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.
For example, the definitions of addiction and pseudoaddiction in pain medicine are based on interpretations of observed behaviour and responses to treatment, rather than theories of neural disruption caused by specific chemicals. I’ve read many articles in pain medicine journals and textbooks but discussions of the neurochemistry of pseudoaddiction are notably absent. Questions about the differences and similarities between pseudoaddicted brains and addicted brain do not arise because these conditions are not constituted as neurological. My point isn’t that this is a shortcoming of pain medicine, a case of a field failing to keep up with the latest science. Rather it demonstrates the divergent ‘styles of thought’ in two medical fields. Nikolas Rose explains that a style of thought is ‘not just about a certain form of explanation, about what it is to explain, it is also about what there is to explain’.[ii] What addiction is in pain medicine is not what it is in addiction science.
What About This, Dr. Feelgood?
Pain medicine isn’t alone in its continued attachment to a resolutely non-neurological vision of addiction. In its introduction to the revisions it proposes for the DSM-V, the substance disorder work group does not mention neuroscience or the brain. The diagnostic criteria proposed for addictive substance use disorder in the DSM-V do not include the observable changes in neural function or structure which are the basis of the brain disease model. Instead the clinical diagnosis of addiction continues to be based on the evaluation of feelings and conduct, for example, ‘craving or a strong desire or urge to use a specific substance’ and ‘failure to fulfil major role obligations at work, school, or home’. Here addiction remains an intransigently hybrid concept which combines the medical and moral.
[i] Courtwright, D. (2010) The NIDA brain disease paradigm: History, resistance and spinoffs. Biosocieties 5/1.
[ii] Rose, N, (2007) The Politics of Life Itself, Princeton University Press, p. 12.