The Serpent and the Rainbow

7 Columns on a Blackboard

ON EASTER SUNDAY I passed through United States Immigration at Kennedy Airport in New York carrying a kaleidoscopic Haitian suitcase constructed from surplus soft drink cans. The specimens inside included lizards, a polychaete worm, two marine fish, and several tarantulas—all preserved in alcohol—as well as several bags of dried plant material. Two rum bottles contained the antidote, while the poison itself was in a glass jar wrapped in red satin cloth. There was also a dried toad, several seed necklaces, a dozen unidentified powders, and two vodoun wangas, or protective charms. Two human tibia and a skull were at the bottom of the case. A cardboard box was full of herbarium specimens, and concealed inside in a duffle was a live specimen of the bouga toad. The customs agent opened the cardboard box, took a quick look, and told me he didn’t even want to hear about it. He never saw the toad.

There was no one in when I rang Nathan Kline from the airport, so I left word on his answering machine and caught the next plane for Boston, arriving in Cambridge slightly after dusk. I found the Botanical Museum deserted. I was tired, and when I entered my office I placed the tin suitcase on my desk and, without turning on the lights, lay back in a hammock I had strung across a corner. It was amusing to look at that colorful case so symbolic of an entire nation. Haiti, it is said, is the place to discover how much can be done with little. Tires are turned into shoes, tin cans into trombones, mud and thatch into lovely, elegant cottages. Material goods being so scarce, the Haitian adorns his world with imagination. Yet if there was anything silly about the suitcase, there certainly was not about its rank contents. If the mystery of the zombi phenomenon was to be solved, these specimens were the most important clues. Without them, there was nothing concrete. With them, I could take full advantage of the resources of the university.

I stood up and emptied the case, placing the specimens in a long row across the back of my desk. Then I took a piece of chalk and drew a column at either end of a large blackboard that covered much of one wall. On the left I listed the ingredients in Marcel’s poison: human remains, the two plants, the sea worm, toad, lizards, and fish. On the right I wrote the medical symptoms of Clairvius Narcisse at the time of his death: pulmonary edema, digestive troubles with vomiting, pronounced respiratory difficulties, uremia, hypothermia, rapid loss of weight, and hypertension. After a moment’s recollection, I added cyanosis and paresthesia, for both Narcisse and his sister had mentioned that his skin had turned blue, and that he felt tingling sensations all over his body. In between the two lists was a very large blank space.

Early the next morning I passed through the dark corridors of the Museum of Comparative Zoology and deposited the animal specimens with the museum’s various specialists for identification. Then I returned to the Botanical Museum to have a look at the plants. I had three initial questions. Did the plants have pharmacologically active compounds that might cause a dramatic decrease in metabolic rate? If so, were the strength and concentration of the compounds sufficient to be effective in the doses used by Marcel Pierre? And finally, were they topically active, or did they have to be ingested? All three were tempered by an important consideration. Very often in folk preparations, different chemicals in relatively small concentrations effectively potentiate each other, producing a powerful synergistic effect—a biochemical version of the whole being greater than the sum of the parts. Thus my primary concern was to demonstrate whether or not any of the plant or animal ingredients contained interesting chemical compounds. Once the specimens were identified, I would find most of this preliminary information in the library.

Late that afternoon the museum secretary interrupted me with a message from Kline asking me to return as soon as possible to New York.

The door to the apartment was open. I went in, stood rather tentatively for a moment in the alcove, then wandered into the living room. The decor was unchanged, but the late afternoon sun left the air hot and compressed and tinged every object with color.

“You seem to be all right.” I turned around, and Kline’s daughter Marna was behind me, smiling and leaning against the doorway to the kitchen. “Welcome back.”

“Hello, Marna. Sorry if I’m barging in.”

“It’s fine. Father told me you’d be coming. How was Haiti?”

“It’s a good place.”

“And the work?”

“Okay.”

“Was he right?”

“Your father?”

She nodded. “No, don’t tell me, don’t say anything. Wait until he gets here. Can I pour you a drink?”

“That’d be nice.”

“Some rum, or have you had it?”

“I’ll take a whiskey.”

Marna went back into the kitchen to get some ice and then walked over to the bar. “He was worried, you know.”

“Your father? Why?”

“Weren’t you a week late getting back?”

“I don’t think so.”

“He expected you several days ago.”

“There were a few delays,” I said. “Where’s your father now?”

“Oh, I’m sorry. He just stepped out. He should be right back. Bo Holmstedt is with him. Do you know him?”

“He is? Yes I do.” This was a surprise. Bo Holmstedt is a professor at the Karolinska Institute in Stockholm and one of the world’s foremost toxicologists. He and Schultes were good friends and had collaborated on a number of projects in the Amazon.

Marna and I were having a second drink when her father and Holmstedt returned. Nathan Kline seemed a different man from our first meeting—warm, even affectionate as he greeted me.

“There you are. All in one piece, I’m glad to see. You know Bo Holmstedt?”

“Professor.”

“Hello, Wade.”

“Bo was on his way to the airport, but I’ve persuaded him to wait until he hears what you’ve got to tell us.”

“Now, Nathan, don’t put the lad on the spot,” Holmstedt said. “Marna, haven’t you got a quick drink for an old sot?” He spoke with the accent of a Scandinavian educated in Britain. An elderly man, short and heavyset, he was dressed conservatively in gray flannels and a blazer. We chatted informally until all were comfortably settled, and then I began my account. In a necessarily anecdotal way, and responding to frequent questions, I shared my instincts for the country, its history and unique social structure, stressing repeatedly the importance of the vodoun religion as the axis around which so much of Haitian life revolves. Then I recounted the events that led up to my obtaining the preparation from Marcel Pierre. Finally, the conversation turned to the poison itself.

“I haven’t got all the determinations yet on the animals, but I have identified the plants. One is a liana known to the Haitians as pois gratter, the ‘itching pea.’ It’s Mucuna pruriens, and like just about everything else in the genus the fruits are covered with vicious urticating hairs.”

“Anything on its chemistry?” Kline asked.

“Not much. I spoke with Professor Schultes, and he seems to think the seeds are psychoactive. He’s also seen it used medicinally in Colombia to treat cholera and internal parasites.”

Holmstedt joined in. “There is a species of Mucuna called … Damn it, what is it? Yes, flagellipes. It’s used in central Africa as an arrow poison. Has something in it not unlike physostigmine. You know, of course, the literature on the Calabar bean?”

It was a good thing I did, for Holmstedt had written a large portion of it. I reviewed briefly the hypothesis I had come up with, and explained that there was no evidence that the plant had reached Haiti.

