Beyond the Brain: Reassessing the Brain Disease Model of Addiction Through a Systems Neuroscience Lens

Abstract

Addiction remains a complex and persistent public health crisis, often framed through the Brain Disease Model of Addiction (BDMA), which conceptualizes addiction as a chronic, relapsing brain disorder rooted in pathological changes. While the BDMA has contributed valuable insights into neurobiological mechanisms like dopamine dysregulation, prefrontal cortex impairments, and stress system activation, it has been critiqued for reducing addiction to individual pathology and sidelining social and environmental factors. This thesis critically evaluates the BDMA’s core assumptions– not to reject the model, but to extend it– arguing that addiction is best understood as a multi-systemic condition shaped by dynamic interactions between neurobiological, social, environmental, and stress-related systems. Drawing on neuroscience, epigenetics, and stress physiology, this thesis explores how these systems co-regulate each other through recursive feedback loops that drive both the biological and behavioral dimensions of addiction Rather than viewing social and environmental factors as peripheral risk contributors, this work positions them as core mechanisms that actively shape addiction’s neurobiology and behavioral patterns. By integrating these perspectives, the thesis moves beyond linear disease frameworks, proposing a dynamic systems model that aims to reflect the complex realities of addiction and offer a new pathway for research and intervention.