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*AMARNA KINGS,ANAEMIAS AND PARASITIC LIVER DISEASE*
Thomas M. Simms (tsimms@nbnet.nb.ca)
Thu, 10 Aug 1995 08:30:03 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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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 (13861347 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 Frlich's Syndrome 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 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
survived.{53} The young man in question suffered heavy schistosome
infestation. He showed clear signs of bleeding from the urinary
tract. He showed obvious evidence of severe liver cirrhosis and
of a greatly enlarged spleen. The latter ruptured shortly before
death.){54}
Inherited anaemias might have caused the deaths of the three
Kings under discussion, but, as explained, could not have caused
the peculiar iconography of their reigns, an iconography so
insistent that the embalmers attempted to continue the image by
overstuffing Tut Ankh Amen's abdomen.{55} The periostitis seen in
Smenkh Ka Ra's bones could have come from the anaemia of parasitic
liver infestation or from inherited anaemia. The epigraphic
evidence helps us decide. Likewise, the parallel nearly
contemporary physical and somatic evidence of Nekht helps us.{56}
Then we can take what we know of the opportunities for infestation.
We can couple that with what we know of the progression of the
outward signs of the disease. Finally, we can compare this
information with what see in the epigraphic record surviving from
the time of the Amarna Kings.
Amen Hetep III excavated a lake, the remains now called Birket
Habu, in front of his palace at Malqata. The palace lies just on
the desert edge of the wide plain forming the western bank of the
Nile at modern Luxor.{57} The opportunities for Bilharzias
infestation would have increased immensely. He gave Queen Tiye in
the eleventh year of his reign a similar newly dug lake at the
doors of her palace at Tahta.{58} The construction would have created
another epidemic of schistosomes affecting his whole family.
These two massive explosions of opportunities for Bilharzias
infestation could very likely have caused the death of the first
Crown Prince, Djehuti (Thoth) Meses. Given equal insults, his
adult parents would have enjoyed a much stronger immunity than
their eldest son.{59} In addition, by the greater and more playful
mobility of youth, the chances for infestation by the prince were
much greater. And the god status of his parents meant they did
not take part in the extensive lustrations of "The Pure", the
priesthood. These lustrations used "living" water, the most
infective kind.{60} They also involved the most intimate contact.{61}
The young princes had plenty of opportunities for exposure to
infestation by schistosomes. Contrary claims therefore rest on
uncertain foundations.
The career of the sixteen year old weaver, Nekht, took place in
sight of the palace of Amen Hetep III at Malkata and within two
centuries of the rules of the Amarna Kings.{62} As a temple staff
member, he had regular priestly duties. This alone put him at risk
if his nearness to the hydraulic works didn't. He likely enjoyed
as reasonable a diet as did the Amarna Kings. His viscera
survived. Theirs did not in any useful way. His showed all the
signs just elaborated.{63} He died at some time between fourteen and
eighteen, likely sixteen.{64} The prince likely died near or just
before that age.{65} The comparison passes suggestion.
Please note that Nekht's opportunity for infestation had
stabilized from the greater hazard present when the hydraulic
constructions were new.{66} Nonetheless his priestly duties presented
an additional hazard.
The next prince, Amen Hetep, did not expect to rule. On the
record, he held no priestly offices, although he had his own
estate.{67} His exposure therefore had to be purely adventitious, not
due to intimate lustrations. If he had moved to Thebes from Mem-
phis with his father at the end of his youth, his exposure would
be less again.
With moderate exposure, as we've noted, the disease becomes
chronic, the body compensates. The signs of the acute stage become
permanent. The change from the normal iconography of the first
year or so of Amen Hetep IV's reign{68} to the new images apparent in
the Jubilee Temple of the second year of his reign now has a
reason.{69} Failing some other insult, from the first several years
of his reign a life span of ten to fifteen years is likely. During
that time vigorous living is possible.{70} There even is a certain
immunity to further infestations.{71} So the record confirms. Once
the body compensated for the infestation, the outward appearances
would change little. In fact, the lack of change as the body
otherwise assumes its fully adult configuration would suggest a
return to normal. This effect offers an explanation for the more
normal iconographic appearances of the later years of the reign of
Akhu En Aten.{72}
The next prince, Smenkh Ka Ra, almost certainly lived all his
life in the midst of the new constructions. Like his older
brother, he too was not subject to much priestly opportunity for
infestation. However, because his father's construction project
continued unabated, he was at greater general risk.{73}
Smenkh Ka Ra's light, non-robust skeleton, with its evidence of
periostitis,{74} coupled with his consistently Amarna iconographic
appearances, suggests strongly the disease affected him young.
