Reevaluating the brain disease model of addiction

Abstract

The brain disease model of addiction has dominated public and scientific discourse on addiction (termed substance use disorder [SUD] in the DSM-5) over the past 3 decades. The model framed addiction as a chronic and relapsing brain disease caused by structural and functional brain alterations. The purpose of this model was purportedly dual, as both an aetiological theory and a tool to reduce stigma. Weak empirical support and concerns about the model downplaying fundamental psychosocial causes of SUDs have led to stark disagreement as to whether addiction should be conceptualised as a brain disease. In this Personal View, we argue that the absence of an agreed, clear, and consistent definition of a brain disease—coupled with frequent recourse to concepts with divergent or shifting meaning—have obstructed productive debate and a coherent advance in knowledge and understanding of addiction. Borrowing from the philosophy of psychiatry, we show that both narrow and broad views of brain disease coexist and inform addiction research, though often implicitly and inconsistently. The narrow view of brain disease posits that a mental condition qualifies as a brain disease only if it manifests similarly to a paradigmatic brain disease, resulting from either known or unknown structural and functional damage. The broad view of brain disease suggests that brain disease status should be granted automatically to mental disorders, as all mental activity resides in the brain. We examine theoretical assumptions, empirical evidence, and treatment implications for each view and propose ways of moving beyond them.