King Tutankhamun’s Family and Demise

LETTERS

King Tutankhamun’s Family and Demise

To the Editor: In their study, Dr Hawass and colleagues1

reported ancient DNA data from 11 royal Egyptian mum-mies and used microsatellites to ascertain kinship amongspecimens. We question the reliability of the genetic datapresented in this study and therefore the validity of the au-thors’ conclusions. Furthermore, we urge a more critical as-sessment of the ancient DNA data in the context of DNAdegradation and contamination.

The long-term survival of DNA is determined by theenvironmental history of the samples, and Gilbert et al2

argued in reference to mitochondrial DNA that “inmost, if not all, ancient Egyptian remains, [ancient DNA]does not survive to a level that is currently retrievable.”The age of the mummies (more than 3300 years beforethe present) coupled with their preservation historysuggests that DNA survival is highly unlikely. Long-term survival of nuclear DNA sequences, as accessed byHawass et al, is even less likely than mitochondrial DNA,given lower copy numbers per cell. Success in theretrieval of putative nuclear DNA sequences is also sur-prising given the use of traditional polymerase chainreaction techniques rather than newly developed captureapproaches coupled with second-generation sequencingthat allow for successful capture of degraded (shorter)DNA sequences.3

Contamination is a major obstacle in human ancient DNAresearch.4 Although laboratory members involved in the studywere genotyped, no persons handling the specimens priorto the study were included, raising a question of the reliabilityof the microsatellite profiles. Precautions such as genotyp-ing of associated nonhuman remains and including infor-mation on the microsatellite allele frequencies in present-day Egypt would have clarified the issue of moderncontamination.

Another cause for concern is the lack of reported qualitycontrol measures in the genotyping of microsatellites. Po-tential genotyping errors include allelic stutters, allelic drop-out, short allele dominance, and null alleles, all of whichcan result in the incorrect identification of alleles. Even smallerror rates (0.01 per allele) can lead to high error rates indownstream applications, such as false paternity exclusionin kinship testing.5

Eline D. Lorenzen, [email protected] Willerslev, DScCenter for GeoGeneticsNatural History Museum of DenmarkCopenhagen, Denmark

Financial Disclosures: None reported.

1. Hawass Z, Gad YZ, Ismail S, et al. Ancestry and pathology in King Tut-ankhamun’s family. JAMA. 2010;303(7):638-647.2. Gilbert MT, Barnes I, Collins MJ, et al. Long-term survival of ancient DNA inEgypt: response to Zink and Nerlich (2003). Am J Phys Anthropol. 2005;128(1):110-114.3. Briggs AW, Good JM, Green RE, et al. Targeted retrieval and analysis of fiveNeandertal mtDNA genomes. Science. 2009;325(5938):318-321.4. Willerslev E, Cooper A. Ancient DNA. Proc Biol Sci. 2005;272(1558):3-16.5. Hoffman JI, Amos W. Microsatellite genotyping errors: detection approaches,common sources and consequences for paternal exclusion. Mol Ecol. 2005;14(2):599-612.

To the Editor: Based on computed tomography (CT), thestudy of King Tutankhamun’s family by Dr Hawass and col-leagues1 purported an age of 35 to 45 years for the KV55male (Table 1), older than previously thought. Prior stud-ies that refute this claim were dismissed and no substantia-tion for a much older age range was given in the text or on-line content.

The KV55 skeletal remains were thoroughly analyzed af-ter their 1907 discovery by Sir Grafton Elliot Smith,2 whoestimated an age of 25 to 26 years based on direct observa-tion of epiphyseal union throughout the skeleton. Re-examination by Ronald Harrison and Ahmed el Batrawi in1963 augmented macroscopic examination with radio-graphs to ascertain the degree of fusion in some bones andassessed morphology of the right pubic symphysis to de-rive an age of 20 years at death.3 Both anatomists reportedthat the epiphyses of the medial clavicle; heads and tu-bercles of some ribs; and the inferior epiphyses of the fourthand fifth cervical, fourth thoracic, and superior fifth tho-racic vertebrae are unfused, while the iliac crests and mostrib epiphyses are partially fused, cranial sutures are en-tirely open, and the right maxillary third molar is not fullyerupted (although the others are). These observations in-dicate an age range of 18 to 23 years. Further documenta-tion, including union of all scapular epiphyses except thevertebral border, confirms this range.3

Although age estimation from morphology of the pubicsymphysis was not available in Smith’s day, Harrison’s

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Letters Section Editor: Robert M. Golub, MD, Senior Editor.

