Food Addiction and Obesity

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