His death at twenty is therefore not a surprise, for no image shows
him driving a chariot, and at least one image shows him supporting
himself with a staff.{75}
On the contrary, the last prince, Tut Ankh Aten, lived much of
his young life at Akhuet Aten in the North Palace area with his
mother.{76} We can argue he lived near the new hydraulic works at
Thebes only in his earliest years.
Tut Ankh Amen's skeleton suggests a more vigorous, robust person
than his brother Kings.{77} Chariot driving is no mean task. The
ones buried with him were made to use. They weren't just for
display.{78}
The bows buried with him, both his and those of his brother,
Smenkh Ka Ra, also were made to use.{79} Just who used them is
difficult to prove. An Egyptian compound bow is a powerful weapon,
even by today's standard, and is not easy to string, as Homer
relates.{80} We suspect from the epigraphic evidence the youngest
King put them to most use.
Nonetheless, the iconography of his reign and the treatment of
his mummy suggest the disease had reached an acute stage and he was
at risk.
The unhealed abrasion on his left cheek{81} may show evidence of
a final insult. However, it may also be the result of a trivial
accident brought on by weakness in the acute stage. There is no
evidence of underlying tissue damage. However, like the weaver
Nekht, whose autopsy has been mentioned, his spleen may have
ruptured.{82} Harrison considered that the unhealed abrasion was
"...likely to represent a skin lesion resulting from some injury
such as falling off a horse for example".{83} (To those who might
suggest that Egyptian Kings drove chariots and did not ride horses,
the riding crop from the tomb of Tut Ankh Amen teaches its own
lesson. The inscription on it says that the King "appeared upon
his horse like Re when he shone".{84} Such a fall might have ruptured
his spleen. In those days, that meant death. Without the fall,
he might have lived on. The unhealed nature of the abrasion argues
strongly it was associated with his death.Because they were
brought up in a similar location, the Amarna Kings were as casually
exposed as the unfortunate Nekht, save for the exceptions noted.
So schistosome infestation accounts for each peculiarity of the
Amarna iconography and explains such evidence as we have from the
remains of two of the Kings of the era.
In future, non-intrusive tomographic examination of all of the
present remains of the central personnel of the Amarna era might
definitively settle the issue. Paleobiology may reach the point
where ancient tissues yield full information, even to the point of
supplying the entire genetic code.{85} Perhaps too, the visceral
remains might yield more information than they have at present.
Of course, discovery of the remains of Akhu En Aten might solve
the problem. For the present, pathology offers the simplest
explanation of the course of many of the events of the Amarna
period.
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NOTES
{a} An earlier, less complete version of this paper was read by title at the
Amarna Centennial Symposium held at the Oriental Institute of the University of
Chicago in February, 1987. It appears in the Proceedings of the Symposium, now
in press.
The author thanks Dr. S.E. Naguib, pathologist at Carleton Memorial Hospi-
tal, Woodstock, N.B., and Mrs. Emery Perkins, Laboratory Technician there, for
their seminal help with this study. Ms. Janice Dimock-Cummings, D.V.M.,
suggested the ascites consequences.
The author especially thanks Prof. Howard Savage of the Department of
Anthropology, University of Toronto, who pointed out the Schistosome evidence in
the autopsy of Nacht, ROM I. The present author had viewed the television
program demonstrating the autopsy without appreciating those findings.
{1} The dates bridging the period are on p. 238, K. A. Kitchen Pharaoh Trium-
phant: The Life and Times of Ramesses II. Mississauga, Ontario: Benben Public-
ations, 1985.
{2} The view here follows Cyril Aldred's analysis of the relationships among
the four kings as summed up on p. 293 in his text, Akhenaten King of Egypt, New
York: Thames and Hudson, 1988.
{3} Figures 1 and 2 - Davies, N. de G. The Tomb of the Vizier Ramose, [London:
1941, pls. xxix and xxxiii. The captions of the figures and the datings of the
panels as well as the proposition the changes reflect reality derive from
Aldred, C. Op. cit., pp. 89-94 and his discussions inter alia about pls. 26, 27
and 28. In Figure 1, the present author takes that the presence of the phrase
"great in the duration of his life" directly below the Sa Ra, Amen Hetep
cartouche indicates with certainty that the damaged cartouche beside it read
Nefer Kheperu Ra Ua En Ra. There can be no doubt the king pictured is Amen
Hetep IV/Akhu En Aten.
{4} Aldred, C. and Sandison, A. T. `The Pharaoh Akhenaten: A Problem in Egypt-
ology and Pathology', Bull. Hist. Med. 36, 1962, p. 293.
{5} Harrison, R. G. `The Anatomical Examination of the Pharaonic Remains
Purported to be Akhenaten.' J. E. A., 52, 1966, pp. [95-119.
