Python Biology: Nature’s Blueprint for Human Medicine?
When Skip Maas adopted Agrapina, a mottled ball python, she hadn’t eaten in 14 months. Yet she remained a taut coil of spring-loaded muscle — strong enough to strike, constrict, and devour a rat the moment one was offered.
That display of raw power after prolonged fasting is precisely what makes pythons extraordinary — and what has a team of researchers at the University of Colorado Boulder convinced these snakes may hold keys to treating human disease.
Maas, a molecular biologist who recently completed his Ph.D. in Leslie Leinwand’s lab at CU Boulder, observed Agrapina’s post-meal metabolism accelerate dramatically to break down the sudden influx of protein and fats. It’s a feat pythons are known for — and one that could have profound medical implications.
An Extreme Metabolism
“Pythons ramp up their metabolism from 10 to 40 times following a feeding, depending on the size of the meal,” says Tommy Martin, an assistant professor at the University of Nebraska Medical Center and a former researcher in Leinwand’s lab.
Jack Gugel, a molecular biologist at CU Boulder and another former Leinwand student, puts that in perspective: It’s the equivalent of a Kentucky Derby racehorse at rest compared to when it’s sprinting around the track. But pythons sustain that high metabolic state for days as they digest.
To handle the demand, the python’s body undergoes a dramatic renovation. Organs actually grow — including the heart, which enlarges to pump more blood and oxygen for digestion. Then, roughly a month after feeding, the heart returns to its previous size.
The Heart of the Matter
Human hearts can enlarge too, but when that growth stems from high blood pressure or a heart attack, the enlargement is permanent and the heart stiffens — often with fatal consequences. “Some people, no matter what they do, even if they have the perfect diet and they’re exercising every day, they’re still going to have heart disease,” says Gugel.
The python’s ability to grow and then shrink its heart reversibly caught the researchers’ attention. Gugel’s central question: What signals tell the heart to enlarge, and what signals tell it to return to normal?
Yuxiao Tan, a molecular biologist at CU Boulder supervised by Leinwand, has uncovered another key insight in a soon-to-be-published study. Python cardiac muscle cells don’t just grow larger after feeding — they increase in number. In humans, heart muscle cells cannot proliferate, which is why heart attacks leave permanent scar tissue.
Resisting Muscle Atrophy
Pythons also defy conventional biology when it comes to muscle preservation. Agrapina, after months without food and barely moving, lost very little muscle tone. “I know of no other creature that can do this kind of fasting without losing muscle function,” says Leinwand, who believes this ability could eventually lead to treatments for age-related muscle atrophy.
A Molecular Gold Mine
Leinwand points to the countless small molecules pythons produce as they digest a meal as a potential “gold mine” for drug discovery. This spring, she and collaborators from multiple institutions published a paper in Nature Metabolism describing a molecule found in the blood of both Burmese and ball pythons that surged a thousand-fold after feeding.
The molecule, called pTOS, appears to function as an appetite suppressant by targeting the hypothalamus. “When we give this molecule to obese mice, they eat less and they lose weight,” says Gugel.
Leinwand’s instinct was straightforward: “If I were a betting person, I’d bet that something that changes a thousand-fold is probably doing something important.”
Evolution’s Natural Experiments
Jasmin Camacho, an evolutionary biologist at the Stowers Institute for Medical Research who was not involved in the python research, sees this work as part of a broader strategy of mining extreme biology for medical breakthroughs. “By going to this extreme animal, that molecule was expressed at a higher level in a way that it just stood out,” she says.
Camacho studies nectar-feeding bats that consume large amounts of sugar without apparent health consequences — a trait she believes could inform diabetes research. “Evolution’s been running natural experiments for hundreds of millions of years,” she says. “So by studying these adaptations, we start to think of other ways that our bodies can work.”
The parallel is already proven. GLP-1 weight-loss drugs like Ozempic emerged from research on the venomous Gila monster lizard. Gugel hopes for a similar trajectory for pTOS. “I think that there’s big potential in the market for a drug that specifically can inhibit appetite in the brain to help people with weight loss,” he says.
Two decades ago, Leinwand first proposed that python biology could translate into medical treatments. Today, her lab’s ongoing work — spanning cardiac remodeling, muscle preservation, and metabolic regulation — suggests she may have been right all along. Nature, it turns out, has already run the experiments. The question is whether we can read the results.