“A good hypothesis is never wasted. Now what else have you got?”

“Albizzia lebbeck. The Haitians call it tcha-tcha. It’s a native of West Africa introduced into the Caribbean some years ago as an ornamental shade tree.”

“You may be onto something there. What did you find out about it?”

“The bark and seedpods contain saponins. In small concentrations quite effective as a vermifuge. But dosage is critical.”

“Isn’t it always?” said Kline.

“Some West African tribes use the plant as an insecticide or fish poison,” I said.

“How’s it work on fish?” Marna asked.

“They put the crushed seeds in shallow bodies of water. The saponins act on the gills to interfere with breathing. The fish suffocate, float to the surface, and the people gather them up. Doesn’t affect the meat.”

“You will find that killing a mammal with saponins is somewhat more complicated,” Holmstedt said. “But it can be done. In East Africa, the roots of Albizzia versicolor make a bloody fine arrow poison. But it’s no good putting it in someone’s food. Saponins aren’t absorbed by the intestines. You’ve got to get the stuff into the blood.”

“But isn’t that what they say they do in Haiti?” Marna asked.

“Yes,” I replied, “through the skin. Professor Holmstedt, what are the symptoms of saponin poisoning?”

“In sufficient dosage, nausea, vomiting, eventually excessive secretions into the respiratory passages. In simpler terms, the victim drowns in his own fluids.”

“With pulmonary edema as an interim result?” I asked.

“Yes, of course.” It was the condition that headed my list of Clairvius Narcisse’s symptoms at the time of his death.

“You will find that Albizzia has one more secret,” Holmstedt went on. “Many species of the genus contain a special class of compounds known as sapotoxins that are absorbed by the intestines. They work in a rather nasty fashion by interfering with cellular respiration throughout the body. They kill you by actually weakening your every cell. Incidentally, the Efik traders of Old Calabar used the bark of Albizzia zygia in a potion known as ibok usiak owo, which means in their language ‘a medicine for mentioning people’—a sort of native truth serum, I would say. They administer it orally as an ordeal poison. You see, Wade, you come back full circle to your hypothesis.”

“Have you got anything yet on these lizards and toads and whatever else they put in?” Kline asked.

“Nothing encouraging,” I replied. “There’s a polychaete worm that Marcel sequesters with the toad. It had bristles on it that some say inflict a mild paralysis. They may be venomous, but the reports are vague. The herpetologists up at the museum knew the lizards right away. Neither is known to be poisonous. In Dominica, they say one of them can make the hair fall out and turn your skin green. But the people eat it anyway. Another species in a related genus plays havoc with housecats in Florida, but it doesn’t kill them. But it wasn’t a lizard that took down Narcisse, that’s for sure.”

“What about the toad?” Holmstedt asked.

“Bufo marinus.”

“You’re certain.”

“It’s unmistakable. The people at Herpetology confirmed it.”

Holmstedt paused to consider. “Quite,” he said finally, and looking straight at me, “Wade, I’d say you’re onto something.”

The next morning when I returned to Cambridge, there was no new information for me. The first botanical determinations did show that Marcel Pierre was exploiting plants with both pharmacologically active compounds and proven African connections, but isolated reports drawn from over half a continent explained very little. The Calabar hypothesis, despite Holmstedt’s words of encouragement, seemed to have led me nowhere. I had found no evidence of the Calabar bean in Haiti, and while datura had been present, its connection to the zombi phenomenon remained uncertain.

It was discouraging, but my luck would change by the end of the day. The more I read about the large bouga toad, the ingredient that had so caught Holmstedt’s interest, the brighter my mood became. I learned that the paratoid glands on its back are virtual reservoirs of toxic compounds.

Although Bufo marinus is a native of the New World, it apparently reached Europe very soon after the voyages of Columbus, and there it was well received by nations long familiar with toad venom. Europeans believed that toads derived their poisons from the earth by eating mushrooms (hence the English name toadstool). As early as Roman times, women used toads to poison their husbands. Soldiers in the Middle Ages believed that a discreet means of wounding an enemy was to rub his skin with the secretions of Bufo vulgaris, the common European species. And not long after Bufo marinus reached the Old World, poisoners found that by placing the toad in boiling olive oil, the secretions of the glands could be easily skimmed off the surface. In Italy early in the sixteenth century, poisoners devised sophisticated processes for extracting toad toxins into salt, which could then be sprinkled on the intended victim’s food. In fact, so highly regarded was the toxicity of toad venom that at the beginning of the eighteenth century it was actually added to explosive shells. Presumably the commanders felt that if the cannon did not kill their enemies, the toad toxins would.

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 compounds, 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 difficulties 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.

The Japanese prefer and pay premium prices for four species of puffer, all in the genus Fugu, and all known to be violently poisonous. Why would anyone play Russian roulette with such a creature? The answer, of course, is that fugu is one of the few substances that walks the line between food and drug. For the Japanese, consuming fugu is the ultimate aesthetic experience. The refined task of the fugu chef is not to eliminate the toxin, it is to reduce its concentration while assuring that the guest still enjoys the exhilarating physiological aftereffects. These include a mild numbing or tingling of the tongue and lips, sensations of warmth, a flushing of the skin, and a general feeling of euphoria. As in the case of so many stimulants, there are those who can’t get enough of a good thing. Though it is expressly prohibited by law, certain chefs prepare for zealous clients a special dish of the particularly toxic livers. The organ is boiled and mashed and boiled again and again until much of the toxin is removed. Unfortunately, many of these chefs succumb to their own cooking. It was such a dish that caused the controversial death in 1975 of Mitsugora Bando VIII, one of Japan’s most talented Kabuki actors, indeed, an artist who had been declared a living national treasure by the Japanese government. He, apparently, like all of those who eat the cooked livers, was among those who, in the words of one fugu specialist, enjoy “living dangerously.”

Because of its popularity as a food and the relatively high incidence of accidental poisonings, the fugu fish has generated an enormous medical and biomedical literature. Exploring that literature for clinical descriptions and case histories, I was immediately struck by the parallels to the zombi phenomenon. In describing his experience to me Clairvius Narcisse recalled remaining conscious at all times, and although completely immobilized could hear his sister’s weeping as he was pronounced dead. Both at and after his burial his overall sensation was that of floating above the grave. He remembered as well that his earliest sign of discomfort before entering the hospital was difficulty in breathing. His sister recalled that his lips had turned blue, or cyanotic. Although he did not know how long he had remained in the grave before the zombi makers came to release him, other informants insist that a zombi may be raised up to seventy-two hours after the burial. The onset of the poison itself was described by several houngan as the feeling in victims “of insects crawling beneath your skin.” Another houngan offered a poison that would cause the skin to peel off the victim. Popular accounts of zombis claim that even female zombis speak with deep husky voices, and that all zombis are glassy-eyed. Several houngan suggested that the belly of the victim swells up after he or she has been poisoned.

