As summarized previously, several common brain circuits have been identified by imaging studies as being relevant in the neurobiology of drug abuse/addiction and obesity. Here, we highlight four of these circuits: (i) reward/saliency, (ii) motivation/drive, (iii) learning/conditioning, and (iv) inhibitory control/emotional regulation/executive function. Note that the two other circuits (emotion/mood regulation and interoception) also participate in modulating the propensity to eat or take drugs but for simplicity are not incorporated into the model. We propose that a consequence of the disruption of these four circuits is an enhanced value of one type of reinforcer (drugs for the drug abuser and high-density food for the obese individual) at the expense of other reinforcers, which is a consequence of conditioned learning and resetting of reward thresholds secondary to repeated stimulation by drugs (drug abuser/addict) and by large quantities of high-density food (obese individual) in vulnerable individuals.
A consequence of the impairment in the reward/saliency circuit (processes mediated in part through NAc, ventral pallidum, medial OFC and hypothalamus), which modulates our response to both positive and negative reinforcers, is a decreased value to stimuli that otherwise would motivate behaviours likely to result in beneficial outcomes while avoiding behaviours that could result in punishment. For the case of drug abuse/addiction, one can predict that as a result of dysfunction in this neurocircuit the person would be less likely to be motivated to abstain from drug use because alternative reinforcers (natural stimuli) are much less exciting and negative consequences (e.g. incarceration, divorce) are less salient. For the case of obesity, one can predict that as a result of dysfunction in this neurocircuit the person would be less likely to be motivated to abstain from eating because alternative reinforcers (physical activity and social interactions) are less exciting and negative consequences (e.g. gaining weight, diabetes) are less salient.
A consequence of disruption of the inhibitory control/emotional regulation circuit is the impairment of the individual to exert inhibitory control and emotional regulation (processes mediated in part through the DLPFC, CG and lateral OFC), which are critical components of the substrates necessary to inhibit prepotent responses such as the intense desire to take the drug in an addicted subject or to eat high-density food in an obese individual. As a result, the person is less likely to succeed in inhibiting the intentional actions and to regulate the emotional reactions associated with the strong desires (either to take the drug or to eat the food).
The consequences of the involvement of memory/conditioning/habits circuit (mediated in part through hippocampus, amygdala and dorsal striatum) are that repeated use of drugs (drug abuser/addict) or repeated consumption of large quantities of high-density food (obese individual) results in the formation of new linked memories (processes mediated in part through hippocampus and amygdala), which condition the individual to expect pleasurable responses, not only when exposed to the drug (drug abuser/addict) or to the food (obese individual) but also from exposure to stimuli conditioned to the drug (i.e. smell of cigarettes) or conditioned to the food (i.e. watching TV). These stimuli trigger automatic responses that frequently drive relapse in the drug abuser/addict and food bingeing, even in those who are motivated to stop taking drugs or to lose weight.
The motivation/drive and action circuit (mediated in part through OFC, dorsal striatum and supplementary motor cortices) is involved both in executing the act and in inhibiting it and its actions are dependent on the information from the reward/saliency, memory/conditioning and inhibitory control/emotional reactivity circuits. When the value of a reward is enhanced owing to its previous conditioning, it has greater incentive motivation and if this occurs in parallel to a disruption of the inhibitory control circuit this could trigger the behaviour in a reflexive fashion (no cognitive control; ). This could explain why drug-addicted subjects report taking drugs even when they were not aware of doing so and why obese individuals have such a difficult time in controlling their food intake and why some individuals claim that they take the drug or the food compulsively even when it is not perceived per se as pleasurable.
Figure 5 Model of brain circuits involved with addiction and obesity: reward/saliency motivation/drive, memory/conditioning and inhibitory control/emotional regulations. Disrupted activity in brain regions involved with inhibitory control/emotional regulation (more ...)
In this model, during exposure to the reinforcer or to the cues conditioned to the reinforcer, the expected reward (processed by memory circuit) results in overactivation of the reward and motivation circuits while decreasing the activity in the cognitive control circuit. This contributes to an inability to inhibit the drive to seek and consume the drug (drug abuser/addict) or the food (obese person) despite the attempt to do so (). Because these neuronal circuits, which are modulated by DA, interact with one another, disruption on one circuit can be buffered by the activity of another, which would explain why an individual may be better able to exert control over their behaviour to take drugs or food on some occasions but not on others.