4.2.3. Neuropsychological and Brain Activity Risk Factors

The brain is central to basic research, prevention and treatment in the context of obesity and EDs [56]. Until very recently, little was known about the neuropsychological mechanisms of EDs and obesity. Mesocorticolimbic mechanisms that increase "liking" include brain hedonic hotspots, specific subregions that can causally increase the hedonic effect of palatable tastes. In contrast, a much larger mesocorticolimbic circuit generates the motivation to "want" or induce to obtain and consume food rewards [57].

Theorists focused on the reward circuit because eating palatable food increases activation in reward-related regions, including the ventral and dorsal striatum, midbrain, amygdala, and orbitofrontal cortex, and causes dopamine release in the dorsal striatum in both humans and other animals [58]. Functional, molecular and genetic neuroimaging has highlighted the existence of brain abnormalities and neural fragility factors associated with obesity and EDs, such as overeating or anorexia nervosa [58]. A better understanding of wanting and linking mechanisms tailored to individual types of EDs and obesity could lead to better therapeutic strategies, and perhaps help people who wish to more effectively create stop signals to their own needs [57].
