The dopaminergic system is involved in a large number of behaviors including reward processing and motivated behavior. Thus, all drugs of abuse increase the extracellular concentration of dopamine (DA) in the striatum and associated mesolimbic regions [7]. Di Chiara’s group has extensively showed that addictive drugs (e.g. amphetamine and cocaine) increase extracellular DA in the nucleus accumbens (NAc), a primary site for reinforced behaviors [7]. Likewise, microdialysis has shown that exposure to rewarding food stimulates dopaminergic transmission in the NAc [8].

Furthermore, neuroimaging studies show that our brain response is similar in the presence of food and drug abuse: increased cell activation in the NAc, the brain’s pleasure center [9–11]. Neuroimaging studies in humans have also shown similarities between obesity and addiction. For example, both obesity and addiction are associated with fewer D2 dopamine receptors in the brain [12, 13], suggesting that they are less sensitive to reward stimuli and more vulnerable to food or drug intake. Thus, for example, individuals with the largest body mass index (BMI) had the lowest D2 values [13].

Specifically, this reduction in striatal D2 density correlates with reduced metabolism in cerebral areas (prefrontal and orbitofrontal cortex) that exert inhibitory control over consumption [12]. Thus, obese subjects show greater activation of reward and attention regions than normal weight subjects do in response to palatable food images versus control images [14, 15]. This observation suggests that a deficit in reward processing is an important risk factor for the impulsive and compulsive behaviors showed by obese individuals. Taken together, these data could explain why in obesity and drug addiction the consummatory behaviors persist despite negative social, health and financial consequences. All these neurobiological data suggest that obesity and drug addiction may share similar neuroadaptive responses in brain reward circuits or action mechanisms.