Date of Award


Document Type


Degree Name


Organizational Unit

College of Arts Humanities and Social Sciences, Psychology

First Advisor

Sarah Watamura


Stress, Health, Cortisol, Child psychology


Early life stress is known to have an enduring impact on individuals’ health trajectories, however, some show greater resiliency to early life stress than others. The exploration of candidate genes and gene-environment interactions may be one promising window on risk versus resilience trajectories. However, prior work involving three polymorphisms (COMT Val158Met, MAOA-LPR, and 5-HTTLPR) has yielded well publicized but inconsistently replicated associations with mental health. Part of this inconsistency may be due to the limited exploration of mechanistic explanations for how these gene-environment interactions lead to variations in health. Thus, this dissertation examines gene-gene and gene-environment interactions in predicting basal cortisol at age eight (assayed from a single blood sample). Data for this project comes from 813 families participating in the Avon Longitudinal Study of Parents and Children (ALSPAC). Early environmental risk is characterized by three well-documented factors (maternal depression, maternal stress exposure, and child stress exposure) compiled across the developmentally salient 0-6 year age range. Contrary to expectation, genetic risk was not related to children’s basal cortisol in middle childhood, and neither were the tested gene-environment interactions. Most measures of environmental risk were also unrelated to children’s cortisol, however maternal stress exposure when the child was 48-61 months old was related to higher basal cortisol. Analyses and discussion describe patterns of environmental risk exposure across early childhood in an effort to better characterize risk trajectories in this sample. Although the current findings do not support HPA axis dysregulation as a mechanism by which gene-environment interactions impact health, methodological limitations likely contributed to these null findings. Future studies should continue to explore such mechanistic explanations in order to create effective interventions for children at high risk for stress related disease.

Publication Statement

Copyright is held by the author. This work may only be accessed by members of the University of Denver community. The work is provided by permission of the author for individual research purposes only and may not be further copied or distributed. User is responsible for all copyright compliance.

Rights Holder

Irena Y. Pikovsky


Received from author

File Format




File Size

104 pgs