The Innate Immune System, Energetics, and the Early-Life Environment
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AbstractHuman immune function is sensitive to ecological context, yet knowledge about immune function primarily derives from a few populations that are relatively unique ecologically, both in comparison to other populations globally and to conditions likely experienced during human evolution. In this dissertation I use life history theory and the emerging field of ecological immunology to situate an investigation into variation in human immune function.
Using data from three populations, I test several hypotheses concerning how innate immune function may evidence sensitivity to energetic resources, and how non-acute immune function may be influenced by the early-life environment. First, working with data from a sample of adolescent girls in the Gambia, I analyze how C-reactive protein (CRP) may be related to energetics. I find that non-acute immune function has relationships with both energy reserves and growth rates, but not energy balance. I then use data from a research project established in Connecticut to test hypotheses concerning how the early-life environment may influence within-individual stability of CRP. Working with Ecuadorian immigrants who experienced different early-life ecological circumstances than those common in the United States, I find that CRP is stable within-individual, but overall levels of CRP are low. In the final study, I utilize comparative data from the Shuar Health and Life History Project to understand how immigrants compare to individuals who remain in their natal communities. I find that CRP is indistinguishable between these two samples, but that indicators of chronic disease risk have shifted. Immigrants have significantly higher glucose levels, and higher waist circumference than non-immigrants. However, these changes are not accompanied by changes in CRP levels, and CRP is inconsistently related to the indicators of the metabolic syndrome in both populations.
The sensitivity of the immune system to both energetics and the early-life environment suggests that the higher levels of inflammation seen in affluent populations may result from multiple, compounding processes. Critically, these results strongly suggest it is not appropriate to use categorical levels of CRP to describe metabolic risk across populations, and some individuals assume risk factors for chronic disease without accompanying changes in inflammatory proteins.
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