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Drug, Food Addiction Share Common Source

A new study shows that the same molecular mechanisms that drive an individual into drug addiction are behind the compulsion to overeat, pushing an individual into obesity. An individual rat, at least. The finding supports the hypothesis that people with obesity have been making for years — that, like addiction to other substances, junk food binging is extremely difficult to stop.
The new study, conducted by Associate Professor Paul J. Kenny and graduate student Paul M. Johnson of Scripps Research Institute, was published in an advance online edition of the journal Nature Neuroscience. The study demonstrates that in rat models, the development of obesity coincides with a progressively deteriorating chemical balance in a rat’s reward brain circuitry.
The very same changes occur in the brains of rats that over-consume cocaine or heroin, and are thought to play an important role in the development of compulsive drug use. Kenny, a scientist at Scripps Research’s Florida campus, said that the study, which took nearly three years to complete, confirms the “addictive” properties of junk food. 
“They always went for the worst types of food,” Kenny said, “and as a result, they took in twice the calories as the control rats. When we removed the junk food and tried to put them on a nutritious diet – what we called the ’salad bar option’ – they simply refused to eat. The change in their diet preference was so great that they basically starved themselves for two weeks after they were cut off from junk food. It was the animals that showed the “crash” in brain reward circuitries that had the most profound shift in food preference to the palatable, unhealthy diet. These same rats were also those that kept on eating even when they anticipated being shocked.”
What happens in addiction is lethally simple, Kenny explained. The reward pathways in the brain have been so over stimulated that the system basically turns on itself, adapting to the new reality of addiction, whether it is cocaine or cupcakes. “The body adapts remarkably well to change—and that’s the problem,” said Kenny.  “When the animal over stimulates its brain pleasure centers with highly palatable food, the systems adapt by decreasing their activity. However, now the animal requires constant stimulation from palatable food to avoid entering a persistent state of negative reward.”
After showing that obese rats had clear addiction-like food-seeking behaviors, Johnson and Kenny next investigated the underlying molecular mechanisms that may explain these changes. They focused on a particular receptor in the brain known to play an important role in vulnerability to drug addiction and obesity – the dopamine D2 receptor. The D2 receptor responds to dopamine, a neurotransmitter that is released in the brain by pleasurable experiences like food, sex or illegal drugs. 
In cocaine abuse, for example, the drug alters the flow of dopamine by blocking its retrieval, flooding the brain and over stimulating the receptors, something that eventually leads to physical changes in the way the brain responds to the drug.  The new study shows that the same thing happens in junk food addiction.  “These findings confirm what we and many others have suspected,” Kenny said, “that over consumption of highly pleasurable food triggers addiction-like neuroadaptive responses in brain reward circuitries, driving the development of compulsive eating. Common mechanisms may therefore underlie obesity and drug addiction.”
Consistent with common mechanisms explaining addiction and obesity, levels of the D2 dopamine receptors were significantly reduced in the brains of the obese animals, similar to previous reports of what happens in human drug addicts, Kenny noted.  Remarkably, when the scientists knocked down the receptor using a specialized virus, the development of addiction-like eating was dramatically accelerated.  “This addiction-like behavior happened almost from the moment we knocked down the dopamine receptors,” Kenny noted. 