Lindenbaum 1979: Kuru Sorcery
Research among the Fore by Sherley Lindenbaum in the 1960s in South Fore, Papua New Guinea
First: psychosomatic phenomenon, directly associated with the threat of fear of what was
believed to be an attack of sorcery.
Later: Kuru is a slow virus infection spread by the ingestion of human flesh.
CJD is a clearly defined neurological disease cased by a PRION, was thought o be a slow virus
infections
KURU is an indigenous explanatory framework for symtomps of trembling, laughing, strange
behaviour,
Kuru is caused by malevolent activities by Fore sorcerers
Kuru means “trembling of fear”
symptoms:
loss of balance, incoordination, ataxia, slurng of speech, ataxic eye movements, tremor, initial
shivering, involuntarily body movements, then motoric incapacity, death in about 1 year
laughing disease
FORE KINSHIP SYSTEM
•
•
•
•
•
•
•
Bilateral, horizontally, only 2 generations deep, open, social
Kuru was thought to be hereditary till anthropologists analysed Fore kinship system
brother-sister bond very strong, husband-wife bond loose
“Fagina” with whom you shared food, fluid kin, dependent on movement
“Nagaya” age mates, had strong priority over the brother, died and were buried together
“Waboli” warrior mates
”Nagkwa” Namesakes: life time bondage
SORCERY IN KURU
•
Sorcerer required body part (nail, clothes, blood feces)
1
•
•
burying of body parts and pit toilets were common to prevent sorcery
healers’ method: bloodletting
THEORY OF ENDOCANNIBALISM
•
•
•
•
•
1960s: wild animal became rare, led to cannibalism,
women ate the brains which were infected
Kuru was considered sorcery, therefore bodies were eaten
Bodies of sick people were not consumed
Beth Conklin 2001: CONSUMING GRIEF analysed reasons for cannibalism (
psychoanalytic approach)
2
Kannibalismus in der prähistorischen Forschung
Heidi Peter-Röcher 1994
Universitätsforschungen zur prähistorischen Archäologie
In Kommission bei Dr. Rudolf Habelt GmbH, Bonn.
first studies in 1957 by D.C. Gajdusek, received Nobel Price in 1976
incubation time: 4 – 20 years
disease: death in 3-9 months
first hypotheses: Infection through endo-cannibalism, while preparing the flesh, contact with
infectious brain substances. infection with kuru virus was most probably through cuts in the skin
or from nose picking, eye rubbing or mucosal injury.
Cannibalism was never observed, the photos taken by Gajdusek showed pork meat.
Among the fore: children of both sexes and mainly women were affected.
Unusual demographic profile as since 1950s number of diseases were less and less,
both sexes were affected.
R. Glasse did ethnographic research in the same region from 1961-63.
He also confirms cannibalism among the Fore without ever having witnessed the event. At that
time Kuru was not associated with cannibalism, but he noticed that the South fore were not
engaged in cannibalism (p209)
Peter-Röcher argues that at that time apparently cannibalism was constructed to suit the kuru
disease image.
It was common in entire Papua New Guinea to deal with dead corpse and take out the buried
skulls, which was practised mainly by women. (208)
According to Peter-Röcher it was enough to deal with the dead corpses in an unhygienic way to
be infected. It was observed that the fore never washed their hands after dealing with corpses.
3
Cannibalism is not necessary to explain the infection. It is apparently a construct of the
ethnologists and perhaps their (male?) informants. (210).
Kuru: the old epidemic in a new mirror
IN: Microbes and Infection
Volume 4, Issue 8 , July 2002, Pages 875-882
Lev G. Goldfarb 2002
The kuru epidemic lasted almost a century; it started in 1901–1902, reached
epidemic proportions in the mid-1950s, and disappeared in the 1990s.
Kuru is the prototype member of a group of disorders known as transmissible spongiform
encephalopathies (TSEs) or prion diseases.
Creutzfeldt–Jakob disease is a variant of Kuru.
The kuru epidemic in the Eastern Highlands of New Guinea took the lives of 3000
individuals; more than 80% of the known kuru fatalities were recorded in a
limited area populated by the Fore people.
200 new cases annually by the mid-1950s
no individual born after 1960 has ever developed kuru.
by the late 1950s, cannibalism was completely abandoned, and exposure to kuru infectivity
ceased.
breakthrough in studies of kuru was the demonstration of its
transmissibility to experimental apes and other animals extremely long
incubation time, relatively slow disease progression, absence of inflammatory
pathology, and an always fatal outcome.
