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INTRODUCTION

1 In the lower montane forests of the Eastern Highlands of Papua New Guinea, a population of some 14,000 slash-and-burn horticulturalists known as the Fore (pronounced FOR-AY! tend gardens of sweet potato, taro, yam, corn, and other vegetables. They also grow sugarcane and bananas, keep pigs, and, in the sparsely populated regions near their south­ ern boundaries, still hunt for birds, mammals, reptiles, and cassowaries. Unlike the open country to the north around Kainantu or Goroka, where long-established grasslands prevail, this part of the Eastern Highlands con­ sists of mixed rainforest broken by small clearings and grasslands of no great age. The forest includes oak, beech, Ficus, bamboo, nut-bearing Castanop­ sis, feathery Albitzia, red-flowered hibiscus, and many other species used for food, medicines, and stimulants, as well as salt, fibers, and building materials. 1 Pandanus grows at higher altitudes. The ground is covered with a wealth of edible shrubs, delicate tree ferns, fungi, and creepers. Red, white, and salmon-colored impatiens sparkle in the shafts of sunlight beside forest paths, and ferns, orchids, and rhododendron grow as epiphytes in the canopy overhead. The forest rings with the sound of birds feeding on tall fruit trees.

The Fore-speaking population lies in the wedge created by the Kratke Mountains to the north, and the Lamari and Yani Rivers to the east and west. Although the terrain ranges in altitude from the mountains at 9,000 feet to southern valleys at 2,000, gardens and hamlets are scattered across the zone between 7,500 and 3,500 feet, where the population has access to

Traditional Fore hamlet near the edge of the forest. photo and legend by Dr. E. R. Sorenson from The Edge of the Forest, Smithsonian Institution Press, 1976.

Nona THIS MATERIAl MAY 81

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MAP 2 The Fore and Their Neighbors

SOURCE: Adapled from E. Richard Sorenson. The Edge of the Forest (Washington. D.C: Smithsonian Ins!. 1976), p 20 © SmIthsonian

both montane and lowland encironments. Hamlets typically consist of sev­ enty to 120 people, living in twelve to twenty houses, and their adjacent gardens. Surrounded on three sides by populations speaking Gimi, Keiagana, Kanite, Kamano, Auyana, Awa and Kukukuku lalso known as AngaJ, the Fore are reluctantly penetrating the uninhabited region to the south. Stories of illness and hardship characterize their view of existence in these frontier communities.

The Fore represent the most southerly extension of the East New Guinea Highland linguistic stock,2 but they have much greater genetic heterogeneity than most linguistic groups in the Eastern Highlands. The

5

c, with a remarkably flexible kinship system, do not constitute an iso­ c,d breeding population. Genetic studies show their close association

. ,h populations in two directions. To the northwest, they are most closely l1ciated with the Kamano, Gimi, and Keiagana, and to the southeast with . Awa, Auyana, and Tairora.3 Kukukuku populations across the Lamari Jky and the Yar-Pawaian groups beyond the uninhabited zone appear to long to different linguistic, genetic, and cultural communities.

The Fore are afflicted with a rare disease. Since record-keeping began 1957, three years after the Australian administration established a patrol ,L at Okapa, some 2,500 people in this region have died from kuru, a l:JCute degenerative disorder of the central nervous system. Appro xi­ ctcly 80 percent of all kuru deaths have occurred among Fore-speaking

.;lple, with the remaining 20 percent striking neighboring populations. In ,~ ~arly years of investigation, over 200 patients died annually, which at

'. ~l time approached I percent per annum of the affected population.4 In ~nt years, kuru rates have steadily declined, and in 1977 only 31 persons

:J of the disease. Following several decades in which kuru was the major 'se of death among the Fore, the disease is rapidly disappearing.

My main focus is on the 8,000 South Fore. Identified by Australian :anment officials in the 1950'S as a single census division within the :1pa Subdistrict, South Fore is separated from North by a low mountain ~e (Wanevintil that hinders but does not preclude contact between the

:, populations. Marriage partners, trade goods, food, refugees, illnesses, d ideas move between North and South, but South Fore social life is 'lj3ed on the lands sloping southward from the mountain barrier. There I) dialect groups (Atigina and PamousaJ with a high frequency of cognate

.' rds are recognizable. The two southern dialects have more in common ::n either has with Ibusa, the dialect of the North Fore.6 It is among the .Jeh Fore that the incidence of kuru has been highest. Between 1957 and ;S, over 1,100 kuru deaths occurred in a South Fore population of 8,000, I most cases reported for 1976 and 1977 come from this region. Since

;'11 is predominantly a disease of adult women-the childbearers, pig .Jers, and gardeners-its effects on Fore society have been particularly :mging. When the incidence of kuru reached a peak, in the 1960'S, the

.! th Fore believed their society was coming to an end. And indeed, with 'ic high female mortality and low birth rates, in the early 1960'S their :nbers were truly declining. South Fore were aware that the disease was :::ing them hardest.

This book discusses the Fore response to kuru in the 1960'S, when the ,demic was at its height. In Chapter 2, I trace the interest of Western ,.'ntists in the disease, from the time they learned about it in the early jO'S to the present. Chapter 3 surveys Fore medical disorders, and shows L apart from kuru, their health status resembles that of kuru-free popu­

:ons in the Eastern Highlands of New Guinea. Chapter 4, an analysis

6

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........ v \V1\ALL AREAS \ ....-\

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~UTHFO~ [7 \ V \ /\

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NORTH FORE

'\....­ ~ 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60

YEAR OF BIRTH

30

en I10 l­ « w o LL o 0 IT: lli 20 ~ => Z

10

20

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FIGURE 1 Number of Persons Dying of Kuru (since 1963) for each year of birth from 1945.

