The exact organisational form and structure the ATN willtake and the range of activities it will engage in is stilldeveloping and under discussion. However, occasional face-to-facemeetingsareconsideredessential.Thefirstsuchmeeting was the European launch of the network by meansof a symposium held at the Annual Conference of theNewDirections in the Study of Alcohol Groupin Weston-super-Mare, Somerset, UK on 12 May 2017. The symposium waschaired by Professor Betsy Thom of Middlesex Universityand a panel discussion following the presentations was mod-erated by Derek Heim. There were six presentations, each ofwhich is summarised by its author(s), in the order in whichtheyweredeliveredattheconference,inthepresenteditorial.If obesity is also a brain disease, what are theimplications for the brain disease model ofaddiction?Matt FieldNora Volkow, one of the most high-profile proponents ofthe BDMA (Volkow et al.2016), has argued that obesityshould be considered a brain disease that shares many fea-tures with the addiction brain disease (Volkow et al.2008,2013). The central tenets of the brain disease model of obes-ityarethat,invulnerableindividuals,consumptionofenergy-dense food results in powerful momentary increasesin dopamine activity in the reward system. This eventuallyoverrides homeostatic control mechanisms that govern foodintake and leads to a number of enduring changes in brainstructure and function, resulting in loss of control over foodintake. The brain disease model of obesity is supported byobservations that obesity is characterised by structural andfunctional changes in regions of the brain that underliereward sensitivity, incentive motivation, and self-control, andthat these changes are largely indistinguishable from thoseseen in the‘addicted brain’(Volkow et al.2008,2013).This is an interesting development. The most influentialneurobiologicalmodelsofaddiction(i.e.,‘braindisease’models) emphasise that the functional or structural changesin the brain that underlie the transition from recreationaldrug use to addiction occur after repeated consumption ofaddictive drugs (alcohol, nicotine, cocaine, opiates etc.), butare not an inevitable consequence of repeated consumptionofallrewards,includingnaturalrewardssuchasfood,warmth and sex (Robinson and Berridge1993; Koob and LeMoal1997; Goldstein and Volkow2002). Therefore, the sug-gestion that similar brain changes may, in fact, also ariseafter repeated exposure to food represents a quiet abandon-ment of those earlier claims that there is something specialabout addictive drugs that leads to brain disease if vulnerablepeople consume them in sufficient quantities.There have been challenges to the claim that obesityshould be characterised as a brain disease, including observa-tions that brain responses during anticipation and consump-tionoffood,and differencesinbrainfunctionbetweenobeseandnormalweightindividuals,arenotconsistent
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