Impact of Maternal Trauma-Related Psychopathology and Life Stress on HPA Axis Stress Response

• In Event: Risk and Protective Factors in the Regulation of Maternal and Infant Cortisol

Abstract

Introduction: To better understand and curb the intergenerational transmission of stress-related disorder, it is important to identify how trauma-related psychopathology in mothers impacts their psychophysiological stress regulation, particularly in the context of parenting their own infants. Research on the association between trauma-related psychopathology and hypothalamic-pituitary-adrenal (HPA) axis function has revealed mixed findings for hypo- vs. hyperresponsiveness (Brand et al., 2009; Juul et al., 2016; Maes et al., 1998). Additionally, it is unknown whether trauma symptoms and/or diagnoses moderate the effect of background life stress on acute HPA axis stress responding, especially in the face of a personally salient stressor such as a parenting interaction.
Hypotheses: In this study we investigated relations of mothers’ trauma-related psychopathology (i.e., PTSD or trauma symptoms) and life stress with HPA axis responding to a personally relevant stressor (infant separation stress) in a non-clinical sample followed longitudinally over the first year and a half postpartum. We hypothesized that trauma-related psychopathology would predict blunted maternal cortisol responding to infant stress, either as a main effect and/or as a moderator dampening the effects of life stress across the postpartum.
Sample and Methods: Hypotheses were tested in a community sample of low-income mothers (n=73) and their infants who completed laboratory sessions at 3, 6, 12, and 18 months postnatal. At the 6-, 12-, and 18-month sessions mothers completed dyadic stress tasks with their infants, and HPA function was assessed with four salivary cortisol samples collected before and after the stress task. Mothers completed the Structured Clinical Interview for DSM-IV (SCID) at the initial (3-month) visit and self-reported their trauma-related symptoms (TSC-40) and life stress (PERI Life Events Scale) at each time. A three-level hierarchical linear model of repeated cortisol measures nested within sessions within dyads was used to test predicted associations between maternal psychopathology (PTSD diagnosis, mean TSC symptoms) and life stress (mean life events) and cortisol response trajectories.
Results: Model results revealed nonsignificant main effects of trauma-related psychopathology on maternal cortisol responding, but there was evidence that both a diagnosis of PTSD and ongoing trauma symptoms blunted effects of life stress on cortisol reactivity. Region of significance analyses indicated that life stress predicted more pronounced cortisol reactivity only among mothers who did not show trauma-related psychopathology (PTSD, elevated symptoms); for those with trauma-related psychopathology, life stress was unrelated to cortisol responding. These effects held when controlling for childhood trauma and previous (prenatal) maternal symptoms, suggesting they did not reflect ongoing impacts of past trauma exposure and/or psychopathology.
Conclusions: The above findings suggest that mothers experiencing harmful impacts of trauma tend to shut down psychophysiological reactivity to normal postpartum stressors. While this may represent a self-protective response, it may also prevent effective behavioral responding to infant needs during a critical developmental period. Implications for the transmission of stress sensitivities and mental health from parent to child will be discussed.

Authors

• Dawn L. Ramdas-Neal, University of Illinois at Urbana-Champaign
  Presenting Author

• Marissa D. Sbrilli, University of Illinois at Urbana-Champaign
  Non-Presenting Author

• Heidemarie Laurent, Pennsylvania State University, University Park
  Non-Presenting Author