THE
AMARNA KINGS, ANAEMIAS AND PARASITIC LIVER DISEASE{a}
by
Thomas 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
Bilharzias infestation and Amarna portraiture, and looks at possible future
paleobiological research on the Amarna period.
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Fig. 2 Copy
in line of a relief in the tomb of the vizier Ramose, with the royal pair on
the palace balcony in the Gem Pp Aten at Karnak bestowing golden gifts upon
the tomb owner. |
The wealth, culture and
political power of Ancient Egypt reached a peak during the rule of Amen Hetep
III (1386-1347 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 Frolich'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 hookworms, 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. Heterozygotic 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 disease.{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 individuals 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 (Bilharzias).{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 schistosomes 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 schistosomiasis.{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 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 Ä 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 Memphis 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 Hospital, 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 additionally 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
Triumphant: The Life and Times of Ramesses II. Mississauga, Ontario: Benben
Publications, 1985.
{2} The view here follows
Cyril Aldred's analysis of the relationships among the four kings as summed up
on p. 292 ff. 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 Egyptology 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.
{8} Harrison, R. G. and
Abdalla, A. B. `The remains of Tutankhamun.' Antiquity, XLVI, 1972, pp. 8-14.
{10} Ibid., p. 12.
Harrison, 1982, Personal Communication, reaffirmed that conclusion.
{11} Harrison, R. G. `The
Anatomical Examination of the Pharaonic Remains Purported 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.
{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: Harmondsworth, 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.
{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.
{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.
{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.
{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.
{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.
{55} Derry, Douglas, M. D.,
in Carter, H. The Tomb of Tutankhamen.
London: 1972., p. 229.
{56} Lewin, P. K., Ibid.,
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. Ibid., p. 147,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 investigation.' 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 preserved 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.
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