Chronological distribution of enamel hypoplasias and weaning in a Caribbean slave population.

Dental enamel hypoplasia is a putative marker of childhood morbidity (nutritional or infectious stress) which can he analyzed by age-of-occurrence using a calcification standard. We have recorded age-specific occurrence of (a) minor linear hypoplasias, (b) pits, (c) major growth-arrest lines, and (d) combined hypoplasias in 103 specimens of 17-19th century Caribbean slaves. This population is probably unique in terms of environment, nutritional deficiency and other severe environmental stresses, and (especially) association with historical resources that might allow more specific correlation of stresses with hypoplasia chronology. Barbados slaves have a clearly defined central age tendency of 3-4 years at formation of hypoplasias. The lateness of the mode, the percent concentration between 3-4 years, and the residual occurrences at 4+ years are relatively pronounced compared to other reported populations (notwithstanding differences in counting techniques). The age of first hypoplasia occurrence per individual is also probably later in slaves than in other populations. The 3-4 year age range encompasses the year following the historically-documented relatively late time that slave children were weaned (at 2-3 years). Other non-industrial populations show a hypoplasia peak at 2-3 years following a presumed weaning at 1-2 years. Thus the weaning hypothesis and other historical factors (such as periodic food shortages and famine conditions) help explain the mode and the residual distribution of hypoplasia. The historical sources also support the general expectation that the postweaning period was one of high risk. Following studies of extant populations (Sarnat and Schour, 1941; ElNajjar et al. 1978; Infante and Gillespie, 1974, 1977; Moller et al. 1972; Ainamo and Cutress, 1982; Gruenwald, 1973), dental enamel hypoplasia has recently become popular as a marker of childhood morbidity in excavated remains (Goodman e t al. 1980, 1984; Schulz and McHenry, 1975; Cook and Buikstra, 1979; Hillson, 1979; Black, 1979; Clarke, 1980; Corruccini et al. 1982). Although precise causes of this interruption in enamel deposition are multiple (Pindborg, 1982; Fraser and Nikiforuk, 1982; ElNajjar et al. 1978), much of the hypocalcemia leading to hypoplasia formation is generally assumed to reflect metabolic stress, temporarily disturbing amelogenesis, due to malnutrition and/or infection. 'Department of Anthropology, Southern Illinois University, Carbondale, Illinois, 62901. Human Biology, December 1985, Vol. 57, No. 4, p p . 699-711. 8 Wayne State University Press, 1985 700 Robert S . Corruccini, Jerome S . Handler and Keith P. Jacobi * In an earlier analysis of a slave osteological sample from the Caribbean island of Barbados, we assumed that relatively high hypoplasia prevalence el would be consistent with this etiology (Corruccini et al. 1982). The historb ical evidence indicates Caribbean slaves experienced nutritional deprivation and severe developmental disruption (e.g., Dirks, 1978; Sheridan, 1985: 201-219, 234-239; Kiple and Kiple, 1980). Results generally confirmed our expectations (see also Handler and Corruccini, 1983). We also briefly noted a tendency for more numerous and serious hypoplasias to occur in laterather than early-calcifying teeth; this tendency was possibly related to a late weaning period in Caribbean slaves. The logical relation between hypoplasia peak and a society's typical weaning age (the post-natal time of maximum environmental/metabolic stress on children in non-industrial societies) is the major theme of many hypoplasia studies (Hillson, 1979; Black, 1979; Clarke, 1980; Goodman et al. 1980). In this paper we give a more detailed analysis focused on the chronology and classification of enamel hypoplasias in Barbados slaves, with special reference to the weaning hypothesis and the integration of historical and biological data.