Once again, recall the list of medical symptoms from the right-hand side of my blackboard. At the time of his reputed death Narcisse suffered digestive troubles with vomiting, pronounced respiratory difficulties, pulmonary edema, uremia, hypothermia, rapid loss of weight, and hypertension. Note that these symptoms are quite specific and certainly peculiar.

Now compare Narcisse’s constellation of symptoms with the following specific description of the effects of tetrodotoxin [italics mine]:

The onset and types of symptoms in puffer poisoning vary greatly depending on the person and the amount of poison ingested. However, symptoms of malaise, pallor, dizziness, paresthesias of the lips and tongue and ataxia develop. The paresthesias which the victim usually describes as a tingling or prickling sensation may subsequently involve the fingers and toes, then spread to other portions of the extremities and gradually develop into severe numbness. In some cases the numbness may involve the entire body, in which instances the patients have stated that it felt as though their bodies were floating. Hypersalivation, profuse sweating, extreme weakness, headache, subnormal temperatures, decreased blood pressure, and a rapid weak pulse usually appear early. Gastrointestinal symptoms of nausea, vomiting, diarrhea and epigastric pain are sometimes present. Apparently the pupils are constricted during the initial stage and later become dilated. As the disease progresses the eyes become fixed and the pupillary and corneal reflexes are lost…. Shortly after the development of paresthesias, respiratory distress becomes very pronounced and … the lips, extremities and body become intensely cyanotic. Muscular twitching becomes progressively worse and finally terminates in extensive paralysis. The first areas to become paralyzed are usually the throat and larynx, resulting in aphonia, dysphagia, and complete aphagia. The muscles of the extremities become completely paralyzed and the patient is unable to move. As the end approaches the eyes of the victim become glassy. The victim may become comatose but in most cases retains consciousness, and the mental faculties remain acute until shortly before death. [See Halstead, Annotated Bibliography.]

Several physicians report this most peculiar state of profound paralysis, during which time most other mental faculties remain normal. One notes “the patient’s comprehension is not impaired even in serious cases. When asked about his experiences he can describe everything in detail after recovery.” Other documented and pronounced symptoms of tetrodotoxin poisoning include pulmonary edema, hypotension, cyanosis, hypothermia, nausea and vomiting. Respiratory distress is almost always the first symptom of the poisoning, and many victims develop distended bellies. The third day after exposure to tetrodotoxins, large skin blisters may appear; by the ninth day the skin begins to peel off. A Chinese patient admitted to the Queen’s Hospital in Honolulu complained that he felt “numb from neck to toes with a feeling of ants crawling over him and biting him.”

This list is not exhaustive. In all, Narcisse shared twenty-one or virtually all the prominent symptoms documented in known cases of tetrodotoxin poisoning.

Not only did the individual symptoms of zombification and tetrodotoxication sound remarkably similar, but entire case histories from the Japanese literature read like accounts of the living dead. A Japanese peddler shared a dish of chiri with several mates and suffered all the classic symptoms of puffer poisoning. The physicians gave up, certain that the man was dead, but the individual recovered, and not fourteen hours after he had eaten the poisonous food he walked out of the hospital. A Korean miner and his son ate the ovaries of a species of Sphoeroides and within an hour were taken to the hospital. The father retained “clear consciousness” until he died; his son suffered complete immobility for about two hours but recovered naturally without treatment.

These two accounts illustrate one of the most eerie characteristics of puffer poisoning. Tetrodotoxin induces a state of profound paralysis, marked by complete immobility during which time the border between life and death is not at all certain, even to trained physicians. I need hardly express the significance of this in terms of the zombi investigation. It became quite clear that tetrodotoxin was capable of pharmacologically inducing a physical state that might actually allow an individual to be buried alive.

In Japan, apparently, it had already happened. One physician reported:

A dozen gamblers voraciously consumed fugu at Nakashimamachi of Okayama in Bizen. Three of them suffered from poisoning; two eventually died. One of these being a native of the town was buried immediately. The other was from a distant district … under the jurisdiction of the Shogun. Therefore the body was kept in storage and watched by a guard until a government official could examine it. Seven or eight days later the man became conscious and finally recovered completely. When asked about his experience, he was able to recall everything and stated that he feared that he too would be buried alive when he heard that the other person had been buried.

What happened to the unfortunate individual who was buried is not explained. The second case was equally dramatic.

A man from Yamaguchi in Boshy suffered from fugu poisoning at Osaka. It was thought that he was dead and the body was sent to a crematorium at Sennichi. As the body was being removed from the cart, the man recovered and walked back home. As in the case previously cited, he too remembered everything.

These two cases were by no means unique. In fact such incidences are apparently frequent enough that in some parts of Japan a person declared dead from eating puffer fish is customarily allowed to lie alongside his or her coffin for three days before burial. On Christmas Eve 1977 a forty-year-old resident of Kyoto was admitted to a hospital after being poisoned by fugu. The patient soon stopped breathing, and all symptoms were consistent with brain death. Physicians immediately initiated artificial respiration and other appropriate treatments. These did not help, but twenty-four hours later the patient spontaneously began to breathe. He eventually recovered completely, and later remembered hearing his family weeping over his still body. His senses were unimpaired. He wanted desperately to let them know that he was alive, but he was unable to. “That,” he later told medical investigators, “was really hell-on-earth.”

These reports cast the zombi investigation in a totally different light. Suddenly it seemed not only possible but likely that Marcel’s poison could cause a state of apparent death. Now a dozen more specific questions came to mind. Did the species of puffers used by Marcel contain the critical toxin? If so, could they have survived the preparation? Recall that Marcel had placed the dried fish on a charcoal grill and broiled them to an oily consistency; heat destroys many chemical compounds. What about the way the zombi poison was reputedly applied? How would the bokor assure that the victim did not die from the poison? Once again, many of these questions could be answered from the literature.

Marcel added two species of puffers to his poison—Diodon hystrix and Sphoeroides testudineus—both known to contain tetrodotoxin. It was a species of Diodon that poisoned the Dutch sailors on the Postilion as it rounded the Cape of Good Hope. Members of the genus Sphoeroides are closely related to the Japanese fugu fish, and are known to be particularly virulent. In the mid-1950s an elderly tourist in south Florida ate the liver of Sphoeroides testudineus. Forty-five minutes later she died, after suffering all the horrible symptoms of the disease. Clearly, the species Marcel had used could contain tetrodotoxin.

