AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY 123:23–29 (2004) An Ill Child Among Mid-Holocene Foragers of Southern Africa Susan Pfeiffer1,2* and Christian Crowder1 1 2 Department of Anthropology, University of Toronto, Toronto, Ontario M5S 3G3, Canada Department of Archaeology, University of Cape Town, 7700 Rondebosch, South Africa KEY WORDS rickets; South Africa; Khoisan; infant mortality; infanticide ABSTRACT The skeletal remains of an infant from a southwest South African rock shelter at Byneskranskop show pervasive abnormalities that are consistent with the effects of hypertrophic (hyperplastic) rickets. Diagnostic features include beading of the costochondral junctions of the ribs, ﬂaring and tilting of the metaphyses, and cupping of the distal ulna, as well as general skeletal hypertrophy. With an uncalibrated accelerator mass spectrometry (AMS) radiocarbon date of 4820 ⫾ 90 BP (TO-9531), this is a very early instance of the condition, among foragers whose environment and diet make dietary shortages of active vitamin D or dietary calcium improbable. Carbon The characteristics of those children who fail to survive should tell us something about the stressors faced by their society. In many parts of the world, the burials of past foraging peoples are rare and geographically dispersed. As a result, we know little about their health, as reﬂected through palaeopathology. Relative to more sedentary groups, huntergatherers may have had less exposure to infectious and nutritional diseases, and more experience with accidental skeletal trauma (Cohen, 1989; Larsen, 1997; Bogin, 2001). The rarity of birth defects and serious chronic diseases among the skeletons of foragers is consistent with scenarios suggesting that the frail may not have been maintained within the group, and that the option of perinatal infanticide was part of the culture. Information about how past foraging groups managed ill health is important to our understanding of human biosocial adaptation. The Later Stone Age of sub-Saharan Africa is an especially rich source of information about foraging adaptations. Until approximately 2,000 years ago, human groups who appear to be ancestral to modern Khoisan-speaking peoples moved through various habitats, subsisting on hunted, ﬁshed, and collected food resources (Deacon and Deacon, 1999). Populations appear to have favored the Cape region, in which the climate is Mediterranean, with mild, wet winters and hot, dry summers, and both terrestrial and aquatic resources are available for exploitation (Deacon and Lancaster, 1988). Well-preserved human skeletal remains have been excavated, especially from rock shelters in the Cape Fold Mountains, which were used for burial rituals during the © 2004 WILEY-LISS, INC. and nitrogen stable isotope ratios indicate a mixed diet, including marine as well as terrestrial protein. Solicitous care maintained the sick infant to an estimated age of 3.5–5 months; it was buried in a manner like that of other deceased group members. This case suggests that if infanticide was practiced, it was an option only during the immediate perinatal period, when this infant would have appeared normal. This is consistent with documentation of infanticide practices among historic foragers from southern Africa. Am J Phys Anthropol 123:23–29, 2004. © 2004 Wiley-Liss, Inc. Holocene. While mature skeletons from the Later Stone Age have been studied for indications of palaeodiet and habitual behaviors (cf. Churchill and Morris, 1998; Sealy and Pfeiffer, 1999; Stock and Pfeiffer, 2001), juvenile remains have received less attention. It was in the context of a broader documentation that the infant skeleton described here was noted. The study of Later Stone Age skeletal remains may be informed by data from historically documented foragers of southern Africa, now limited to the interior regions of Botswana, Namibia, and northern South Africa. Studies from the era of the Harvard Kalahari Research Group (ca. 1963–1970; Lee, 1976) are particularly useful, because the application of a biosocial model caused researchers to ask speciﬁc questions about health and mortality. Studies of adult care of infants and children among Kalahari foragers indicate solicitous care, with relatively late weaning as the norm (Konner, 1976; Grant sponsor: Social Sciences and Humanities Research Council of Canada *Correspondence to: Susan Pfeiffer, Department of Anthropology, University of Toronto, 100 St. George St., Toronto, Ontario M5S 3G3, Canada. E-mail: Pfeiffer@chass.utoronto.ca Received 