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AMARNA KINGS, ANAEMIAS AND PARASITIC LIVER DISEASE -I
Thomas M. Simms (tsimms@nbnet.nb.ca)
Sat, 18 Jan 1997 09:28:09 AST
THE AMARNA KINGS, ANAEMIAS AND PARASITIC LIVER DISEASE{a}
T. M. SIMMS
ABSTRACT
Reviews ancient Nile Valley inherited and parasitic anaemias,
describes the progress and outcome of those diseases, outlines
recent research on the physiology and physiognomy of the three
Kings Akhu En Aten, Smenkh Ka Ra, and Tut Ankh Aten/Amen,
draws tentative conclusions about their lives and deaths,
points out an unusual link between certain effects of Bilhar-
zias infestation and Amarna portraiture, and looks at possible
future paleobiological research on the Amarna period.
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| [Figure 1.] | [Figure 2.]
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Amen Hetep IV Amen Hetep IV
with his mother as Maat with Queen Nefert Iti
The wealth, culture and political power of Ancient Egypt reached
a peak during the rule of Amen Hetep III (1386Ä1347 B.C.).{1} Three
sons, Amen Hetep/Akhu En Aten, Smenkh Ka Ra, and Tut Ankh Aten/Amen
succeeded him, the last dying in 1331 B.C..{2} The first of these
built a new capital at Tel El Amarna on the east bank of the Nile
twenty-five miles north of modern Asyut. All three lived there.
So they have the name of the "Amarna Kings", and the period of
their rule the "Amarna" period or era.
Conventional Ancient Egyptian pictorial representations changed
noticeably during the Amarna period. Stick-like arms, spindly
shanks, fat thighs, noticeable breasts on males, and bloated,
sagging bellies became the standard. One of the earliest examples
occurred in two panels from the tomb of the Vizier Ramose made
before the son, Amen Hetep IV, changed his Sa Ra name to Akhu En
Aten.{3}
Style might have explained some of the new conventions and the
changes, but without an underlying reality the changes made no
sense.
Aldred and Sandison supposed the cause of the physical changes
to be Fr”lich's Syndrome Ä a pituitary disorder.{4} Dr. R. G.
Harrison's examination of the purported remains of Akhu En Aten in
1966 did not find support for their hypothesis and for other
suggestions such as hydrocephalus. Nonetheless, it did identify
beyond a reasonable doubt the remains as those of Smenkh Ka Ra.{5}
Harrison at that time noted in Smenkh Ka Ra's remains radiologic
evidence of periostitis, a destructive inflammation of the membrane
surrounds bones and their joints.{6} He pointed out in his remarks
that its radiological appearances are similar to those occurring
in syphilis, bejel, yaws, and certain haemoglobinopathies or blood
disorders.{7} He made no review of the symptomology of those
disorders. He made no comparisons of any observable characteristics
of the disorders with similar visible characteristics of the new
iconography.
As a consequence of this examination, Harrison, with A. B.
Abdalla, performed a post mortem examination of the remains of Tut
Ankh Amen.{8} They concluded the two kings were brothers.{9} They
noted that the radiographs of the limb bones were "not very
informative".{10} Simply stated, because of the corrosive effect of
consecrating unguents outside of the head and extremities, major
features such as epiphyses of long bones were visible but little
else.
In the post mortem of the remains of Smenkh Ka Ra, Harrison
noted that Syphilis was unknown in Ancient Egypt{11} and supported
his position by citing other studies.{12} He then argued that without
further information he could not be specific about the cause of the
periostitis.{13} He left the matter there.