Other answers were suggested by a remarkable account handed down by the Mexican historian Francisco Javier Clavijero. In 1706, while searching for a new mission site in Baja California, four Spanish soldiers came upon a campfire where indigenous fishermen had left a roasted piece of the liver of a botete (Sphoeroides lobatus). Despite the warnings of their guides, the soldiers divided the meat. One of them ate a small piece, another chewed his portion without swallowing, and the third only touched it. The first died within thirty minutes, the second shortly thereafter, and the third remained unconscious until the next day.

Two critical points came across. That the soldiers were poisoned by roasted meat exemplifies the important fact that heat—frying, boiling, baking or stewing—does not denature tetrodotoxins. Secondly, although tetrodotoxin is one of the most poisonous chemicals known, like any drug its effects depend on dosage and the way it is administered. Having studied over a hundred cases of tetrodotoxication, the Japanese investigators Fukada and Tani distinguished four degrees of poisoning. The first two they characterized by progressive numbing sensations and the loss of motor control; the equivalent, perhaps, of having one’s entire body “fall asleep.” The third degree includes paralysis of the entire body, difficulty in breathing, cyanosis, and low blood pressure—all suffered while the victim retains clear consciousness. In the final degree, death comes very quickly, as a result of complete respiratory failure. If the poisonous material is ingested, the onset of the third degree is usually very rapid. The sailors on the Postilion typically died within seventeen minutes. If tetrodotoxin somehow enters the bloodstream directly its potency is enhanced forty to fifty times. However, tetrodotoxin is also topically active, and some of the preliminary symptoms have shown up in individuals who merely handle the toxic organs. In other words, whether or not the victim of the zombi poison survived would depend on just how he or she was exposed to the poison.

Marcel had recognized the potency of his preparation and had acknowledged at least implicitly the importance of proper application and correct dosage. He most emphatically stated that it was never placed in the victim’s food. Now I understood why. Ingested orally it would more than likely kill the victim; applied repeatedly to the skin or open wounds, or blown across the face of the victim so that it was inhaled, it could bring on a state of apparent death.

One final point was critical. Those who are poisoned by tetrodotoxin generally reach a crisis after no more than six hours. If the victim survives that period, he or she may expect a full recovery, at least from the effects of tetrodotoxin. This made it at least theoretically possible for a poison victim to appear dead, be hastily buried, and then recover in the coffin.

The implications of these conclusions were extraordinary. Here was a material basis for the entire zombi phenomenon—a folk poison containing known toxins fully capable of pharmacologically inducing a state of apparent death. That the peculiar symptoms described by Clairvius Narcisse so closely matched the quite particular symptoms of tetrodotoxin poisoning suggested that he had been exposed to the poison. If this did not prove that he had been a zombi, it did, at least, substantiate his case. And there was one more especially haunting fact. Every indication pointed to the possibility that Narcisse had remained conscious the entire time. Totally paralyzed, he may have been a passive observer of his own funeral.

As soon as I had these results I contacted Nathan Kline and, on his instructions, forwarded an unmarked sample of the poison to a Professor Leon Roizin at the New York State Psychiatric Institute. The next step was straightforward. Before initiating an expensive series of chemical studies, Roizin would see what the powder could do to laboratory animals. To avoid any possible bias in the experiments, I told Roizin neither what the powder contained nor what it was reputedly used for. He was merely instructed to prepare an emulsion and apply it topically to the animals. I heard from him within a week. He had worked very fast, and was ready to see me.

The elevator opened onto a congested hall that smelled of laboratories. I took a few steps along the short corridor and paused, flanked on both sides by photographic montages of monkeys under the influence of megadoses of various drugs. I was in no position to cast judgment, but I had to acknowledge that these photographs were more gruesome than anything I had witnessed in any bokor’s collections.

Roizin worked in a cluttered office. He was short, almost dwarfed by his white lab coat. Discussing his experiments, we spoke clinically.

“What you have here,” he began, “is a very strong neurotropic substance. Most peculiar. You have no idea what it contains?”

I shook my head. I didn’t like to deceive him, but I wanted first to hear what he had discovered. Explanations could come later.

Roizin reached into a folder and passed me two photographs of white rats. Both appeared dead. “First we shaved the dorsal surface and applied a thick emulsion containing the powder. Within a quarter hour spontaneous activity decreased, and within forty minutes the animals moved only when stimulated. Soon after that all mobility ceased, and the rats held a single position for three to six hours. Breathing became superficial. We could still get a heartbeat, and there was some response to sound and corneal stimulation. After six hours all movement completely ceased. They looked comatose and showed no response to any stimuli. Yet we could still register a heartbeat on the EKG. We also picked up brainwaves. They remained that way for twenty-four hours.”

“And they were alive?” I asked.

“Yes, but totally tranquilized. But there is much more. Most tranquilizers do not act as anesthetics. This one does. Look at the second photograph.” I glanced down. “We stuck that needle into its tail, and there was absolutely no response of any kind. Whatever you have here acts peripherally as an anesthetic. And it acts very quickly, without affecting the heart even in the toxic stage.”

“Were there any other behavioral changes?”

“Yes, one that comes to mind. Early in the experiment while there was still some mobility, the rats clustered together, and their extremities were noticeably cool. It was as if they were attempting to keep warm.”

“How much of the powder was administered to each animal?”

“Five milligrams per one hundred gram weight. But there is something else I want to show you.” Roizin lifted his phone to make a call. I took the opportunity to discreetly make a calculation on my notepad based on the dosage administered to rats. Extrapolating to the weight of an average man, Roizin had used the equivalent of 3.5 grams of the crude poison.

“The technician is ready down in the studio,” he said as he hung up. “When we got these results with the rats I decided to record what happened to the monkeys.” He got up and indicated I should follow him out of his office. “Ever worked with rhesus monkeys before?” he asked as he led me away.

“Never had to,” I replied.

“You’re most fortunate, then. But you ought to experience the animals at least once before you see the film.” Roizin took me through a maze of cinderblock corridors that led to the animal facility of the institute. The sound as we approached the room that housed the cages of monkeys was deafening. The last time I had heard any monkey had been in the rain forest of the northwest Amazon. But that had been the deep roar of a howler, free and majestic and fearsome. Here, an entire wall of metal cages rattled with the frantic movements of animals that had never called a mate. Out of the dozen sterile screams, Roizin picked one and tapped its cage menacingly. The captive lunged violently, knocking its teeth against the thin bars. “Passive they are not,” he said loudly and close to my ear. His point made, he turned out of the room.