6 September 2002; accepted 7 February 2003. DOI 10.1002/ajpa.10297 24 S. PFEIFFER AND C. CROWDER Draper, 1976). Chronic maladies, like malnutrition and gastroenteritis, were rare among children, and child mortality was chieﬂy associated with epidemics (Truswell and Hansen, 1976). During the postnatal care of infants in the Kalahari environment, it is reported that mothers would use their leather capes to protect their infants from intense sunlight, to the extent that infants occasionally showed craniotabes. This term refers to the softening of the parietal bone and the widening of fontanels that occur chieﬂy in rickets. Once the babies were exposed to the sun, the rickets would disappear (Truswell and Hansen, 1976). While it is difﬁcult from any ethnographic study to calculate the incidence of infanticide, its occasional practice at the discretion of the mother is unquestioned in the Kalahari setting (Howell, 1976, 1979). An expectant mother normally gave birth in solitude, and if an infant was deformed or was one of twins, or if the mother seriously doubted that the child’s life could be sustained, it was her prerogative or duty to smother it (Shostak, 1981). Schapera (1930) reported that among some historic Khoisan, unwanted babies, such as those born while mothers were still breastfeeding a child too young to wean, were disposed of immediately after birth in a burrow or hole in the ground. Several ethnographic accounts (Schapera, 1930; Silberbauer, 1981; Shostak, 1981; Barnard, 1992) describe how babies were named a few days or weeks after their birth, after which time they were seen as part of the family group and other extended relationships. MATERIALS AND METHODS Two cave sites in the Byneskranskop limestone hill, Bredasdorp District, South Africa, were excavated in 1980 and reported by deVilliers and Wilson (1982). The sites are roughly 160 km east-southeast of Cape Town, straddling the southern and southwestern Cape regions. The lowest occupation layers date to about 12,500 years ago, while sheep bones in the upper layers indicate dates of less than 2000 BP. Most of the deposit is artifactually characteristic of the Wilton complex or tradition, known for its high incidence of backed bladelets and of segments or “crescents” (Deacon and Deacon, 1999). With the sea coast 5– 6 km away, mollusc shells and the bones of seal, ﬁsh, and sea birds occur, as well as terrestrial large and small prey species (Klein, 1981). Eight human skeletons, four of them immature, were excavated from shelters BNK 1 and BNK 3. Three skeletons were radiocarbon dated to dates between 1480 –3190 BP (deVilliers and Wilson, 1982). The infant described here, Burial 6, was loosely ﬂexed on its right side in BNK3. It shows red ochre staining on its skull. Some apparently unrelated postcranial elements were initially comingled, presumably from a prior burial that was disturbed by this interment. While a ﬁeld photograph and an inventory of the skeleton were published, the abnormal nature of the bones was not noted. The focus of that initial study was the determination that the people associated with the Wilton complex were of Khoisan rather than black African background. The remains of Burial 6 are designated in the collections at Iziko Museums, Cape Town, as SAM-AP 6060. Another BNK3 infant of very similar age, Burial 7 (SAM-AP 6059), is used for comparison. The remains were studied during research visits in 2000, 2001, and 2002. Seven right ribs were used for chronometric dating and light stable isotope analysis. Casts of the destroyed material were provided to the Museum. RESULTS Isotopic analysis The stable carbon and nitrogen isotope ratios were measured from collagen (C/N ⫽ 3.0, yield 15.1%), following standard procedures of light-stable isotope analysis (Sealy, 1997; Sealy and Pfeiffer, 2000). The value for ␦13C ⫽ ⫺16.6‰, and the value for ␦15N ⫽ 13.2‰. The uncalibrated accelerator mass spectrometry date (TO-9531) is 4820 ⫾ 90 BP. The proper calibration of this date should address both its southernhemisphere location and the effect of the dietary incorporation of carbon from the “older” marine system. The Southern Hemisphere ’98 Curve, developed by the Quaternary Dating Research Unit (Pretoria, South Africa), is based on INTCAL with a southern hemisphere correction. When applied, it yields dates of 3631 BC, 3564 BC, and 3541 BC, with one-sigma ranges of 3652–3507 BC and 4327–3386 BC. Recognizing the effect of marine carbon on radiocarbon dating, the Pretoria Laboratory developed the West Coast ’93 (WC93) calibration