The obesity epidemic in the US and abroad has increased interest in neurobiological mechanisms that contribute to eating in the absence of energy demand or hunger (overeating). Overeating, sometimes called ‘hedonic’ feeding because foods consumed are usually palatable and high in sugars and fats, is the leading cause of overweight and obesity in the US. One important factor that contributes to obesity is overeating triggered by sights, sounds, and smells (food cues) associated with palatable food (Stice et al, 2013; Tang et al, 2012). For example, obese and overweight people report greater food craving and consume larger portions in response to food cues. A wealth of preclinical studies have demonstrated that these cue-triggered motivational responses are mediated by brain mesocorticolimbic circuits, particularly dopamine and glutamate transmission within the nucleus accumbens (NAc). In humans, the magnitude of activations in the NAc in response to food cues predicts future weight gain in normal-weight people and inability to lose weight after obesity onset. This suggests that differences in NAc function may mediate enhanced cue-triggered urges to eat in susceptible individuals both before and after weight gain. The overlap in the neural systems involved and similarities between responses to food, addictive drugs, and cues associated with them have sparked vibrant discussion about ‘food addiction’ (Carter et al, 2016), despite some obvious differences between food and drug (eg, food does not have psychoactive properties in the pharmacological sense, nor is there a clear dose-response relationship, etc.). So, can overeating that produces common obesity really be considered a form of addiction?

In a recent preclinical study we found that, prior to any diet manipulation, those rats that show the strongest motivational responses to a food cue subsequently gained the most weight when given free access to a fatty, sugary, ‘junk-food’ diet (Robinson et al, 2015). Obesity-prone rats are also more sensitive to the locomotor-activating effects of cocaine, indicating enhanced responsivity of mesolimbic systems, and have greater excitability of medium spiny neurons in the NAc core prior to the development of obesity (Oginsky et al, 2016a, b). Taken together, our data suggest that pre-existing enhancements in NAc responsivity may render obesity-susceptible individuals more sensitive to the motivational properties of food cues. In addition, consumption of fatty, sugary foods alters NAc function in ways that also vary by susceptibility to obesity. For example, consumption of junk food enhances NAc glutamatergic transmission and produces an upregulation of calcium-permeable AMPA receptors (CP-AMPARs) in obesity-susceptible rats (Brown et al, 2015; Oginsky et al, 2016a). Interestingly, increases in CP-AMPARs were found prior to obesity onset, suggesting that they may drive enhanced motivational responses that promote weight gain (see Oginsky et al, 2016b for further discussion).

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