“What you will see, of course, are but preliminary results,” he told me as we entered the studio. “We used exactly the same procedure as with the rats.” A technician dimmed the lights, and the fuzzy image of Roizin came on the video monitor. Beside him was a single cage, with an aggressive rhesus monkey just like those we had seen. Roizin’s voice on tape was difficult to understand, but the images spoke for themselves. Twenty minutes after application of the emulsion this same monkey appeared noticeably sedated. Even when prodded it did not lunge at the bars. Rather, it slowly retreated to one corner of the cage, assuming, as Roizin explained, a stereotypic catatonic position. When stimulated, it reacted at best passively, opening its mouth in a vain imitation of its normal threatening posture. The monkey maintained that position for three hours. At that point the technician and Roizin had been called away on other business. When they returned six hours later the monkey was still in the same position.

“Now we can increase dosage and do any number of things,” Roizin told me once we were back in his office, “but I think for now the point is made. Whatever this powder contains, it acts very quickly and completely modifies behavior.” Roizin leaned back in his chair. “I can promise you one thing for certain. For many years I have worked for Professor Kline, and some pretty odd drugs have passed through this laboratory. This, without doubt, is the most peculiar.”

“Do you have any idea what it might be used for?” I asked.

“There’s no way of knowing right now.”

“Don’t you have any guesses?”

“Perhaps cardiovascular surgery. It is curious how the heart remains unaffected while the body is totally anesthetized. Also in psychiatry, it might be of use treating something like psychotic excitement.”

“As a tranquilizer?”

“Of a sort. There is one more thing. Did Nate Kline ever talk to you about experimental hibernation?”

These preliminary lab results should have delighted me. They demonstrated experimentally what all the literature could only suggest as a possibility. Marcel’s powder did contain pharmacologically active compounds that acted very rapidly to lower the metabolic rate of the victim. Yet even as I received congratulatory letters and calls from Kline and Lehman, and from Schultes as well, I was more deeply perplexed than ever. Before these results the entire notion of zombis had remained strictly an idea, a curiosity, an abstraction. I went to Haiti skeptically, knowing nothing about the country or the people, and the assignment dropped me into an enchanted land whose spiritual rhythms took me utterly by surprise and moved me profoundly. Despite this, or perhaps because of it, I had never actually paused to consider whether or not zombis truly existed. It wasn’t that I didn’t believe, and it wasn’t that I did. I just hadn’t passed judgment. The formula of the poison, the correlations from the literature and the case of Narcisse, and now the preliminary but concrete laboratory results changed everything. Now I had to face just how little I understood about a phenomenon that suddenly appeared hauntingly real.

There were so many loose ends. Every report received from Haiti, for example, had mentioned an antidote. Yet while Marcel had prepared a potion that he believed counteracted the effects of the poison, the way it was used and the ingredients themselves suggested that it was pharmacologically inactive. Tetrodotoxin has no known medical antidote, nor, from what is known of the action of the toxin, would the zombi makers require one. Victims of puffer fish poisoning either live or they die, and those who survive recover on their own, as presumably would the zombis. Still, this information notwithstanding, the persistent reports of an antidote begged further investigation. As colleagues often remind me, absence of evidence is not evidence of absence.

Yet in all this obsession with the drug and elusive antidote, I was, in one sense, missing the point entirely. All that the formula of the poison explained was how an individual might be made to appear dead. Clearly the same thing occurred in Japan, however infrequently, but just as clearly those who succumbed to toxic fugu preparations were not zombis; they were merely poison victims. Any psychoactive drug has within it a completely ambivalent potential. Pharmacologically it induces a certain condition, but that condition is mere raw material to be worked by particular cultural or psychological forces and expectations. This is what experts call the “set and setting” of any drug experience. Set in these terms is the individual’s expectations of what the drug will do to him; setting is the environment—both physical and, in this case, social—in which the drug is taken. For example, in the northwest rain forests of Oregon there are a number of native species of hallucinogenic mushrooms. Those who go out into the forest deliberately intending to ingest these mushrooms generally experience a pleasant intoxication. Those who inadvertently consume them while foraging for edible mushrooms invariably end up in the poison unit of the nearest hospital. The mushroom itself has not changed.

This did not suggest that the zombi poison might be only a pleasant hallucinogen. But like the mushroom, its potential was latent. The Japanese victim lying conscious but paralyzed while his family mourned his death might, upon recovery, rationalize his terrifying experience within the expectations of his society. Everyone knows that is what fugu poisoning is like. Without doubt, in the phantasmagoric cultural landscape of Haiti, Clairvius Narcisse had his own expectations that he carried with him literally into and out of the grave. Of what was going on in his mind, I had no idea, and until I did I would know nothing about zombis. But I did have available to me—and the opportunity to explore it before my return to Haiti—a literature that would provide a context for understanding.

8 Voodoo Death

COUNT KARNICE-KARNICKI was a compassionate man, and his invention made him the rage of Europe. The count was a Russian nobleman, the chamberlain to the czar, but his inspiration had come in Belgium while attending the funeral of a young girl. As the first shovefuls of dirt landed on the wooden coffin, a pitiful scream rose from the earth, staggering the officiating priest and causing a number of young women to faint. It was a sound that the count would never forget. He, like so many of his generation in all corners of Victorian Europe, became obsessed by the threat of premature burial.

His invention, introduced just before the turn of the century, was a simple contraption, efficient and inexpensive enough to be well within reach of rich and poor alike. For the truly destitute, the apparatus was available for rent. It consisted of a hermetically sealed box and a long tube that would be fixed into an aperture in the coffin as soon as it was lowered into the ground. On the chest of the dead person was placed a large glass ball attached to a spring linked to the sealed box. With the slightest movement of the glass ball, as would occur if breathing began, the spring would be released, causing the lid of the box to fly open and admit both light and air to the buried coffin. At the same time the spring initiated a mechanical chain reaction worthy of Rube Goldberg. A flag sprang four feet above the box, a bell began to ring and continued for thirty minutes, and an electric lamp ignited. The long tube was envisioned not only to admit oxygen, but also to serve as a megaphone, amplifying the presumably weak voice of the almost dead. Not a hundred years ago, at the turn of this century, this peculiar apparatus was heralded as a technological breakthrough. Many thousands of Frenchmen left specific instructions in their wills to ensure that it would be placed on their tombs. In the United States it was so popular that societies formed to promote its subsidized use.