curve, based on the marine data set of Stuiver and Brazunias (1993), with a local correction. The ␦13C value for SAM-AP 6060, ⫺16.6‰, suggests that carbon was being incorporated from both terrestrial and marine systems, a “mixed” diet. Assuming that approximately half of the carbon in the infant’s bones was marine-derived, recalibrating using the WC93 curve, averaging the intercepts with the results of the calibration based on SH98, yields dates of 3267 BC, 3234 BC, and 3222 BC. Error terms are not available for this adjustment. Skeletal inventory The dentition is represented by 11 unerupted deciduous tooth crowns: 3 maxillary incisors (Ri2, Ri1, and Li1), and 8 mandibular crowns (ﬁrst deciduous molars, canines, and all incisors). The cranial vault bones are somewhat fragmented and remain slightly distorted, but all major vault bones are nearly complete, i.e., paired frontal bones and parietals, occipital squamae, and basilar and lateral parts. The temporal bones are represented by the petrous portions, which appear “weathered” in a manner that may instead reﬂect premortem bone remodeling of an abnormal type. There are small fragments of the sphenoid. Both maxillae are extant, although broken distally and missing frontal processes. The man- HYPERTROPHIC RICKETS dible consists of the anterior body (fused mesially) and a portion of the right ascending ramus. The postcranium includes 19 vertebral bodies (most being lumbar, sacral, and cervical), two halves of the atlas, 9 other unfused cervical arch halves, 22 unfused thoracic arch halves, 5 fused or partially fused lumbar arches, 10 left ribs, and 8 right ribs. Long bones include 10 hand/foot long bone shafts, plus one ﬁrst metatarsal; paired scapulae, ilia, ischia, and pubes; paired femora, tibiae, and humeri; and one unsided ﬁbula, right ulna, right radius, and right clavicle. There are no epiphyses that clearly match these bones. One epiphysis from a scapular fossa may be from SAM-AP6060, but the match is equivocal. Estimated age The formation of each tooth crown was assessed using the standards of Moorrees et al. (1963). There is consistency throughout the dentition; maturation is consistent with an age of 0.3– 0.4 years, i.e., approximately 3.5–5 months of age. Skeletal maturation is consistent with this estimated age, except for the posterior fusion of the lumbar arches, which would be expected at a slightly later age. While there are few Later Stone Age infants of similar age available for comparison, the infant’s longitudinal growth appears to have been retarded. Long bone lengths are shorter than those of two infants with comparable dental ages. Lengths are very similar to those of a slightly younger, normally developed infant from Byneskranskop. The younger infant, SAM-AP 6059, has a dental age of 2–3 months, and has arm bones slightly longer and leg bones slightly shorter than in SAM-AP 6060. The diaphyseal diameters and distal diaphyseal widths of SAM-AP 6060 are always greater than those of SAM-AP 6059, by a ratio of about one third. There is no radiographic evidence of episodic disruptions (growth arrest lines), so the slow growth was probably persistent. 25 Fig. 1. Two frontal bones of SAM-AP 6060, demonstrating rough and irregular new bone deposited supraorbitally, and diffuse porosity of orbits. Region of red ochre staining is immediately superior to region of abnormal bone. Fig. 2. Cross section of left frontal bone, illustrating additional new bone, deposited ectocranially. Diploic bone shows normal thickness, but diploe appear sclerosed. Abnormal skeletal morphology Probably the most obvious abnormal feature of SAM-AP6060 is the thickening of the supraorbital portions of the frontal bones. The bone is 12 mm thick at the fronto-malar junction, and of similar thickness along the metopic suture superior to the glabella (Fig. 1). The interorbital distance is wide (18 –19 mm). In the thickened regions, the ectocranial bone is rough and irregular, and on cross section it appears to be superimposed on the diploic bone (Fig. 2). Exposed diploic trabeculae appear sclerosed. The superior orbits are porous, but not in the focal manner seen in the cribra orbitalia. Other cranial and jaw bones appear normal. The palate and nasal ﬂoor appear normal. No deformation of the very short right ascending ramus is apparent on the fragmentary mandible, but the bone is damaged on all edges. There is a horizontal notch near the tip of one deciduous canine crown, suggesting the possi- Fig. 3. Radiograph of SAM-AP 6060, including (clockwise