brain disease in the absence of other kinds of determinant and some that it is

Brain disease in the absence of other kinds of

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brain disease in the absence of other kinds of determinant, and some that it is not best seen as brain disease of any kind or in any way. At the same time, criticisms come from various vantage points that may seem to have little in common with each other from philosophy, psychology and behavioural science, social science and even from neuroscience. This is not the place to attempt to identify all the objections to the BDMA that cur- rently exist or might conceivably exist, but the question can be asked, in the midst of this diversity, what is the point of forming a network dedicated to challenging the brain disease model. Perhaps the best answer to this question is that all adher- ents of the ATN share an objection to what they perceive as the dogma of the BDMA the repeated, public pro- nouncements that science has already clearly established that addiction is a chronic, relapsing brain disease and that it is surprising anyone should continue to doubt the truth of this assertion (Volkow et al. 2016 ). At the same time, anyone who does voice such doubts is often castigated as reckless and irresponsible, ignorant of the realities of addiction and as potentially placing the lives of addicts at risk. In other cir- cumstances such dogma might be harmless and could be jus- tifiably ignored but the problem is that it is a dogma that has come to dominate public discourse and national policy on addiction, at least in the USA and increasingly, we fear, in other countries of the world. Research linked to the BDMA has also come to swallow up almost all the funding for research on addiction on the planet, resulting in a demise in funding for research on the prevention of addiction and approaches other than pharmacotherapy to its treatment. This self-perpetuating research agenda has also tended to appropriate all available data on neurobiological change in addiction, thus side-lining interpretations that stress neuro- psychological development and neuroplasticity in contrast to pathology (Lewis 2017 ). And the dominance of the BDMA has limited the dissemination of approaches to addiction that are known to be cheap and effective in reducing harm (Hall et al. 2014 , 2015 ). We therefore see the future tasks of the ATN as the clari- fication and articulation of the main grounds for criticising the BDMA, and their dissemination both to the scientific and addiction professional communities and to the general public and decision-makers. The network will hopefully pro- vide the opportunity for colleagues in different geographical areas and/or from different scientific disciplines to form col- laborations to work towards these ends. While network members may differ in their specific objections to the BDMA, there may also be disagreement on what models of addiction should replace it. Nevertheless, the ATN will hope- fully foster collaborations on developing new ways of under- standing addiction and their consequences for the prevention and reduction of harm. Lastly, as a counterpoint
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