Please note Dr. Davis is interested in taking students for Fall 2017
Areas of expertise/research interests
- The early/developmental origins of health and disease
- Stress and stress hormones during pregnancy, infancy and childhood
- Fetal, infant, child and adolescent brain development
- Individual differences in development of HPA axis regulation
- The influence of stress and stress hormones on brain development
- Sex differences in vulnerability to early life stress
Current Research and Projects
The multidisciplinary research that is conducted in my lab examines biological and social/behavioral processes in human pregnancy and in fetal, infant and child development. This research addresses a major health issue involving the role of early experiences in determining the risk for health and disease across the lifespan. Specifically, my program of research evaluates the way that prenatal exposure to maternal psychosocial stress and stress hormones is incorporated into the developmental program and the influence this has on adaptation to the postnatal world. I have used two complementary approaches to evaluate the influence of prenatal stress and stress hormones for development. The first approach evaluates the effects of prenatal exposure to synthetic glucocorticoids and the second identifies the consequences of natural variations in maternal psychosocial stress and stress hormones. These projects, supported by grants from NICHD and NIMH, investigate the role that fetal exposure to stress and stress hormones play in programming individual differences in stress and emotional regulation, cognitive functioning and brain development.
Fragmented Early Life Environment Influences Emotional and Cognitive Vulnerabilities during Childhood and Adolescence
Mental disorders affect 15 to 20% of the US population, primarily originate early in life, have a peak onset of disease during adolescence, and vulnerabilities are sex dependent. This project is part of a NIMH Silvio O. Conte Center(P50 MH 096889) and will test specific hypotheses about how prenatal and early postnatal maternal signals, experienced during transitional periods of rapid changes in brain and behavior, determine risk for cognitive and emotional vulnerabilities to mental illness. The long term consequences of exposure to fragmented maternal signals during fetal and early postnatal life will be tested with a prospective longitudinal investigation of two cohorts followed from early in gestation and assessed during infancy/toddlerhood and childhood/adolescence.
Prenatal Influences on Child Brain Development
Rapid changes in the developing fetal brain render it vulnerable to both organizing and disorganizing influences. Current research evaluates the consequences of prenatal influences such as synthetic glucocorticoids exposure, maternal stress, and maternal infection for child brain development (evaluated with structural MRI, fMRI and DTI). We have recently published in Biological Psychiatry evidence that fetal exposure to synthetic glucocorticoids has neurologic consequences that persist for at least 6 to 10 years. Children with fetal glucocorticoid exposure have a thinner cortex primarily in the rostral anterior cingulate (rACC). Consistent with the possibility that these neurologic changes may indicate prodromal risk for mental health problems, we show that a thinner rACC predicts increased child affective problems.
Prenatal Exposure to Maternal Stress and Stress Hormones Influences Infant and Child Development
These projects evaluate the impact of naturally occurring individual variations in prenatal maternal psychosocial stress and stress hormones exposures on fetal, infant and child development. Prospective evaluations of pregnant women and their infants and children determine the influence of prenatal stress exposures on cognitive functioning, temperament and stress regulation. Our data consistently demonstrate that children exposed to higher levels of stress hormones during gestation have heightened HPA axis reactivity, fearful temperament during infancy and anxiety during childhood. Recently we have published in PNAS evidence fetal programming of child affective problems may be mediated through effects of maternal cortisol on the development of the amygdala.
The Synergistic Relation between the Prenatal and the Early Postnatal Environment
Several ongoing projects include the evaluation of the joint role of the prenatal and the early postnatal environment in the determination of child health and development. These data will address important questions such as: "Can high quality maternal care ameliorate the negative effects of prenatal stress?" and "Does the prenatal environment prepare the infant for functioning in the postnatal world?"
Prenatal Exposure to Glucocorticoids has Persisting Consequences for Development
This 5-year longitudinal study, supported by NICHD (R01 HD065823), is designed to identify individuals who are vulnerable to glucocorticoid treatment, a standard of care for women in preterm labor. This prospective longitudinal study involves evaluation of changes in stress and reproductive hormones in response to glucocorticoid treatment during the prenatal period, birth outcome and infant development.
Preconception and Prenatal Influences on Child Development
This project supported by NICHD (R01 HD72021) is a unique investigation of the role of maternal stress prior to pregnancy on both prenatal outcomes and infant and child development. This multi-site collaborative project involves collaborations with researchers at University of Denver, University of California, Los Angeles, North Western, and Virginia Technical Institute.
PhD, University of Minnesota, 2002
BA, Vassar College, 1996
- Davis, E.P. & Sandman, C.A. (2010). The timing of prenatal exposure to maternal cortisol and psychosocial stress is associated with human infant cognitive development. Child Development, 81 (1), 131-138.
- Davis, E.P., Glynn, L.M., Waffarn, F. & Sandman, C.A. (2011). Prenatal maternal stress programs infant stress regulation. Journal of Child Psychology and Psychiatry, 52(2), 119-129.
- Davis, E.P., Waffarn, F. & Sandman, C.A. (2011). Prenatal exposure to synthetic glucocorticoids impairs stress regulation among healthy full term infants. Developmental Psychobiology, 53(2), 175-183.
- Davis, E.P., Buss, C., Muftuler, T., Head, K., Hasso, A. Wing, D.A., Hobel, C. & Sandman, C.A. (2011). Children's brain development benefits from longer gestation. Frontiers in Psychology. 2, 1-7.
- Muftuler, L.T., Davis, E.P., Buss, C., Head, K., Hasso, A. & Sandman, C.A. (2011). Cortical and subcortical changes in typically developing preadolescent children. Brain Research, 1399, 15-24.
- Hatfield, T.*, Wing, D.A., Buss, C., Muftuler, L.T., Head, K. & Davis, E.P. (2011). Magnetic resonance imaging demonstrates long term changes in brain structure in children born preterm and exposed to chorioamnionitis. American Journal of Obstetrics & Gynecology. 205(4): 384 e1-384 e8.
- Sandman, C.A., Davis E.P., & Glynn, L.M. (2011). Prescient human fetuses thrive. Psychological Science. 23(1): 93-100. PMID: 22173740.
- Davis, E.P. & Sandman, C.A. (2012). Exposure to prenatal maternal psychobiological stress increases anxiety in preadolescent children. Psychoneuroendocrinology. PMID: 22265195
- Baram, T.Z., Davis, E.P., Obenaus, A., Sandman, C.A., Small, S., Solodkin, A., Stern, H. (2012). Fragmentation and unpredictability of early-life experience in mental disorders. American Journal of Psychiatry. PMID: 22885631
- Buss, C.*, Davis, E.P., Shahbaba, B., Pruessner, J.C., Head, K. & Sandman, C.A. (2012). Maternal cortisol over the course of pregnancy and subsequent child amygdala and hippocampus volumes and affective problems. Proceedings of the National Academy of Sciences.
- Muftuler, L.T., Davis, E.P., Buss, C., Solodkin, L., Su, M. Y., Head, K., Hasso, A. & Sandman, C.A. (2012). Development of white matter pathways in typically developing preadolescent children. Brain Research 1399: 15-24. PMID: 22634375
- Davis, E.P., Sandman, C.A., Buss, C., Wing, D.A., & Head, K. (2013). Fetal glucocorticoid exposure is associated with preadolescent brain development . Biological Psychiatry.