from upper left) clavicle, two representative ribs showing expansion at sternal ends, ﬁrst rib, and ilia showing dense cancellous pattern that accompanies abnormal bone thickness. bility of some disruption in enamel formation in utero, but this possible abnormality is very slight. The ribs of SAM-AP6060 are ﬂared at their sternal extremities, expanded, and ﬁlled with cancellous bone. The irregular bones (especially the ilia and 26 S. PFEIFFER AND C. CROWDER Fig. 5. Tibiae of SAM-AP 6060 are central, in anterior-posterior view, compared with tibiae of SAM-AP 6059, an infant with normal skeletal morphology who died at a slightly younger age. Note angle of distal metaphyseal surfaces on affected tibiae, which could have contributed to bowing of lower limbs, in life. DISCUSSION Fig. 4. Radiograph of selected long bones from SAM-AP 6060 in anterior-posterior view, including humeri, ulna, and radius (upper row); grouped tibiae and femora (lower row). All long bones show expanded diaphyses, narrowed medullary spaces, and cortical bone that is less dense than normal. scapulae) are thickened with cancellous bone, and show indistinct surface morphology (Fig. 3). All of the long bones, including the clavicle, are expanded along their extent (Fig. 4). The shafts show cortical thickening, with some surface irregularity caused by patches of irregularly structured bone. The hand and foot bones are widened, with a sausage-like appearance. The left tibia is slightly bowed, medially. The metaphyses are ﬂared, especially in the lower extremities, and the cortex is thick but not dense. Metaphyseal surfaces appear rougher than normal (as per Ortner and Mays, 1998). Radiographs reveal narrow medullary cavities. Some muscle attachment areas, especially the linea aspera and those of the elbow region, are particularly rough, and show longitudinal cortical excavations. The popliteal line and the deltoideus region look smooth and unexcavated. The distal right ulna appears distinctly cupped. The metaphyseal ends of the distal femora and tibiae appear laterally tilted as compared to normal infant bones (Fig. 5), so there may have been more bowing of the legs than is apparent in the extant diaphyses. The stable isotope values from the bone collagen of SAM-AP 6060 can provide information on both diet and health. However, neither interpretation is straightforward in an infant of this young age from this ecosystem. The site is situated between the southern Cape, where terrestrial vegetation includes both C3 and C4 species, and the southwestern Cape, a region with predominantly C3 terrestrial ﬂora. Hence, the degree of marine resource exploitation is most reliably assessed using different approaches in the two regions. Marine exploitation should indicate dietary access to vitamin D-rich fatty ﬁsh. Because breastfeeding is associated with trophic-level enrichment in both nitrogen and carbon (Katzenberg, 2000), comparisons should focus on other infants and young children. Isotopic values for juveniles are not directly comparable with those of adults, because of the trophic-level effect produced by breastfeeding. A further complication to interpretation is the possibility that metabolic imbalances that stimulate rapid bone remodeling may enrich the 15N/14N ratio (Katzenberg and Lovell, 1999). Published juvenile ␦13C values from the coastal southern Cape site of Oakhurst range from ⫺10.4‰ to ⫺16.4‰ for infants (N ⫽ 6, mean ⫽ ⫺14.3‰; Sealy et al., 1992), thus tending to be less negative than those from the southwestern Cape, and less negative than the value for SAM-AP 6060. The isotope values of SAM-AP 6060 are intermediate between those of Later Stone Age infants and juveniles from inland and coastal sites of the southwestern Cape (Table 1). Applying the interpretive framework that was developed for the southwestern Cape ecosystem (cf. Sealy et al., 2000), it appears that the ill child was breastfeeding from a mother whose diet included both terrestrial and marine protein sources. It does not appear as a dietary outlyer. 