Had he looked beyond the case at hand, he might have led us to
a wider understanding. He would quickly have eliminated bejel and
yaws. Bejel and yaws, as is syphilis, are caused by Treponema,
protozoan organisms parasitic in the blood.{14} Bejel's visible
symptomology in no way matches the new Amarna style.{15} Yaws, being
a disease with clearly visible skin effects and only tropical in
distribution, need not concern us here either.{16} In both bejel and
yaws, no bloated bellies or other trunk deformities occur except
in the very terminal stages of the diseases.{17}
However, he might have reviewed the visible characteristics of
various blood disorders. Some haemoglobinopathies have very
distinctive visible physical characteristics. Those associated
with severe liver dysfunction have many of the hallmarks of the
physical condition lending itself to the Amarna appearance.{18}
One researcher, Dr. P. Ghalioungui, suggested these visible
characteristics could have come from liver cirrhosis secondary to
Bilharzias infestation.{19} (Bilharzias are Schistosomes, that is,
blood flukes.{20} Liver flukes could yield similar effects. However,
they don't occur in Egypt.{21} Intestinal and lung flukes are not a
consideration.{22})
Risse, discussing the work of Ghalioungui, noted Ghalioungui
questioned Akhu En Aten's opportunity to exposure to Bilharzias
infestation.{23} Risse also argued there was no chronological order
for portraits of the King which Ghalioungui used so the progression
of the disease was purely hypothetical.{24} W. S. Smith firmly
rejected the argument.{25} Lately, Cyril Aldred argued convincingly
the order was quite clear.{26}
Certain haemoglobinopathies occurred in the Ancient Nile Valley.
S. W. Hillson examined skulls from ancient gravesites in Middle
Egypt, Upper Egypt and Nubia.{27} He found that four chronic anaemias
occurring in modern Nile Valley inhabitants also occurred in
antiquity: sickle cell anaemia, beta-Thalassaemia anaemia, combination
sickle cell/beta Thalassaemia anaemia, and chronic iron
deficiency/bleeding due to parasitic infestations such as hook-
worms, malaria, and Bilharzias.{28}
According to Hillson, parasite-caused anaemias occurred less
frequently in Ancient Nubia than in Upper and Middle Egypt because
the Nubian Nile Valley was rocky and narrow with few stagnant pools
and irrigation canals necessary to the life cycles of the
parasites.{29}
Middle and Upper Egypt were much more richly supplied with such
sites. The comparison is less apt today.{30}
Sickle cell anaemia results from a single gene change. Heterozy-
gotic individuals live normal lives and are protected against
malaria. Homozygotics are very severely affected and rarely live
into their twenties. Loss of vigor, tissue wastage, inability to
resist many diseases, ending in general collapse, models the dis-
ease.{31} For the victim, normal life does not exist. However, only
in the final stages of the disease does abdominal bloating occur.{32}
This effect eliminates sickle cell anaemia from our consideration
unless we collapse the entire reign of Akhu En Aten into a few
months.
Beta-Thalassaemia anaemia results from changes either at one gene
locus or at a group of closely-related loci. Homozygotic in-
dividuals are severely affected, but because the loci are not
always exactly matched, the length of survival is somewhat more
variable than with sickle cell anaemia. Heterozygotic individuals,
on the other hand, are not so fortunate as sickle cell victims.
They may suffer from some small degree of anaemia. Suspicion that
the genes for this disorder are maintained by a malarial protection
mechanism continues but is not yet confirmed by research. Progress
of the disease is similar to sickle cell anaemia only more variable
in the speed of its development.{33} However, the time spans of the
lives the three individuals and the lack of major variability of
the epigraphic evidence after the initial change does not match the
progressions of beta-Thalassaemia anaemias.
Curiously, and contrary to expectation, the combination sickle
cell/Beta-Thalassaemia usually causes only mild anaemia, so survival
to adulthood is common.{34} The three Amarna Kings might have been
victims except for the observed lack of erosion in the x-rays of
the two surviving skulls. Measures similar to Hillson's were not
made, therefore the issue might be open.{35} However, the iconography
of the era, the abdominal bloating and heavy thighs, do not
characterize mild anaemias.{36} Therefore we must consider other
factors.
Chronic iron deficiencies/bleeding from parasitic infestation
resulted mostly from malaria and water borne schistosomes (Bilhar-
zias).{37} Because the ancient diet was mostly vegetarian, hookworm
or tapeworm infestation which comes from poorly cooked meat,
especially pork, ought not to have been a large concern.
