DeLTA Center Symposium

"The Effects of Stress on Development"

How does stress affect biological and behavioral development? Join us to hear Stacy Drury (Tulane University), Hanna Stevens (University of Iowa), Birdie Shirtcliff (Iowa State University), and Molly Nikolas (University of Iowa) discuss studies with animal models, infants and mothers, children, and adolescents.


Location

Lindquist Center, N300 on the University of Iowa Campus.
240 South Madison Street, Iowa City, Iowa 52240


Schedule

12:30 p.m.: Stacy Drury, MD, PhD (Tulane University)

Rethinking mom’s and the prenatal environment: Epigenetic evidence of transgenerational effects of maternal life course and prenatal stress from neighborhoods to telomeres

Abstract:

Stacy Drury

Maternal prenatal stress, broadly defined, has been implicated in a range of negative outcomes across the life course. Despite this recognition, efforts to both decrease prenatal stress as well as mitigate the negative effects on the offspring remain insufficient as is our understanding of the molecular mechanisms.  Biological markers of exposure that track on to the different factors in a mother’s life that lead to lasting effects on the infant have the potential to significantly increase our knowledge of this important contributor to long-term health and potential differences by race and sex.  This presentation will present data from the Infant Development Study, an NIH funded study to examine the impact of prenatal and maternal life course stress on infant development, physiology and molecular markers.  Leveraging this prospective study of over 400 mothers recruited prenatally and followed over the first years of infant life. Data will be presented linking maternal early life stress to infant telomere length, a marker of cellular aging and stress.  Additionally, we will present data linking maternal neighborhood level violence exposures to infant cortisol regulation and telomere length across the first year of life. Lastly we will present evidence of racial differences in cellular aging in the placenta and discuss the implications of this for the persistence of racial differences in preterm birth. Overall this presentation expects to present novel findings linking cellular aging and allostasis to both maternal life course and prenatal exposures and the implications of these findings for child health and development as well as health disparities.

1:45 p.m.: Hanna Stevens, MD, PhD (University of Iowa)

Prenatal Stress Effects on Developmental Processes in the Offspring Brain

Abstract:

Hanna StevensPrenatal stress is a known risk factor for neuropsychiatric disorders, including autism spectrum disorders (ASDs), ADHD, Tourette syndrome and schizophrenia.   However, the pathophysiology of these disorders and how early stress modification of brain development may influence this pathology is poorly understood. In particular, very little is known about the influence of prenatal stress on developmental processes of embryonic neural progenitors, particularly those for inhibitory neurons which are implicated in ASD, Tourette and schizophrenia. Here, we examined the effects of prenatal stress on embryonic neurodevelopment using a well-validated mouse model of repetitive daily physiological stress. We found multiple effects of prenatal stress on inhibitory neuron progenitors including delayed migration, increase in mitochondrial number, increased cellular proliferation and reduction in telomere length. Of interest, the latter two effects showed sexual specificity. We discuss the implications of these findings for understanding developmental psychopathology.

3:00 p.m.: Birdie Shirtcliff, PhD (Iowa State University)

Riding the Physiological Roller-Coaster: Why Life Stress Alters Stress Responsive Physiological Systems

Abstract:

Birdie ShirtcliffA popular vantage point of stress hormones or stress exposure emphasizes the deleterious consequences or problems of stress and, by extension, stress hormones like cortisol. This perspective is juxtaposed with a different view which emphasizes the adaptive nature of stress physiology. In order to understand stress regulation, and biomarkers like cortisol, it is important to understand why these biomarkers are released and what they function to accomplish within the individual.  High (or rising) cortisol has advantages and disadvantages that must be understood within a context to understand how individual differences unfold. A functional, dynamic, and context-dependent perspective helps advance understanding of how and why stress impacts physiological systems and shapes early development.

The proposed talk will discuss adaptive theories about stress and stress biomarkers, and then considers whether emerging data fits with such an adaptive view.  Future directions are then considered, including an exploration of new technology that will allow the context-specific role of stress hormones to be better appreciated.

4:15 p.m.: Molly Nikolas, PhD (University of Iowa)

Impact of Developmental Stressors on the Etiology and Course of Attention-Deficit Hyperactivity Disorder

Abstract:

Molly NikolasNeurobiological processes have been shown to make substantial contributions to the development of attention-deficit hyperactivity disorder (ADHD).  However, recent work has also emphasized the critical role of environmental stressors in shaping the developmental course of ADHD.  Further, stress may have a greater impact on psychopathology, including ADHD, at particular critical periods in development.  Here, I will describe a series of studies of youth and adults with ADHD that emphasize the role of stress and its interaction with neurobiological risk factors.  I will specifically focus on the effects of prenatal stress, stress related to the pubertal transition, and chronic family conflict on ADHD severity, developmental persistence, and neurocognitive functioning as well as potential genetic moderation of these effects.  I will also describe some preliminary work underway that aims to identify potential epigenetic targets of prenatal stress and their association with early risk factors for neurodevelopmental disorders.