{6} Ibid., p. 105
{7} Ibid., p. 105.
{8} Harrison, R. G. and Abdalla, A. B. `The remains of Tutankhamun.' Anti-
quity, XLVI, 1972, pp. 8-14.
{9} Ibid., p. 13.
{10} Ibid., p. 12.
Harrison, 1982, Personal Communication, reaffirmed that conclusion.
{11} Harrison, R. G. `The Anatomical Examination of the Pharaonic Remains Pur-
ported to be Akhenaten.' J. E. A., 52, 1966, p.105.
{12} Ruffer, and Rietti, J. Path. Bact. 16, 1912, p. 439, and Salib, J. Bone Jt.
Surg., 44B, 1962, p. 944.
{13} Harrison, R. G., Op. cit., p. 105.
{14} Moody, Peter. `Yaws, Pinta and Begel' in Braude, A. I., ed. Medical
Microbiology and Infectious Diseases, Vol. II. Philadelphia: W. B. Saunders
Company, 1981, pp. 1613-1620.
{15} Ibid., p. 1614.
{16} Ibid., p. 1613.
{17} Ibid. pp. 1616 and 1618 and illustrations on those pages.
{18} Dennert, Gunther. `Schistosomiasis.' in Braude, A. I., ed. 1981, Op. cit.,
p. 1099.
{19} Ghalioungui, P. `A medical study of Akhenaten,' A.S.A.E., 1947, 47, 29-46.
Ghalioungui, P. `Some body swellings illustrated in two tombs of the
ancient Empire and their possible relation to Aaa', Z..S.,1962, 87, p. 114.
Ghalioungui, P. Magic and Science in ancient Egypt. London: 1963, p. 56.
{20} Pawlowski, Z. S. `Trematoda (Flukeworms)', in Braude, A. I., ed. 1981, Op.
cit., p. 726.
{21} Ibid. See Fig. 3 and `Epidemiology', pp. 732-33.
{22} Symptomologies not congruent. See preceding footnote.
{23} footnote 36 in Risse, Guenter B. `Pharaoh Akhenaton of Ancient Egypt:
Controversies among Egyptologists and Physicians Regarding His Postulated
Illness'. J. Hist. Med., January 1971, pp.3-17.
{24} footnote 37 in Risse, Guenter B. Ibid.
{25} Smith, W. S. Art and Architecture in Ancient Egypt. London: Harmonds-
worth, 1965, p. 174.
{26} Aldred, C. Akhenaten King of Egypt. London: Thames and Hudson, 1988, pp.
234, 235.
{27} Hillson, S. W. `Chronic Anaemias in The Nile Valley.' MASCA Journal, 1(6),
1980, pp. 172-174.
{28} Ibid., p. 174.
{29} Ibid., p. 174.
{30} `Nubia', p. 20 and pp. 178-185, and `Upper Nubia', pp. 186-187, in Baines,
J., and Malek, J. Atlas of Ancient Egypt. New York: Facts on File, 1985.
{31} Hillson, 1980, Op. cit., p. 173.
{32} Dennert, Gunther. Op. cit., p. 1099.
{33} Hillson, 1980, Op. cit., p.173.
{34} Ibid., p.173.
{35} Harrison, R.G. Personal Communication.. 1982.
{36} P. 85 under `Anaemias' in Bennington, James L., Ed. Saunders' Dictionary
and Encyclopedia of Laboratory Medicine and Technology. Philadelphia: W. B.
Saunders, 1984.
{37} Hillson, 1980, Op. cit., p. 173.
{38} Lewin, P. K. `Mummies That I Have Known.' American Journal of Diseases of
Children, Vol. 131, March, 1977, p. 350.
{39} Dennert, Gunther. Op. cit., pp. 1094 and 1104.
{40} Ibid., p. 1094.
{41} Ansari, N. Epidemiology and Control of Schistosomiasis (Bilharziasis).
Basel: S. Karger, 1973, as reported on p. 732 in Pawlowski, Z. S. Op. cit., pp.
726-733.
{42} Dennert, Gunther. Op. cit. p. 1095.
{43} Ibid. p. 1095.
{44} Ibid., pp. 1097.
{45} Ibid., p. 1100, including Fig. 6.
{46} P. 86 under `Anaemias' in Bennington, James L., Ed. Op. cit.
{47} Dennert, Gunther. Op. cit., pp. 1100-1102.
{48} Ibid., p. 1097.
{49} Ibid., pp. 1102-1104.
{50} Hillson, 1988, Personal communication.
{51} The present author prefers Nekht to Nacht. The details of such a decision
are not the concern of this paper.
