by Wade Davis
The toxic properties of toads had certainly not been overlooked by the natives of the Americas. The Choco Indians of western Colombia, for example, learned to milk poisonous toads by placing them in bamboo tubes suspended over open flames. The heat caused the creature to exude a yellow liquid, which dripped into a small ceramic vessel where it coagulated into the proper consistency of curare, the arrow poison. According to an early and perhaps exaggerated report, these preparations were extremely potent; a deer struck by an arrow survived two to four minutes, a jaguar perhaps ten. Of course, arrow poisons work in many different ways. Those based on the lianas of the northwest Amazon act as muscle relaxants, causing death by asphyxiation. The skin of Bufo marinus, on the other hand, contains chemical substances resembling the strongest of the African arrow poisons. These latter are derived from a plant, Strophanthus kombe, and they act in a quite different way. The active principle is a chemical called ouabain, and it is a powerful stimulant of the muscles of the heart. In moderate dosage ouabain is used today to treat emergency heart failure; in excessive doses it makes the heart go crazy, pumping wildly until it collapses.
Not surprisingly, European physicians incorporated toad venom into their materia medica at a very early point, and in fact powdered toad remained a prominent therapeutic agent well through the eighteenth century. But as in so many things, the Chinese were far ahead. For centuries they had been forming the venom into round, smooth dark disks, which they named ch’an su, or “toad venom.” According to the Pentsao Kang Mu, a famous herbal written at the end of the sixteenth century, the venom was used to treat toothache, canker sores, inflammations of the sinus, and bleeding of the gums. Taken orally as a pill, it was said to break up the common cold.
From this list of rather mundane afflictions, it is difficult to appreciate that the Chinese were dealing with an extremely toxic preparation. When ch’an su was analyzed early in this century it was found to contain among other active principles two powerful heart stimulants known as bufogenin and bufotoxin.
Powerful is perhaps an understatement. Virtually any contemporary victim of heart disease depends on a daily dose of digitalis, a drug extracted from the common European foxglove, a plant used as a cardiotonic in England since the tenth century. Bufotoxin and bufogenin have been found to be fifty to one hundred times more potent than digitalis. What does this mean? When a cat, in one experiment, was injected with as little as one-fiftieth of a gram of crude ch’an su, its blood pressure tripled almost immediately, and then it collapsed following massive heart failure. If a human responded in the same way, this would mean that as little as half a gram of dried venom applied intravenously would do similar punishment to a 150-pound man. Applied topically, one would at least expect a rapid increase in blood pressure. A quick glance at my list of Narcisse’s symptoms allowed me to draw a line between Bufo marinus and hypertension.
Given the toxicity of these compounds it is perhaps difficult to appreciate a controversy that has developed in recent years over whether or not Bufo marinus was used as a hallucinogen by New World Indians. The problem is that the glands of the toad secrete another chemical known as bufotenine, a compound that is found in a hallucinogenic snuff made from a plant by Indians of the upper Orinoco in Venezuela. In Central America the toad seems to be a prominent feature of Mayan iconography, and at one Postclassic Mayan site, in Cozumel, Mexico, an archaeologist found that virtually all amphibian remains were Bufo marinus. This report coincided well with an earlier and similar discovery at San Lorenzo that led one prominent archaeologist to suggest that the Olmec civilization used Bufo marinus as a narcotic. As it turns out, however, Bufo remains the dominant amphibian component of middens throughout many parts of Central America, leading other archaeologists to believe that pre-Columbian Indians didn’t get high from the toad, but ate it only after carefully cutting away the skin and paratoid glands. Today in Peru, for example, the toad is commonly eaten in this manner by the Campa, a tribe of the upper Amazon. This seems to be the most reasonable idea, especially when one considers what kind of intoxication the toad would offer. It is unlikely that the Maya would have been interested in selectively poisoning vast numbers of their priesthood, who presumably would have been the ones taking the drug. Only if some very complex process had been developed that selectively neutralized its toxic compounds could Bufo marinus have been much of a ritual hallucinogen.
