Browsing by Author "Thomas, Jenna C."

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    Adverse childhood experiences and HPA axis function in pregnant women
    (Elsevier, 2018-05-28) Thomas, Jenna C.; Magel, Chantelle; Tomfohr-Madsen, Lianne; Madigan, Sheri L.; Letourneau, Nicole Lyn; Campbell, Tavis S.; Giesbrecht, G. F.; APrON Study Team
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    Biological embedding of perinatal social relationships in infant stress reactivity
    (Wiley, 2017-02-21) Thomas, Jenna C.; Letourneau, Nicole Lyn; Bryce, Crystal I.; Campbell, Tavis S.; Giesbrecht, G. F.; APrON Study Team
    Whereas significant advances have been made in understanding how exposure to early adversity "gets under the skin" of children to result in long-term changes in developmental outcomes, the processes by which positive social relationships become biologically-embedded remain poorly understood. The aim of this study was to understand the pathways by which maternal and infant social environments become biologically-embedded in infant cortisol reactivity. Two hundred seventy-two pregnant women and their infants were prospectively assessed during pregnancy and at 6 months postpartum. In serial mediation analyses, higher perceived social support from partners during pregnancy was associated with lower infant cortisol reactivity or larger decreases in cortisol in response to a stressor at 6 months of age via lower self-reported prenatal maternal depression and higher mother-infant interaction quality. The findings add to our understanding of how perinatal social relationships become biologically-embedded in child development.
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    Intergenerational transmission of adverse childhood experiences via maternal depression and anxiety and moderation by child sex
    (2018-07-23) Letourneau, Nicole Lyn; Dewey, Deborah; Kaplan, Bonnie J.; Ntanda, Henry N.; Novick, Jason; Thomas, Jenna C.; Deane, Andrea J.; Leung, Brenda My; Pon, Kylie; Giesbrecht, G. F.; APrON Study Team
    Adverse childhood experiences (ACEs) of parents are associated with a variety of negative health outcomes in offspring. Little is known about the mechanisms by which ACEs are transmitted to the next generation. Given that maternal depression and anxiety are related to ACEs and negatively affect children's behaviour, these exposures may be pathways between maternal ACEs and child psychopathology. Child sex may modify these associations. Our objectives were to determine: (1) the association between ACEs and children's behaviour, (2) whether maternal symptoms of prenatal and postnatal depression and anxiety mediate the relationship between maternal ACEs and children's behaviour, and (3) whether these relationships are moderated by child sex. Pearson correlations and latent path analyses were undertaken using data from 907 children and their mothers enrolled the Alberta Pregnancy Outcomes and Nutrition study. Overall, maternal ACEs were associated with symptoms of anxiety and depression during the perinatal period, and externalizing problems in children. Furthermore, we observed indirect associations between maternal ACEs and children's internalizing and externalizing problems via maternal anxiety and depression. Sex differences were observed, with boys demonstrating greater vulnerability to the indirect effects of maternal ACEs via both anxiety and depression. Findings suggest that maternal mental health may be a mechanism by which maternal early life adversity is transmitted to children, especially boys. Further research is needed to determine if targeted interventions with women who have both high ACEs and mental health problems can prevent or ameliorate the effects of ACEs on children's behavioural psychopathology.
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    Prenatal bisphenol a exposure and dysregulation of infant hypothalamic-pituitary-adrenal axis function: findings from the APrON cohort study
    (Springer Nature, 2017-05-19) Giesbrecht, G. F.; Ejaredar, Maede; Liu, Jiaying; Thomas, Jenna C.; Letourneau, Nicole Lyn; Campbell, Tavis S.; Martin, Jonathan W.; Dewey, Deborah; APrON Study Team
    Background: Animal models show that prenatal bisphenol A (BPA) exposure leads to sexually-dimorphic disruption of the neuroendocrine system in offspring, including the hypothalamic-pituitary-adrenal (HPA) neuroendocrine system, but human data are lacking. In humans, prenatal BPA exposure is associated with sex-specific behavioural problems in children, and HPA axis dysregulation may be a biological mechanism. The objective of the current study was to examine sex differences in associations between prenatal maternal urinary BPA concentration and HPA axis function in 3-month-old infants. Methods: Mother-infant pairs (n = 132) were part of the Alberta Pregnancy Outcomes and Nutrition study, a longitudinal birth cohort recruited (2010–2012) during pregnancy. Maternal spot urine samples collected during the 2nd trimester were analyzed for total BPA and creatinine. Infant saliva samples collected prior to and after a blood draw were analyzed for cortisol. Linear growth curve models were used to characterize changes in infant cortisol as a function of prenatal BPA exposure. Results: Higher maternal BPA was associated with increases in baseline cortisol among females (β = 0.13 log μg/dL; 95% CI: 0.01, 0.26), but decreases among males (β = −0.22 log μg/dL; 95% CI: -0.39, −0.05). In contrast, higher BPA was associated with increased reactivity in males (β = .30 log μg/dL; 95% CI: 0.04, 0.56) but decreased reactivity in females (β = −0.15 log μg/dL; 95% CI: -0.35, 0.05). Models adjusting for creatinine yielded similar results. Conclusions: Prenatal BPA exposure is associated with sex-specific changes in infant HPA axis function. The biological plausibility of these findings is supported by their consistency with evidence in rodent models. Furthermore, these data support the hypotheses that sexually dimorphic changes in children’s behaviour following prenatal BPA exposure are mediated by sexually-dimorphic changes in HPA axis function. Keywords: Bisphenol-A, Fetal exposure, Cortisol, Hypothalamic-pituitary-adrenal axis, Infant stress reactivity
