The heterogeneity of youth at risk of prediabetes and diabetes: A latent class analysis of a United States national sample.

Binge eating is a significant behavioral problem, characterized by recurrent episodes of consuming large quantities of food accompanied by a sense of loss of control, and is closely linked to obesity and food addiction (). Food addiction (FA) is a syndrome marked by compulsive overeating of highly processed foods (HPF) and is associated with tolerance and withdrawal symptoms (). Both FA and binge eating have clinical significance and share clinical features (). That is, binge eating and FA are each associated with numerous physical and mental health issues, including obesity, diabetes, cardiovascular disease, and psychiatric disorders (; ; ). And while HPF consumption is not considered an eating disorder symptom, binge eating like FA is associated with increased HPF consumption (; ; ). Yet, despite the evident overlap between binge eating and FA, there remains a notable gap in understanding their shared or distinct mechanisms. Reward responsiveness, the degree to which an individual responds to rewarding stimuli, represents a potential shared mechanism underlying binge eating and FA. Reward responsiveness is also associated with increased intake of HPF, which include foods that are calorically dense, typically high in sugar and saturated fats, and engineered to be intensely rewarding and addictive (; ; ; ). Trait reward responsiveness has also been linked to dysregulated eating behavior such as binge eating and FA; although, research suggests some inconsistency in size and magnitude of effects (; ). Overall this evidence suggests heightened sensitivity to reward, especially food rewards, may drive individuals to overeat HPF in pursuit of the pleasurable feelings these foods induce, even in the absence of hunger. Over time, the brain’s reward system may become conditioned to seek out these foods repeatedly, reinforcing patterns of binge eating and increasing the risk of FA (Alonso-Alonso et al., 2015). However, associations between reward responsiveness, HPF consumption, and binge eating and FA have been somewhat mixed. Obesity and excess weight gain can alter reward responsiveness (), which may partially explain disparate findings in the literature. Consistent with theoretical models (i.e., incentive salience theory, mechanistic staging model of reward processing in binge eating, and the dynamic vulnerability model of obesity), heightened reward responsiveness may predispose individuals to repeatedly seek out and overeat reinforcing HPF, resulting in increased binge eating, FA symptoms, and excess weight gain (; ; ). However, over time, excessive and repeated dopamine release caused by overconsumption of palatable HPF may lead to down-regulation of striatal dopamine receptors, paralleling neuroadaptations observed in the context of substance abuse (; ; , ). In turn, this could result in blunted responses to consumption of rewards that potentiates compulsive overconsumption, as individuals need to consume increasing amounts to attain similar subjective pleasure from HPF they initially experienced. Consequently, once overweight or obesity is established, a negative association between reward responsiveness and binge eating and/or FA symptoms may emerge. depicts these conceptual associations. This also complements prior research that found reward responsiveness was positively associated with body mass index (BMI) among adults and children with normal to overweight BMI, yet negatively associated with BMI among those with obesity (; ). As such, it is imperative to examine how individual differences in BMI interact with reward responsiveness and HPF consumption in predicting dysregulated eating such as binge eating and FA.