Evolutionary anthropologists can be an argumentative lot, a professional trait due, perhaps, to the often speculative nature of their research. One proposition, however, generates little disagreement: Over many thousands of years human genes have been selected to maximize our ability to take in calories and put on fat.
In the prehistoric milieu where food insecurity was a given, a genetic predisposition toward eating and weight gain would confer an obvious advantage. In lean times, humans who consumed and retained fat would starve less quickly. Those who starved less quickly would have a better shot at sniffing out that next life-sustaining meal.
Thus did our early brains evolve to seek out calorie-rich foods. And to ensure that our ancestors didn’t push back from the woolly mammoth too soon, their hungry minds also released feel-good chemical enhancements, certain endogenous boosters, that made gorging pleasurable. Trouble is, what’s good for the Homo erectus is not necessarily good for the Homo sapien — especially when said Homo sapien is contemplating a Chili Cheese Thickburger at the Hardee’s drive-through.
“A key to curbing the obesity epidemic in America is controlling the desire to binge eat,” says Matthew Will, a behavioral neuroscientist and assistant professor of psychological sciences at MU. “Humans have more programming to start and continue eating than to stop eating, especially when they have a bowl of ice cream in front of them.”
How might we unlearn this propensity to overindulge? Will says one way forward involves determining which areas of brain circuitry make binge eating pleasurable, then instructing those circuits not to fire.
His latest research, the results of which were published in the August edition of the journal Behavioral Neuroscience, moves scientists closer to that goal. The study involved deactivating a group of lab rats’ basolateral amygdala (BLA), an area of the brain involved in regulating emotion.
Will hypothesized that fatty food overconsumption might have more to do with the emotions of eating—as driven by pleasure-producing opioids—rather than the strict need for sustenance. So Will compared how the deactivated BLAs would affect differing forms of high-fat bingeing; one driven by the administration of opioids, another by hunger produced via 24 hours of food deprivation.
After the procedure, Will discovered the opioid group no longer felt a desire to binge. “Confirming previous reports,” he wrote, “inactivation of the BLA completely prevented the opioid-induced enhancement of high-fat diet intake but had no effect on feeding in hungry rats.”
That the procedure didn’t diminish feeding in food-deprived rats was particularly intriguing. “The finding that the basolateral amygdala only appears involved in the opioid-produced consumption was the most surprising part of the study,” Will says. “Normally, if a rat stops eating, he will go lie down and take it easy. In this case, they showed all the signs of still wanting to eat, but didn’t.”