The citizens who embraced Count Karnice-Karnicki’s invention were responding to an epidemic of premature burials that had colored the popular press and confounded medical authorities. A typical report appeared in the London Echo in March of 1896. Nicephorus Glycas, the Greek Orthodox metropolitan of Lesbos, was pronounced dead in his eightieth year. According to the traditions of his church he was immediately garbed in his episcopal vestments and placed on a throne, where his body was exposed day and night to the faithful, and guarded constantly by priests. On the second night, the old man suddenly awoke and stared with amazement and horror at the parade of mourners at his feet. His priests, according to the report, were no less startled to realize that their leader had not been dead but had merely fallen into a deathlike trance. The Echo correspondent impassionately questioned what might have happened had the metropolitan been a layman, and then concluded that he would have been buried alive.

A second popular account was that of a Reverend Schwartz, an Oriental missionary who was reportedly aroused from apparent death by his favorite hymn. The congregation celebrating his last rites was stunned to hear a voice from the coffin joining in on the refrain.

Though today both of these cases may appear preposterous, at the time they were not only seriously discussed, they were believed, and they helped fuel a hysterical fear of premature burial that swept late Victorian Europe. In 1905 an English physician and member of the Royal College of Surgeons edited a volume in which were documented 219 narrow escapes from premature burial, as well as 149 cases in which the body was actually interred while still alive. Also noted were ten instances in which autopsies were erroneously performed on the living, and two cases in which consciousness returned to the “corpse” during the process of embalming.

Many people were not about to take any chances. Hans Christian Andersen constantly carried a note in his pocket instructing what should be done with his body in the event of his death. The English novelist Wilkie Collins placed a similar precautionary note by his bedside table each night. So did Dostoyevsky, who urged that his burial be delayed five days lest his apparent death be but a trance. Certain leading members of the British aristocracy took more drastic measures, which incidentally were remarkably similar to certain Haitian practices that their countrymen would no doubt have condemned. The vodounist, fearing that a family member will be raised as a zombi, has been reported to drive a blade through the heart of the dead. Fearing premature burial, the noted British antiquary Francis Douce requested in his will that the surgeon Sir Anthony Carlisle be permitted to sever his head from his body. So did a certain Harriet Martineau. A well-known actress of the era, Ada Cavendish, left instructions in her will that her jugular be sliced. Lady Burton, widow of the famous African explorer and writer Sir Richard Burton, provided that her heart be pierced with a needle. Bishop Berkeley, Daniel O’Connell, and Lord Lytton had similar fears and ordered that their burials be delayed, and that one or more of their veins be opened so that their blood would drain and thus assure that they were truly dead.

By the turn of this century fear of premature burial had grown into an overriding public concern. It was discussed in all the learned medical journals, and in England it generated parliamentary inquiries that led to the Burial Act of 1900, which among its many statutes specified the length of time that had to transpire between the pronouncement of death and actual interment. On the Continent prizes were offered for the discovery of a conclusive sign of death. In France in 1890 a certain Dr. Maze was awarded the prestigious Prix Dusgate and twenty-five hundred francs simply for asserting that the only reliable sign of death was putrefaction. The earnest scientific interest in establishing the difference between real and apparent death is evident in an academic textbook on the subject published in 1890 whose bibliography lists no fewer than 418 citations.

Actually, a satisfactory means of diagnosing death has both obsessed and eluded man since earliest times. Of course the fundamental signs of death have always been known, and they have not changed. They are: cessation of respiration and heartbeat, changes in the eye, insensibility, rigor mortis, pallor and discoloration due to the settling of the blood. The problem, as Kline had expressed so forcefully when we first met, has always been that not one of these is foolproof. And once that is recognized and admitted, a floodgate of possibilities opens.

But there was something else going on in the minds of Victorian society. Just how serious a threat premature burial was in the late nineteenth century is uncertain. Even at the time many insisted that reports were greatly exaggerated. Yet the very fact that the debate flourished in the Houses of Parliament and the halls of the Royal Academy was as significant as its outcome. An already uneasy public undoubtedly took note that the subject was being seriously considered within institutions that were the very pillars of the Victorian world and, by extension, of reason itself. As physicians outlined the difficulties of diagnosing death, politicians debated how long the dead should be kept from the grave, and salesmen pitched Count Karnice-Karnicki’s invention, the public mood was further aroused by certain popular accounts. One of these was the notorious case of a Colonel Townsend. According to a panel of physicians called upon to witness the event, this officer willingly reduced his heart rate and entered a self-induced trance, or, as some described it, a state of suspended animation. Heartbeat ceased, respiration stopped, and the entire body assumed the icy chill and rigidity of death. The color fled from Townsend’s face; his eyes became glazed and fixed. After he had been comatose for thirty minutes, the physicians actually certified him dead and prepared to go home. As they did so, Townsend began to recover slowly, and by the next day he was well enough to repeat his feat. This case was widely quoted not only in the press but in academic textbooks of medical jurisprudence, and it undoubtedly lent credence to contemporary statements such as “the difference between trance and death has never been quite understood by the majority of mankind.”

This statement perfectly encapsulated the Victorians’ dilemma. At the root of the hysterical fear of premature burial was the fact that physicians recognized, and patients suffered, a number of peculiar conditions characterized by immobility and insensibility, and known variously as trance, catalepsy, cataplexy, and suspended animation. As far as the public was concerned, any one of these clinical diagnoses could be the ominous prelude to accidental interment. Victorian physicians noted that catalepsy was marked by the singular absence of will or volition; the body of the patient remained in whatever position it was placed. Trance was said to most nearly resemble the condition of a hibernating animal, with the patient suffering complete mental inertia. Cataplexy was a modification of the same conditions, only the patient simply collapsed limply to the ground with the eyes closed, completely immobile, unable to speak, yet conscious and totally aware of all that was going on around him. Medical writers of the era even discussed a fourth clinical condition, marked by immobility, which they termed ecstasy, but this was not a state that might lead to premature burial. The ecstatic patient was described typically as having a “radiant, visionary expression and a tendency to fix himself in statuesque poses whilst concentrating upon some object of adoration.”

Needless to say, these conditions are no longer recognized by the medical profession. Certain aspects of the cataleptic condition have been subsumed under “catatonic schizophrenia,” but trance has been reduced to a feature of hypnosis research, and ecstasy and cataplexy have disappeared as clinical diagnoses. But for the Victorians these ailments did exist, and they were discussed seriously by the leading medical authorities precisely because people were succumbing to them. Where did they come from? Cataplexy, for example, is described in the old medical textbooks as “being precipitated by strong emotion and persisting until such emotion be controlled,” which sounds not unlike another common feature of Victorian life, also now abandoned—the fainting spell. Recently some have suggested that women of the era simply suffered the physical consequences of wearing impossibly tight corsets, but this interpretation misses the point. Fainting was a socially conditioned response; in certain clearly recognized and predictable situations it was virtually expected. Young women of the elite, in particular, found fainting a convenient means to avoid or modify uncomfortable social predicaments. Some learned to attain their desires simply by cleverly faking, while others actually did pass out, and in some cases it was assumed by physicians that they were dead. In other words, a socially conditioned act became a physiological reality.

