Frequency and chronological distribution of dental enamel hypoplasia in enslaved African Americans: A test of the weaning hypothesis

Abstract

The dentition of 27 enslaved African Americans from archaeological sites in Maryland and Virginia were examined. All 17 males and 7 of the 10 females in this study exhibited enamel hypoplastic defects indicative of systemic nutritional and disease stresses interfering with amelogenesis. Estimates of the ages of occurrence of these defects show that most occur between 1.5 and 4.5 years of age, 0.5-3.75 years later than historically documented weaning age (9-12 months of age) in similar plantation populations. Comparisons are made with studies of dental enamel hypoplasia in contemporaneous enslaved and free African American populations, including our data on 75 individuals from the First African Baptist Church cemetery in Philadelphia. These populations were highly stressed. While there appears to be a modest effect of early weaning stress, no direct relationship of peak frequencies to weaning age can be shown. These data raise questions about the attribution of peak hypoplasia frequencies to age at weaning or "post-weaning" stresses in previous paleopathological studies. High hypoplasia frequencies during the middle years of enamel development are more likely the result of a combination of 1) multiple environmental stresses, 2) differences in hypoplastic susceptibility in enamel, and 3) random factors.

What can developmental defects of enamel reveal about physiological stress in nonhuman primates?

“…2 Bioarcheological applications have involved documenting an increase in the prevalence of enamel hypoplasia in the transition from hunting and gathering to agricultural subsistence systems in various regions of the globe [12][13][14] and reporting a high prevalence of enamel hypoplasia in slave populations. 15,16 Although Colyer 17,18 published findings on nonhuman primate enamel hypoplasia in 1936 and 1947, it is only during the last 15 years that this topic has become a strong focus of research interest and activity. 19 -38 There is growing recognition that if developmental defects in enamel can help answer questions about the conditions under which humans experience stress, then they may also be valuable in answering these questions about nonhuman primates.…”

Osteobiography of a high‐status burial from the lower Río Verde Valley of Oaxaca, Mexico

“…These seasonal variations can reflect disturbances that also affect adults in a population. Childhood diseases and high fevers can also create periods of cessation in enamel development (Blakey et al, 1994;Hillson, 1996). Weaning not only directly affects ingestion of nutrients but also exposes individuals to new environmental insults directly through the food itself, increasing the potential for exposure to such things as parasites, bacteria and viruses (Kent, 1986;Reinhard, 1988).…”

“…A permanent record of health disturbances both in utero and during childhood, enamel defects are caused by disease (such as scurvy, rickets or measles), infections, fevers, gastrointestinal disorders (such as chronic diarrhoea), malnutrition, premature birth, anaemia, and, in some instances, from inherited factors or trauma. Dental hypoplasias formed on deciduous dentition in utero are also an indirect indicator of the mother's health status (Goodman & Armelagos, 1988;Goodman & Rose, 1990: 59-110;Blakey et al, 1994;Hillson, 1996;Cucina & Iscan, 1997;Rankin-Hill, 1997;Wright, 2006). Determination as to when such disruptions in enamel formation took place are carried out by measuring from the cemento-enamel junction (CEJ), to the occlusal/superior border of the linear enamel hypoplasias.…”

Infectious disease among enslaved African Americans at Eaton's Estate, Warren County, North Carolina, ca. 1830-1850

“…Rose 1985, Hutchinson 1987, Owsley et al 1987, Rathbun 1987, Jacobi et al 1992, Blakey et al 1994, Rankin-Hill 1997, Rathbun & Steckel 2002) have explored the prevalence of infectious diseases and other disorders. Diseases noted in these studies and of particular interest here, given their potential to produce dental defects and other lesions observed in the Eaton Ferry skeletal series, include congenital syphilis (Rose 1985, Rathbun 1987, Jacobi et al 1992, tuberculosis (Rose 1985, Rankin-Hill 1997, marasmus (Blakey et al 1994), rickets, scurvy (Rose 1985, Rankin-Hill 1997, and sickle-cell anemia , Rathbun 1987. The cranial, dental, and postcranial signs of these diseases/disorders Roberts et al 1994;j: Lambert 2002. are described in Table IV.…”