Behaviorial Neuroscientists point of view: the DSM-5 [118] does not recognize FA in itself, but it identifies different forms of substance-related and addictive disorders (including gambling) that can be used as a reference framework for our discussion. In this context, if we accept the existence of FA, then the neurobiological characteristics of substance-related and addictive disorders should reveal common patterns between food and drug abuse. The point is that the FA construct must be supported by precise definitions, as well as dedicated neurobiological and neuroimaging studies. These definitions must be supported by concrete data and not only by shortcuts based on analogies with obesity or food abuse. Even though we must assume that substance addiction always starts with substance use, not all obese and/or bingeing ED-subtype patients have FA, and not all “food addicts” are obese. All these data support the existence of a specific FA brain phenotype that can be detected in normal-weight, overweight, or obese individuals and that is characterized by anomalies in the reward and inhibitory control processes, with likely corollary consequences in the limbic/emotional and cognitive/attentional spheres (Figure 2). Even though a recent meta-analysis of fMRI studies defends an addiction model of obesity, characterized by reduced cognitive control and interoceptive brain responses [141], this vision is probably restricted to part of the obesity spectrum and cannot be generalized to all forms of obesity