The concept of food addiction is an area of growing scientific interest and ongoing debate. Animal models suggest that rats given highly palatable foods (e.g., icing, bacon, cheesecake) or intermittent access to sugar will display neurobiological and behavioral indicators similar to those observed in models of drug addiction [1, 2]. In humans, overlapping neurobiological systems (e.g., mesolimbic dopamine system) appear activated by both drugs of abuse and highly palatable foods [3•]. Individuals with addiction or eating-related problems (e.g., obesity, binge eating disorder) exhibit similar patterns of neural reactivity to drug or food cues, respectively [4•, 5]. Higher scores on the Yale Food Addiction Scale (YFAS)
[6], which applies the diagnostic criteria for substance dependence to the consumption of highly palatable foods, are associated with increased body mass index (BMI), more frequent binge eating, greater impulsivity, and stronger cravings for fatty, processed foods [7]. Patterns of neural response and genetic profiles implicated in addiction have also been related to higher YFAS scores [8, 9]. Although these findings are important and provide support for food addiction as a clinically relevant concept, more scientific inquiry is needed before the “food addiction” concept can be either accepted or rejected and applied routinely in clinical settings. A major obstacle to evaluating whether an addictive process contributes to problematic eating may involve potential misconceptions about what an addiction perspective means when applied to eating behavior. In the current paper, we will address many of these notions and highlight important gaps that should be addressed to empirically evaluate whether an addictive process contributes to problematic eating behavior.