Scientific Understanding of Consciousness
Junk Food Addiction
Nature Neuroscience Published online 28 March 2010
Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats
Paul M Johnson & Paul J Kenny
Laboratory of Behavioral and Molecular Neuroscience, Department of Molecular Therapeutics, The Scripps Research Institute-Scripps Florida, Jupiter, Florida, USA.
We found that development of obesity was coupled with emergence of a progressively worsening deficit in neural reward responses. Similar changes in reward homeostasis induced by cocaine or heroin are considered to be crucial in triggering the transition from casual to compulsive drug-taking. Accordingly, we detected compulsive-like feeding behavior in obese but not lean rats, measured as palatable food consumption that was resistant to disruption by an aversive conditioned stimulus. Striatal dopamine D2 receptors (D2Rs) were downregulated in obese rats, as has been reported in humans addicted to drugs. Moreover, lentivirus-mediated knockdown of striatal D2Rs rapidly accelerated the development of addiction-like reward deficits and the onset of compulsive-like food seeking in rats with extended access to palatable high-fat food. These data demonstrate that overconsumption of palatable food triggers addiction-like neuroadaptive responses in brain reward circuits and drives the development of compulsive eating. Common hedonic mechanisms may therefore underlie obesity and drug addiction.
Feeding is influenced by pleasure and reward, and obtaining food reward can powerfully motivate consumption. Activity in the dorsal and ventral striatum, which are core components of brain reward circuits, increases markedly in response to images of food. This suggests that the striatum is important in hedonic aspects of feeding behavior. It was shown recently that activation of the striatum in response to highly palatable food is blunted in obese individuals when compared with lean controls. These and similar observations have led to the proposal that deficits in reward processing may be an important risk factor for the development of obesity, and that obese individuals may compulsively consume palatable food to compensate for reward hyposensitivity. Notably, it is unclear whether deficits in reward processing are constitutive and precede obesity, or whether excessive consumption of palatable food can drive reward dysfunction and thereby contribute to diet-induced obesity.
A defining characteristic of overweight and obese individuals is that they continue to overeat despite the well known negative health and social consequences. Indeed, many overweight individuals express a desire to limit their food consumption, yet struggle to control their intake and repeatedly consume beyond their energy requirements. Development of feeding behavior that is insensitive to negative outcome is analogous to the compulsive drug-taking behavior seen in human drug addicts, which is similarly impervious to negative consequences. Here we investigated the effects of extended access to a palatable high-fat diet on the sensitivity of brain reward systems in rats. We also examined the link between diet-induced hedonic dysregulation and the emergence of compulsive food seeking.
In summary, we found that over-stimulation of brain reward systems through excessive consumption of palatable, energy-dense food induces a profound state of reward hyposensitivity and the development of compulsive-like eating. These maladaptive behavioral responses in obese rats probably arise from diet-induced deficits in striatal D2R signaling. Overconsumption of drugs of abuse similarly decreases striatal D2R density, induces a profound state of reward hypofunction and triggers the emergence of compulsive-like drug-taking behaviors. Our findings therefore support previous work in indicating that obesity and drug addiction may arise from similar neuroadaptive responses in brain reward circuits.
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