In all fairness to Hostess, it's not just Ding-Dongs. The cream-filled chocolate snack cakes were just one of the "high-fat, palatable foods" that Kenny and Johnson used to test if obesity in rats could alter the neurological chemistry of their brains the same way that cocaine or heroin use did. And the answer they discovered was: yes, it can.
In the brains of rats (and humans), a neurotransmitter called dopamine is released by pleasurable experiences. So the initial intake of highly palatable foods (or use of a drug like cocaine) releases dopamine, stimulates something called the dopamine D2 receptors, and causes a good psychological feeling. But what Kenny and Johnson found was that as their test rats ate more and more of the high-fat food, and became obese, the resulting regular overstimulation of the D2 receptors caused the brain to compensate -- just like it apparently does in the case of cocaine users. The D2 receptors became less sensitive. So what began as impulsive behavior became compulsive behavior: the rats had to keep overindulging in the high-fat food just to keep their D2 receptors stimulated enough to avoid feeling bad.
"What we found, in essence, was that the rats were in a persistent state of withdrawal," Kenny said.
The researchers also found that the obese rats' need for the high-fat food became so great that they would continue to seek it out even when it was associated with electric shocks. And when the high-fat food was taken away, the obese rats chose not to eat at all rather than partake of more healthy food, even though they were hungry. It wasn't a matter of normal choice anymore. The rats had become, quite literally, addicted to the food.
"This whole notion of being addicted to food is kind of fascinating and strange," Kenny said. "I mean, in a sense, we kind of all are [addicted to food]." But the especially yummy, high-fat foods created the same changes in brain chemistry, and the same shift from impulsive to compulsive use, as had previously been observed with cocaine or heroin.
"One of the important things we found was that access to palatable foods mattered," Kenny noted. "The more access [the rats] had, the more likely they were to 'use' a ding dong. And the more often they 'used' it, the more likely they were to 'use' it again."
Kenny and Johnson even tested how a genetic predisposition to addiction might affect the rats' response to the high-fat food. They gave one group of rats a virus that knocked down the activity of their D2 receptors, simulating the brain chemistry of people who are thought to have "addictive personalities," or a DNA inclination toward addiction. (In human studies, people with low D2 receptor levels have been found to have a greater inclination toward risky, impulsive behavior -- and a greater vulnerability to drug use and addiction.) Kenny and Johnson found that the rats with the artificially-lowered D2 levels did, indeed, become compulsive eaters of the high-fat food more quickly than their control group counterparts.
What are the implications of all this? Well, for starters, the research offers a far scarier take on the hazards of unhealthy eating. It's one thing to resist overindulging in cheesecake and Ding-Dongs because they'll get you fat -- and potentially bring on physical health problems thought to be associated with obesity. But it's far more sobering to think that the very act of eating too much high-fat food can alter our brain chemistry, making us dependent on more of it. Especially because, as Kenny said, reversing those "addictive" changes in psychological/neurological brain chemistry takes far longer, and is a far greater challenge, than overcoming any physical withdrawal or need for a substance.
The results also offer a new twist in how we view persistent obesity. If an obese person has to keep eating high-fat food to avoid the psychological crash of withdrawal, losing weight isn't just an easy matter of making better food choices. It's a far more complex and daunting challenge that might need to be approached like we now approach drug rehabilitation. Of course, Overeaters Anonymous has intuitively understood this for years. But Kenny and Johnson's research potentially offers a cellular, neurological underpinning for that idea.
But more than anything else, Kenny and Johnson's research underscores just how important Michelle Obama's new crusade is. If access to junk food is a big factor in the development of an addiction, and the changes in brain chemistry are far tougher to undo than they are to avoid, then getting parents and schools to limit that access for children is really critical. Not just for kids' physical health, but for their long-term neurological health as well. And while Kenney's research didn't specifically test whether rats with lower D2 levels from overeating were then more inclined to undertake other risky behaviors, that would certainly be another argument for fighting childhood obesity.
Admittedly, it's a little hard to think of cheesecake in the same category as cocaine. It's like the Brazilian caipirinha: a drink so light, fruity, and yummy that it's hard to believe it packs the punch of a double martini. But Kenny and Johnson's research at least helps explain why eating dessert and junk food feels sooooo good. It's because they're titillating a lot more than just our taste buds. And if junk food really does mess with our brain chemistry over time, or if we gain too much weight from it, it's a pretty compelling reason to make smarter food choices -- while we still have the control to make them.
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