and bounded rationality. NEURAL NETWORKS, 116, 269-278 [10.1016/j.neunet.2019.04.022].

Addiction beyond pharmacological effects: the role of environment complexity and bounded rationality

Ognibene D
Primo
;
2019

Abstract

Several decision-making vulnerabilities have been identified as underlying causes for addictive behaviours, or the repeated execution of stereotyped actions despite their adverse consequences. These vulnerabilities are mostly associated with brain alterations caused by the consumption of substances of abuse. However, addiction can also happen in the absence of a pharmacological component, such as seen in pathological gambling and videogaming. We use a new reinforcement learning model to highlight a previously neglected vulnerability that we suggest interacts with those already identified, whilst playing a prominent role in non-pharmacological forms of addiction. Specifically, we show that a dual-learning system (i.e. combining model-based and model-free) can be vulnerable to highly rewarding, but suboptimal actions, that are followed by a complex ramification of stochastic adverse effects. This phenomenon is caused by the overload of the capabilities of an agent, as time and cognitive resources required for exploration, deliberation, situation recognition, and habit formation, all increase as a function of the depth and richness of detail of an environment. Furthermore, the cognitive overload can be aggravated due to alterations (e.g. caused by stress) in the bounded rationality, i.e. the limited amount of resources available for the model-based component, in turn increasing the agent’s chances to develop or maintain addictive behaviours. Our study demonstrates that, independent of drug consumption, addictive behaviours can arise in the interaction between the environmental complexity and the biologically finite resources available to explore and represent it.
Articolo in rivista - Articolo scientifico
Reinforcement learning; addiction; Computational psychiatry;
English
2019
116
269
278
reserved
Ognibene, D., Vincenzo Guido, F., Xiaosi, G. (2019). Addiction beyond pharmacological effects: the role of environment complexity and bounded rationality. NEURAL NETWORKS, 116, 269-278 [10.1016/j.neunet.2019.04.022].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/301345
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