SOURCE: Adapted from Hornabrook & Moir 1970

of South Fore kinship, indicates that Fore establish ties by demonstrat­ ing commitment to a relationship. Kinship is as often based on common interest and support as it is on heredity.

In Chapters 5 and 6, I present Fore views of the cause of disease, and suggest that Fore beliefs are appropriate to a particular way of life and period of time-that is, to communities of partially intensive swidden horticul­ turalists in the 1960'S. In the three decades since the Australian administra­ tion at Port Moresby sent the first patrol through Fore territory, both their mode of existence and Fore beliefs about it have undergone rapid change, allowing us an opportunity to observe the ways that philosophical systems depend on context. A new way of life gave rise to greater manipulation of the environment, and to differences in rank requiring the coercion of others in order to maintain an elevated position. New diseases also took their toll. As these changes occurred, ghosts of the dead and spirits of the forest re­ ceded, displaced by growing numbers of sorcerers.

The early 1960'S were crisis years for the Fore. They hunted for sorcer­ ers and consulted curers IChapter 7), and finally they called great public

7

j·..::etings (Chapter 8). There, they denounced the performance of sorcery ,at was decimating their women and creating a wasteland. Sorcerers were :;id to be the agents of all that was wrong with the human condition. They :ere seen as the negative of all that is fine, good, and moral, as instruments i impoverishment and decline, and as a burden on the community (Chapter \. Notions of sorcery, witchcraft, and pollution emerge as ideologies of J!ltainment, by which wielders of power attempt to degrade their oppo­

;::l1ts, coerce social inferiors, and allocate resources. Sorcerers, witches, and ':lluters therefore have universal attributes. They appear in different man­ ,cstations and with varying powers of retaliation in New Guinea and lscwhere. The direction from which they project their feared energies is a

-lLle to an asymmetrical interchange, either between individuals or between _:~ions (Chapter 10).

In the search for the cause of kuru, Western science unraveled a ~ological mystery; the solution has applications for neurological afflictions ",;It range far beyond the borders of New Guinea. The Fore analysis of the ;nblem revealed more about victimization, and told us more about our­ ..:ives. While their medical observations were frequently accurate, they 'ere embedded in social codes, and in messages about the nature of exis­

_,:nce. In their statements about the cause of disease, the Fore also consid­ ;"t.:d those conditions under which a threatened society might ultimately ,:dure.

KURU AND SORCERlJ

2 As he passed through the hamlets at Arnusi during an Australian govern­ ment patrol in the South Fore region, Patrol Officer McArthur made a sig­ nificant notation. "Nearing one of the dwellings," he wrote in August 1953, "I observed a small girl sitting down beside a fire. She was shivering vio­ lently and her head was jerking spasmodically from side to side. I was told that she was a victim of sorcery and would continue thus, shivering and unable to eat, until death claimed her wi thin a few weeks."1 Although the disease had been mentioned in earlier government reports,2 this was the first official description of kuru, a fatal neurological disorder very common among Fore, and present to a lesser degree among neighboring groups, but unknown elsewhere in the world. The discussion that follows presents kuru as a disease entity as perceived by Western observers, and follows the evolu­ tion of medical thought over more than two decades. Western scientists now consider kuru to be a slow virus infection spread by the ingestion of human flesh. This view contrasts with that of the Fore, who remain con­ vinced that the illness results from the malevolent activities of Fore sorcerers.

CLINICAL FEATURES OF KURU

A Fore word meaning trembling or fear, kuru is marked primarily by symptoms of cerebellar dysfunction-loss of balance, incoordination (ataxia), and tremor. An initial shivering tremor usually progresses to com­ plete motor incapacity and death in about a year. Women, the prime victims

8 9

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the disease, may withdraw from the community at the shock of recogniz­ .~ the first symptoms-pain in the head and limbs, and a slight unsteadi­ 55 of gait. They resume their usual gardening activities a few weeks later, Ilggling to control their involuntary body movements until forced by

,):;s physical incoordination to remain at home, sedentarily awaiting llh.

The clinical progress of kuru is remarkably uniform. It has been di­ vided into three stages by Dr. Carleton Gajdusek, who has made extensive clinical studies of the disease:

The first, or ambulant, stage is usually self-diagnosed before others in the community are aware that the patient is ill. There is subjective [self-perceived] unsteadiness of stance and gait and often of the voice, hands and eyes as well. Postural insta­ bility with tremor and titubation [body tremor while walking] and ataxia of gait are the first signs. Dysarthria [slurring of speech] starts early and speech progressively deteriorates as the disease advances. Eye movements are ataxic.... A convergent

A woman in the primary stage of kuru, steadied by her husband. Note abo normal position of her left arm and hand.

10

strabismus [crossed eyes] often appears early in the disease and persists. Tremors are at first no different from those of slight hypersensitivity to cold; the patient shivers inordinately. In­ coordination affects the lower extremities before progressing to involve the upper extremities. Patients arising to a standing posture often stamp their feet as though angry at them. In at­ tempting to maintain balance when standing, the toes grip and claw the ground more than usual. Very early in the disease the inability to stand on one foot for many seconds is a helpful diagnostic clue.... In the latter part of this first stage, the patient usually takes a stick to walk about the village unaided by others.

The second, or sedentary, stage is reached when the patient can no longer walk without complete support. Tremors and ataxia become more severe and a changing rigidity of the

Pregnant young kuru victim goes to work in her garden supported by stick. She was dead a few months later, less than a year after the first symptoms appeared. Photo by Dr. D. Carleton Ga;dusek.

A middle-aged kuru vic­ tim braces herself with both arms to maintain balance while sitting. Photo by Dr. D. Carle­ ton Ga;dusek.

