by Wade Davis
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 o
f 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 co
ol. 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.