{52} Hart, G.D., Millet, N.B., Scott, J.W., and Cockburn, A., editors. `Autopsy
of an Egyptian Mummy {Nacht - ROM I}.' Canadian Medical Association Journal,
Vol 117, 1977, pp.461-477.
{53} Ibid., p.464.
{54} Ibid. p. 464.
{55} Derry, Douglas, M. D., in Carter, H. The Tomb of Tutankhamen. London:
1972., p. 229.
{56} Lewin, P. K. `Mummies That I Have Known.' American Journal of Diseases of
Children, Vol. 131, March, 1977, p. 350.
{57} P. 85 in Baines, J., and Malek, J. Op. cit.
{58} Aldred, C. The Egyptians. London: Thames and Hudson, 1984, p. 70.
{59} Dennert, Gunther. Op. cit., p. 1102
{60} White, J. E. Manchip. Ancient Egypt Its Culture and History. New York:
Dover, 1970, p. 41 (a reprint and revision of a 1952 text), notes the ritual
use, as does Budge, Sir E. A. Wallis. The Dwellers On The Nile. New York:
Dover, 1977, p. 147 (a reprint of a 1926 edition). Dennert, Gunther. Op.
cit., p. 1094, describes the infective hazard.
{61} Budge, Sir E. A. Wallis. The Dwellers On The Nile. New York: Dover, 1977,
p. 147(a reprint of a 1926 edition) quotes the Egyptian description of the
intimate nature of the contact.
{62} Millet, N. B. `Archaeological Background.' in Hall, Millet, Scott, and
Cockburn, eds. 1977, Op. cit., p. 462.
{63} Reyman, T. A., Zimmerman, M. R.and Lewin, P. K. `Histopathologic investi-
gation.' in Hart, Millet, Scott, and Cockburn, editors. 1977, Op. cit., pp.470-
471.
{64} D. F. Rideout. `Radiological examination'. in Hart, Millet, Scott, and
Cockburn, editors. 1977, Op. cit., p. 463. Dr. Rideout notes the difficulty
even simple dehydration presents in making age estimates. Hip joints, deep in
the body, suggested an age of 18 years. Knee joints, subjected to a different
protocol of desiccation, suggested 14 years. The cited author split the
difference at 16 years. The present author takes these discrepancies as notice
the best estimates of age come from sites deep in the body of anciently pre-
served remains. He considers that radiographic protocols for desiccated or
dehydrated tissues do not have sufficient experience to make exact age
estimates. It seems for the present, therefore, visual notices have to have
predominant weight.
{65} Aldred, C. Op. cit., p. 259.
{66} Dennert, Gunther. Op. cit., pp. 1102 and 1104.
{67} Redford, D. B. Akhenaten, The Heretic King. Princeton, N. J.: Princeton
University Press, 1984, pp.58-59.
{68} Budge, Sir E. A. Wallis. Tutankhamen, Amenism, Atenism, and Egyptian
Monotheism. London: 1923, p. 78.
{69} Redford, D. B. Op. cit., p.57 and following.
{70} Dennert, Gunther. Op. cit., p. 1099.
{71} `Immunology', p. 731 in Pawlowski, Z. S. Op. cit.
{72} Aldred, C. Akhenaten King of Egypt. London: Thames and Hudson, 1988,
pls. 1, 17, 21, and 25 with discussions.
{73} Dennert, Gunther. Op. cit., p. 1104.
{74} Harrison, l966, Op. cit., p. 105.
{75} DesRoches-Noblecourt, Christiane. Tutankhamen. Boston: New York Graphic
Society, 1963, p. 166, pl. 98.
{76} P. 169 in DesRoches-Noblecourt, Christiane. Op. cit.
{77} Harrison, R. G. Personal Communication, 1982.
{78} Hoving, T. Tutankhamun The Untold Story. New York: Simon and Schuster,
1978, p. 121.
{79} McLeod, W. Composite Bows from the Tomb of Tutankhamen. Oxford: Tutankh-
amun Tomb Series, 1970., p. 10, 12.
McLeod, W. Personal Communication, 1991.
{80} McLeod, W. `The Bow and The Axes', in Studies Presented to Sterling Dow On
His Eightieth Birthday. Durham, N. C.: Duke University, 1984, p. 205.
{81} Harrison, 1982, Op. cit.
{82} Reyman, T. A., Zimmerman, M. R.and Lewin, P. K. `Histopathologic investi-
gation.' in Hart, Millet, Scott, and Cockburn, editors. 1977, Op. cit., p. 472.
{83} Harrison, 1982, Op. cit.
{84} DesRoches-Noblecourt, Christiane. Op. cit., p. 66.
{85} Pabo, S. `Molecular Cloning of Ancient Egyptian Mummy DNA.' Nature, Vol.
314, 18 April 1985, pp. 644-45.
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