The exact organisational form and structure the ATN will take and the range of

The exact organisational form and structure the atn

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The exact organisational form and structure the ATN will take and the range of activities it will engage in is still developing and under discussion. However, occasional face- to-face meetings are considered essential. The first such meeting was the European launch of the network by means of a symposium held at the Annual Conference of the New Directions in the Study of Alcohol Group in Weston-super- Mare, Somerset, UK on 12 May 2017. The symposium was chaired by Professor Betsy Thom of Middlesex University and a panel discussion following the presentations was mod- erated by Derek Heim. There were six presentations, each of which is summarised by its author(s), in the order in which they were delivered at the conference, in the present editorial. If obesity is also a brain disease, what are the implications for the brain disease model of addiction? Matt Field Nora Volkow, one of the most high-profile proponents of the BDMA (Volkow et al. 2016 ), has argued that obesity should 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- ity are that, in vulnerable individuals, consumption of energy-dense food results in powerful momentary increases in dopamine activity in the reward system. This eventually overrides homeostatic control mechanisms that govern food intake and leads to a number of enduring changes in brain structure and function, resulting in loss of control over food intake. The brain disease model of obesity is supported by observations that obesity is characterised by structural and functional changes in regions of the brain that underlie reward sensitivity, incentive motivation, and self-control, and that these changes are largely indistinguishable from those seen in the addicted brain (Volkow et al. 2008 , 2013 ). This is an interesting development. The most influential neurobiological models of addiction (i.e., brain disease models) emphasise that the functional or structural changes in the brain that underlie the transition from recreational drug use to addiction occur after repeated consumption of addictive drugs (alcohol, nicotine, cocaine, opiates etc.), but are not an inevitable consequence of repeated consumption of all rewards, including natural rewards such as food, warmth and sex (Robinson and Berridge 1993 ; Koob and Le Moal 1997 ; Goldstein and Volkow 2002 ). Therefore, the sug- gestion that similar brain changes may, in fact, also arise after repeated exposure to food represents a quiet abandon- ment of those earlier claims that there is something special about addictive drugs that leads to brain disease if vulnerable people consume them in sufficient quantities. There have been challenges to the claim that obesity should be characterised as a brain disease, including observa- tions that brain responses during anticipation and consump- tion of food, and differences in brain function between obese and normal weight individuals, are not consistent
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