Trial Lecture – time and place
See Trial Lecture.
Adjudication committee
- First opponent: Assistant Professor Bizu Gelaye, Harvard T.H. Chan School of Public Health, USA
- Second opponent: Deputy Director Siri Eldevik Håberg, Centre for Fertility and Health, Norwegian Institute of Public Health
- Third member and chair of the evaluation committee: Professor Randi Ulberg, Faculty of Medicine, University of Oslo
Chair of the Defence
Professor II Trond H. Diseth, Faculty of Medicine, University of Oslo
Principal Supervisor
Professor Einar Røshol Heiervang, Faculty of Medicine, University of Oslo
Summary
Early-life stress has been shown to affect an infant’s long-term development, but the underlying biological mechanisms have not yet been fully understood. One current hypothesis is that prenatal maternal stress influences an infant’s epigenetic marks. Prenatal maternal stressors can be investigated either through psychological or biological maternal measurements. Data from the Little in Norway study was used to investigate associations between prenatal maternal stress and infant DNA methylation.
Discussions on the different forms of early-life stress led to the primary study of the associations between maternal biological stress and psychological stress. This was performed by studying associations between maternal hair cortisol concentrations and self-reported symptoms of depression during pregnancy. In this study, no associations were detected. The results did not fully clarify what measure of maternal stress must be used for the epigenetic analyses, thereby resulting in the two studies of associations between biological or psychological prenatal maternal stress and infant DNA methylation.
The biological study investigated the associations between maternal prenatal hair cortisol concentrations and infant HPA axis gene DNA methylation. No associations were found, but the study showed homogeneous DNA methylation patterns for all HPA genes studied. The psychological study investigated maternal prenatal depressive symptoms and infant genome-wide DNA methylation at 6 and 52 weeks. No associations were found.
The negative associations between maternal prenatal depressive symptoms and infant DNA methylation between 6 and 52 weeks led to the investigation of whether there are any changes in infant DNA methylation during this period at all. This study found clear differences between the two time points, and on further analyses significant changes in DNA methylation were found in 42 genes. As infants experience rapid development during the first year of life, the expectation was that the DNA methylation results would show changes indicating increased gene expression. However, the changes indicated decreased expression. These findings suggest that the changes in DNA methylation may represent a decelerating mechanism after the rapid development in fetal life.
In summary, this study did not find associations between maternal prenatal stress and infant DNA methylation. However, it found an unexpected increase in infant DNA methylation during the first year of life, possibly indicating a biological decelerating mechanism.
Additional information
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