Nonetheless for some classes of ancient society such as temple
workers and the upper classes suffered from tapeworm infestation
from eating poorly cooked pork. This paper discusses an example
later. Today in Egypt because of religious dietary laws the
problem no longer exists.{38}
The course of parasitic infestation from water borne schis-
tosomes is much more variable. First of all, the rate or severity
of infestation depends on the local environment allowing the stages
of development of the parasite outside its human host to occur.
A necessary condition is the live presence of a small water snail.
Without it and the banks of stagnant water bodies it inhabits, the
infestation ceases. Without exposure of the human host to such
waters, infestation does not occur.{39} Further, if drinking water
from those areas is allowed to stand a day and a half, the stages
of the schistosomes free to move in the water die and the water is
safe to drink.{40}
"In endemic areas, the transmission is usually continuous and
results in frequent infection of rather low intensity, due either
to infrequent exposure or to some degree of concomitant immunity,
or to both. Epidemics of trematode infection are usually caused
by changes in environmental or social factors. Thus, epidemics of
Schistosoma haematobium occur around man-made lakes or in new
irrigation systems that introduce the parasite or intermediate host
into susceptible areas".{41}
The adult schistosomes common to Ancient Egypt, Schistosoma
haematobium and S. mansoni, breed in the pelvic and vesical venous
plexes or in the mesenteric veins of humans, and produce eggs. The
eggs are intended to reach the lumen of the bladder and intestine,
thereby being excreted. However, most are trapped in tissues along
the way, causing serious tissue damage by being capsulated in
granuloma.{42}
The host tolerates this damage well and compensates for it until
the number of adult flukes rises to the point that the eggs
produced are not excreted but are "swept back" into the portal
system to the liver or to ectopic localization in the lungs or
central nervous system. The granuloma formation around these eggs
accounts for the manifestations of established, chronic schis-
tosomiasis.{43}
The pathologic reaction is a series of chronic inflammatory
lesions elicited mostly by the encapsulated eggs but also by dead
adult worms. The severity of the disease varies with the severity
of infection. Because small vascular lesions are easily repaired,
a heavy burden of worms and ova is necessary to produce significant
disease, showing as progressive tissue destruction and formation
of fibrous tissue mostly in the liver, although sometimes ova
affect the lungs and the spinal cord.{44}
If the infestation to begin with is large, the damage in the
liver is substantial and the spleen is greatly enlarged. If the
body compensates for this insult, life goes on. If the body does
not compensate, a variety of results follow: anaemia, ascites,
gynecomastia, and emaciation.{45}
Anaemia leads to tissue wastage and emaciation.{46}
Ascites is an abnormal fluid build-up within the abdomen similar
to the fluid retention in extremities from congestive heart failure
and for essentially the same reason, inefficient blood transport,
although with ascites the cause is vascular damage within the
abdomen. The pressure of ascites causes bloating of the thighs and
buttocks by interfering with venous returns from those areas. It
also causes bloating of the mammaries or gynecomastia, sometimes
leading to lactation in both sexes. The host-parasite balance
adjusts even to such potentially lethal damage.{47}
Without further reinfestation or until the worms begin to die
(they live an average dozen years), life can go on. No mental
dysfunction occurs. The victim seems only at slightly greater risk
to the other hazards of living. When the worms die, serious
complications for the victim arise. The result may be fatal.{48}
As a rule, the earlier the infestation--given a certain standard
of insult--the sooner the fatal outcome. A child might die before
his twenties, a young adult in his thirties.{49}
(Hillson cautioned taking too precisely his ancient data.{50}
However. the pathologies he describes clearly existed in remains
which survive to modern times. An autopsy done in Toronto on
Nekht,{51} a sixteen year old weaver at the funerary chapel of Set
Nekht, and who died in the reign of Ra Meses III, indicates his caution
was groundless.{52} In the case cited, the ancient undertakers simply
wrapped the remains. The Egyptian climate did the embalming.
Accordingly, we received an essentially unadulterated body from
the past. However, the preservation was uneven. Because the
ancient undertakers did not remove the brain. that tissue putrefied
and the head disintegrated, leaving bones but no appearances. On
the other hand, the contents of the abdomen dehydrated and
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