One central area of anthropological inquiry is the effect of stress on human populations, with a common interpretation that stress episodes are “unhealthy” as they represent disruptions in physiological function. Bioarchaeological research emphasizes the interaction between environment, biological needs, cultural buffering, and psychosocial trauma as contributing factors to physiological stress response, integrating aspects of life history and cultural context (Reitsema and McIlvaine 2014). Goodman et al. (1984) modeled stress episodes as a linear process beginning with stressors, such as extreme climate, or limited resources, such as famine. Cultural behavior in turn could buffer or introduce stress; Temple and Goodman (2014) suggested that cultural food systems could be altered to mitigate the effects of a famine or shortage, but political systems could exacerbate a stress episode by limiting food production. In this model, both the physical and cultural environment interact with an individual, but different host resistance factors, such as sex and age, may further buffer or exacerbate the physiological reaction to the stressor (Goodman et al. 1984). If the environmental, cultural, and host responses cannot remain in homeostasis, then physiological disturbance occurs (Goodman et al. 1984; Temple and Goodman 2014). Goodman and Armelagos (1989) defined physiological disturbance (stress) in terms of skeletal manifestations: growth disruptions, disease, and death. The hypothesized effects on the population at large were decreased health, decreased work capacity, decreased fertility, and cultural disruption. Though several skeletal stress indicators are available, stress markers used in this study included cribra orbitalia, porotic hyperostosis, and dental enamel hypoplasia (Goodman et al. 1988: 179, Table 1) (See Figures 1-2).
Figure 1: Left - porotic hyperostosis, right parietal, FC#5700, early adult female, Middle Monongahela – Bunola site. Right - cribra orbitalia, right orbit, FC#1491, adult female, Middle Monongahela – Bunola site
Figure 2: LEH, right mandibular canine, FC#7493, late child, Early Monongahela – Murphy Old House site
2.3.1.1 Etiology: Physiological Stress
Cribra orbitalia and porotic hyperostosis are formed by the expansion of hemopoietic bone marrow in the skull. Cribra orbitalia can be described as “sieve like” lesion of the upper eye orbit, consisting of increased porosity or
expansive changes that have a spicule-like appearance in severe cases (Wapler et al. 2004). Porotic hyperostosis is characterized by the appearance of microporosity on the ectocranial surface of the skull, usually involving the parietals (Waldron 2008; Wapler et al. 2004). The specific etiology of the marrow expansion process is debated. These lesions are rarely seen in clinical contexts (DeWitte and Stojanowski 2015), but anthropologists have traditionally linked cribra orbitalia with iron deficiency anemia following Britton et al. (1960). Histological and clinical research has shed some doubt on this widely used diagnosis, as it is unlikely that iron deficiency anemias cause the expansive marrow changes that form cribra orbitalia (Walker et al. 2009; Wapler et al. 2004). This type of marrow expansion is more commonly seen in genetic hemolytic and megaloblastic anemias such as thalassemia (Walker et al. 2009). Because the etiology of cribra orbitalia and porotic hyperostosis is debatable (Walker et al. 2009) they should be interpreted as an indicator of stress rather than of a specific condition due to multifactorial etiology (DeWitte and Stojanowski 2015).
Dental enamel hypoplasias (DEH) are described as areas of decreased dental enamel thickness (Goodman and Rose 1990). Dental enamel is entirely inorganic in its structure and is laid down on the developing tooth dentin by specialized cells known as amelobasts during infancy and childhood (Goodman and Rose 1990). Ameloblasts are responsible for secreting enamel matrix, and it is during this secretory phase that DEHs form. Ameloblastic activity has been shown to be particularly sensitive to perturbations in development caused by a number of factors: diet, low birth weight, infections, systemic illnesses, and genetic conditions (Pindborg 1982; Hillson 2005). Due to this multifactorial etiology, these defects are generally classified as non-specific indicators of stress episodes during childhood (Goodman and Rose 1990). They are most commonly identified as visible rings of decreased enamel thickness, also known as linear enamel hypoplasias (LEH) (Goodman and Rose 1990).
2.3.1.2 Discussion: Physiological Stress indicators and Gender
Gendered differences in the expression of non-specific stress indicators have been investigated with respect to the general pattern of health and nutritional deficiency in past populations (Guatelli-Steinberg and Lukacs 1999; Ribot and Roberts 1996; Sullivan 2005). Nutrition, social status and gender are of particular relevance to reconstructions of gender in the past. Sullivan (2005) examined the rate of cribra orbitalia as a possible indicator of iron deficiency anemia in medieval York. Among individuals of lower social status, cribra orbitalia was more prevalent than in cohorts of higher status. Low status women were disproportionately affected by these lesions and more likely to have the condition than males in other social classes. It was argued that iron deficiency anemia factored in the lives of medieval York women and that high demands on reproductive systems along with cultural factors such as social class exacerbated this pattern (Sullivan 2005).
Patterns of childhood stress are often used as proxies for general population health for past populations through evaluation of rates of pathology and growth curves (Mays et al. 2009; Ribot and Roberts 1996). The interpretation of these results is complicated by the fact that there are often no significant differences between stressed and unstressed cohorts in terms of skeletal growth in bioarchaeological studies (Lewis 2002; Mays et al.
2009; Wakefield 2009). The long-term effects of childhood stress may be over-estimated, though studies of specific conditions have shown differential rates of childhood disease according to biocultural factors. Ortner et al. (2001) studied scurvy in North American skeletal collections, and noted that the frequencies of the condition varied among populations and were highest in those with high maize consumption. Thus, high rates of skeletal indicators of stress may suggest a more general pattern of dietary intake, as well as the interplay between environment and resource exploitation (Ortner et al. 2001).
DEH are one of the most frequently recorded stress indicators, and gendered social practices along with biological buffering may have some influence on differential rates between the sexes (Guatelli-Steinberg and Lukacs 1999). Non-human primate studies have demonstrated that males have a longer period of tooth formation, resulting in increased “recording” of stress events via enamel hypoplasias and sex influenced female buffer for hypoplasia formation was suggested due to this developmental difference (Guatelli-Steinberg and Lukacs 1999). However, sex differences were not statistically significant for many samples, and it was emphasized that cultural practices can influence LEH formation. For example, there may be a sex preference in parental investment during episodes of stress; male children in indigenous groups in Mexico were more likely than girls to receive adequate nutrition in times of food insecurity (Guatelli-Steinberg and Lukacs 1999).