An elderly kuru victim who can no longer walk waits for the other women to return from their gardens. Despite the heat of the sun, she feels chilled.

12

limbs often develops, associated with widespread [repetitive muscular spasms], or sometimes shock-like muscle jerks and occasionally coarser [irregular, involuntary] movements, espe­ cially when the patient is thrown into an exaggerated startle response by postural instability, or by sudden exposure to noise or bright light. Deep tendon reflexes are usually normal. Al­ though muscle activity is poorly maintained there is no real weakness or muscle atrophy. Emotional lability, leading to out­ bursts of pathological laughter [is] frequent, sometimes even appearing in the first stage of the disease, and smiling and laughter are terminated slowly.... Some patients, especially adolescent and young adult males, become depressed, and a rare patient develops a pathological belligerence [in response to] disturbances by family members or others. Mental slo.wing is apparent, but severe dementia is conspicuously absent. No sensory changes have been noted....

The third, or terminal, stage is reached when the patient is unable to sit up without support, and ataxia, tremor and dysarthria become progressively more severe and incapacitat­ ing. Tendon reflexes may become exaggerated.... Some cases show characteristic ... defects of posture and movement. Ter­ minally, urinary and faecal incontinence develop and dysphagia [difficulty swallowing] leads to thirst and starvation and the patient becomes mute and unresponsive. Deep ulcera­ tions [of the skin over bony prominences and] pneumonia appear in this stage and the patient finally succumbs, usually emaciated, but occasionally quickly enough t-o be still well nourished.J

HEORIES OF THE ETIOLOGY OF KURU

_.t first, kuru was thought by Westem observers to be a psychosomatic )henomenon, "directly associated with the threat and fear of what was :,clieved to be a particularly malignant form of sorcery."4 A provisional ,Iedical diagnosis of the first case sent to the Australian govemment hospi­ .•1 at Kainantu for close observation in r955 elicited a diagnosis of "acute ;?steria in an otherwise healthy woman."s In r957, Drs. Vincent Zigas :orking for the Papua New Guinea Department of Health) and Gajdusek

\(rom the United States National Institutes of Health) began an intensive Ludy of the disease, and Gajdusek was soon to write in a note to the ,! thropologist Ronald Bemdt:

We cannot yet claim any clues to its pathogenesis, and infectious and toxic factors which might be responsible for its etiology have thus far eluded us. However-and most unfortu­ nately for us-all the guidance is pointing toward the vast group of chronic-progressive-heredo-familial degenerations of

the central nervous system.... We have recently had the assis­ tance and advice of Dr. Sinclair, Director of Psychiatry from the Royal Melbourne Hospital, and he agrees with our current opinion that fatal kuru ... cannot by any stretch of the imagi­ nation be identified with hysteria, psychoses or any known ... psychologically-induced illnesses ... the evidence for direct central nervous system damage is far too great in the strabis­ mus, and pictures ... of advanced neurological disease shown by the advanced cases.6

Later the same year, 1957, Gajdusek and Zigas published their first medical assessment. They emphasized the high incidence of kuru in cer­ tain families and hamlets, its localization to the Fore and adjacent peoples with whom they intermarried, and its predilection for children and adult women. 7

The boundaries of the kuru region as defined by these investigators in 1957 have changed little since that time, although the region of high inci­ dence has gradually been contracting.8 The kuru region comprises most of the Okapa Subdistrict of the Eastern Highlands District, a population of over 40,000, belonging to nine language groups and representing about one­ fifth of the population of the Eastern Highlands District. The Lamari River to the southeast and a large expanse of uninhabited country to the south­ west sharply separate the southernmost Fore villages, which are regularly afflicted with kuru, from the Kukukuku and Yar populations, who have never experienced the disease. Elsewhere, the boundaries of kuru incidence are not sharply defined. To the east, Awa and Auyana peoples rarely contract kuru. North of Fore, kuru has occurred in Usurufa villages and in the adjoin­ ing part of Kamano. Some Yate and Yagaria peoples to the northwest have been affected, and to the west kuru is found in those parts of Kanite, Keiagana, and Gimi which border Fore territory.

Because kuru seemed to run in families and was localized to a small interrelated population, a genetic basis for the disease was suspected. In the late 1950'S, it was proposed that kuru was a hereditary disorder, determined by a single autosomal gene that was dominant in females but recessive in males. 9 The implications of such a hypothesis were somber. By the mid­ 195 0 'S, Highland men had been encouraged to participate as migrant labor­ ers under the provisions of the Highlands Labour Scheme, administered from Goroka. Each worker signed a two-year contract. Although the gov­ ernment employed some of these men on public works, the majority were under contract to private copra, cocoa, and rubber plantations in coastal and island regions of Papua New Guinea, where labor w:lS scarce. The laborers received food, clothing, lodging, transport, and medical attention. Half their low wages was deferred and paid in a lump sum at the termination of the contract. Government officials and kuru investigators debated whether it would now be possible to erect an invisible fence aroWld the Fore, to pre­

14 15

vent their participation in the Highlands Labour Scheme, and to discourage the exodus of the affected population from the region. Only if such a plan were found feasible and morally acceptable, it was said, could other peo­ ples be protected against the lethal kuru gene. In the meantime, Fore would continue to transmit the disease one to the other until their tragic extinction.

