An Exploratory Study of Maternal Prenatal Stress, Immunogenetic Risk, and Pediatric Asthma: Identifying Temporal-and Sex-specific Associations Öffentlichkeit

Abstract

Pediatric asthma is among the most prevalent chronic illnesses in the world. Persisting prevalence rates and associated health burdens justify greater exploration of the genetic and environmental susceptibilities that may put some children at a heightened risk for future asthma development. The current study examined the role of psychological stress experienced by the mother during pregnancy in the development of asthma in offspring. Although prenatal stress and asthma associations have previously been found, the operationalization of prenatal stress is often inconsistent and warrants further study. The study aimed to explore potentially differential effects of objective versus subjective prenatal stress on asthma outcomes. In addition, it explored the moderation effects of biological sex and genetic risk on the relationships between prenatal stress exposure and asthma outcomes. The investigation utilized the archival data of the longitudinal Mater Misericordiae Mothers’ Hospital-University of Queensland Study of Pregnancy (MUSP). Participants were 444 Australian young adults, ages 22–25 years, drawn from the MUSP birth cohort of 7,775 children for a genetic sub-study. Maternal prenatal stress was measured both during pregnancy and 3 to 5 days after birth, operationalized as objective life events and subjective stress. Asthma was measured using a maternal report at youth ages 5 and 15 years. Hypotheses were tested using logistic regression models. Results showed maternal reports of objective stressful events in the last six months of pregnancy were correlated with elevated asthma risk in offspring at age 5 years. Biological sex was found to moderate the association between maternal prenatal reports of subjective stress and offspring asthma at age 15 years. Specifically, and in line with our hypotheses, prenatal stress predicted post puberty asthma in girls, but not boys. Our genetic analyses resulted in unexpected findings, detecting a possible protective effect of the IL1β-511 TT genotype in the context of maternal objective stress during pregnancy and offspring asthma at age 15 years. Together, these results reinforce the importance of timing, perception and experience in the prenatal stress-asthma connection. Future directions and clinical implications are discussed.

Keywords: asthma, maternal prenatal stress, objective stressful life events, genotype, inflammation, biological sex.

Table of Contents

Table of Contents

 

Introduction………………………………………………………………………………………..1

            Prenatal Stress and Pediatric Asthma Risk…………………………………….....2

            A Model of Moderation………………………………………………………………...3

            Biological Sex and Asthma Risk: The Puberty “Switch”……………………….3

Biological Sex, Prenatal Stress and Asthma Risk……………………………………......4

The Genetics of Asthma………………………………………………………………......…...6

Prenatal Stress, IL6-174G>C, TNF-308G>A and IL1β-511C>T and Asthma

Development…………………………………………………………………………..…..........8

The Current Study……………………………………………………………..……...…..…...9

Method……………………………………………………………………………………….…...10

            Participants……………………………………………………………………………..10

            Procedure…………………………………………………………………………….....11

                        Prenatal Stress Measures…………………………………………………...12

                        Asthma………………………………………………………………………..…13

                        Immunogenetic Measures …………………………………………….……13

                        Potential Confounds………………………………………………………....14

            Data Analytic Plan……………………………………………………………………..14

Results…………………………………………………………………………………………..…15

            Preliminary Analysis…………………………………………………………………..15

                        Covariates…………………………………………………………………..…...15

                        Prenatal Stress and Asthma..……………………………………………….16 

            Biological Sex as a Moderator……………………………………………………….16

            Immunogenetic Moderation…………………………………………………………16

Discussion………………………………………………………………………………………...17 

            Limitations and Strengths…………………………………………………………...20

Future Directions……………….......…………………………………………………....…...21

Conclusion……………………………………………………………………………..........….22

References………………………………………………………………………………………..24

Tables and Figures………….…………………………………………………...……………..31

About this Honors Thesis

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School	Emory College
Department	Psychology
Degree	B.A.
Submission	Honors Thesis
Language	English
Research Field	Psychology, Developmental Psychology, Clinical Health Sciences, Immunology
Stichwort	Australia IL6-174 IL1β-511 longitudinal disease mothers biological sex immunogenetics prenatal risk puberty stressful life events TNF-308 genotype inflammation Asthma stress development
Committee Chair / Thesis Advisor	Patricia Brennan, Emory University
Committee Members	Vernon Robbins, Emory University Andrew Kazama , Emory University

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