Still, such a process was not inconceivable. Several years ago a colleague of Professor Schultes dispatched an intrepid young anthropologist by the name of Timothy Knab to search the backcountry of Mexico for a contemporary cult that might have preserved the ancient knowledge. After months of effort Knab finally located an old curandero in the mountains of southern Vera Cruz who knew the formula of a preparation that had not actually been used by his people for fifty years. The old man ground the glands of ten toads into a thick paste, to which he added limewater and the ashes of certain plants. The mixture was boiled all night, or until it no longer smelled foul, and then was added to corn beer and filtered through palm fiber. The liquid was mixed into cornmeal and then placed in the sun for several days to ferment. Finally, the mixture was heated to evaporate the remaining liquid, and the resulting hardened dough was hidden deep in the forest.
Although Knab had persuaded the curandero to prepare the drug, under absolutely no conditions would the recalcitrant old man actually sample it. Only very reluctantly did he consent to give a dose to Knab. From what happened it appears that he knew something the anthropologist did not. Knab’s intoxication was marked by sensations of fire and heat, convulsive muscle spasms, a pounding headache, terrifying hallucinations, and delirium. For six hours he lay immobilized in a specially excavated depression in front of the curandero’s fire.
Knab never did find out whether or not the preparation actually neutralized any of the most toxic compounds found in the glands of the toad. But even if it had, it seems that bufotenine alone would be enough to ruin any experience. In the late 1950s Howard Fabing, a medical doctor, obtained permission to inject bufotenine intravenously into a number of inmates at the Ohio State Penitentiary. In the mildest dose an inmate complained of a prickling sensation in his face, nausea, and slight difficulty in breathing. In a higher dose these symptoms became more pronounced, and the face and lips became purplish. The final doses caused mild hallucinations and delirium, and the skin turned the color of an eggplant, indicating that the drug was keeping oxygen from getting into the blood. Further experiments led this audacious physician to conclude that the symptoms produced by bufotenine coincided curiously with the conditions of the berserkus of Norse legend. Our expression going berserk pays homage to these warriors who, according to Fabing, ingested a psychoactive substance that put them into a state of frenzied rage, reckless courage, and enhanced physical strength. True or not, it was worth considering his conclusions in light of the zombi investigation. Fabing’s descriptions of his experimental subjects closely matched those of the zombis when they first come out of the ground. Marcel Pierre had suggested that as many as three men might be required to subdue the zombi; and Narcisse had mentioned that he had been beaten and bound as soon as he came out of the ground.
Again I considered Narcisse’s symptoms at the time of death, and was gratified to find that they included both cyanosis (the bluing of the face) and paresthesia (the tingling sensations).
By the end of the day some interesting patterns were appearing on the blackboard. With some confidence I had eliminated the two species of lizards. The polychaete worm was more problematic, as there was very little information on the nature of its reputed toxin. The two reports I had found had been vague. My tendency was to accept the interpretation of the vodounists themselves, who had suggested that the role of the worm was simply to agitate the toad, and thus increase the quantity of toxic secretions. One of the plants did have recognized toxins that were topically active and caused pulmonary edema. And of course the toad had a slew of pharmacologically active compound
s, all topically active, some of which might cause severe hypertension, cyanosis, and paresthesia as well as behavioral changes marked by delirium and a confused state of sham rage.
Yet clearly it was not enough simply to evaluate chemical properties of the ingredients and compare them with the symptoms of Narcisse. Albizzia lebbeck, for example, can cause pulmonary edema, but so might a dozen other substances. Missing from this data was any evidence of a potent compound that might bring about the most critical requisite condition—a profound reduction in metabolic rate that would actually cause the victim to appear dead.
By the middle of the week I had still not heard from the fish experts, so I decided to drop by their lab to see what was going on. I found the man who was working on my specimens in a dark corner of their basement catacomb, staring down the tiny mouth of an incredibly ugly creature. I think he was counting teeth.
“Got anything on those Haitian fish yet?” He looked up from his specimen, struggling both to remember who I was and to refocus his attention on something of human dimensions.
