New work from Paul Johnson and Paul Kenny (Scripps Research Institute, Jupiter, FL) has elucidated the neurobiology underlying compulsive eating. Their results suggest that rats with easy access to high-fat diets may become addicted to the 'junk' food.
Johnson and Kenny used three groups of rats in their studies, all of which had unlimited access to standard rat chow. In addition to rat chow, one group also had limited access (1 hour per day) to junk food, and another group had almost unlimited access (18–23 hours per day) to junk food. The junk food included high-fat, high-calorie items such as bacon, sausage, cheesecake, pound cake, frosting and chocolate. After 40 days, the high-fat diet was removed and all the groups were given only standard rat chow. The researchers monitored the rats' body weight and caloric intake throughout the experiment, as well as the responsiveness of the rats' brain reward systems.
Rats given the most access to junk food consumed almost twice as many calories as control rats and quickly became obese (Nat. Neurosci. published online 28 March 2010; doi:10.1038/nn.2519). Overconsumption of the high-fat foods triggered a gradual increase in reward thresholds, such that the rats' brains required more of the foods in order to feel satisfied, indicating that the reward system had become unbalanced and unresponsive. The rats also developed compulsive, binge-like eating behavior, possibly as a result of the unresponsiveness of their brain reward systems. These rats would continue bingeing on the high-fat diet even when they knew they would receive a shock if they did; control rats stopped eating when they knew a shock would be coming.
The brain circuit changes in these rats were similar to those observed in rats allowed to self-administer cocaine or heroin, suggesting that overconsumption of junk food and drug addiction may share a similar neurological mechanism. To investigate this mechanism further, the researchers focused on dopamine D2 receptors, which are known to be involved in vulnerability to obesity and addiction. Dopamine is a neurotransmitter released by pleasurable experiences. They found that expression of D2 receptors was decreased in brains of obese rats. Additionally, when they used a lentivirus to reduce expression of D2 receptors in rats with extended access to the high-fat diet, development of compulsive eating and brain circuit changes was much faster.
Although these results can't be applied directly to humans, they suggest that common mechanisms may be involved in both obesity and addiction.