A new study suggests ghrelin — the hunger hormone — plays a key role in triggering individuals to indulge in high-calorie, high-fat comfort foods in response to stress.
Using a mouse model, researchers believe ghrelin is responsible for initiating unhealthy eating behavior.
“This helps explain certain complex eating behaviors and may be one of the mechanisms by which obesity develops in people exposed to psychosocial stress,” said Dr. Jeffrey Zigman, senior author of the study.
“We think these findings are not just abstract and relevant only to mice, but likely are also relevant to humans.”
The study is published online and will be found in a future print edition of the Journal of Clinical Investigation.
Prior research has found that fasting causes ghrelin to be released from the gastrointestinal tract, and that the hormone then plays a role in sending hunger signals to the brain.
Zigman’s lab at the University of Texas Southwestern Medical Center has previously shown that chronic stress also causes elevated ghrelin levels, and that behaviors generally associated with depression and anxiety are minimized when ghrelin levels rise.
In mice, these stress-induced rises in ghrelin lead to overeating and increased body weight, suggesting a mechanism for the increased prevalence of weight-related issues observed in humans with chronic stress and depression.
In the current study, researchers developed a mouse model to determine which hormones and what parts of the brain may play a role in controlling more complex eating behaviors that occur upon stress, particularly those that lead to the indulgence of comfort foods.
They subjected mice to a standard laboratory technique that induces social stress by exposure to more dominant “bully” mice. Such animals have been shown to be good models for studying depression and the effects of chronic stress and depression in humans.
Wild-type mice subjected to the stress gravitated toward a chamber where they had been trained to find pleasurable, fatty food – the mouse equivalent of “comfort food.”
However, genetically-engineered mice, which were not able to respond to stress-induced increases in ghrelin, showed no preference toward the fatty food-paired chamber, and when exposed to the fatty food, did not eat as much as the wild-type animals.
“Our findings show that ghrelin signaling is crucial to this particular behavior and that the increase in ghrelin which occurs as a result of chronic stress is probably behind these food-reward behaviors,” Zigman said.
The researchers discovered ghrelin influences the transmission of nerve signals to the area of the brain associated with pleasure and reward behaviors.
The findings, he said, may make sense when considered from an evolutionary standpoint.
Our hunter-gatherer ancestors needed to be as calm as possible when it was time to venture out in search of food, or risk becoming dinner themselves, said Zigman, who pointed out that ghrelin’s antidepressant effects and its actions to help efficiently secure calorically dense, tasty foods may have provided a survival advantage.
“Though it might have been beneficial to have these actions of ghrelin linked, now it seems to be a cause of a lot of morbidity in our modern society,” Zigman said. “Ultimately, these linkages also may present a large challenge to the development of therapeutics to treat and/or prevent obesity.”
Researchers now plan to study the molecular action by which ghrelin acts to cause these stress-associated food-reward behaviors.
Source: UT Southwestern Medical Center