Abstract
Exposure to social adversity has been associated with cortisol dysregulation during pregnancy and in later childhood; less is known about how prenatal exposure to social stressors affects postnatal cortisol of infants. In a secondary analysis of data from a longitudinal study, we tested whether a pregnant woman’s reports of social adversity during the third trimester were associated with their infant’s resting cortisol at 1, 6, and 12 months postnatal. Our hypothesis was that prenatal exposure to social adversity would be associated with elevation of infants’ cortisol. Measures included prenatal survey reports of social stressors and economic hardship, and resting cortisol levels determined from infant saliva samples acquired at each postnatal timepoint. Data were analyzed using linear mixed effects models. The final sample included 189 women and their infants (46.56% assigned female sex at birth). Prenatal economic hardship was significantly associated with infant cortisol at 6 months postnatal; reports of social stressors were not significantly associated with cortisol at any time point. Factors associated with hardship, such as psychological distress or nutritional deficiencies, may alter fetal HPA axis development, resulting in elevated infant cortisol levels. Developmental changes unique to 6 months of age may explain effects at this timepoint. More work is needed to better comprehend the complex pre- and post-natal physiologic and behavioral factors that affect infant HPA axis development and function, and the modifying role of environmental exposures.
Acknowledgments
We would like to acknowledge the contributions of other members of our research team, Sandra Niemann and Nina Ahlers, as well as the original study participants without whom this work would not have been possible.
Disclosure statement
The authors have no conflicts of interest to declare that are relevant to the content of this article. The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; or decision to submit the manuscript for publication.
Availability of data and material
Data used in this study are available on reasonable request.
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Notes on contributors
Victoria F. Keeton
Victoria F. Keeton is Assistant Professor of Research at the University of California, Davis School of Nursing. Her research focuses on stress as a physiologic contributor to metabolic disease and emotional dysregulation in children who experience social adversity.
Thomas J. Hoffmann
Thomas J. Hoffmann is Professor of Epidemiology and Biostatistics at the University of California, San Francisco. His applied work in statistics and computer science encompasses a wide variety of genetic association studies related to human health.
Kalisha Moneé Goodwin
Kalisha Moneé Goodwin is an independent community research consultant focused on supporting birth equity and justice for women and birthing people of color.
Bree Powell
Bree Powell is an independent community research consultant focused on supporting birth equity and justice for women and birthing people of color.
Sophia Tupuola
Sophia Tupuola is an independent community research consultant focused on supporting birth equity and justice for women and birthing people of color.
Sandra J. Weiss
Sandra J. Weiss is Professor and Robert C. and Delphine Wentland Eschbach Chair in Mental Health at the University of California, San Francisco, School of Nursing, and Director of the Weiss Stress and Depression lab. She investigates neuroendocrine and other physiologic vulnerabilities and interactions with adverse events during pregnancy and infancy.