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    Social buffering of the maternal and infant HPA axes: Mediation and moderation in the intergenerational transmission of adverse childhood experiences
    (Cambridge University Press, 2018-08-02) Thomas, Jenna C.; Letourneau, Nicole Lyn; Campbell, Tavis S.; Giesbrecht, G. F.; APrON Study Team
    Supportive social relationships can reduce both psychological and physiological responses to stressful experiences. Recently, studies have also assessed the potential for social relationships to buffer the intergenerational transmission of stress. The majority of these studies, however, have focussed on social learning as a mechanism responsible for the intergenerational transmission of stress. Evidence of biological mechanisms is lacking. The objective of the current study was, therefore, to determine whether the association between maternal adverse childhood experiences (ACEs) and infant hypothalamic-pituitary-adrenal (HPA) axis function is mediated by maternal HPA axis function during pregnancy and moderated by social support. Data were from 243 mother-infant dyads enrolled in a prospective longitudinal cohort (the Alberta Pregnancy Outcomes and Nutrition Study). Maternal history of ACEs was retrospectively assessed while maternal perceived social support and salivary cortisol were assessed prospectively at 6-22 weeks gestation (Time 1) and 27-37 weeks gestation (Time 2), and infant cortisol reactivity to a laboratory stressor and maternal perceived social support were assessed at 5-10 months postnatal (Time 3). Results revealed that maternal HPA axis function during pregnancy mediated the effects of maternal ACEs on infant HPA axis reactivity, suggesting that the maternal HPA axis is a mechanism by which maternal early life stress is transmitted to offspring. Furthermore, social support in the prenatal and postnatal periods moderated the cascade from maternal ACEs to infant HPA axis reactivity. Specifically, prenatal social support moderated the association between ACEs and maternal HPA axis function during pregnancy, and postnatal social support moderated the association between maternal HPA axis function and infant cortisol reactivity. These findings highlight the social sensitivity of the HPA axis and suggest the utility of social relationships as an intervention target to reduce the effects of maternal early life stress on infant outcomes.
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    The Intergenerational Transmission of Stress: Investigating Mediators and Moderators of the Association between Maternal Adverse Childhood Experiences and Child Development
    (2018-08-27) Thomas, Jenna C.; Giesbrecht, Gerald; Campbell, Tavis S.; Curtin, Suzanne; Noel, Melanie
    Objective: The intergenerational transmission of adverse childhood experiences (ACEs) has been observed, however the biological mechanisms underlying these associations have yet to be elucidated. Given the dearth of research examining prenatal biological mechanisms, the overall objective of this dissertation was to understand the role of the maternal hypothalamic-pituitary-adrenal (HPA) axis during pregnancy in transducing the effects of maternal ACEs to child developmental outcomes. A subsequent aim was to evaluate social support as a moderator that may buffer the intergenerational transmission of stress. Methods: Data were from 356 pregnant women and their children enrolled in the longitudinal Alberta Pregnancy Outcomes and Nutrition (APrON) study. Maternal HPA axis function was assessed via self-collected salivary cortisol samples collected over multiple days in early (6-22 weeks) and late (27-37 weeks) pregnancy. Maternal ACEs, mental health, and social support were assessed via self-report measures. At 6 months of age, infant HPA axis reactivity was assessed via salivary cortisol samples at baseline and 20 minutes after a standardized laboratory stressor. At 4 years, child behaviour problems were assessed via a standardized maternal report. Results: Maternal ACEs were associated with higher morning cortisol levels and a flattened diurnal slope, consistent with a pattern of cortisol hypersecretion. Maternal HPA axis alterations mediated the association between maternal ACEs and infant HPA axis reactivity to stress at 6 months. These mediated effects were moderated by social support indicating that social support may be a factor that buffers the intergenerational transmission of stress. Maternal ACEs were associated with higher child internalizing problems at 4 years of age, and there were multiple mediators of this association including maternal HPA axis function, prenatal depression, and gestational age at birth. Unexpectedly, the HPA axis pathway predicted lower child internalizing problems and may represent a biological resiliency pathway in an otherwise healthy low sociodemographic risk sample. Conclusions: These studies provide the first evidence that prenatal maternal HPA axis function is a biological mediator of the association between maternal ACEs and child outcomes, and offers some insights into potential avenues for preventing the intergenerational transmission of stress.