©2010 American Medical Association. All rights reserved. (Reprinted) JAMA, June 23/30, 2010—Vol 303, No. 24 2471

description and photographs of the right pubic symphysissupported his estimate.3 Clear billowing (ridges and fur-rows) with an ossific nodule on the upper extremity butwithout delimitation of the upper or lower margins corre-sponds to phase 1 in the Suchey-Brooks system (themethod most commonly used by osteologists4), yielding a95% confidence interval of 15 to 23 years for males with amean of 18.5 years.5

These age indicators from previously published descrip-tions and photographs contradict the estimate of 35 to 45years in the study by Hawass et al, indicating that KV55 isnot old enough at the age of death to be the pharaohAkhenaten. Additionally, the purported pathology sharedwith Tutankhamun, including a partial cleft palate, de-formed maxillary third molar, and scoliosis,1 are not sup-ported by these prior analyses of the KV55 skeleton. Thisman must be another son of Amenhotep III based on hisage at death.

Brenda J. Baker, [email protected] of Human Evolution and Social ChangeArizona State UniversityTempe


1. Hawass Z, Gad YZ, Ismail S, et al. Ancestry and pathology in King Tut-ankhamun’s family. JAMA. 2010;303(7):638-647.2. Smith GE. Catalogue General Antiquites Egyptiennes du Musee du Caire, Nos61051-61100: The Royal Mummies: Cairo: Service des Antiquites de L’Egypt, Im-primerie de L’institut Francais D’archeologie Orientale; 1912 [Reprinted]. Lon-don, England: Duckworth; 2000.3. Harrison RG. An anatomical examination of the pharaonic remains purportedto be Akhenaten. J Egypt Archaeol. 1966;52:95-119.4. Komar DA, Buikstra JE. Forensic Anthropology: Contemporary Theory andPractice. New York, NY: Oxford University Press; 2008.5. Brooks ST, Suchey JM. Skeletal age determination based on the os pubis: a com-parison of the Acsadi-Nemeskeri and Suchey-Brooks methods. Hum Evol. 1990;5:227-238.

To the Editor: Based on my review of the radiographic im-ages in the study by Dr Hawass and colleagues,1 I disagreewith the authors’ conclusion that Tutankhamun had a leftclubfoot. In talipes equinovarus, or clubfoot, the hindfootis in equinus, and the navicular is medially displaced on thetalus.2,3 The images in Figure 4 of the article show the leftfoot to have a normal hindfoot and a normal talonavicularrelationship. Thus, Tutankhamun’s left foot is not in equi-nus and not in varus, and is not a clubfoot.

However, the relationship of the calcaneus to thecuboid is consistent with a habitually supinated foot. Theimages in Figure 5 show chronic pathology of the secondand third metatarsal heads, so it is reasonable to assumethat Tutankhamun walked with a stick and with his leftfoot in supination to relieve pressure on the diseasedmetatarsal heads.

Tutankhamun does not have oligodactyly as he has 5 toes.He does not have hypophalangism as the proximal and dis-tal phalanges are normal and symmetrical with the right side.It is unclear why he is missing the middle phalanx of thesecond toe. It is arguable whether the lateral view of the right

foot (Figure 4A) represents a pes planus or simply a low-arched variation of normal; however, it is unreasonable topropose the causation of pes planus to be “transferred ad-ditional joint load to the right foot” in the absence of evi-dence suggesting either neuromuscular disease or chronicrupture of the posterior tibial tendon.

James G. Gamble, MD, [email protected] of Orthopaedic SurgeryStanford University Medical CenterStanford, California


1. Hawass Z, Gad YZ, Ismail S, et al. Ancestry and pathology in King Tut-ankhamun’s family. JAMA. 2010;303(7):638-647.2. Ponseti IV. Congenital Clubfoot. Oxford, England: Oxford University Press; 1966:8-20.3. Bridgens J, Kiely N. Current management of clubfoot (congenital talipesequinovarus). BMJ. 2010;340:c355.

