Journal
BRAIN BEHAVIOR AND IMMUNITY
Volume 31, Issue -, Pages 23-30Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbi.2012.08.010
Keywords
Inflammation; High sensitivity C-reactive protein; Psychoneuroimmunology; Infectious disease; Cardiovascular disease; Developmental origins of adult disease; Human ecological immunology
Categories
Funding
- National Institutes of Health [RO1HL085144, 5RO1TW05596]
- Fogarty International Center [5RO3TW008133]
- Interdisciplinary Obesity Center [RR20649]
- Center for Environmental Health and Susceptibility [ES10126, 7-2004-E]
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Chronic inflammation is a potentially important pathway through which psychosocial stressors increase risk for cardiovascular disease. However, prior research on stress and inflammation has been conducted almost exclusively in high income, industrialized populations with low levels of infectious disease. In this study we test the hypothesis that psychosocial stressors are associated with elevated concentrations of C-reactive protein (CRP) among young adults in the Philippines (n = 1622), who have grown up in an ecological and epidemiological setting that differs substantially from that of the US. In addition, we apply a developmental, ecological perspective to consider whether microbial and nutritional environments in infancy alter patterns of association between stressors and CRP. Data come from the Cebu Longitudinal Health and Nutrition Survey, a prospective cohort study that began collecting data in 1983-1984 when participants were in utero. A series of regression models indicate trends toward significant interactions between perceived stress and environmental factors in infancy, including exposure to animal feces, season of birth, and birth weight. Parental absence in childhood was a significant predictor of CRP in adulthood in interaction with exposure to animal feces in infancy. Positive associations between stressors and CRP were only evident for individuals with lower levels of microbial exposure in infancy, or lower birth weight. These results suggest that early environments influence the development of inflammatory phenotypes in ways that moderate sensitivity to psychosocial stressors in adulthood, and they underscore the value of a comparative, developmental approach to research on social environments, inflammation, and disease. (c) 2012 Elsevier Inc. All rights reserved.
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