“Ah, yes. Haitian fish. Nasty little beasts.” He slipped into the back room and returned with my specimens. “Schultes have you working for the CIA, or what?” He laughed out loud.
“How do you mean?”
“I mean the puffers.” He rattled off a list of scientific names that meant nothing to me.
“What do they have in them?”
“Good Lord, I thought you people were drug experts. Not very up on your literature, either.” I must have looked confused. “James Bond. Last scene in From Russia with Love, one of the great moments in ichthyotoxicology. British agent double-oh-seven utterly helpless, paralyzed and unconscious after a minute wound from a hidden knife.” He stood up and perused his bookshelf, somehow managing to look scholarly even as he pulled the small paperback from between the thick rows of anonymous journals.
“Knew it was here somewhere. Here you go.” He quoted: “‘The boot with its tiny steel tongue flashed out. Bond felt a sharp pain in his right calf…. Numbness was creeping up Bond’s body…. Breathing became difficult…. Bond pivoted slowly on his heel and crashed to the wine-red floor.’” He returned the paperback to the bookshelf. “Double-oh-seven never had a chance,” he lamented. “Terribly clever of Fleming, too. You have to read the next book to find out. The blade was poisoned with tetrodotoxin,” he confided. “He tells you in the first chapter of Dr. No.”
“What is it?”
“A nerve toxin,” he replied, “and there is nothing stronger.”
It didn’t take me long to realize that the original hunch of Kline and Lehman had proved correct: the zombi poison included one of the most toxic substances known from nature. Marcel had recognized two varieties of fish—the fou-fou, which was Diodon hystrix, and the crapaud de mer, or sea toad, which was Sphoeroides testudineus. In English we know these as blowfish or puffer fish because of their ability to swallow large amounts of water when threatened, and thus assume a globular shape, making it more difficult for their predators to swallow them. One would hardly think such a passive defensive mechanism necessary. Both creatures belong to a large pan-tropical order of fish, many of which have tetrodotoxin in their skin, liver, ovaries, and intestines. This deadly neurotoxin is one of the most poisonous nonprotein substances known. Laboratory studies have shown it to be 160,000 times more potent than cocaine. As a poison it is, at a conservative estimate, five hundred times stronger than cyanide. A single lethal dose of the pure toxin would be about the amount that would rest on the head of a pin.
Tetrodotoxin’s role in human history reaches literally to the dawn of civilization. The Egyptians knew of the poison almost five thousand years ago; a figure of a puffer fish appears on the tomb of Ti, one of the pharaohs of the Fifth Dynasty. The deadly Red Sea puffer was the reason for the biblical injunction against eating scaleless fish that appears in the Book of Deuteronomy. In China the toxicity of the fish is acknowledged in the Pentsao Chin, the first of the great pharmacopeia, supposedly written during the reign of the mythical Emperor Shun Nung (2838 B.C.-2698 B.C.). In the East there is a continuous record that reflects an increasingly sophisticated knowledge of the biology and toxicology of the fish. By the time of the Han Dynasty (202 B.C.-A.D. 220), it was recognized that the toxin was concentrated in the liver; four hundred years later, during the Sui Dynasty, an accurate account of the toxicity of the liver, eggs, and ovaries appears in a well-known medical treatise. The last of the Great Herbals, the Pentsao Kang Mu (A.D. 1596), recognizes that toxin levels vary in different species and that within any one species they may fluctuate seasonally. It also offers a succinct but vivid description of the results of eating the liver and eggs: “In the mouth they rot the tongue, if swallowed they rot the gut,” a condition that “no remedy can relieve.” This is but one of the injunctions mentioned in the herbal warning of the dangers of the fish. Yet the Pentsao Kang Mu also reveals an extraordinary development that had taken place in Mandarin society. Despite the obvious risks, by 1596 the fish had become something of a culinary delicacy. Several recipes describe in great detail methods of preparing and cooking the fish that are said to eliminate some of the toxin and render the flesh edible. One account suggested soaking the roe overnight in water; another heralded the delight of eating “salted eggs and marinated testes.” Just how much range of error these methods allowed is uncertain. The herbal also records a folk saying that remains popular to this day in China and Japan: “To throw away life, eat blowfish.”