To the Editor: Dr Hawass and colleagues1 assessed the re-lationship between Tutankhamun, Akhenaten, and severalother members of Egypt’s 18th dynasty. However, some oftheir claims regarding possible inherited disorders amongthe 11 royal mummies they examined appear to be incon-sistent. The Abstract reported that “[n]o signs of gyneco-mastia and craniosynostoses . . . were found,” but the textstated that “putative breasts in Tutankhamun and his fa-ther Akhenaten (KV55) cannot be determined, because KV55is a mummified skeleton and Tutankhamun lacks the fron-tal part of the chest wall.”

In their Results section, the authors stated that “Akhenatenhas [a cephalic] index of 81.0 and Tutankhamun anindex of 83.9, indicating brachycephaly. . . . ThutmoseII . . . show[s] dolichocephaly, with [a cephalic index] of73.4.” Nevertheless, these skulls are visibly abnormally elon-gated, having the “family head” of the 18th dynasty. Three-dimensional CT scans of Tutankhamun’s skull2 andimages of Akhenaten’s skull3 by these authors showabsent to poorly developed interdigitated cranial sagittal su-tures consistent with premature fusion seen in craniosyn-ostosis.

The authors also reported that “Macroscopic and radio-logic inspection of the mummies did not show . . . defi-ciency in cytochrome P450 oxidoreductase.” However,such genomic analyses were not described. Therefore, thisstudy does not exclude the possibility that the elongatedheads and gynecomastia of numerous royal members ofthis dynasty were due to a genetic disorder analogous toAntley-Bixler syndrome,4 in which a single mutant gene(POR) induces both craniosynostosis and defective ste-roidogenesis. Classic cases exhibit insufficient estrogenproduction leading to deformed, underdeveloped genitaliain both sexes. We have proposed an as yet undescribedvariant of the syndrome, associated with excess (ratherthan deficient) estrogen production as in the aromataseexcess syndrome.5 The observation of Hawass et al that

LETTERS

2472 JAMA, June 23/30, 2010—Vol 303, No. 24 (Reprinted) ©2010 American Medical Association. All rights reserved.

Tutankhamun’s penis was well developed would beexpected in this putative syndrome. This hypothesis couldbe tested by appropriate genomic analysis.

Irwin M. Braverman, [email protected] of DermatologyYale Medical SchoolNew Haven, ConnecticutPhilip A. Mackowiak, MD, MBAVeterans Affairs Medical CenterBaltimore, Maryland


1. Hawass Z, Gad YZ, Ismail S, et al. Ancestry and pathology in King Tut-ankhamun’s family. JAMA. 2010;303(7):638-647.2. Williams AR. Modern technology reopens the ancient case of King Tut. NatlGeogr Mag. 2005:2-21.3. King Tut unwrapped: pharaoh forensics. Discovery Channel Web site. http://dsc.discovery.com/videos/king-tut-unwrapped-pharaoh-forensics.html. Ac-cessed March 15, 2010.4. Flück CE, Tajima T, Pandey AV, et al. Mutant p-450 oxidoreductase causes dis-ordered steroidogenesis with and without Antley-Bixler syndrome. Nat Genet. 2004;36(3):228-230.5. Braverman IM, Redford DS, Mackowiak PA. Akhenaten and the strange phy-siques of Egypt’s 18th dynasty. Ann Intern Med. 2009;150(8):556-560.

To the Editor: Dr Hawass and colleagues1 suggested Plas-modium falciparum malaria in conjunction with Köhler dis-ease II as a possible cause of death for Tutankhamun. Fal-ciparum malaria was endemic in ancient Egypt. Althoughdetection of plasmodial MSP1, STEVOR, and AMA1 gene frag-ments in the mummy may prove presence of P falciparum,we are not convinced that the disease pattern suggested bythe authors was the primary cause of Tutankhamun’s earlydeath. In endemic areas, malaria is a life-threatening dis-ease commonly affecting children until the age of 6 to 9 years,not semi-immune adults of 18 to 19 years,2 the age that Tut-ankhamun apparently reached.