27 HYPERTROPHIC RICKETS TABLE 1. Stable carbon and nitrogen isotope values comparing SAM-AP 6060 with Later Stone Age, pre-2000 BPt, infants and young children, South Africa1 Specimen Estimated age (years) ␦13C (‰) ␦15N (‰) SAM-AP 6060 (Byneskranskop) WVR 16 (Watervalsrivier) Eland Cave 1 Eland Cave 2 UCT 388 (Faraoskop) SAM-AP 6314 (Steenbokfontein Cave) SAM-AP 6054A (Malmesbury) SAM-AP 6054B (Malmesbury) SAM-AP 6054C (Malmesbury) 0.3–0.4 2–2.5 3 6.5 6–7 NB 12 5–6 2–3 ⫺16.6 ⫺18.6 ⫺18.8 ⫺18.7 ⫺18.8 ⫺12.8 ⫺11.7 ⫺14.8 ⫺15.2 13.2 14.0 13.2 12.8 15.2 15.9 15.1 15.7 References This study 1 1 1 2 3 4 4 4 1 Among southwestern Cape samples, ﬁrst four comparators are from inland sites. Latter four are from sites near coast. References: 1, Sealy et al., 2000; 2, Sealy et al., 1992; 3, Jerardino et al., 2000; 4. Sealy and van der Merwe, 1988. There is no indication that rapid, pathological bone remodeling heightened the ␦15N value, but the comparator group is small. TABLE 2. Infant skeleton compared against criteria that indicate rickets in juvenile skeletal remains (as per Ortner and Mays, 1998) Diagnostic characteristics Differential diagnosis While most causes of juvenile morbidity and mortality do not affect the skeleton, rickets is an exception. Rickets is a metabolic disturbance of the ability to deposit calcium and phosphorous within bone tissue, resulting in the failure of osteoid to properly calcify. It commonly occurs in children aged 6 months to 2 years, although it may appear in children as old as 15 years (Passmore and Eastwood, 1986; Steinbock, 1976; Stuart-Macadam, 1989; Aufderheide and Rodriguez-Martin, 1998). Most commonly, the condition occurs when the body obtains insufﬁcient effective vitamin D from the environment, either through lack of vitamin D in the diet or lack of exposure to sunlight. Symptoms of the condition are rarely seen in infants that are less than 4 months old, because the newborn’s liver stores placentally derived vitamin D (Ortner and Putschar, 1981). The presence of rickets and of its adult counterpart, osteomalacia, often highlight maladaptive aspects of culture change. The potentially deleterious effects of rickets are a key feature of one of the most popular scenarios for depigmentization of European populations (cf. Molnar, 1998), although cases in the paleopathological literature tend to come from skeletons of the past two millennia, often from relatively complex societies (Littleton, 1998; Ortner and Mays, 1998). Many of the abnormal features of this infant are consistent with the skeletal criteria of juvenile rickets (Ortner and Mays, 1998) (Table 2). The deformation of the sternal rib ends, in the manner of the well-known “rachitic rosary,” the cupping of the distal ulna, and the slight bowing of several long bones are consistent with rickets (Jaffe, 1972). However, there are also skeletal features that are not consistent with rickets as it is commonly described. While the ribs show the characteristic shape, the expanded ends are ﬁlled with cancellous bone. Indeed, there is no evidence of low bone mass in the skeleton. Further, there is no involvement of the parietal bones and no craniotabes. SAM-AP6060 Cranial vault porosity, craniotabes Orbital roof porosity Deformation of mandibular ramus Deformation of arm bones Portion of frontal only Yes No No, but cupped distal ulna Deformation of leg bones Yes, slight bowing of tibia Flared costo-chondral ends of ribs Yes Irregular and porous cortex of ribs Yes Thickening of long bones, especially Yes metaphyses Roughened metaphyseal surfaces Yes Teeth poorly mineralized1 Equivocal 1 Criterion from Mankin (1974). A less common cause of rickets arises not from environmental perturbations but from a defect in metabolism, such that the effective vitamin D cannot be used for bone formation. The most common source of renal tubular disfunction leading to vitamin D-resistant rickets is the X-linked dominant condition of hypophosphatemia (Albright et al., 1937; Blondiaux et al., 2002), but there are many skeletal growth disorders that can disrupt the normal bone formation pathway (Ortner and Putschar, 1981; Aufderheide and Rodriguez-Martin, 1998). Understandably, this type of rickets has received less anthropological attention. However, the most ancient examples and examples from very early infancy may represent this type of rickets. Formicola (1995) argued that an adult male skeleton from an Italian cave, radiometrically dated to over 10,000 BP, shows symptoms of a life lived with X-linked vitamin D-resistant rickets. The man’s long life illustrates the variable clinical expression of this condition. Nonrachitic conditions that might explain at least some of the abnormalities were explored, including infantile syphilis (Caffey, 1939), hypervitaminosis A, infantile scurvy, and infantile cortical hyperostosis (Caffey’s disease). While infantile syphilis can lead to increased bone density in both diaphyses and metaphyses as seen here, it characteristically appears in focal zones, accompanied by necrosis, with 28 S. PFEIFFER