The investigation of kuru in the 1950'S was hampered by a lack of information about Fore kinship. As we shall see in Chapter 4, many of the supposedly related kuru victims were not closely related biologically, but were kin in an improvised, non-biological sense. An analysis of the Fore kinship system does not support a purely genetic interpretation of the dis­ ease. Moreover, as John Mathews, a physician whose study of kuru began in 1963, noted:

This purely genetic model, if true, implied that kuru must have been of remote evolutionary origin and that it ought to have been in epidemiological equilibrium. It was soon apparent that kuru was too common and too fatal to be a purely genetic disorder unless the hypothetical kuru gene was maintained at high frequency by a mechanism of balanced polymorphism. There was no evidence to support the latter suggestion. to

In other words, an inevitably fatal genetic disorder could not reach the incidence kuru then had among the South Fore without soon killing off the host population, unless the gene for kuru in some other way conferred a selective survival advantage.

Anthropological evidence gathered in 1962 by Robert Glasse and my­ self from dozens of Fore informants indicated that kuru had spread slowly through Fore villages within living memory, and that its progress through Fore territory followed a specific, traceable route. Entering from a Keiagana village to their northwest around 1920, the disease, according to Fore tes­ timony, proceeded down their eastern border, and then swung westward into central South Fore. From this point, it turned again to the north and also continued to move south. Its appearance in the extreme south was thus relatively late, and many people gave persuasive accounts of their first en­ counter with the disease.

Owata lnot his real namel of Wanitabe was about 55 years of age when he described his experience with kuru:

When I was a young boy, I didn't know anything about kuru. I was initiated [at 9 or 10 years] and I still hadn't seen kuru. It wasn't until I was married that I first saw it. That was true of many places around here. I visited Purosa and Aga Yagusa, and it wasn't there. I heard rumors of it at Kasokaso before it came to Wanitabe. My mother died of kuru at Wanitabe. I was mar­ ried then, but it was before I had any children. She wasn't the

first to die of it here; a few other women died of it before her. When I heard it arrived at Kamila, I went to Kamila to

look at it. Men asked at first, /lIs it sickness or what? 1111 Then they said that men worked it [Le., caused it by sorcery]. We fought against Kamila after this. We were angry with them be­ cause all the women were dying of kuru. We asked them where we would get wives from if this continued.... Then some men of Wanitabe purchased it [Le., paid for knowledge of the sorcery technique] from Kamila, and now we get it here too. Now it has spread everywhere. In the past, we fought only with bow and arrow. Then kuru came and killed the women one by one. I can't see of course, since I am blind, but I hear others talking about it, and they say it kills everyone now.

This places the arrival of kuru at Kamila in the late 1920S, and at Wanitabe by about 1930. The first cases at Purosa, six miles south of Wanitabe, are also associated with a sorcery purchase from Kamila at about the same time, in the early 1930'S. A week after the death from kuru of a twenty-year-old Purosa youth in 1962, his mother llnatal, his mother's mother IAsa'inal, and her husband ITano) speak of the first appearance of the disease at Purosa:

Asa'ina (grandmother): Kuru came to Purosa only recently. I had carried all my children and my hair was white before it came here.

Question: Was Inata married? Inata (mother): Yes, I had given birth to all my five chil­

dren.... my first child, a son, was about ten years old. Inata (in response to question): We were afraid when we first

saw kuru. We asked the men what kind of sickness it was, and they told us it was kuru.... When it first ar­ rived, only one woman would get it, then a little later, another. Now, since the tetegina [red people, that is, "whites"] have arrived, plenty of people get the disease.

Question: Can you remember the names of the first people here to get kuru?

Tano (husband of Asa'ina, interjecting): These two can't re­ member. I can. The first woman to get it here was Agiso. She lived in a house on this hill. We were free of it in the past. Then we heard rumors of this trembling thing, this kuru, at Kasokana. From Kasokana it came to Wanikanto where four women got it. Still we didn't have it, we had only heard of it. Then the men of Kamila had four women who died of it, and still we had only heard of it. Then Agiso, who was a Kamila woman, came here to live and she wasn't here long before she died of it. She left her

16 17

The site of the first case of kuru in the region is a UWAMI, maner of controversy between the peoples involved

(KEIAGANA)-- -- - -- -'-.,

KAGA AWANDE " 1941 (NORTH FORE)

PAIGATASA '-' 1942 ...........

"-- MIARASA "­ ~41 \

YASUBI 1940

\ KEIAGASA

/1940

AMORA ) /'" 1933 '-­

KANIGATASA, WANIKANTO

1935 - KUME '- I 1927 \ 1934 WANITABEMENTILE~ ·1~ 1934 KAMILA

')940:;:>1'. \ WAISA / 1927 ~ASOKANA 1930 1922

U~9~A _ TAKAI . ILESA 1937 ~ PUROSA 1946 ~

./ 1933 AWAROSA

IVAKI ~ ~ 1940 1936 "'- AGAKAMATASA

1938

MAP 4 Epidemiological Map of Kuru

SOURCE: Adapted from J.D. Mathews 1971, Page 134. (unpublished thesis)

husband at Kamila and came to marry a man here at Purosa. She was a young woman when she died, about eighteen or twenty years old [her age is conveyed by comparing her to another girl now living]. The next to die of it was a woman called Alakanto ... and we saw that it had come to us and we wondered who had purchased it and brought it here.... I was married with one child, a

18

daughter called Tabelo who was about five years old [in­ dicating a child of similar age in the group] when Agiso died.... This was a child of my first wife. I married Asa'ina later.

From scores of such accounts there emerges a broad chronology of the spread of kuru, with its arrival in some northwestern and southeastern areas convincingly dated as late as the 1940'S.

Fore accounts had a ring of epidemiological accuracy. They noted the initial incidence of kuru among women, and describe its subsequent shift to children of both sexes and to adult men. They also indicated uncertainty in the diagnosis of early cases. At Umasa, the first case occurred in a woman who had arrived recently from the North Fore. A young widow, she had been inherited in marriage by her husband's age-mate, and people at Umasa were puzzled by her illness. Noting that her tremor resembled the swaying of the casuarina tree, they supposed that she had a shaking disorder called cassow­ ary disease, by the further analogue that cassowary quills resemble waving casuarina fronds. They fed the victim pork and casuarina bark, a homeopathic treatment that gave little relief. When the woman's brothers came to visit her, they, having already seen the disease, told the people of Umasa what it was.