In addition, translucent bone areas of 2 metatarsals of theleft foot and shortening of the second toe, likely signs of os-teonecrosis, osteomyelitis, or ulcerative osteoarthritis, arevisible in Figure 5 of the article. These radiological signs arecompatible with osteopathologic lesions seen in sickle celldisease (SCD), a hematological disorder that occurs at genecarrier rates of 9% to 22% in inhabitants of Egyptian oases.3

The SCD gene HbS may appear homozygously or in com-bined heterozygosity with �-thalassemia mutations, caus-ing disease. Therefore, it is reasonable to include SCD inthe differential diagnosis of Tutankhamun’s paleoradio-logic findings.

Ischemic osteonecroses, inflamed by osteomyelitis and sep-ticemia (eg, due to Salmonella or Staphylococcus infec-tions), are frequent SCD complications and often triggeredby malaria episodes.4 Heterozygous and homozygous HbScarriers are not protected from P falciparum infection perse and may exhibit significant parasitemia.4,5 However, al-though heterozygous carriers are protected from severecourses of falciparum malaria, homozygous carriers are proneto childhood or early adulthood fatality from SCD and its

complications. The age of 25 to 45 years attributed to Tut-ankhamun’s parents and the age of approximately 50 yearsof other relatives are reconcilable with segregation of theHbS trait and, thus, resistance to severe courses of malariain the royal pharaonic family. The possible occurrence ofSCD in Tutankhamun is strengthened by the consanguin-ity suspected in his parents.

We suggest that, if possible, the authors include in ge-netic testing of their royal mummies the HbS variant on chro-mosome 11p15.5 (rs334) and common variants causing�-thalassemias.

Christian Timmann, [email protected] G. Meyer, MDDepartment of Molecular MedicineBernhard Nocht Institute for Tropical MedicineHamburg, Germany


1. Hawass Z, Gad YZ, Ismail S, et al. Ancestry and pathology in King Tut-ankhamun’s family. JAMA. 2010;303(7):638-647.2. Snow RW, Gilles HM. The epidemiology of malaria. In: Warrell DA, Gilles HM,eds. Bruce-Chwatt’s Essential Malariology. 4th ed. London, England: Arnold Pub-lishers; 2002:85-106.3. El-Beshlawy A, Youssry I. Prevention of hemoglobinopathies in Egypt.Hemoglobin. 2009;33(suppl 1):S14-S20.4. Makani J, Komba AN, Cox SE, et al. Malaria in patients with sickle cell anemia:burden, risk factors, and outcome at the outpatient clinic and during hospitalization.Blood. 2010;115(2):215-220.5. Williams TN, Mwangi TW, Wambua S, et al. Sickle cell trait and the risk of Plas-modium falciparum malaria and other childhood diseases. J Infect Dis. 2005;192(1):178-186.

In Reply: Drs Lorenzen and Willerslev are incorrect regard-ing insufficient contamination prevention and quality con-trol measures during our study. In addition, authentic, ad-equately preserved DNA can indeed be obtained fromEgyptian mummy tissue (FIGURE 1) but requires specifi-cally adapted extraction protocols.

The following aspects substantiate authenticity. (1) Allgenerally accepted criteria for ancient DNA authentica-tion1,2 were strictly adhered to before, during, and after ge-netic analysis experiments, as described in our article. (2)Putative contamination by people handling the mummiesbefore the sampling and during the experiments was moni-tored. (3) All female mummies were negative for Y-chromosomal markers. (4) All male mummies showed ho-mozygous (ie, hemizygous) Y-chromosomal profiles. (5) Theprofiles and haplotypes of the whole set of mummies showedindividual differences and therefore could not have origi-nated from the same source of putative contaminant DNA.(6) The combination of nuclear data (Y- and autosomal chro-mosome–related markers) complemented each other. (7) Re-producible genotypes were obtained from different biop-sies and extractions per mummy. (8) Subsets of the data wereindependently replicated in a second, separate ancient DNAlaboratory staffed by a separate group of personnel, who re-confirmed the authenticity of the results. (9) DNA isolatedfrom Egyptian mummies was highly informative when pro-cessed with next generation sequencing.

