Electronic Thesis and Dissertation Repository

Degree

Doctor of Philosophy

Program

Psychology

Supervisor

Dr. Elizabeth P. Hayden

Abstract

Purpose: Individual differences in early-emerging vulnerability to mood and anxiety disorders have been linked to genetic and environmental influences, with psychophysiological reactivity potentially mediating this vulnerability. However, research seeking to identify influences on the development of psychophysiological reactivity, such as the Hypothalamic-Adrenal-Pituitary (HPA) axis, is still in an early stage, with most studies focusing on individual risks, even though such vulnerability is likely etiologically complex. Disentangling the interplay of biology and context in shaping HPA axis responses to stress, indexed via salivary cortisol reactivity, may ultimately aid in the development and application of targeted prevention and early intervention programs. Method: This study examined whether key biological and contextual variables, including specific genes (5-HTTLPR and BDNF val66met), parent psychopathology, poor parenting, and life stress, were related to cortisol reactivity to psychosocial stress in 409 preschool-aged children. Parenting was assessed using questionnaires and observational ratings, and stress and parent psychopathology were assessed using structured interviews. Cortisol reactivity was indexed using both area under the curve and multi-level modelling. Results: Maternal depression interacted with poor parenting and chronic stress to predict child cortisol reactivity. Specifically, evidence was found for dysregulated cortisol reactivity in children with a maternal depression history who were exposed to life stress, including hyperreactivity in the context of chronic stress and hyporeactivity in the context of poor parenting. In contrast, the cortisol reactivity of children with no maternal depression history was unrelated to these environmental influences. However, the pattern of findings differed depending on the index of cortisol reactivity being examined (AUC versus MLM). Paternal depression had a stronger influence on baseline or trait-like cortisol relative to cortisol reactivity. Conclusion: Findings suggest that children with a history of maternal depression and exposure to early stress may be at the greatest risk for HPA dysregulation, and that this risk is manifested differently depending on which type of early stress is experienced. Findings highlight a potential mechanism, cortisol stress reactivity, through which familial depression risk and the early environment influence children’s vulnerability. Results also speak to the importance of methodological factors when examining cortisol reactivity to stress.

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