Many people first called the disease negi nagi, a Fore term meaning silly or foolish person, because women afflicted with the ailment laughed immoderately. In those early days, our informants said, they joked and took sexual levities with the sick women as they do with those who manifest temporary mental derangement or bizarre behavior. When it became appar­ ent that the victims were uniformly dying, they were forced to conclude that the matter was more serious than they had thought, and that sorcerers were at work. Early medical reports also emphasized the sufferers' emo­ tional lability, leading to the unfortunate characterization of kuru in the Australian press as "the laughing death." Only a minority of the patients examined in the 1960'S were said to smile or laugh inappropriately; it is possible that the clinical features of the disease have changed.12

CANNIBALISM

In 1962 and 1963, Robert Glasse and I presented evidence gathered in two extended stays among the Fore that kuru had spread through the Fore popu­ lation in recent times, and that its high incidence in the early 1960'S was related to the cannibal consumption of deceased kuru victims. We also provided evidence that for the South Fore, the depletion of women was a recent phenomenon. 1J Our cannibalism hypothesis seemed to fit the epidemiological evidence. The first Australian government patrols in the late 1940'S reported cannibalism throughout the entire kuru region. By

19

T \)5 I, the Berndts, living on the North Fore borders, noted that government 'ntcrvention had put a stop to cannibalism in that area, although it was still 'I ;Icticed surreptitiously farther afield. The South Fore confirmed the

:'.cmdt's observation. One elderly man from Wanitabe said in 1962 that the ,:xhortations of the first patrol (1947) were disregarded. "We hid and ate "cople still. Then the luluais [government-appointed localleaders]and tul­ ,~11s [their appointed assistants] tried to stop us, but we hid from them, too. 'Je only stopped when the big road came through from Okapa to Purosa I l) 55]." Thus, in the South Fore, the area with the highest incidence of .uru, cannibalism had continued later than in the North.

When a body was considered for human consumption, none of it was :iscarded except the bitter gall bladder. In the deceased's old sugarcane ~:nden, maternal kin dismembered the corpse with a bamboo knife and :wne axe. They first removed hands and feet; then cut open the arms and ,\~gs to strip out the muscles. Opening the chest and belly, they avoided ~;pturing the gall bladder, whose bitter contents would ruin the meat. After :vering the head, they fractured the skull to remove the brain. Meat, vis­

,era, and brain were all eaten. Marrow was sucked from cracked bones, and '1metimes the pulverized bones themselves were cooked and eaten with ~! cen vegetables. In North Fore, but not in the South, the corpse was buried If several days, then exhumed and eaten when the flesh had "ripened" and

he maggots could be cooked as a separate delicacy.14 Thus, little was wasted, but not all bodies were eaten. Fore did not eat

lcople who died of dysentery or leprosy, or who had had yaws. Kuru victims, :!Owever, were viewed favorably, the layer of fat on those who died rapidly :i~ightening the resemblance of human flesh to pork, the most favored pro­ .:.:in. Nor were all body parts eaten by everyone. For instance, the buttocks It Fore men were reserved for their wives, while female maternal cousins

{cccived the arms and legs. Most significantly, not all Fore were cannibals. Although cannibalism by males occurred more frequently in the North, ,()uth Fore men rarely ate human flesh, and those who did (usually old men)

',::li.d they avoided eating the bodies of women. Young children residing apart ; rom the men in small houses with their mothers, ate what their mothers ':lVe them. Initiated boys moved at about the age of ten to the communal ;(luse shared by the adult men of the hamlet, thus abandoning the lower­ :!::lSS world of immaturity, femininity and cannibalism. As will be discussed

: II greater detail in Chapter 10, men in this protein-scarce society claimed [:1': preferred form of protein (wild boar, domestic pigs), whereas women ,upplemented their lesser allotment of pork with small game, insects, frogs, 'nd dead humans. Women who assisted a mother in childbirth ate the ,y!acenta. Both cannibalism and kuru were thus largely limited to adult ",,'omen, to children of both sexes, and to a few old men, matching again the :pidemiology of kuru in the early 1960'S.

As mentioned earlier, body parts were not randomly distributed. The

Young girl holds up rat she caught and will cook with the bagged vegetables at her feet.

corpse was due those who received pigs and valuables by rights of kinship and friendship with the deceased (primarily maternal kin), and the gift 'had to be reciprocated. Pig and human were considered equivalent. The death of a breeding sow in 1962 evoked the following speech of mourning: "This was a human being, not a pig. One old woman among us has died." Pig and human were dismembered and allocated in similar fashion. Among South Fore, a man's brain could be eaten by his sister, and in the North, by his sister as well as his son's wife and maternal aunts and uncles. A woman's brain, perhaps the most significant body matter in transmission of the dis­ ease, was said to be given to her son's wife or her brother's wife.

Ethnographic accounts of the consumption of the first kuru victim in a certain location also describe cases four to eight years later among those who had eaten the victim. IS Moreover, the average risk of kuru in wives of kuru victims' brothers was three to four times as great as that in a control group of women who were not related either genetically or by marriage to kuru victims. Furthermore, the risk of kuru in females related to kuru victims by marriage only (4 I percent) was almost as high as the risk in females genetically related to kuru victims (5 I percent), 16 This conforms to the stated regulation that brothers' wives receive the victim's brain, and the

20 21

lpportunity of these women to participate in kuru cannibalism along with Lhe victim's mother, sisters, and daughters. The distribution of human flesh ~\!r consumption thus crossed genetic lines much as the distribution of !~uru did.

