Abstract
Increased availability of tasty, energy-dense foods has been blamed as a major factor in the alarmingly high prevalence of obesity, diabetes, and metabolic disease, even in young age. A heated debate has started as to whether some of these foods should be considered addictive, similar to drugs and alcohol. One of the main arguments for food addiction is the similarity of the neural mechanisms underlying reward generation by foods and drugs. Here, we will discuss how food intake can generate reward and how behavioral and neural reward functions are different in obese subjects. Because most studies simply compare lean and obese subjects, it is not clear whether predisposing differences in reward functions cause overeating and weight gain, or whether repeated exposure or secondary effects of the obese state alter reward functions. While studies in both rodents and humans demonstrate preexisting differences in reward functions in the obese, studies in rodent models using calorie restriction and gastric bypass surgery show that some differences are reversible by weight loss and are therefore secondary to the obese state.