Abstract
Meat-eating was an important factor affecting early hominin brain expansion, social organization and geographic movement. Stone tool butchery marks on ungulate fossils in several African archaeological assemblages demonstrate a significant level of carnivory by Pleistocene hominins, but the discovery at Olduvai Gorge of a child's pathological cranial fragments indicates that some hominins probably experienced scarcity of animal foods during various stages of their life histories. The child's parietal fragments, excavated from 1.5-million-year-old sediments, show porotic hyperostosis, a pathology associated with anemia. Nutritional deficiencies, including anemia, are most common at weaning, when children lose passive immunity received through their mothers' milk. Our results suggest, alternatively, that (1) the developmentally disruptive potential of weaning reached far beyond sedentary Holocene food-producing societies and into the early Pleistocene, or that (2) a hominin mother's meat-deficient diet negatively altered the nutritional content of her breast milk to the extent that her nursing child ultimately died from malnourishment. Either way, this discovery highlights that by at least 1.5 million years ago early human physiology was already adapted to a diet that included the regular consumption of meat.
Highlights
We report the discovery of porotic hyperostosis on Olduvai Hominid (OH) 81, two refitting right parietal fragments of a,2year-old child (Hominidae gen. et sp. indet.) from the 1.5-millionyear-old (Ma) SHK (Sam Howard Korongo) site, Olduvai Gorge, Tanzania (Fig. 1)
The exact relationship of porotic hyperostosis to various anemias is debated [1,6,7,8,9,10] but current research hypothesizes its production in infants and young children through the combined effects of hypoferremia and gastrointestinal infections [2]
Given that porotic hyperostosis is often documented in human infants of roughly the same estimated age as OH 81 from regions free of malaria [7], we conclude that serious nutritional stress at a key phase in the development of the OH 81 individual was the most likely cause of the porotic hyperostosis observed on the fossil
Summary
We report the discovery of porotic hyperostosis on Olduvai Hominid (OH) 81, two refitting right parietal fragments of a ,2year-old child (Hominidae gen. et sp. indet.) from the 1.5-millionyear-old (Ma) SHK (Sam Howard Korongo) site, Olduvai Gorge, Tanzania (Fig. 1). The exact relationship of porotic hyperostosis to various anemias is debated [1,6,7,8,9,10] but current research hypothesizes its production in infants and young children through the combined effects of hypoferremia (induced by the ingestion of breast milk depleted in vitamin B12 or loss of access to vitamin B12 through weaning) and gastrointestinal infections [2] Such an etiology fits with observations of OH 81, which consists of two refitting pieces of the posterior portion of a right parietal (one piece is 53.93 mm long [major axis] and 32.33 mm wide, the other 47.31 mm long [major axis] and 24.56 mm wide; refitted, OH 81 is 65.35 mm long anteroposteriorly and 53.38 mm wide superoinferiorly). Taking into account that OH 81 derives from a smaller-brained hominin species than is H. sapiens, the relative morphology and size of the fossil parietal matches those of some estimated two-year-olds in a sample of XVIIIth century modern human crania from the necropolis of the Nuestra Senora de la Asuncion Church (Chinchon, Madrid) (see Methods)
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