THE ADOPTION OF CANNIBALISM

Fore had not been cannibals for long. Within the zone of cannibal peoples to the east and south of Goroka, they may have been among the last to include human flesh in their diet. Cannibalism was adopted by the Kamano and ;~eiagana-Kanite before it became customary among Fore. North Fore say they were imitating these northern neighbors when they became cannibals around the tum of the century, while among South Fore, cannibalism began as recently as fifty or sixty years ago, or about a decade before the appear­ :mce of kuru there. Old people in the South Fore, whose memory of the matter appears unclouded, describe their attraction to human flesh. There was no thought of acquiring the power or personality of the deceased. Nor is it correct to speak of ritual cannibalism, although many medical and jour­ nalistic accounts do so.17 While the finger and jaw bones of some relatives were retained for supernatural communication, Fore attitudes toward the hodies they consumed revolved around their fertilizing, rather than their moral, effect. Dead bodies buried in gardens encouraged the growth of crops. In a similar manner human flesh, like pig meat, helps some humans regenerate. The flesh of the deceased was thought particularly suitable for invalids.

As a Wanitabe man born about 1890 said: "The Ibusas [North Fore] were visiting the Kamano and saw them stealing and eating good men. They heard it was sweet to taste, and tried it themselves. I was about ten years old when we heard these stories." North of Fore, then, aggressive exocan­ nibalism, or the eating of dead enemies, appears to have been the prevailing practice. Among South Fore, however, it was usual to eat kin or people of one's own residential group after they had died (endocannibalism).

A variable enthusiasm for human flesh runs from Goroka through the Fore area, coming to an abrupt halt in the southeast, where the Awa, in contrast to their Fore neighbors, were not cannibals at all. This is a gradient that matches an environmental shift from grassland groups for whom hunt­ ing plays but a small part in the diet18 to the Fore, who have not yet denuded their land of forest and for whom until recently wild game was readily available. By 1962, traditional gifts of wild protein between matrilateral kin were rare in the South Fore; possum and cassowary were being replaced by chicken and canned fish purchased at the local trade store. The last wild boar injury in Wanitabe occurred around 1940, and by 1970 South Fore groups who had supplied feathers for the northward trade began to buy them from the forest-dwelling Kukukuku further south. A less agricultural recent

A hamlet and ad;oining gardens recently carved out of the forest. Grass and scrub are overtaking the older, abandoned site above. Photo and legend by Dr. E. R. Sorenson from The Edge of the Forest, Smithsonian Institu­ tion Press, 1976.

23 22

";lSt is portrayed in Fore stories of men and their humanoid dogs encounter­ ~lg possum, birds, snakes, and flying foxes. Fore also have an elaborate :uological classsification system, which represents a relict of vanishing :l\lnting habits. 19

Population increases in the region and the conversion to the sweet ;Jil(ato as a dietary staple thus appear to have lead to the progressive re­ :Iloval of forest and animal life, to cultivation methods involving more ~omplete tillage of the soil, and to the keeping of domestic pig herds, which ~()mpensate for the loss of wild protein. As the forests protein sources be­ ::ame depleted, Fore men met their needs by claiming prior right in pork, .':hile women adopted human flesh as their supplemental habus, a Melane­ :;ian pidgin term meaning "meat" or "small game." Fore still refer to the human corpse and the stillborn infant as "the true habus of women." Men .tt Awarosa, who insisted that cannibalism was a female habit, argued that

LEFT One stage in slash-and-bum agriculture: felled trees are drying before the garden is set afire.

BELOW A mixed garden of sweet potato, surgarcane, and beans.

in this southeastern Fore region there was "plenty of habus in the forest for men." They noted, in addition, that "if we men ate people, we would fall ill with respiratory disorders and our flesh would waste away," a rationale they also gave for their initial rejection of chicken/lmore will be said about these attitudes in relation to pollution in Chapter 10). Traditional male curers guarded their powers and are said never to have practiced cannibalism.

The case of the non-cannibal, grass-dwelling Awa does not weaken the supposition that human flesh is ingested as a relevant source of dietary protein. 20 Fore at Awarosa report the neighboring Awa as saying they have never been cannibals. "We have no forests of our own," they reportedly told the Fore, "so we give you Our sisters in marriage, and in exchange we eat your habus." The Awa SOurces of protein were pigs given them as brideprice, and subsequent gifts of wild protein received as birth payments each time their sisters gave birth to children. Ronald Berndt also takes seriously Fore statements on the value of human flesh. Noting that in the 1950'S pigs were not plentiful, he records a story in which Fore first taste human flesh. "This is sweet," they said. "What is the matter with us, are we mad? Here is good food and we have neglected to eat it."21

Epidemiological evidence reported in the mid-1960'S indicated that the age and sex distribution of kuru was changing. Young children were less often affected, and the disorder was mOre often seen in adolescents and young adult men and women, as well as in older women. Moreover, the overall incidence fell in all areas except the Gimi.22 A purely genetic expla­ nation of kuru no longer seemed plausible.

KURU AS A SLOW VIRUS

After the first clinical descriptions of kuru were published, this unusual disorder attracted considerable international attention. In England, W J. Hadlow, working on scrapie, a degenerative disease of the central nervous system in sheep, pointed to the remarkable similarities in the clinical and pathological features of kuru and scrapie. Moreover, the disease of sheep was transmissible by inoculation.23 Unlike most infectious disorders, which have a relatively short incubation period, scrapie did not become manifest until many years after inoculation. Stimulated by the parallel with scrapie, Gajdusek and his coworkers at the National Institutes of Health in Bethesda, Maryland, injected the brains of chimpanzees with brain material from Fore patients who had died of kuru, and in 1966 they reported that after incubation periods of up to fifty months, the chimpanzees had de­ veloped a clinical syndrome astonishingly akin to human kuru.24 Kuru, like scrapie, thus appeared to be a viral disease of extraordinarily long incuba­ tion, a "slow virus infection."

