Addiction is a Brain Disease (But Not Always?)

Closing out her stint as a Guest Blogger, Helen Keane notes the gap between the way pain management experts and neuroscientists think about addiction.

The currently dominant scientific paradigm of addiction is that of a ‘chronic, relapsing, brain disease’ which develops as a result of persistent consumption of drugs of abuse. Over time, according to this model, drug use produces long-term changes in brain structure and function, and what began as a voluntary behaviour becomes an uncontrollable compulsion. The process is driven by the effect of dopamine on brain reward pathways, and the ability of drugs to ‘hijack’ these pathways which evolved to reinforce behaviours necessary for survival such as eating and sex.

In addiction science journals the brain disease paradigm is celebrated as a major breakthrough which promises a new era of enlightened treatment, prevention and research.

This Explains Everything!

But as David Courtwright outlined in a recent article  it has also been met with ‘indifference’, ‘suspicion’ and ‘resistance’ from a range of  interested parties including politicians, clinicians and (perhaps least surprisingly) social scientists.[i]  From a sociological and historical perspective there are many things questionable about the neuroscientific discourse of addiction, including, to cite Joseph Gabriel’s recent post, the idea that drug effects on the body can be understood as theoretically prior to the social and cultural contexts in which they occur. But the apparently limited impact of the brain disease model on medical understandings of addiction is more surprising.

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