4
Currently known transmissible spongiform encephalopathies (TSEs) include:
sporadic, familial and iatrogenic Creutzfeldt–Jakob disease (CJD);
Gerstmann–Sträussler–Scheinker disease (GSS);
fatal familial insomnia (FFI); and
variant Creutzfeldt–Jakob disease (vCJD).
The critical event in the pathogenesis of TSE is believed to be a conformational switch in the
normal cellular prion protein (PrP-c), a predominantly -helical molecule, into its pathogenic
isoform PrP-sc that is rich in -sheet structures, partially protease-resistant and Infectious.
Until recently, kuru was the only example of oral transmission occurring in
humans. The latest TSE member, vCJD linked to consumption of contaminated beef from
animals incubating bovine spongiform encephalopathy, has a phenotypic similarity to kuru .
These two disorders are expected to share other basic
disease mechanisms. Therefore, the results of extensive kuru studies can be used
in current attempts to curb and eliminate the epidemic of vCJD in Great Britain
and other European countries.
Historic background of the kuru epidemic
Eastern Highlands Province of New Guinea
Fore is one of the groups, a Stone Age culture that, until the 1950s, practiced endo-cannibalistic
consumption of dead kinsmen as a rite of mourning.
Early anthropological studies were conducted in
1951–1952 and 1952–1953, at which time the presence of kuru in this area was
first observed
The Fore always believed that kuru was one kind of sorcery (among 34 other
variants) To induce kuru, the sorcerer had to obtain some object intimately
associated with the victim. He then placed the object with pieces of bark and
leaves in a bundle and buried the bundle in boggy ground. The sorcerer returned
5
intermittently to beat the bundle, and with each beating, it was believed, the
illness intensified.
How exactly kuru first appeared in the Fore people is unknown. The most likely
possibility is that the kuru epidemic started with a single individual who died
of sporadic CJD and was then consumed by tribesmen in the traditional ritual
cannibalism fashion.
THE HINDU
Online edition of India's National Newspaper
Thursday, Apr 24, 2003
http://www.hinduonnet.com/seta/2003/04/24/stories/2003042400030200.htm
Were we cannibals long ago?
DID MAN ever eat man? He eats just about every form of life — fungus, bacteria, plants, insects
and animals in water, land or air. Is there a biological difficulty about it, or is it a cultural
restriction? Many animals do it, some of them eating their own young. Alex Pacheco, the
Chairman of People for the Ethical Treatment of Animals, writes that he had seen starving dogs
eat their own kind. In the book "Chimpanzee Politics: Power and Sex among the Apes", authors
Frans de Waal and Desmond Morris claim that the great apes too practice cannibalism, albeit less
frequently. Did evolution equip us to eat other men, and culture stop it?
Historical accounts on cannibalism are not clear, since they are invariably mixed with prejudice,
self-aggrandisement of the colonial and religious or cultic pronouncements. Columbus chronicled
that he encountered a man-eater tribe called the Caniba in the Caribbean, and that gave us the
term cannibal. It is not clear whether the caniba really ate their fellow men, or whether this was
an allegation by an unfriendly neighbouring tribe. In any event, Pope Innocent IV decreed it to be
a sin, which led Queen Isabella to order the Spanish colonialists to legally enslave natives
thought to be cannibals. This provided the licence, plus the economic interest, to the colonists in
making such allegations and conquer territory.
A dispassionate and unprejudiced history of cannibalism is hard to come by. Whenever someone
in history reported that they saw men eating human flesh, it was not clear whether it was because
of lack of any other food, or done in a more token or ritualistic manner for cultural, religious or
medicinal purposes. The fierce Bhairavas of Tantrik Hinduism seem to engage in it, using blood
and certain other parts ceremonially. Medieval European medicine men prescribed blood and
certain other parts of the human body as cures for epilepsy, porphyria, and arthritis. And the tribe
called Fore in Papua New Guinea, chronicled to be man-eaters, appear to do so as part of a
religious ritual. The Nobelist Dr. Carleton Gajdusek, who studied a particularly deadly form of
brain disease called Kuru among the Fore people, kept a detailed dairy on his visits and stay
there. He found that the family and neighbours of a dead Fore ceremonially chewed on the dead
person's brain in order to ensure a safe after-life for the deceased. Not studying a practice in
context and in detail can lead one to jump into conclusions that would support preconceived
notions.