The subtleties of safely preparing puffer fish were quite unknown to the first European explorers to reach the Orient, and as a result they have left some of the most vivid accounts of just what these toxins are capable of. During his second circumnavigational voyage, Captain James Cook ignored a warning from the two naturalists he had on board and ordered the liver and roe of a puffer dressed for his supper. Cook insisted that he had safely eaten the fish elsewhere in the Pacific, and then in the unassuming way of a captain in the Royal Navy, he invited the two naturalists to eat with him. Fortunately, the three men merely tasted the morsel. Nevertheless, between three and four in the morning they were “seized with an extraordinary weakness in all our limbs attended with a numbness or sensation like that caused by exposing one’s hands or feet to a fire after having been pinched much by frost.” Cook wrote, “I had almost lost the sense of feeling; nor could I distinguish between light and heavy bodies … a quart pot full of water and a feather being the same in my hand.” Cook and his naturalists were lucky. Two sailors on the Dutch brig Postilion rounding the Cape of Good Hope some seventy years later fared less well. This account is offered by the physician who arrived at the bodies not ten minutes after they had eaten the fish (a species of Diodon, as it turned out). The boatswain
lay between decks, and could not raise himself without the greatest exertion; his face was somewhat flushed; his eyes glistening, and pupils rather contracted; his mouth was open, and as the muscles of the pharynx were drawn together by cramp, the saliva flowed from it; the lips were tumid and somewhat blue; the forehead covered with perspiration; the pulse quick, small and intermittent. The patient was extremely uneasy and in great distress, but was still conscious. The state of the patient quickly assumed a paralytic form; his eyes became fixed in one direction; his breathing became difficult, and was accompanied with dilation of the nostrils; his face became pale and covered with cold perspiration; his lips livid; his consciousness and pulse failed; his rattling respiration finally ceased. The patient died scarcely 17 minutes after partaking of the liver of the fish.
The sailor’s partner suffered the same symptoms, except that he vomited several times, which made him feel momentarily relieved. He expressed some hope until “a single convulsive movement of the arms ensued, whereupon the pulse disappeared and the livid tongue was protruded from between the lips.” His death occurred about one minute after that of his shipmate.
While Cook and the rest of the Europeans were having their diffi
culties on the high seas, the Japanese had adopted the Chinese passion for the puffer fish and carried its preparation to the level of art. The ardor with which the Japanese consumed their fugu fish bewildered early European observers. Engelbert Kaempfer, a physician attached to the Dutch embassy in Nagasaki at the turn of the eighteenth century, noted that “the Japanese reckon [this] a very delicate fish, and they are fond of it, but the Head, Guts, bones and all the garbage must be thrown away, and the flesh carefully wash’d and clean’d before it is fit to eat. And yet many people die of it….” He also observed that the fish was so dangerous and yet so popular that the emperor had been obliged to issue a special decree forbidding his soldiers to eat it. Curiously, though Kaempfer seems to have witnessed many individuals eating and enjoying the puffer, he concludes, “the poison of this sort is absolutely mortal, no washing nor cleaning will take it off. It is therefore never asked for, but by those who intend to make away with themselves.” This Dutchman, like countless generations of Western visitors who came after him, missed the point of the puffer experience completely. As the Japanese explain in verse, “Those who eat fugu are stupid. But those who don’t eat fugu are also stupid.”
Today the Japanese passion for puffers is something of a national institution. In Tokyo alone puffers are sold by over eighteen hundred fish dealers. Virtually all the best restaurants offer it, and to retain some semblance of control the government actually licenses the specially trained chefs who alone are permitted to prepare it. Generally the meat is eaten as sashimi. Thus sliced raw, the flesh is relatively safe. So are the testes, except that they are sometimes confused with the deadly ovaries by even the most experienced chefs. Yet many connoisseurs prefer a dish known as chiri, partially cooked fillets taken from a kettle containing toxic livers, skins, and intestines. Lovers of chiri are invariably among the hundred or more fatalities that occur each year.