Graduation Year

2015

Document Type

Dissertation

Degree

Ph.D.

Degree Name

Doctor of Philosophy (Ph.D.)

Degree Granting Department

Anthropology

Major Professor

Erin Kimmerle, Ph.D.

Committee Member

Lorena Madrigal, Ph.D.

Committee Member

Christian Wells, Ph.D.

Committee Member

Julia Irwin, Ph.D.

Committee Member

David Hunt, Ph.D.

Keywords

Developmental origins of health and disease, Epidemiological transition, Lifecourse, Paleopathology

Abstract

Although the association between social inequality and poor adult health is well established, the mechanisms by which inequality is translated into poor adult health are less clear. Increasingly, evidence suggests that many adult health problems and health disparities have their origins in early life; the developmental origins of health and disease (DOHaD) hypothesis provides an explanatory mechanism linking adverse early life conditions with permanent structural or functional changes that increase the risk for disease. This hypothesis is consistent with bioarchaeological research noting reduced lifespan among individuals exhibiting signs of childhood stress.

The principal aim of this dissertation is to contribute a bioarchaeological perspective to health disparities research by investigating how health disparities can be measured and understood in the past. This study focuses on early life conditions as a source of adult health disparity by examining a skeletal sample for the association between childhood stress and adult longevity; the relationship between childhood stress and the presence of adult health conditions; and sex, ancestry, and regional differences in these relationships.

The study sampled 830 age-documented, U.S. born African American males and females and Euro-American males from the Terry and the Hamann-Todd anatomical collections, representing socially-marginalized individuals from the late 19th- to early 20th centuries. Enamel hypoplasia, femoral length, and vertebral neural canal diameters represented childhood stress; skeletal fractures, tibial periostosis, and the diseased, missing, and filled tooth index represented adult health. Longevity was modeled with Kaplan-Meier survival curves and adult health relationships were modeled with logistic regression. Additionally, cause of death data from historic health department publications and the study sample morgue records were examined for disparity in the epidemiological transition from infectious to degenerative cause of death.

The study found mixed results for all analyses. There was no reduction in longevity for the presence of enamel hypoplasia, short femoral length, or reduced thoracic neural canal diameter. African American males had statistically significant reduced longevity for small lumbar vertebral neural canal diameters. African American males from the Hamann-Todd Collection and Euro-American males from both collections had significant relationships between vertebral neural canal diameters and adult conditions; these relationships varied among the groups but in most cases demonstrated reduced odds for having the adult condition for individuals with smaller canal diameters. African American females had no differential survival or relationships between variables over the lifecourse. All groups except for the Terry Collection Euro-American males continued to have more infectious disease deaths than degenerative disease deaths. The study results contribute to disparities research by demonstrating that the consequences of childhood stress varied by sex and ancestry and by demonstrating within-population variation in timing of the epidemiological transition. Additionally, the study results support the contention of greater male sensitivity to environmental conditions and contributes evidence supporting the DOHaD hypothesis.

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