The Triumph of Seeds (27 page)

I knew this history when I sat down to sample a few of the roasted seeds with my dissertation adviser, and coauthor of all my
almendro
papers, Steve Brunsfeld. The fact that he was a liver cancer survivor didn’t faze us. In botany, tasting weird things goes with the job description—flavors and smells are often valuable tools in identifying plants. Still, we limited ourselves to a few nibbles, just enough to appreciate what struck me as a combination of vanilla and cinnamon, with a citrus finish. Steve wrinkled his mustache and described
the flavor more simply: “These things taste like furniture polish.” The comment was typical Steve: sharp, funny, and straight to the point. But our
almendro
-tasting moment was also deeply ironic. At the time, neither of us knew that Steve’s cancer had reawakened and spread to other parts of his body, and that within a few months his doctors would probably start prescribing a variation of the very compound we’d been joking about.

Since the heyday of tonka beans, scientists have found traces of coumarin in a wide range of plants. It adds to the cinnamon fragrance of cassia bark, and it freshens the smell of cut hay from any field containing vernal grass or sweet clover. But scientists also noticed that something strange happens when plants containing coumarin start to rot. The presence of blue mold and other common fungi changes coumarin from a moderate liver toxin into a blood thinner potent enough to
kill a full-grown cow. This discovery solved the riddle of why spoiled fodder sometimes wipes out a farmer’s stock. But once researchers mastered that small chemical tweak, it led to billion-dollar advances in two industries: pest control and pharmaceuticals.

Named
warfarin
after the group that funded the research (the Wisconsin Alumni Research Foundation), this modified coumarin quickly became the most widely used rat poison in the world. Mixed in with a tempting food bait, it kills rodents by causing anemia, hemorrhaging, and uncontrollable internal bleeding. But in people, a small dose thins the blood just enough to prevent dangerous clots inside the veins, one of the most common and deadly side effects of cancer and its treatment. Sold under the trade name Coumadin, a warfarin prescription often goes hand in hand with chemotherapy, particularly when the cancer spreads widely, like Steve’s. It’s also commonly used by stroke and heart patients, and remains one of the world’s top-selling drugs over half a century after its discovery.

All the while Steve and I worked on the
almendro
project, his body was fighting cancer. It was a situation that sick botanists must face all the time: struggling against diseases whose treatment may come from the very plants on their herbarium sheets and microscope
slides. Steve never told me whether he was taking warfarin, but it wouldn’t have been the first time his research had overlapped with the medicine cabinet. He spent much of his career studying willow trees, the original source of aspirin, and once helped a biotechnology company find a good natural supply of false hellebore, a member of the lily family whose toxic seeds, leaves, and roots contain promising anticancer alkaloids.

In the end, no prescription was enough—Steve died a few short weeks before I defended my dissertation. It bothered him to leave things unfinished, in the lab as well as in his personal life, and he kept working long past the point where most people would have thrown in the towel. But while nothing could buy him more time on earth, he did live long enough to get some answers, to know what the research meant. And, for a curious mind like his, that was at least some reward. In the years since, I’ve often missed not only Steve’s friendship, company, and wicked sense of humor, but also his keen intellect. He had that rare ability to cut right through extraneous information, what he would have called “the bullshit,” and get at the heart of things. That’s a valuable skill both for conversation and for science, because, in nature, even straightforward ideas are rarely as simple as they seem.

On the surface, the notion of lethal seed poisons seems to make perfect sense. It’s a natural extension of the same adaptations that led to spices, caffeine, and other defensive compounds. After all, what better way to protect your seeds than to kill anything that tries to eat them? But in practice, taking that evolutionary step from disagreeable to deadly is more complicated. When a seed is attacked, the plant’s first imperative is to make the attacker stop, which is why bitterness, pungency, and burning sensations are so common. Immediate physical discomfort drives seed-eaters away and teaches them not to try again, a lesson they can even pass along to others. Poisons, on the other hand, may take hours or days to have an effect, which does nothing to stop a seed attack in progress. A flavorless toxin like ricin makes it theoretically possible for an animal to
consume and destroy every seed on a castor bean plant, then wander off and die without even knowing the cause. (And certainly without developing and passing on a “castor-bean-avoidance” behavior!) So while chemicals that cause unpleasantness can discourage whole groups of seed predators, deadly poisons eliminate only individuals, a battle that must be fought again and again. This raises the question of what evolutionary incentive causes some toxins to keep getting stronger, to reach the almost absurd potency of compounds like ricin.

“There don’t seem to be any obvious answers,” Derek Bewley told me when I posed this question. I hadn’t contacted him in a while, but this “god” of seed research was always a generous resource when I ran into puzzles I couldn’t solve. He explained that seed poisons often affect different attackers in different ways. Something that evolved to give one animal a modest stomachache (and teach it not to eat that seed again) might prove utterly deadly to another. Or a poison that took days to dispatch large creatures might kill insects in seconds, thereby stopping an attack just as quickly as a foul taste. “Or, the whole thing might be a fortuitous accident,” he mused, and pointed again to the castor bean example. “Ricin is an easily and early mobilized storage protein, and its toxic properties might be just a useful side-effect.”

