The prevalence of obesity in the United States continues to increase, with more than 85% of adults projected to be overweight or obese by 2030 [1]. Health care costs associated with obesity currently comprise almost 10% of national health care expenditures [2] and are projected to increase to 15% over the next 15 years [1]. There has been little success at preventing excessive weight gain or developing weight loss treatments that are effective long-term [3]. Multiple causes contribute to the obesity epidemic, such as increased energy intake, increased availability and ease of access to foods, larger portion sizes, and decreased physical activity [4–6]. Although the causes of obesity are multifactorial, one potential contributing factor is the idea certain foods may be capable of triggering an addictive response in some individuals, which may lead to unintended overeating.

Gearhardt et al. [7] developed and validated the Yale Food Addiction Scale (YFAS), which uses DSM-IV criteria for substance dependence to quantify symptoms of addictive-like eating (see Table 1). “Food addiction” is characterized by symptoms such as loss of control over consumption, continued use despite negative consequences, and an inability to cut down despite the desire to do so [8]. Addictive-like eating has been associated with increased impulsivity and emotional reactivity, which are similarly implicated in substance-use disorders [9]. Thus, “food addiction” may share common behavioral attributes with other addictive disorders. Neuroimaging studies have also revealed biological similarities in patterns of reward-related dysfunction between “food addicts” and substance-dependent individuals. Individuals endorsing symptoms of “food addiction” exhibit increased activation in reward-related regions (e.g., striatum, medial orbitofrontal cortex) in response to food cues, consistent with other addictive disorders [10]. Further, higher scores on the YFAS have been associated with a composite genetic index of dopamine signaling [11]. This multilocus genetic profile has been related to dopamine signaling capacity, which may also be a risk factor for addictive disorders [12,13].