Like the fainting spell, catalepsy, cataplexy, trance, and ecstasy were socially conditioned ailments, and their cause lay somewhere deep within the psyche of the age. Their manifestations were concrete and isolated to a particular time. The fear of premature burial undoubtedly was accentuated because people really believed such states of sham death possible. And just because they did exist for the Victorians, some unfortunate souls may well have ended up in the ground wishing that their relatives had rented from Count Karnice-Karnicki.

Part of what was going on in Victorian England was related to a phenomenon that Western anthropologists had noted in “primitive” societies but overlooked in their own culture. For just as an individual’s sickness may have a psychosomatic basis, it is possible for a society to generate physical ailments and conditions that have meaning only in the minds of its people. In Australia, for example, aborigine sorcerers carry bones extracted from the flesh of giant lizards, and when these slivers are pointed at a person while a death spell is recited, the individual invariably sickens and almost always dies. According to one scientific report the victim

stands aghast, with his eyes staring at the treacherous pointer, and with his hands lifted as though to ward off the lethal medium which he imagines is pouring into his body. His cheeks blanch and his eyes become glassy and the expression on his face becomes horribly distorted … he attempts to shriek but usually the sound chokes in his throat, and all that one might see is froth at his mouth. His body begins to tremble … he sways backwards and falls to the ground … writhing as if in mortal agony. After awhile he becomes very composed and crawls to his [shelter]. From this time onwards he sickens and frets, refusing to eat and keeping aloof from the daily affairs of the tribe.

At this point only the nangarri, or medicine man, may save him by initiating a complex ritual. But should the nangarri refuse to cooperate, the victim will almost certainly die.

What happens to the Australian aborigine is an example of something that occurs in many cultures. It is a phenomenon every bit as real, and every bit as enigmatic, as the ailments generated by the Victorian mind. Its basic pattern is consistent. An individual breaks a social or spiritual code, violates a taboo, or for one reason or another believes himself a victim of putative sorcery. Conditioned since childhood to expect disaster, he then acts out what amounts to a self-fulfilling prophecy. Often the death knell is sounded by a hex or, as in Australia, a simple gesture rife with meaning. Sorcerers may use props as media of transmission: African witch doctors have knucklebones, and European witches carved wooden dolls. Or transmission is direct. Even to day in Greece the harbinger of death need merely squint the evil eye.

In Haiti, there are literally dozens of methods, and that is perhaps why anthropologists call the entire phenomenon voodoo death.

Voodoo death has been so commonly reported, and so frequently documented and verified by scientific observers, that its existence is no longer a matter of debate. Of course, no scientist would believe that there is a direct causal relationship between the death of the victim and, for example, the physical act of pointing a bone. Clearly it is the victim’s mind that mediates the sorcerer’s curse and the fatal outcome. What remains to be discovered is the mechanism that actually allows this to occur. Three possible explanations have been offered.

The first scientists seriously to consider the phenomenon of voodoo death were not anthropologists but physicians, many of them affected by the peculiar cases they witnessed on the battlefields of Europe during the First World War. In the nightmare of despair and death on the Western Front, certain traumatized soldiers who had not suffered any wound inexplicably died of shock, a medical disorder normally brought about by a critical drop in blood pressure due to excessive bleeding. When these physicians later became familiar with cases of voodoo death, they saw a connection. They suggested that individuals terrified by a magic spell suffered, like the soldiers, from an over-stimulation of the sympathetic-adrenal system, which led to a form of fatal shock. Fear, in other words, could initiate actual physiological changes that quite literally led to death.

Many anthropologists, less familiar with the complex workings of the autonomic nervous system, have considered voodoo death as a psychological process, emphasizing the power of suggestion. If faith can heal, they argue, fear can kill. Psychologists have studied, for example, something that most of us take for granted—that the likelihood of becoming ill or even dying depends to a large extent on our frame of mind. Feelings of depression, hopelessness, or despair do not cause diseases, but somehow they make us vulnerable. Loneliness would seem hardly a fatal affliction, yet a disproportionate number of spouses die in the first year after the death of their mates. Psychologists label this the “giving up/given up complex.” According to this view, the victim of voodoo death becomes caught in a vicious cycle of belief that indirectly kills him, perhaps, as some suggest, by making his body susceptible to pathogenic disease. His psychological state can be imagined. He is doomed to die by a malevolent curse that both he and all those around him deeply believe in. He becomes despondent, anxious, and fearful. His resignation is both recognized and expected by other members of his society. They join him in speculating how long he may survive, or who is the source of the curse. And then a strange thing happens. A consensus is reached that the end is near, and his friends and family retreat as from the smell of death. They return, but only to wail and chant over the body of this person they consider already dead. Physically the victim still lives; psychologically he is dying; socially he is already dead.

A third group, also anthropologists, agree with this perspective but carry it further by suggesting an actual mechanism to account for physical death. They point out that in many cases the victim of voodoo death is not merely a benign presence but, having by definition crossed into the realm of the spirits, has become an actual threat that must be removed. And in the case of the Australian aborigines, this is precisely what happens. Weakened by the long ordeal, the victim of sorcery receives no relief from even his closest relatives. On the contrary, these former supporters actually take food and water away, on the theory that a dead person has no need for either and with the motive, as one physician was told, “if real close up finish, take water away so spirit goes.” In the deserts of Australia, where the daytime temperatures average over one hundred degrees Fahrenheit in the shade, death by dehydration occurs in about twenty-four hours.

Not all cases of voodoo death are as clearly explicable as these examples reported from Australia, where because of the harsh climate a relatively simple act by the kin eliminates the victim’s life supports. More usual in voodoo death, but again more enigmatic, the victim dies despite the fact that his family offers succor.

All that can be ascertained is that voodoo death occurs, and that as a process it involves a number of complementary factors. Fear probably does initiate physiological changes. Certainly it makes the victim psychologically vulnerable, and this in turn affects the physical health. Neurophysiologists still do not fully understand the process, though the response of the victim’s family and society would seem inevitably to influence both his psychological and his physical well-being. So, while a universal mechanism to account for voodoo death has not been identified, the basic assumption is clear. As one researcher has put it, the brain has the power to kill or maim the body that bears it.