AND C. CROWDER osteochondritis and considerable periosteal bone formation. The pervasive, diffuse nature of the bone changes in SAM-AP6060 are inconsistent with infantile syphilis. Hypervitaminosis A is another condition that causes periosteal new bone formation (Jaffe, 1972; Ruby et al., 1974; Walker et al., 1982). The metaphyses of long bones can appear irregular and cuplike in shape, and there is widening of the epiphyses, often associated with transient demineralization of cortical bone. In cases that we reviewed, there was no speciﬁc discussion of cranial changes. While it may be possible that some unusual source of vitamin A was ingested by the nursing mother and passed on to the infant, this pathological condition does not match the case under study. The bone shows no areas of demineralization, and the metaphyses are widened, but not irregular. While infantile scurvy (Jaffe, 1972; Stuart-Macadam, 1989) causes periosteal bone formation in response to hemorrhagic activity, the pattern of bone changes differs from that seen in this case. The new periosteal bone tends to be very tenuously attached to the cortex, and the radiopacity of rib ends and metaphyses is due to calciﬁed cartilage matrix, rather than cancellous bone within the diaphyses. The cranial pattern of bone change seen in infantile scurvy, along chewing muscle attachment sites (Ortner et al., 2001), is not seen here. Infantile cortical hyperostosis (Caffey, 1945) is an idiopathic condition characterized by multiple cortical hyperostoses scattered throughout the extremities, ribs, clavicle, face, mandible, and scapular regions. The mandible is always affected; other sites are variable. Cortical thickening of extremities does not extend to the terminal segments. In that the mandible of SAM-AP 6060 is unremarkable and the terminal diaphyses are affected, this etiology is also unlikely. The most probable etiology for the skeletal changes described here is the hypertrophic or hyperplastic form of rickets, as distinct from the atrophic or porotic form (Caffey, 1939; Jaffe, 1972; Ortner and Putschar, 1981; Steinbock, 1976; Stuart-Macadam, 1989). The bone cortices, although porous, become thickened from the deposition of osteoid by the periosteum. The medullary cavity may be reduced in diameter. Thickening of the frontal and parietals occurs, with most deposition on the outer surface. In hypertrophic rickets, the bones become enlarged, especially around the metaphysis. The epiphyses may become displaced or tilted due to weak connective tissue at the growth plate, causing angulation at weight-bearing sites. The bowing of long bones, the fracturing, and all the other sequellae of osteoporosis that are seen in the atrophic form are not seen in the hypertrophic form of rickets. The hypertrophic form of rickets occurs in wellnourished children, while the atrophic form is generally observed in malnourished children (Jaffe, 1972). Both forms may be the result of a shortage of calcium or active vitamin D in the child’s environment, or a metabolic inability to incorporate vitamin D during the mineralization process, usually through inadequate renal function. The hypertrophic form of rickets is characterized by the exuberant deposition of poorly mineralized osteoid at periosteal and endosteal locations. Response to bonestimulating factors like mechanical loading can lead to the deposition of more than the normal amount of bone, but it is bone of reduced density. It is unlikely that SAM-AP 6060 developed these abnormal features through the X-linked dominant condition of hypophosphatemia. Skeletal changes caused by this condition are rarely manifest until later in infancy, and its familial nature leads to relatives showing indicators of the condition, such as abnormal skull shape and premature synostosis. Such indicators have not been noted in the Later Stone Age skeletons from this region. It is unusual to see such a breadth of rachitic skeletal abnormalities in such a young infant. In both the hypotrophic and hypertrophic forms, the fetal liver is expected to store vitamin D sufﬁcient to maintain normal skeletal growth through the ﬁrst four postnatal months. In the case of SAM-AP 6060, renal malfunction may have been particularly severe, with very early onset of symptoms. Clinical symptoms of a rachitic infant are not restricted to the skeleton. They vary, depending on the cause and severity of the disease. A rachitic infant may be restless and irritable. The infant is prone to respiratory infections, and commonly has gastrointestinal