Silence of the Newts

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Three dead men. No clues. Just a newt. And he wasn’t spilling the beans. 

Spend enough time in the Oregon Coast Range, and you'll hear the local legend of three friends who went hunting for the weekend and disappeared without a trace. How it took weeks for police to locate the bodies. How, when they did, the men were found dead at a campsite with no sign of foul play.

The story’s been told since the 1950s, long before the days of CSI. And while few meaningful clues were found at the scene, there’s a kicker—the fourth corpse, a rough-skinned newt lying in the men’s coffeepot, likely scooped up with the stream water and boiled with the grounds. With no leads, police simply left the case open.

A decade later, that’s the tale Doc Walker, a biology professor at Oregon College of Education, told his student Edmund Brodie Jr. The undergrad had been hunting for a research project, and Walker suggested that Brodie investigate.

“This was not a question anyone thought important,” recalls Brodie. Still, the thought of killer newts intrigued him. Armed with a single syringe, some buckets, a few traps, and a mortar and pestle, Brodie devised an experiment. He started by using the buckets to collect newts in the ponds where they bred. Then he scoured the nearby woods, trapping potential predators—birds, mice, fish. After setting up a tiny lab in an old campus building, Brodie used the mortar and pestle to grind up the newt skin into a fine powder, which he mixed up into different concentrations.

"The first mouse I injected with macerated skin died in my hand before I could put it back in its cage," says Brodie. "I was ghost white."

Stunned by the result, Brodie ran to get Walker, who accompanied him back to the lab. When he repeated the procedure in front of his professor, it happened again. Every animal that received a dose of newt skin fell ill. Depending on the concentration of skin in the shot, the animals would have trouble walking, vomit uncontrollably, stop moving, or die.

Brodie’s fascination with newts blossomed. He continued to study the creatures through his undergrad degree and into his work on a master’s from nearby Oregon State University. Then one day a colleague came into the lab with the latest copy of Science. On the cover was a newt. Unbeknownst to Brodie, a group of chemists at Stanford University had been studying the creatures as well, and they’d made a breakthrough. They’d identified the newt’s poison as tetrodotoxin, or TTX.

Here’s why the toxin’s so deadly: When consumed or absorbed, TTX binds to the sodium channels on the surfaces of neurons, blocking the electrical signals the cells use to communicate. With the nervous system’s lines of communication severed, a TTX sufferer experiences numbness, muscle spasms, dizziness, loss of speech, and paralysis—exactly what Brodie had observed in his test subjects. If the dose is strong enough, an agonizing death comes by cardiac arrhythmia or oxygen depletion. And in a sinister twist, the victim remains completely aware of what’s going on since TTX doesn’t affect the brain.

Brodie was disappointed to get scooped, but the Stanford report excited him. The identification of the toxin freed him up to answer what he thought was the more interesting question: Why did a single newt carry enough TTX to kill a hundred men? Why would one newt need that much poison?


Brodie’s breakthrough occurred when he spotted a garter snake chowing down on a newt in one of his buckets. The little snake, no more than half a pound, downed the entire newt. To Brodie’s amazement, it showed no sign of TTX poisoning.

Up to this point, Brodie had deliberately avoided studying snakes—they gave him the willies. But his fascination trumped his phobia: Brodie began collecting garters and observing them feast on newts. Miraculously, the snakes suffered no ill effects, resisting toxic doses that could have killed animals hundreds of times their size. Was the snakes’ resistance to TTX a by-product of their physiology? Or had it evolved in direct response to the poisonous meals?

Brodie speculated that the snakes’ resistance explained the newts’ extreme toxicity; the two species could be evolving in response to each other, a tit-for-tat adaptation in competing species that biologists call coevolution. Pressure applied by one species drives an adaptation in the other, and that evolutionary response puts pressure back on the first species to deal with it.

Over the next 30 years, Brodie studied the snakes and newts, and his research turned into a family business. His son, Dr. Edmund D. Brodie III, joined the effort, and together the Brodies found that only a handful of the snakes’ genes are involved in developing TTX resistance. More important, the reptiles have the ability to adapt quickly. Through decades of experiments and observations, the two Brodies showed that the newts had indeed developed toxicity as a defense against predators. The snakes, in turn, developed a resistance to the poison so they could continue to eat newts, driving the newts to increase their toxicity. The two species kept adapting to each other’s defenses like two nations developing bigger and badder nuclear weapons—an evolutionary arms race.


The cold-blooded war between newts and snakes rages on today. The animals share space in forests from southern California up through British Columbia. Where low toxicity newts are found, the snakes in the area have lower resistance to TTX; highly toxic newts are neighbors to the most resistant snakes.

But there are a few especially interesting battlegrounds scattered between San Francisco and Vancouver Island. In these spots, the least resistant snakes can eat the most toxic newts. It turns out that newts can keep only a limited amount of toxin in their skin. They’re not big animals, so the most poisonous newts the Brodies have come across max out at a little more than 10 milligrams of TTX. Meanwhile, the most resistant snakes can survive a hit of 100 milligrams, an amount that appears to be well beyond the upper limit of what a single newt can carry.

While it seems the snakes have won the evolutionary battle, don’t count out the newts just yet. The mutation that gives the snakes immunity also appears to make them slower than their less-resistant cousins. If this turns out to hinder their survival, the snakes would be pressured to skimp on their TTX resistance for a little more speed, setting the stage for a thrilling newt comeback.

This story originally appeared in mental_floss magazine. Subscribe here!