UC Santa Barbara

Porous cranial lesions (PCLs) of the orbital roofs (cribra orbitalia) and cranial vault (porotic hyperostosis) are among the most commonly observed pathological findings in archaeological skeletal remains. These lesions develop in childhood but can remain visible throughout adulthood. Though widely used by bioarchaeologists to infer compromised health in past populations, they are largely ignored in clinical practice and have never been studied in a population-representative sample. Consequently, the causes of PCLs and their consequences for health are a subject of on-going bioarchaeological debate. This dissertation takes an ethnobioarchaeological approach to the relationship between PCLs and health in a contemporary subsistence population, using biomedical data from the Tsimane Health and Life History Project to address the adult health correlates of PCLs and the childhood skeletal response to anemia, one known cause of PCLs.

Investigating PCLs in living individuals required that I first validate their visibility on clinical computed tomography (CT) criteria, which I did with an archaeological reference sample (n = 22) of individuals from sites of Pachacamac and Chicama, Peru. I found that porosity in the outer table of the cranial vault (porotic hyperostosis) was best observed on CT using volume-rendered reconstructions, and only porosity with pore diameters larger than the image resolution of the scan could be reliably identified. Porosity in the occipital squama is thus more likely to be visible on CT than porosity in other bones of the cranial vault. In the orbital roofs, porous lesions (cribra orbitalia) were consistently identifiable only when they presented with enlarged diploic spaces.

I then used the resulting CT criteria to identify PCLs on existing CT scans of living adults. Because childhood anemia is one known cause of PCLs, I expected PCLs to be common among the Tsimane, a contemporary population of Amazonian forager-horticulturalists with high prevalence of childhood anemia. Given the established links between childhood stress and adult morbidity and the archaeological evidence that PCLs are associated with younger age at death, I expected the identification of PCLs to be associated with a distinct health signature in Tsimane adults. Using cranial CT scans and longitudinal biomedical data on a population-representative sample of 375 adults (45% female; aged 40+ years), I compared health outcomes for individuals with and without visible PCLs, including immune cell counts, biomarkers of inflammation, clinical diagnoses, and functional disability assessments.

I observed PCLs in 17.2% of the overall sample, with cranial vault lesions in 12.3% and orbital roof porosity in 6.1%. PCLs of the orbital roofs (cribra orbitalia) were associated with 3.8 (95% CI: 1.3, 11.2) times the risk of developing symptomatic tuberculosis and a lower CD4+/CD8+ T cell ratio for age (β = -0.78, (-1.52, -0.06)), an indicator of immunosenescence. However, orbital lesions were not associated with higher incidence of other respiratory infections, other markers of cell-mediated immunity, or adult hemoglobin levels. Vault lesions (porotic hyperostosis) were not associated with meaningful differences in measured health outcomes. These findings suggest that lesion-causing processes in early life can result in heightened lifetime susceptibility to some infections. It is also clear that, even if childhood anemia causes Tsimane PCLs, lesions do not indicate continued risk of anemia in adults.

As a first look at whether Tsimane PCLs could feasibly be caused by specific forms of childhood anemia, I investigated whether anemia was associated with differences in childhood skeletal metabolism—as measured in blood by the bone turnover marker osteocalcin—and whether the skeletal effects of iron-deficiency anemia differed from those of anemia of inflammation. I found that among 362 observations of Tsimane children aged 4 months to 8 years (49% female), iron-deficiency anemia was associated with lower osteocalcin-for-age whereas high inflammation (C-reactive protein and erythrocyte sedimentation rate), with or without anemia, was not. However, because iron-deficient anemia cases (serum transferrin receptor >5 mg/L) tended to have lower hemoglobin than iron-replete cases, it is unclear whether the mechanism behind lower bone turnover is iron deficiency per se or the degree of anemia.

Taken together, this research strengthens the empirical foundations necessary for the study of health in past populations by linking skeletal stress markers to measures of individual health. In the process of doing so, it narrows the gap between skeletal biology research in living and past populations by using health-representative samples of a contemporary population and developing methods for creating comparable PCL data from living and long-deceased individuals.