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Imagine if you could spend a few months each winter in hibernation—you’re curled up in bed, your heart rate, body temperature, and brain activity drastically low. Then you emerge in the spring, ready to get back to your normal routine having recovered from these health changes almost immediately. For animals like bears, snakes, bats, and more, that’s typical. For humans, that would be considered a medical miracle.
However, according to two studies, both published in Science, the recovery superpowers of hibernating animals might not be as foreign to us as we think. Indeed, the very same genetic instructions these animals have might actually be tucked away in our own DNA.
In order to fully understand why this might be the case, it’s important to understand how hibernating animals recover from extreme health changes.
“Hibernating animals go through dramatic physiological shifts. Their body temperature can drop close to the surrounding environment, their heart rate slows dramatically, metabolism falls to just a few percent of normal, and brain activity is greatly reduced. In humans, changes like this would cause serious injury. In hibernators, they are temporary and fully reversible,” says Christopher Gregg, PhD, professor in neurobiology and human genetics at University of Utah Health and senior author of the two new studies.
What allows their recovery is not a special “hibernation organ,” Gregg explains, but a “highly coordinated genetic program.”
“When hibernators rewarm and start eating again, their brains—especially a region called the hypothalamus that controls metabolism—rapidly activate thousands of genes. We found that this refeeding and recovery phase is actually when the biggest molecular changes occur,” he says.
These animals have regulatory DNA switches, called cis-regulatory elements, that control how genes turn on and off during fasting and recovery, according to Gregg. Over millions of years, hibernating animals have evolved subtle changes in these switches, many of which remove the constraints that normally keep metabolism stable all year long.
“The result is extraordinary flexibility: They can safely suppress metabolism, then reboot it without damage,” Gregg says. “In short, hibernators don’t just survive hibernation—they are genetically programmed for safe recovery.”
Understanding how hibernating animals recover from the aforementioned physiological changes could eventually lead to treatments that would help reverse health conditions like type 2 diabetes.
“Type 2 diabetes is, at its core, a disorder of metabolic inflexibility,” Gregg says. “The body struggles to shift between fasting and fed states. Insulin signaling becomes dysregulated, energy storage and use become imbalanced, and tissues accumulate damage.”
Hibernating animals show the opposite pattern, Gregg explains. They intentionally become insulin resistant before hibernation, suppress metabolism, and then reverse those changes when they refeed—without long-term harm. “That tells us the biology of metabolic flexibility already exists in mammals,” he says.
In order to come to this conclusion, Gregg and his colleagues analyzed the genomes of multiple hibernating species and compared them to non-hibernating mammals, including humans.
“We focused on DNA regions that have been conserved for about 100 million years—meaning they are biologically important,” he says. “We then asked: Which of these conserved regulatory regions have changed in hibernators in similar ways across different mammalian species that independently evolved hibernation?”
When he and his colleagues found those overlapping changes, they traced them to the genes they regulate in the brains of mice. Many of those genes control metabolic responses to fasting and refeeding, he explains. Importantly, the same regulatory DNA regions are found in the brains of humans.
“That means humans already carry much of the same genetic circuitry. Hibernators didn’t invent new genes. Instead, they fine-tuned existing regulatory switches,” he says. “The framework for metabolic flexibility is evolutionarily ancient and shared. The difference is how it is wired and deployed.”
He says that if scientists can understand and safely modulate these regulatory switches, they may be able to do the following in the future:
“The goal would not be to make people hibernate. It would be to harness the biology of safe metabolic shutdown and recovery to protect organs during stress—such as in diabetes, obesity, aging, or even surgery—and to enhance biological flexibility and neuroprotection for healthy aging and disease prevention,” Gregg says.
Danielle Zickl is a freelance writer who has 10 years of experience covering fitness, health, and nutrition. She's a graduate of Ithaca College. You can find her work here on Women's Health, and in many other publications including PS, SELF, Well+Good, Runner’s World, Outside RUN, Peloton, Men’s Fitness, and more.
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