This finding lent support to our idea that the disease had reached epidemic proportions among the Fore as a result of the eating of dead kuru

25

iictims. That hypothesis had also assumed that kuru would not strike those :,om after the abandonment of cannibalism, which in South Fore occurred :s a result of government and missionary intervention in the middle to late I9S0'S.25 The prediction now appears substantiated by the virtual disappear­ :nce of kuru among children, and by the earlier decline in childhood cases ,1110ng North Fore, where government influence suppressed cannibalism 'cars earlier than in the South or in the Gimi, where childhood kuru occur­ cd until 1970.26 The Gimi, even more remote from government influence

:han South Fore, continued as cannibals for longer. Epidemiological data gathered between 1970 and 1977 strengthen the

.iypothesis that kuru is a disease transmitted by cannibalism and caused by ) slow virus with an extremely long period of incubation. There has been a ,:ontinued decline in the annual incidence of the disease, particularly in ll'males. The greater decline of new cases in females can be explained by the [Jct that those who ate human flesh as adults were predominantly women, and they have already died of kuru. They leave behind an increasing major­ i ty of new cases resulting from childhood ingestion of the virus, a condi tion :or which both sexes were equally at risk since cannibal flesh was consumed :qually by male and female children. With the passage of time, the sex ratio ,)j new kuru victims should thus approach pari ty. This has already occurred in North Fore, where government influence eliminated cannibalism earlier, :md a similar trend is now appearing in the South.27 Moreover, while there 'Ncre two twelve-year-old patients With kuru in 1970, the youngest current ~ase in May 1978 was more than 20 years old. Thus both childhood and ,dolescent cases have disappeared completely. The only Fore and Gimi cur­ ently coming down With kuru are those who participated in cannibal meals

"rior to 1955. Recent data also allow us to delineate the behavior of the virus more

:nccisely. Since the youngest victim is now twenty-five, while the youngest l<ltients ever seen have been four years of age,28 the virus may be estimated .() have a minimum incubation period of roughly two years [from the first .ligestion of solid meat) and a potential maximum of at least twenty-three ·cars. This upward limit may be raised as data are gathered in the next few

.'Cars, but the pattern already known depicts an extraordinary infectious lilness in which symptoms may appear decades after the causal event.

While the means by which the disease was transmitted thus seems ,'[arified, kuru continues to provoke scientific curiosity. Recent research has :fJcused on the pathogenesis of slow virus infections, on documenting of :,;w epidemiological trends, and on attempts to establish the kuru virus in -issue culture. 29

The pathogenic agent responsible for the disease has recently been :~,olated and transmitted to spider, capuchin, squirrel, rhesus, woolly, and ,narmoset monkeys, as well as to chimpanzees, yet the virus itself has

roved elusive. It seems to elicit in its host none of the usual immune

responses. Kuru does not produce detectable antibodies. Nor has the virus been depicted under the electron microscope. As the first chronic or sub­ acute degenerative disease of humans proven to be a slow virus infection, however, kuru has stimulated the search fo~ virus infections in other sub­ acute and chronic human diseases, particularly of the nervous system. Mul­ tiple sclerosis is the most common central nervous system disorder believed (though in this case not yet proven) to be caused by a slow virus infection.311

The evidence for other neurological diseases is more conclusive. For exam­ ple, it now appears that Creutzfeldt-Jakob disease, one of the presenile dementias (mental deterioration at a relatively young age) that occur spo­ radically and in familial patterns in humans throughout the world, is also transmissible to chimpanzees and monkeys, and is caused by a virus with properties much like those of the kuru virus.31 Moreover, the incidence of Creutzfeldt-Jakob disease among Jews of North African and Middle Eastern origin in Israel is thirty times the rate for Jews of European origin. Since only the former customarily eat the eyeballs and brains of sheep, scrapie­ infected sheep tissue has been suggested as the source of infection.32

Two other rare disorders of the central nervous system-subacute sclerosing panencephalitis (SSPE) and progressive multifocalleukoenceph­ alopathy (PML)-have been shown to be due to slow virus infection. 33 The kuru model may also apply to amyotrophic lateral sclerosis, Al­ zheimer's disease, and other presenile or senile dementias. 34

Thus, as research proceeds, the concept of a related group of diseases of viral etiology has emerged. These are all virally transmitted diseases of the brain, infections that do not provoke the typical inflammatory response, caused by viruses with very unconventional properties. The kuru agent remains stable on storage at 70°e. for many years and after freeze-drying. It is not totally inactivated when subjected to a temperature of 85°e. for thirty minutes. 35 Fore cooking methods therefore did not destroy the kuru virus. After the brain of a dead person was removed from the skull, the tissue was squeezed to a pulp and steamed in bamboo cylinders at temperatures that would not completely inactivate the virus, since in high altitudes water boils at 90-95 0 No serological tests for the virus have been found. There is • no evidence of an immune response, and no antibodies have been detected. Nor is there evidence of an antigen related to any of the more than fifty known virus antigens. 36 Yet the kuru-scrapie agents persist in laboratory cultures of infected brain tissue, and they are readily transmissible in extremely low dilutions by intravenous, intramuscular, or subcutaneous injection, and from tissues other than brain (pooled liver, kidney, spleen, and lymph nodes).37

Kuru has not yet been transmitted to animals via the gastrointestinal tract. Gajdusek therefore has suggested that a likely route of infection from contaminated brain was through the skin, entering either through cuts and sores or upon being rubbed by unwashed hands into the nose or eyes.38

26 27

Research continues on the question of susceptibility to the agent, and on refining our know ledge of its properties. Kuru is already an established l.1ndmark in neurology and virology. In neurology, it is the first human degenerative disease shown to be caused by a virus. In virology, it is the first ;1Uman disease shown to be caused by a novel kind of viral agent. 39 The implications of the discovery of the slow virus etiology of kuru for the understanding of other diseases have only begun to be explored. The Fore experience will be remembered for decades to come as investigators use the kuru model in their search for the cause of disease in other populations of the world.

