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Elysia Davis

Dr. Davis is interested in taking a new graduate student for Fall 2020. She will review applications from students applying to either Affective/Social/Cognitive, Clinical, or Developmental Psychology programs.

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

Our lab evaluates the way that biological and behavioral processes during the prenatal period are incorporated into the developmental program and the influence this has on adaptation to the postnatal environment. Specifically, our lab focuses on understanding the influence of prenatal exposure to signals of stress on fetal development, birth outcome, and subsequent child and adult health and disease risk, and on the role of maternal-placental-fetal neuroendocrine processes as mediators. Our NIH funded research program has contributed to an important shift in our understanding of the role of the prenatal environment in fetal neurodevelopment and the ensuing consequences for child mental health.

Reducing Fetal Exposure to Maternal Depression to Improve Infant Risk Mechanisms (R01 MH 109662)
Mood and anxiety disorders are a significant public health concern, as over 25% of Americans will experience a disorder in their lifetimes, and anxiety and depression are associated with substantial impairments in social, occupational, and educational functioning. Maternal history of depression is a well-established and profound risk factor for later child development of anxiety and depression, and new evidence suggests that prenatal maternal depressive symptoms have a larger consequence for child outcomes as compared to postpartum depressive symptoms. This project would have clear relevance and impact to affect this significant mental health problem by determining whether reducing prenatal maternal depressive symptoms affects the development of infant mechanisms that contribute to risk for psychopathology later in life. This knowledge would provide clear translational impact on when, where, and how to intervene, as well as identify infant risk mechanisms that could become the targets for later intervention development among at-risk offspring.

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 tests 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 are 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 evidence that fetal exposure to cortisol has persisting influences on children's brain development. For example, 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 evidence that 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.


PhD, University of Minnesota, 2002
BA, Vassar College, 1996

Selected Publications

  • 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, 74(9), 647-55. PMID: 23611262
  • Sandman, C.A., Glynn, L.M. & Davis, E.P. (2013). Is there a viability vulnerability trade off? Sex differences in fetal programming. Journal of Psychosomatic Research, 75(4), 327-335. PMID: 24119938
  • Davis, E.P. & Pfaff, D. (2014). Sexually dimorphic responses to early adversity: implications for affective problems and autism spectrum disorder. Psychoneuroendocrinology, 49, 11-25. PMID: 25038479
  • Stout, S.A., Espel, E., Sandman, C.A., Glynn, L.M. & Davis, E.P. (2015). Fetal programming of children's obesity risk. Psychoneuroendocrinology, 53, 29-39. PMID: 25591114
  • Sandman, C.A., Buss, C., Head, K & Davis, E.P. (2015). Fetal exposure to maternal depressive symptoms is associated with cortical thickness in late childhood. Biological Psychiatry, 77(4), 324-34. PMID: 25129235
  • Grant, K.A., Sandman, C.A. Wing, D.A., Dmitrieva, J. & Davis, E.P. (2015). Prenatal programming of postnatal susceptibility to memory impairments: A developmental double jeopardy. Psychological Science, 26(7), 1054-62. PMID: 26063439.
  • Kim, D.J., Davis, E.P., Sandman, C.A., Sporns, O., O'Donnell, B.F., Hetrick, W.P. (2015). Children's intellectual ability is associated with structural network integrity. NeuroImage, 550-6. PMID: 26385010
  • Howland, M., Sandman, C.A., Glynn, LM, Crippen, C. & Davis, E.P. (2016). Fetal exposure to placental corticotropin-releasing hormone is associated with child self-reported internalizing symptoms, Psychoneuroendocrinology, 10-17. PMID: 26855003
  • Edelmann, M., Sandman, C.A., Glynn, LM, Wing, D.A., & Davis, E.P. (2016). Antenatal glucocorticoid treatment is associated with diurnal cortisol regulation in term-born children. Psychoneuroendocrinology, 72, 106-112.
  • Kim, D.J.*, Davis, E.P., Sandman, C.A., Sporns, O., O'Donnell, B.F., Hetrick, W.P. (2016). Prenatal maternal cortisol has sex specific associations with child brain network properties. Cortex, 1-12.
  • Davis, E.P., Buss, C., Head, K. & Sandman, C.A. (2017). Prenatal maternal cortisol concentrations predict neurodevelopment in middle childhood. Psychoneuroendocrinology 75, 56-73.
  • Vohr, B., Davis, E.P., Wanke, C.A, & Krebs, N.F. (2017). Neurodevelopment: The impact of nutrition and inflammation during preconception and pregnancy in low resource settings. JAMA Pediatrics, 139, 1, 38-49.
  • Snyder, H., Hankin, B.L., Sandman, C.A., Head, K. & Davis, E.P. (2017). Distinct patterns of reduced prefrontal and limbic grey matter volume in childhood general and internalizing psychopathology. Clinical Psychological Science.
  • Curran, MM, Sandman, C.A., Davis, E.P., Glynn, L.M., & Baram, T.Z. (2017). Abnormal dendritic maturation of developing cortical neurons exposed to corticotropin releasing hormone (CRH): insights into effects of prenatal adversity? PlosOne.
  • Davis, E.P., Stout, S.A., Molet, J., Vegetabile, B, Glynn, L.M., Sandman, C.A., Hein, K., Stern, H., Baram, T.Z. (in press). Exposure to unpredictable maternal sensory signals influences cognitive development across-species. Proceedings of the National Academy of Sciences.