When Noelle Machnicki investigated the capsaicin in chili peppers, she learned that what began as an antifungal compound ended up influencing everything from insects and birds to the taste buds of mammals, including people. The same complexity applies to seed poisons, and it would probably take a determined doctoral student like Noelle to unravel the story behind any one of them. But there is something certain about all poisonous seeds: no matter how toxic they may have become, the plant must have also invented some way to disperse them. Because there’s no use in keeping your seeds safe if you can’t move them around. In the case of castor beans, the solution is twofold: an explosive pod that hurls the ripe seeds up to thirty-five feet (eleven meters) away from the mother plant, and
a nutritious little package attached to the
outside
of the seed coat, which makes the seeds attractive to ants. Anywhere in the world, the scene near mature castor bean plants is pretty much the same—pods popping open, seeds flying, and thousands of ants busily dragging them home to their underground nests. Once there, they chew off the food packet and leave the seed untouched, safely buried and ready to sprout. Surprisingly, no one has yet looked into whether the food packets are harmless, or if the ants have developed an immunity to ricin. Either way, this clever system allows castor beans to become exceedingly deadly with no risk of compromising their ability to disperse. For
almendro
, on the other hand, the presence of coumarin in seeds is a little harder to explain.

Though it’s not technically rat poison without modification by mold or chemistry, coumarin still seems an unlikely compound for a seed dispersed by rodents. Even in its unadulterated form, it wreaks havoc on their livers. The toxicity that got it banned as a food additive was first noticed in an experiment on laboratory rats. Fed a diet supplemented with coumarin, the rats systematically lost weight, developed liver tumors, and died young. No one has studied this dynamic in the wild, but it’s hard to imagine a diet more rich with coumarin than that of agoutis, squirrels, and spiny rats living beneath an
almendro
tree. Yet these rodents continue feasting on the seeds—and occasionally dispersing them—with no apparent ill effects. Have they developed an immunity? Do their livers recover during other seasons, when
almendro
seeds aren’t available? Or perhaps they are, indeed, dying young, unnoticed in their nests and burrows. Nobody knows the answer, but there is another possibility that is even more intriguing.

Coumarin occurs in a wide variety of plants, but nowhere is the concentration higher than in
almendro
seeds. (That’s why European perfumers continue to get theirs from tonka beans rather than trying to squeeze it out of the vernal grass in their backyards.) Is it possible that the coumarin in
almendro
is on the rise? Could we be witnessing the early stages of a new chemical defense strategy? At the moment,
rodents do indeed disperse
almendro
seeds, but that situation is only a snapshot in evolutionary time. From the plant’s perspective, it’s a messy and chancy business. Agoutis and squirrels will eat and destroy every seed they can, only dispersing the ones they happen to forget about. If
almendro
does develop a coumarin potency strong enough to keep them away, it wouldn’t be the first time a seed defense targeted rodents. Remember that capsaicin, to name but one example, burns the mouths of seed-eating rats and mice, but has no effect on the beaks of the seed-dispersing birds. But the
almendro
could only afford to deter rodents if, like chili peppers, it had an ace in the hole, another option for dispersing its seeds. And after walking hundreds of transects in the jungle, and analyzing thousands of samples in the lab, we realized that is exactly what is going on.

*
Self-medication may be common practice for wild primates, and it probably helped inspire many traditional remedies, but it’s not something to trifle with. Like the ricin in castor beans, many compounds from seeds and other plant parts are highly toxic at the wrong dosage.

Seeds Travel

Each pregnant Oak ten thousand acorns forms

Profusely scatter’d by autumnal storms;

Ten thousand seeds each pregnant poppy sheds

Profusely scatter’d from its waving heads
.

—Erasmus Darwin,

The Temple of Nature
(1803)

CHAPTER TWELVE

Irresistible Flesh

Did Nature have in view our delectation when she made the apple, the peach, the plum, the cherry? Undoubtedly; but only as a means to her own private ends. What a bribe or a wage is the pulp of these delicacies to all creatures to come and sow their seed! And Nature has taken care to make the seed indigestible, so that, though the fruit be eaten, the germ is not, but only planted
.

—John Burroughs,
Birds and Poets
(1877)

“
M
urciélago
,” José breathed. “A bat!” And for the first time in our long work together I saw his cool reserve give way to something like wonder. The
almendro
seeds lay on the ground before us, grouped together in a loose pile. Where we usually felt lucky to find one or two, this trove held more than thirty—a veritable mother lode. And yet we knew there wasn’t a mature
almendro
tree within half a mile (eight hundred meters), too far for any rodent to carry such a horde. I knelt down and we began collecting the seeds, placing each one in a carefully numbered plastic bag. They were still fresh, their hard shells surrounded by a thin green pulp chewed into damp strands. Looking up, I already knew what I would see—the drooping, twelve-foot (four-meter) frond of a young palm tree, favorite perch of the largest fruit bat in Central America.