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The metamorphosis of Clairvius Narcisse from human to zombi was a very special instance of voodoo death. A sorcerer’s spell initiated a long process that exploited the victim’s greatest fears, mobilized the reinforcing beliefs of the community, and finally led to actual death. To the Haitian peasants Narcisse really did die, and what was magically taken from the ground was no longer a human being. Like many sorcerers around the world, the bokor that spun his death had a prop—in this case an ingenious poison that served as a template upon which the victim’s worst fears might be amplified ten thousand times. Still, in the end, it was not the powder that sealed Narcisse’s fate, it was his own mind.

Consider for a moment what he went through. As a Haitian peasant he had been socialized since childhood to believe in the reality of the living dead. This conviction had been enforced throughout his life by both a complex body of folklore and, more importantly, the direct testimony of friends and family; in Haiti virtually everyone has a vivid zombi tale to tell. For Narcisse, a zombi was a being without will, on the very frontier of the natural world, an entity that could manifest itself as either spirit or human. Zombis do not speak, cannot fend for themselves, do not even know their names. Their fate is enslavement. Yet given the availability of cheap labor, there would seem to be no economic incentive to create a force of indentured service. Rather, given the colonial history, the concept of enslavement implies that the peasant fears and the zombi suffers a fate that is literally worse than death—the loss of physical liberty that is slavery, and the sacrifice of personal autonomy implied by the loss of identity. Critically, for Narcisse as for all Haitian peasants, the fear is not of being harmed by zombis, but rather of becoming one. And it is to prevent such a horrid fate that the relatives of the dead may reluctantly mutilate the corpse if there is any suspicion of foul play. Unless, of course, the family itself was involved in the zombification.

Not only did Narcisse believe in zombis, he undoubtedly was aware of how and why they were created. When his world began to close in on him, he was already personally isolated. Within his lakou he had been ostracized because of his antisocial behavior; within his own family he was actively engaged in a dispute with his brother over the question of the right to sell heritable land. Eventually it was, by all accounts, that very brother who sold him to the bokor. Had Narcisse been in the right, and was zombified by his adversary without the support of the community, it is difficult to imagine that the brother would have been tolerated in the community for close to twenty years. But in fact he was, and even today Narcisse is not. In all likelihood, at the time of his demise, Narcisse had support from neither his immediate society nor his kin; his closest relatives may have been his greatest enemies. And since family members were involved, gossip and rumors undoubtedly took their toll, especially when he began to suffer physical symptoms that he had never known. Gradually as these symptoms got worse and worse, he would have realized that he had become a victim of sorcery. And more than likely he knew why.

His symptoms were real and concrete, and they worsened. He consulted houngan, but they did nothing. By now desperate, he entered the alien environment of the Schweitzer Hospital, knowing something the doctors did not. His condition deteriorated rapidly, and then something more extraordinary occurred. We have noted the devastating impact that social death has on victims of voodoo death throughout the world. The Haitian model takes this one step further. Narcisse was actually pronounced dead in a hospital by Western-trained physicians. More incredibly, from the known actions of the toxins in the poison, and from his own testimony, there is every reason to believe that he remained conscious for much of the time. He actually heard himself pronounced dead, was aware of his sister’s weeping, saw the sheet lifted over his face. Like the Japanese victims of tetrodotoxin, he strove desperately to communicate, but with the paralytic poison, he found it impossible.

Then Narcisse entered another realm. Having caused such a dramatic, virtually complete, reduction in metabolic rate, the poison took its victim quite literally to the frontier of death. Indeed, it very nearly killed him … as it may have killed many others. His symptoms remained consistent, yet at one point there seems to have been a qualitative change. Perhaps not surprisingly, the advanced symptoms of known tetrodotoxin poisoning merge with those of what Western physicians have termed the autoscopic near-death experience (NDE). Recall once again his description. He sensed that he was floating above his body at all times. When they placed him in the cemetery, he remained above his tomb, still floating, constantly aware of everything that was going on. He was content, he was without fear. He sensed that his soul was about to take a great journey, and it did travel, he insisted, taking in great passages over the land, timeless passages, immaterial yet powerfully real. His travels were multidimensional, yet they always returned him to the gravesite. His notion of time was lost. His tomb was the only axis of his existence.

Strange things happen to us when we die, at least if we are to believe the word of those who come back. Those who have been close to death speak of an ineffable dimension where all intuitive sense of time is lost. Like a dreamscape, it is timeless, but unlike a dream it is impossibly real, a place of crystal awareness wherein the process of death is acknowledged as something positive, calm, even beautiful.

Like Narcisse, virtually every medical patient who has been to the frontier of death experiences a profound separation between his material body and an invisible, nonmaterial aspect of himself, one that often hovers above the flesh; and in nearly all cases the patient identifies not with the body, but with the spirit. An elderly woman who nearly died during severe complications following surgery in a Chicago hospital wrote her physician, “I was light, airy, and felt transparent.” Often patients distinctly remember floating above their bodies, looking down at their material selves. A cardiac patient noted, “I was going up slowly, like floating … I was looking from up, down … they were working the hell out of me.” Also typical is the amazement of a construction worker from Georgia following cardiac arrest: “I recognized me lying there … [it was] like looking at a dead worm or something. I didn’t have any desire to go back to it.” Sometimes survivors of autoscopic near-death experiences recall conversations between attending physicians and nurses. Often they describe their frustration at not being able to communicate with others physically present at their bedside. “I tried to say something,” one patient remembered, “but she [the nurse] didn’t say nothing … she was like looking at a movie screen that can’t talk back and that doesn’t recognize you’re there. I was the real one and she was unreal. That’s the way I felt.” Certain survivors describe an extraordinary ability to “travel” through space and time. “It was just a thought process,” one explains. “I felt like I could have thought myself anywhere I wanted to be instantly. I could do what I wanted to … it’s realer than here, really.”

And then, those who go through a near-death experience and survive share one thing in common: they all retain a distinct awareness that at one point their immaterial aspect returned to its physical body. It was at this moment, many remember, that they regained consciousness. In hospital patients, this often occurs instantaneously, coinciding with a particular resuscitative procedure. A cardiac patient responded to electric shock: “She [the nurse] picked up them shocker things … I seen my body flop like that … it seemed like I was up here and it grabbed me and my body, and forced it back, pushed it back.” Another experience ended with the sudden arrival of a loved one. The patient explained, “I was up at the ceiling…. Then when someone in the family came to the door and called … I was instantaneously back in my body.”

This, of course, is what Clairvius Narcisse remembers happening. One moment he was floating above his tomb, and then he heard someone call out. But for Narcisse, the voice did not come from a loved one, and when he returned to his body it was not in a hospital bed, it was in a coffin. And for him, the ordeal was only about to begin.