:ORE SORCERY

,(1 this day, Fore universally believe that kuru is caused by malicious sor­ ·.:rcrs in their midst. Early observers of the Fore population were struck not -'lily by the concern of the people with this strange and dramatic disease, .Jut by their more general focus on sorcery. In the report of August 1953 ;uoted at the beginning of this chapter, Patrol Officer McArthur wrote: "In '-] i s area, I regard sorcery as a powerful foe .... Its results are serious. Even nce the last patrol in December 1952, it has caused one tribal fight and two

" <;crtions of ground [evacuations of hamlets] .... There are ... a large t:mber of sorcerers."

Fore have a powerful reputation as sorcerers among other populations J the reginn.~o As far away as Kainantu and Hcnganofi, forty miles and two i three days' walk from Wanitabe, people believe that methods and ingre­ imts can be obtained from Fore,41 while their immediate neighbors view ,ile with considerable anxiety. Gimi have a particular fear of sorcery i);mating from their eastern neighbors,~2 and Kamano confide that they "ke special care not to throwaway scraps of food (which can be used :Jinst them in sorcery bundles I while parties of Fore are visiting. Keiagana !ll1it to a similar caution about providing Fore with potential sorcery :nerials, and when traveling in Fore territory they deposit sweet potato !cl sugarcane skins in their string bags, to discard on the return home. ;llth Fore at Ilesa, by contrast, pay no heed to their food scraps or feces !lile visiting the Awa, but resume Vigilance as soon as they return to home

ri tory. Not only do neighboring peoples fear Fore, but Fore fear one 'Ither.

Patrol Officer Colman's 1955 report describes South Fore hamlets ;ricaded behind wooden constructions and impenetrable canegrass. :uss the entrance corridor to the hamlet lies a small gate. "When all the ":ple are inside after dark," he writes, "this gate is closed and generally a 'try is posted. These precautions stop intending sorcerers from entering

.: hamlet.... Some of the men's houses have an additional encircling ;ckade for the same reason." Commenting on sanitation and hygiene, he

28

adds: liThe fault in most native areas is a shallow latrine," but Fore anxiety to keep excreta from potential sorcerers results in the construction by South Fore of " a latrine hole that seems bottomless."43

In recent years the Fore reputation for sorcery has become widespread. New Guinea and Australian newspapers carry occasional accounts of sorcery-related deaths in the Okapa region,44 and in 1973 the government's Law Department inquired into allegations of fifty to sixty sorcery-linked deaths a year at Okapa said to be caused by professional killers who were being paid up to five hundred dollars for murder "contracts."4S

The distribution of kuru lends credence to the belief that Fore sorcery is vastly more powerful than that of their neighbors. While kuru is present

Barricaded hamlet en­ trance. Photo and legend by Dr. E. R. Sorenson from The Edge of the Forest, Smithsonian Institu­ tion Press, 1976.

29

: n surrounding populations (as mentioned earlier, 20 percent of kuru deaths .::lch year occur among other peoples), the prevalence of the disease is mark­ :dly higher among Fore, particularly South Fore. In 1964 it was estimated ,llat Gimi males had only one chance in twenty-five of dying from kuru, _':hile the risk for South Fore males exceeded one in five. For females, the tllain victims of the disease, the difference was even greater. Eighty-four :'~rcent of Gimi women had a chance of surviving the reproductive period :":ithout a fatal attack of kuru, but fewer than one in ten South Fore women :l1ight do so. The average life expectancy for South Fore women born in the mid- 1 960's was estimated at little over twenty years.

46 That the South Fore were engaged in dangerous sorcery seemed incontestable.

OTHER MEDICAL DISORDERS

3 Apart from kuru, the diseases suffered by Fore are similar to those found in many other Highland peoples. Some of these populations show striking fluctuations in size from year to year, as do the Fore, which points to infec­ tious disease as a major determinant of mortali ty among Highlanders.\

During the late 1930'S and early 1940'S, a number of epidemics swept southward through the Fore region-mumps, measles, whooping cough, and dysentery. Many people died, but the new diseases were not regarded by Fore as new forms of sorcery, although the loss of certain important men lay behind later sorcery accusations between some local groups. The simul­ taneous incapacitation of large numbers of people is what Fore recall most vividly about these epidemics. Disorganization of labor was at times so great that normal agricultural activities were halted, and the ripening com and cucumbers are said to have rotted while people lay recovering in their houses. Aware that the dysentery epidemic of 1943 had swept down upon thein like a great wind from the north, South Fore at Purosa responded by refusing visitors access to their hamlets, and by persuading fellow residents to remain at home until the epidemic had passed. With clinical perception, Fore noted that the second wave of some diseases, sUfh as mumps, was less serious than the first. In 1959 and 1962, however, influenza epidemics caused many deaths, especially among children under the age of five.

Discounting kuru, the commonest problems afflicting Fore at present are upper-respiratory infections, bronchitis, pneumonia, diarrhea, gastroen­ teritis, and complications of childbirth. Meningitis and tetanus also occur, as does anemia in association with hookworm, closely spaced pregnancies,

30 31