upsets and diarrhea or constipation (Mankin, 1974). Other symptoms may include excessive sweating and convulsions. The muscles may become weak, causing the infant to have difﬁculty maintaining a sitting posture (Jaffe, 1972; Mankin, 1974; Stuart-Macadam, 1989). The varying pattern of cortical roughening at muscle attachment sites may indicate that this infant was swaddled in a manner that limited movement, especially at the knees and shoulders. Care of such a child would require extra energy and patience. CONCLUSIONS The health and survival of foragers are of central importance to our understanding of human evolution. Assertions are made regarding what constituted successful adaptive strategies during the millennia in which our ancestors were dependent on hunting and gathering for their subsistence, but solid information is rare. Individual cases, when contexts are ﬁrmly established, can contribute to our understanding of ﬂexibility and decision-making in the foraging context. To our knowledge, this case joins one other illustration of putative rickets from prehistoric hunting and gathering peoples (Formicola, 1995). Evidence from archaeological food waste, bone morphology, and stable isotope values suggests that an etiology of malnutrition (either general or speciﬁc to the nutrients needed for normal bone formation) is improbable in this case. The abnormal bone formation may therefore have been the result of an inborn error of bone metabolism. In burial, the infant was treated in a fashion consistent with that of other deceased group members. HYPERTROPHIC RICKETS ACKNOWLEDGMENTS Stable isotope assessment and radiocarbon date calibration were done by Prof. J.C. Sealy, Archaeometry Unit, University of Cape Town. We thank G. Avery, Iziko Museums of Cape Town, South African Museum, for access to the material. The South African Heritage Resources Agency granted permission for AMS dating and light stable isotope analysis. We thank the manuscript reviewers for their helpful comments. LITERATURE CITED Albright F, Butler AM, Bloomberg E.1937. Rickets resistant to vitamin D therapy. Am J Dis Child 54:529 –547. Aufderheide AC, Rodriguez-Martin C. 1998. The Cambridge encyclopedia of human paleopathology. Cambridge: Cambridge University Press. Barnard A. 1992. Hunters and herders of southern Africa: a comparative ethnography of the Khoisan peoples. Cambridge: Cambridge University Press. Blondiaux G, Blondiaux J, Secousse F, Cotton A, Danze P-M, Flipo R-M. 2002. Rickets and child abuse: the case of a two year old girl from the 4th century in Lisieux (Normandy). Int J Osteoarchaeol 12:209 –215. Bogin B. 2001. The growth of humanity. New York: Wiley-Liss. Caffey J. 1939. Syphilis of the skeleton in early infancy. Am J Roentgenol Radiat Ther 42:637– 655. Caffey J. 1945. Infantile cortical hyperostoses: preliminary report on a new syndrome. Am J Roentgenol Radiat Ther 54:1–16. Churchill SE, Morris AG. 1998. Muscle marking morphology and labour intensity in prehistoric Khoisan foragers. Int J Osteoarchaeol 8:390 – 411. Cohen MN. 1989. Health and the rise of civilization. New Haven: Yale University Press. Deacon HJ, Deacon J. 1999. Human beginnings in South Africa: uncovering the secrets of the Stone Age. Cape Town: David Philip Publishers. Deacon J, Lancaster N. 1988. Late Quaternary paleoenvironments of southern Africa. Oxford: Clarendon Press. deVilliers H, Wilson ML. 1982. Human burials from Byneskranskop, Bredasdorp District, Cape Province, South Africa. Ann S Afr Mus 88:205–248. Draper P. 1976. Social and economic constraints on child life among the !Kung. In: Lee RB, DeVore I, editors. Kalahari hunter-gatherers: studies of the !Kung San and their neighbors. Cambridge, MA: Harvard University Press. p 199 –217. Formicola V. 1995. X-linked hypophosphatemic rickets: a probable Upper Paleolithic case. Am J Phys Anthropol 98:403– 409. Howell N. 1976. The population of the Dobe area !Kung. In: Lee RB, DeVore I, editors. Kalahari hunter-gatherers: studies of the !Kung San and their neighbors. Cambridge, MA: Harvard University Press. p 137–151. Howell N. 1979. Demography of the Dobe !Kung. First edition. New York: Academic Press. Jaffe HL. 1972. Metabolic, degenerative and inﬂammatory diseases of bones and joints. Philadelphia: Lea and Febinger. Katzenberg MA. 2000. Stable isotope analysis: a tool for studying past diet, demography and life history. In: Katzenberg MA, Saunders SR, editors. Biological anthropology of the human skeleton. p 305–328. Katzenberg MA, Lovell NC. 1999. Stable isotope variation in pathological