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The Embodiment of Stress: Do cortisol-immune interactions moderate social influences on health?


Patterns of morbidity and mortality are unequally distributed across and within populations. At the population level, marginalized individuals tend to be at higher risk for poor health from many causes, ranging from psychosocial conditions to infectious and metabolic diseases. Socioeconomic, nutritional, and ecological landscapes often change alongside market integration and development, making it difficult to tease apart the primary agents responsible for changes in health profiles and increases in disease risk. Though differences in health and disease are associated with the affect of stressors on neuroendocrine and immune systems, the complete pathways between environmental conditions and health in developing populations remain poorly understood. This dissertation research seeks to fill that gap by targeting three important but under-studied factors that contribute to health and disease risk: pathogen exposure, inequality, and psychosocial stress. Correlates of health under variable conditions are examined in two populations: the Tsimane of Bolivia and inhabitants of the Honduran island of Utila.

First, I present research that investigates tradeoffs between key life history parameters, growth and immunity, among Tsimane children of the Bolivian amazon. In this high pathogen environment, investment in adaptive immune function should be prioritized. I find that investment in components of adaptive immunity does not vary as a consequence of moderate differences in energetic resources. Further, I find evidence of a trade-off between adaptive immunity and height: children with more robust adaptive immunity are shorter. In the next chapters, I investigate the pathways through which neuroendocrine-immune responses mediate social influences on health. First, I investigate the role perceptions play in mediating how aspects of an individual’s socioeconomic and ecologic landscape influence diurnal cortisol. This chapter utilizes a measure called “perceived lifestyle discrepancy” (PLD) to evaluate variation in perceptions of unmet need, and its link to parameters of physiological stress. PLD significantly predicts cumulative exposure to, and reduced diurnal change in, cortisol. The following chapter focuses on one of the mechanistic pathways through which psychosocial stressors may influence disease risk, by altering the diurnal profiles of cortisol and leukocytes, which together regulate the majority of homeostatic processes in the body. Here, I find that diurnal decline in cortisol is inversely associated with changes in both count and proportion of lymphocytes over the course of the day, driven by the influence of afternoon cortisol on lymphocytes and granulocytes. This suggests evidence for a potential pathway to poor health, by suppressing peripheral lymphocytes, which may further exacerbate damage done by other inflammatory processes. Finally, I test the theory that diverse aspects of social adversity leads to impaired glucose through their common ability to disrupt cortisol-immune interactions resulting in glucocorticoid resistance. I find individuals that are discriminated or depressed show evidence of glucocorticoid resistance, and glucocorticoid resistance also predicts higher fasting glucose.

Taken together, this research project begins to unpack the dynamic processes that shape health and disease risk. Specifically, this research integrates methods and theory from biocultural and evolutionary anthropology, endocrinology, and immunology to investigate how environmental conditions affect health and disease risk among marginalized populations as a function of both diurnal cortisol and its regulation of inflammatory components of immunity.

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