King Tutankhamun, Modern Medical Science, and the Expanding Boundaries of Historical Inquiry

Abstract

TUTANKHAMUN, BETTER KNOWN AS KING TUT, RULED ancient Egypt from 1333 to 1324 BC, during the 18th dynasty (circa 1550-1295 BC) of ancient Egypt’s New Kingdom (circa 1550-1070 BC). His brief reign, youthful visage, and premature death, as well as the rediscovery of his remains and tomb in 1922, have fascinated Egyptologists and other historians alike for decades. Over the years, many scholars have offered a wide variety of explanations for his early demise as well as the seemingly androgynous appearance of his face and gynecomastia portrayed in sculptures and other relics. These diagnoses have included Marfan syndrome, Wilson-Turner X-linked mental retardation syndrome, Frohlich syndrome (adiposogenital dystrophy), Klinefelter syndrome, androgen insensitivity syndrome, aromatase excess syndrome in conjunction with sagittal craniosynostosis syndrome, and Antley-Bixler syndrome or one of its variants. After a series of radiographs taken of Tutankhamun’s mummy in 1968 suggested signs of trauma to the back of the head and an unhealed broken leg, armchair pathologists began suggesting that Tutankhamun’s death was caused by his falling from a chariot, getting kicked in the head by a large beast, septicemia or fat embolism secondary to a femur fracture, or, most sensationally, being murdered by either a blow to the back of the head or poisoning. More recently, an advertisement with the headline “Murder of King Tut Solved” in the October 1, 2009, issue of USA Today announced a new book by a best-selling mystery writer and a historian. Echoing the theories of many others, these authors suggest that the boy pharaoh married his younger sister, Ankhensenamun to produce a male child. The marriage produced no heirs but inspired an imaginative plot— specifically, the queen, a villainous general, and an evil advisor murdered Tutankhamun so they could assume control of the kingdom. Such diverse musings serve as proof of the most enjoyable aspect of retrospective diagnoses: there is always room for debate and, in the face of no definitive evidence, room for new theories and claims. But as Hawass and colleagues demonstrate in their study of King Tutankhamun’s family in this issue of JAMA, the legion of Tutankhamun admirers might be well advised to reconsider several existing theories. Between September 2007 and October 2009, Hawass et al, from Egypt, Germany, and Italy, independently examined 11 royal mummies believed to be from King Tutankhamun’s immediate lineage (circa 1410 to 1324 BC) and another 5 royal mummies from an earlier period (circa 15501479 BC). The objective was to determine the familial relationship of these royal family members and test the mummies for evidence of murder, genetic disorders, and infectious diseases. Unlike the previous hypotheses about Tutankhamun’s death and medical history, this investigation was based on unfettered access to the actual mummies. Using partial Y-chromosomal information, Hawass et al constructed the most plausible 5-generation pedigree to date, whereby Yuya and Thuya are established as the greatgrandparents of Tutankhamun; Pharaoh Amenhotep III and KV35 elder lady (Queen Tiye) are his grandparents; and KV55 male (most likely Akhenaten) and KV35 younger lady are siblings as well as Tutankhamun’s parents. Settling the question of Tutankhamun’s supposed gynecomastia is not possible, because most of the mummy’s chest wall is missing. It is also difficult to assess such abnormalities among the other males in the study because of the mummification process. Nevertheless, the morphological and radiological examinations did not reveal evidence of a feminine physique, leading the authors to suggest that the artistic or “beautified” style of artifacts and portraits of Tutankhamun’s era may have left behind the wrong impression for 20thand 21st-century observers. Although no evidence was found to confirm a diagnosis of either Marfan or Antley-Bixler syndromes, Tutankhamun did have juvenile aseptic bone necrosis of the left second and third metatarsals, which may be consistent with Kohler disease II or Freiberg-Kohler syndrome. More-