LETTERS


Dr Baker questions the accuracy of our CT-based age de-termination for the KV55 mummy. CT technology allows amore accurate age determination and depicts bony land-marks more precisely than in previous studies that used in-accurate and vague age estimation methods3 (and also failedto detect various pathologies of the KV55 mummy de-scribed in our study). The cancellous bone distribution ofthe femur and humerus heads4; epiphysis ossification of thevertebrae, long bones, and iliac crests; and osteophyte de-velopment on many of the vertebral end plates are typicalof an age at death of 35 to 45 years, ruling out the muchyounger age suggested by Baker.

Dr Gamble disagrees with our diagnosis of left clubfootand right pes planus in the Tutankhamun mummy. How-ever, the images to which he refers are not sufficient for aconclusive evaluation when viewed on their own. The dis-

placement of the left navicular and cuboid bone, taken to-gether with the additional adduction and supination of theleft forefoot, indicates a congenital malformation (grade 1clubfoot) rather than an acquired defect, with the right flat-foot having developed through 1-sided strain (FIGURE 2).In our opinion, the missing middle phalanx of the left sec-ond toe is hypophalangism, as the images show no trace ofglue. Moreover, bearing in mind the extensive damage causedby the rough and careless handling of the mummy, it seemsimprobable that such a painstaking and illogical repair at-tempt should have been carried out on a toe.

In contrast to the speculations of Drs Braverman and Mack-owiak, our conclusions are based on direct examination ofthe mummies. Their hypothesis of Antley-Bixler syndromeor other diseases running in the 18th dynasty royal family5

was refuted by Miller,6 who drew attention to the lack of

Figure 1. Agarose Gel Electrophoresis of 12 Representative DNA Extractions From Egyptian Mummies Described in the Original Article

M 1 2 3 4 5 6 L M M 7 8 9 10 11 12

500 bp

75 bp

500 bp

75 bp

Although each aliquot contains only 5 µL of extract (which amounts to 5%-10% of a standard extract), the DNA is clearly visible. Lanes 2, 5, 8, 9, and 11 show DNAextractions that contain fragment sizes up to 500 base pairs (bp) and longer, despite the small volume of the loaded DNA aliquots. Each lane represents a different mummy.

Figure 2. Computed Tomographic (CT) Image of the Left and Right Feet of Tutankhamun From Various Angles

A Axial cross sections B Sagittal CT reconstructions

R L R L Right foot

Left foot

Navicular

Talus

Talus

Navicular

Cuboid

Cuboid

Calcaneus

Calcaneus

The left cuboid and navicular bones are displaced compared with the normal positioning of the right navicular bone.

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2474 JAMA, June 23/30, 2010—Vol 303, No. 24 (Reprinted) ©2010 American Medical Association. All rights reserved.

convincing evidence. We agree with Miller6 and reiterate thatnone of the 16 examined royal mummies showed any anoma-lies symptomatic of Antley-Bixler syndrome,7,8 POR defi-ciency, isolated gynecomastia, or craniosynostoses. Fur-thermore, the suggestion by Braverman and Mackowiak tosearch for a novel disease gene5 would imply positional clon-ing and a subsequent candidate gene approach, a method-ology inapplicable for such a small group of persons of un-defined phenotype.

Drs Timmann and Meyer suggest the possibility of SCDas the origin of the osteopathologic lesions in the mummyof Tutankhamun. This is an interesting and plausible addi-tion to the palette of potential disease diagnoses in AncientEgyptian royalty that we are currently investigating.

Yehia Z. Gad, MDAncient DNA LaboratoryEgyptian MuseumCairo, EgyptAshraf Selim, MDDepartment of RadiologyKasr Al Ainy Faculty of MedicineCairoCarsten M. Pusch, [email protected] of Human GeneticsDivision of Molecular GeneticsEberhard-Karls-UniversityTübingen, Germany