6
It is thus not clear whether the practice occurred due to biological demands of hunger, or cultural
reasons. I should like to believe the latter, at the risk of being thought of as a wimp with a notion
in mind. But it now transpires that there may be a biological disadvantage or risk in at least
certain types of this practice. Dr. John Collidge of University College London got together with
colleagues in Western Australia, and Goroka in Papua New Guinea, to study genetic aspects of
the `cannibalistic' practice of the Fore people.
Kuru is a brain disease, a neurodegenerative disorder that wastes the affected person horribly the equivalent of Scrapie in sheep and the Mad Cow Disease of cattle. Dr. Gajdusek showed that
this occurs due to a "slow acting virus" that was present in the flesh of the deceased. It has now
become clear that the pathogen is not a DNA virus nor an RNA virus, but actually a
malformed miniature protein called a prion (named so, to sound similar to `virion' for a virus).
Misfolded prions act as seeds or nuclei, forcing other, native prions, also to misfold and
clump together into fibrous masses which kill brain cells. The Cruetzfeldt- Jacob Disease
(CJD) is thought to be caused in a similar manner, as are Scrapie and Mad Cow Disease. A
normal protein in the nervous system, called Prp-C loses its normal shape in the disease, turning
into a misfolded wrongly-shaped form, termed Prp-Sc. This sets out a chain reaction, recruiting
more and more of normal Prp-c, misfolding and aggregating it into an insoluble Prp-Sc. Insoluble
like the scales in a coffee kettle, or plaque formed on teeth, this is called the amyloid plaque,
and causes brain cells to misfire and die.
Collidge and group focused on the gene (called PRNP) that codes for the prion protein in humans
and went over to Papua New Guinea to study the PRNP profile of the Fore people. Kuru no
longer affects them, because of a ban on `cannibalism' imposed by the Australian authorities
there in the 1950s. Collidge decided to look at the PRNP genes in elderly Fores who had
practised the ritual before the ban, and in young Fores who had never done it. For
comparison, the PRNP gene profiles of `control' populations from Japan, India, Sri Lanka, Africa,
Europe and Colombia were also studied. The idea was to compare the gene sequences and
mutations, so that the genetic aspects of Kuru could be understood. The approach here is
similar to a similar analysis done on CJD patients earlier. In that instance, it was found that
the people carrying two identical copies of the gene for the prion protein (PRNP) are more
susceptible to developing CJD than those who carry two unmatched variants. This mismatch
seems to protect people against the disease.
When the gene sequences were compared, now for Kuru, Collidge found that all ethnic groups
carried two unmatched variants of the prion gene. The fact that the variants are so widespread
suggests that they have been conserved throughout human history. Based on further comparisons,
and comparison with the chimpanzee DNA, the scientists estimate that the variants in the gene
arose about 500,000 years ago, during the era of prehistoric ancestors of us modern humans. For
most genes, one variant is beneficial for fitness more than the other. The less beneficial
disappears over time. Thus, there is a selection pressure due to adaptation.
Among Fore, the number of women carrying one copy of each variant (heterozygotes)
instead of two copies of one or the other, was particularly high. This suggests that having
one copy of each variant protected many members of the Fore tribe against Kuru. This is
what Collidge refers to as "balancing selection". Some genes are selected thus, the haemoglobin
gene being an outstanding example. One variant of the globin gene causes sickle cell anaemia in
a person who carries two copies of it (one from each parent), but the variant persists because it
protects against malaria if it is coupled with another variant.
But the fact that prion gene variants persist in humans across the world suggests that prion
diseases were widespread in early human history. The group also suggests that frequent
epidemics of prion disease caused by cannibalism in ancient humans would explain
7
existence of protective gene signature ( variant pairing) among today's humans. This is perhaps
why, of the 50 million people in England, only 134 fell victim to the Mad Cow Disease, eating
prion-contaminated beef; so says Dr Simon Mead of Prion Unit of MRC England, who worked
with Dr Collidge. So, was cannibalism prevalent in ancient human history? Collidge thinks so,
and Dr. Tim White of the University of California Berkeley says archeological evidence might
support the idea. But anthropologists are not convinced and argue that evidence from their field is
lacking. We have to wait more in future to know what we did in the past.
D. Balasubramanian
dbala@lvpeye.stph.net
8