“…In the last years, thanks to the support of neuroscience, several neurobiological models of eating disorders emerged; Kaye et al (2009, 2010, 2013, 2015) for example, consider AN as the product of an altered serotonin and dopamine metabolism which in turn may leads to dysfunctional neural process involved in emotion and appetite. Such alterations would contribute to AN trait-related vulnerabilities like anxiety, emotional recognition and regulation deficits (Schmidt et al, 1993; Zonnevijlle-Bendek et al, 2002; Kucharska-Pietura et al, 2004; Schmidt and Treasure, 2006; Harrison et al, 2009; Rowsell et al, 2016), insensitivity to reward (Kaye et al, 2009; Harrison et al, 2010), disturbed perception of physical states (Fassino et al, 2004; Pollatos et al, 2008; see below) and cognitive inflexibility and rigidity (Katzman et al, 2001; Anderluh et al, 2003; Kucharska-Pietura et al, 2004; Tchanturia et al, 2004; Cassin and von Ranson, 2005; Chui et al, 2008; Titova et al, 2013) that may be exacerbated by puberty and social desirability, given rise to the onset of AN.…”