Each spring, a grizzly bear emerges from its den after months of deep hibernation — having eaten nothing, barely moved and slowed its heart and metabolism to a crawl. Yet it wakes up strong, alert and healthy.
Its muscles remain intact. Its organs are unharmed. And any signs of metabolic stress seem to vanish as if they were never there.
What if humans had access to the same biological resilience?
That is the question scientists at the University of Utah asked, and they now believe they might have an answer. Their latest research, stemming from two studies, suggests that the genetic tool kit that enables animals like bears to survive hibernation could also exist in humans, lying dormant within their DNA. If scientists can learn to activate it, it could transform the treatment of chronic diseases like Type 2 diabetes, stroke and Alzheimer’s.
“Humans already have the genetic framework,” said Dr. Susan Steinwand, lead author in one of the studies. “We just need to identify the control switches for these hibernator traits.”
According to the research published in Science, some of the same genetic switches that enable hibernation may already exist in humans, they’ve just never been used.
“There’s potentially an opportunity — by understanding these hibernation-linked mechanisms in the genome — to find strategies to intervene and help with age-related diseases,” said Dr. Chris Gregg, senior author of the studies and professor of neurobiology and human genetics at University of Utah Health.
The DNA link
The study focused on a familiar part of the genome: the FTO locus, known as a major risk factor for obesity in humans. Surprisingly, this same region also plays a central role in hibernating animals’ ability to slow metabolism and survive extreme conditions. By instead studying the genes directly, the Utah team zoomed in on noncoding regions of DNA, specifically stretches of DNA called cis-regulatory elements, or CREs. These elements act like “dimmer switches,” controlling how much or how little nearby genes are expressed.
“What’s striking about this region is that it is the strongest genetic risk factor for human obesity,” Gregg noted.
The researchers likened finding these genetic regions to searching for needles in a “a massive DNA haystack.”
To test their effects, scientists mutated hibernator-specific DNA regions in mice and tracked the results. They saw changes in weight, metabolic rate and even the ability to regulate body temperature, responses similar to those seen in hibernating animals.
“When you knock out one of these elements — this one tiny, seemingly insignificant DNA region — the activity of hundreds of genes changes,” Steinwand said. “It’s pretty amazing.”
In fact, the regions highlighted weren’t genes at all, but control elements, similar to traffic signals directing the flow of genetic activity.
“This means that mutating a single hibernator-specific region has wide-ranging effects extending far beyond the FTO locus,” Steinwand added.
What this could mean for medicine
These findings hope to revolutionize treatments for metabolic and neurological conditions. Understanding hibernators’ metabolic flexibility could lead to better treatments for human metabolic disorders like Type 2 diabetes, the researchers say.
“If we could regulate our genes a bit more like hibernators,” said Elliott Ferris, bioinformatician at U of U Health and first author on the second study, “maybe we could overcome Type 2 diabetes the same way that a hibernator returns from hibernation back to a normal metabolic state.”
A complementary study from Oregon
Scientists at Oregon Health and Science University are also exploring ways to replicate hibernation-like states in humans. In a recent study, researchers identified a brain-based mechanism called thermoregulatory inversion, a process that allows animals to lower their core body temperature without triggering the usual warming responses like shivering or burning a specific type of fat in the body, brown fat. Essentially, it flips the body’s natural survival settings.
“The idea is to reduce the body temperature to a lower level so that tissues like the brain or heart don’t need as much oxygen,” Dr. Domenico Tupone, senior author of the OHSU study, explained. “That could improve outcomes from strokes or heart attacks.”
In typical mammals, exposure to cold triggers heat generation. But in hibernators, that response is flipped — allowing them to survive long periods with little energy use.
“If we had a mechanism that allows us to transform humans into hibernating animals,” Tupone added, “we could achieve and control therapeutic hypothermia much better.”
This could one day allow doctors to safely lower a person’s body temperature during medical emergencies like heart attacks or strokes, giving vital organs more time to survive reduced oxygen flow.
By learning how to activate or mimic these gene switches, researchers from both universities hope to unlock hibernation’s secrets — not to help sleep through winter, but to transform how diseases, injury and aging itself are treated.
“If that’s hidden in the genome that we’ve already got,” Gregg says, “we could learn from hibernators to improve our own health.”