bone. Int J Osteoarcheol 9:316 –324. Jerardino A, Sealy J, Pfeiffer S. 2000. An infant burial from Steenbokfontein Cave, west coast, South Africa: its archaeological, nutritional and anatomical context. S Afr Archaeol Bull 55:44– 48. Klein RG. 1981. Later Stone Age subsistence at Byeneskranskop Cave, South Africa. In: Harding RSO, Teleki G, editors. Omnivorous primates: gathering and hunting in human evolution. New York: Columbia University Press. p 166 –190. Konner MJ. 1976. Maternal care, infant behavior and development among the !Kung. In: Lee RB, DeVore I, editors. Kalahari 29 hunter-gatherers: studies of the !Kung San and their neighbors. Cambridge, MA: Harvard University Press. p 218 –245. Larsen CS. 1997. Bioarcheology: interpreting behavior from the human skeleton. Cambridge studies in biological anthropology 21. Cambridge: Cambridge University Press. Lee RB. 1976. Introduction. In: Lee RB, DeVore I, editors. Kalahari hunter-gatherers: studies of the !Kung San and their neighbors. Cambridge, MA: Harvard University Press. p 3–24. Littleton J. 1998. A Middle Eastern paradox: rickets in skeletons from Bahrain. J Paleopathol 10:13–30. Mankin H. 1974. Rickets, osteomalacia, and renal osteodystrophy: parts I and II. J Bone Surg [Am] 56:101–128, 352–384. Molnar S. 1998. Human variation: races, types and ethnic groups. Fourth edition. Upper Saddle River, NJ: Prentice Hall. Moorrees CFA, Fanning EA, Hunt EE. 1963. Formation and resorption of three deciduous teeth in children. Am J Phys Anthropol 21:205–213. Ortner DJ, Butler W, Cafarellor J, Milligan L. 2001. Evidence of probable scurvy in subadults from archaeological sites in North America. Am J Phys Anthropol 114:343–351. Ortner DJ, Mays S. 1998. Dry-bone manifestation of rickets in infancy and early childhood. Int J Osteoarchaeol 8:45–55. Ortner DJ, Putschar WGJ. 1981. Identiﬁcation of pathological conditions in human skeletal remains. Smithsonian contributions to anthropology no. 28. Washington, DC: Smithsonian Institution Press. Passmore R, Eastwood MA. 1986. Human nutrition and dietetics. London: Churchill Livingston. Ruby LK, Mital MA. 1974. Skeletal deformities following chronic hypervitaminosis A. J Bone Joint Surg [Am] 56:1283–1286. Schapera I. 1930. The Khoisan peoples of South Africa. London: Routledge & Kegan Press. Sealy JC. 1997. Stable carbon and nitrogen isotope ratios and coastal diets in the Later Stone Age of South Africa: a comparison and critical analysis of two data sets. Ancient Biomol 1:131–147. Sealy J, Pfeiffer S. 2000. Diet, body size, and landscape use among Holocene people in the Southern Cape, South Africa. Curr Anthropol 41:642– 655. Sealy J, van der Merwe NJ. 1988. Social, spatial and chronological patterning in marine food use as determined by ␦13C measurements of Holocene human skeletons from the south-western Cape, South Africa. World Archaeol 20:87–102. Sealy J, Patrick MK, Morris A, Alder D. 1992. Diet and dental caries among Later Stone Age inhabitants of the Cape Province, South Africa. Am J Phys Anthropol 100:389 –396. Sealy J, Pfeiffer S, Yates R, Willmore K, Manhire A, Maggs T, Lanham J. 2000. Hunter-gatherer child burials from the Pakhuis Mountains, Western Cape: growth, diet and burial practices in the Late Holocene. S Afr Archaeol Bull 55:32– 43. Shostak M. 1981. Nisa: the life and words of a !Kung woman. Cambridge, MA: Harvard University Press. Silberbauer GB. 1981. Hunter and habitat in the central Kalahari Desert. Cambridge: Cambridge University Press. Steinbock T. 1976. Paleopathological diagnosis and interpretation: bone diseases in ancient human populations. Springﬁeld, IL: Charles Thomas. Stock J, Pfeiffer S. 2001. Linking structural variability in long bone diaphyses to habitual behaviors: foragers from the southern African Later Stone Age and the Andaman Islands. Am J Phys Anthropol 115:4:337–348. Stuart-Macadam P. 1989. Nutritional deﬁciency diseases: survey of scurvy, rickets, and iron deﬁciency anemia. In: Iscan MY, Kennedy KAR, editors. Reconstruction of life from the skeleton. New York: Alan Liss. p 201–222. Stuiver M, Brazunias TF. 1993. Modeling atmospheric 14C inﬂuences and 14C ages of marine samples to 10,000 BC. Radiocarbon 31:137–189. Truswell AS, Hansen JDL. 1976. Medical research among the !Kung. In: Lee RB, DeVore I, editors. Kalahari hunter-gatherers: studies of the !Kung San and their neighbors. Cambridge, MA: Harvard University Press. p 166 –194. Walker A, Zimmerman MR, Leakey REF. 1982. A possible case of hypervitaminosis A in Homo erectus. Nature 296:248 –250.