1. Roberts C, Ingham S. Using ancient DNA analysis in paleopathology: a criticalanalysis of published papers, with recommendations for future work. Int JOsteoarcheol. 2008;18(6):600-613.2. Richards MB, Sykes BC, Hedges RE. Authenticating DNA extracted from an-cient skeletal remains. J Archaeol Sci. 1995;22(2):291-299.3. Hershkovitz I, Latimer B, Dutour O, et al. Why do we fail in aging the skullfrom the sagittal suture? Am J Phys Anthropol. 1997;103(3):393-399.4. Denk W, Szilvassy J, Bauer G. Age determination based on the structure of theproximal parts of the humerus and femur. Beitr Gerichtl Med. 1990;48:673-678.5. Braverman IM, Redford DS, Mackowiak PA. Akhenaten and the strange phy-siques of Egypt’s 18th dynasty. Ann Intern Med. 2009;150(8):556-560.6. Miller WL. Did Akhenaten have the Antley-Bixler syndrome? Ann Intern Med.2009;151(12):892.7. Antley R, Bixler D. Trapezoidocephaly, midfacial hypoplasia and cartilage ab-normalities with multiple synostoses and skeletal fractures. Birth Defects Orig Ar-tic Ser. 1975;11(2):397-401.8. Crisponi G, Porcu C, Piu ME. Antley-Bixler syndrome: case report and reviewof the literature. Clin Dysmorphol. 1997;6(1):61-68.

Physical Activity and Preventing Weight Gainin Women

To the Editor: The observational study by Dr Lee andcolleagues1 found that relatively high levels of physicalactivity among overweight or obese women in the Wom-en’s Health Study were not associated with protectionagainst long-term weight gain. On the other hand, amongwhite women in the US Diabetes Prevention Program,those exposed to a structured lifestyle intervention (com-bining exercise, diet, and coping or problem-solvingskills) experienced about 8 kg of weight loss during the

period of their multidisciplinary, structured support.2

The report from the Women’s Health Study, therefore, isconsistent with less intensive obesity intervention trialsthat found little or no weight loss following exercise ordietary treatments.

If preservation of cardiometabolic health is a majorobjective, these results should not be considered discour-aging. A growing body of evidence confirms that adop-tion of healthy habits can result in reduced abdominalobesity and improved metabolic risk factors despite mini-mal change in weight.3 A failure to lose weight or preventweight gain does not prove that exercise (or dietary)interventions were futile. Weight gain under circum-stances of high physical activity might reflect accumula-tion of salutary lean tissue, especially skeletal muscle.And for adults who gain weight as adipose tissue, a pre-dominant increase in subcutaneous fat may serve tosafely sequester the excessive calorie burden.4 Subcutane-ous lipid sequestration (often in the hips and thighs) mayprotect such adults from lipotoxic damage to the liver,muscle, heart, and pancreas. Accumulation of intra-abdominal adipose tissue, on the other hand, may indi-cate increased cardiometabolic risk.

Rather than focus only on weight loss, health promotionprograms might alternatively pursue reductions in abdomi-nal obesity, improved lipid indices, or greater cardiores-piratory fitness. Health benefits might be better estimated,for example, as improvements in the lipid accumulation prod-uct5 (a continuous variable) or as the reduced populationprevalence of a hypertriglyceridemic waist phenotype.

Henry S. Kahn, [email protected] Center for Chronic Disease Prevention

and Health PromotionCenters for Disease Control and PreventionAtlanta, Georgia

Financial Disclosures: None reported.Disclaimer: The findings and conclusions in this letter are those of the author anddo not necessarily represent the official position of the Centers for Disease Con-trol and Prevention.

1. Lee IM, Djousse L, Sesso HD, Wang L, Buring JE. Physical activity and weightgain prevention. JAMA. 2010;303(12):1173-1179.2. West DS, Elaine Prewitt T, Bursac Z, Felix HC. Weight loss of black, white, andHispanic men and women in the Diabetes Prevention Program. Obesity (SilverSpring). 2008;16(6):1413-1420.3. Ross R, Bradshaw AJ. The future of obesity reduction: beyond weight loss. NatRev Endocrinol. 2009;5(6):319-325.4. Unger RH, Clark GO, Scherer PE, Orci L. Lipid homeostasis, lipotoxicity andthe metabolic syndrome. Biochim Biophys Acta. 2010;1801(3):209-214.5. Kahn HS, Cheng YJ. Longitudinal changes in BMI and in an index estimatingexcess lipids among white and black adults in the United States. Int J Obes (Lond).2008;32(1):136-143.

To the Editor: Dr Lee and colleagues1 examined the rela-tionship between physical activity and weight gain preven-tion. The study concluded that physical activity is in-versely related to weight gain in women of normal weight,but not in women who are overweight. However, this con-clusion may be flawed.

LETTERS


Documents

King Tutankhamun’s Family and Demise