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Panel information
Panel 3. Biological Processes: Psychophysiology

Paper #1
Psychophysiological stress and postpartum bonding among mothers and fathers during the transition to parenthood
Author information	Role
Gabriella Vavala, University of Southern California, United States	Presenting author
Gabriel A. León, University of Southern California, United States	Non-presenting author
Darby E. Saxbe, University of Southern California, United States	Non-presenting author
Abstract
Background The transition to parenthood is a major life event that may introduce mixed emotions, including the stress associated with becoming a first-time parent. Prior studies suggest that heightened parental stress may impair bonding with the infant (Hruschak, Palopoli, Thomason, & Trentacosta, 2022). Although the field has used both psychological and physiological measures to capture stress, these measures do not always track with each other or with parenting experiences. In the present study, we sought to evaluate the relationship between (1) psychological measures of stress and postpartum bonding and (2) physiological measures of stress and postpartum bonding. Additionally, we assessed whether these associations differ for mothers and fathers. Methods We leveraged data from first-time parents (mothers; n=57, fathers; n=57) who participated in the Hormones Across the Transition to Childrearing (HATCH) Study. For psychological measures of stress, we examined the Perceived Stress Scale-14 (PSS-14) and the Parenting Stress Index-Short Form (PSI-SF) collected at six months postpartum. The PSS-14 is an instrument used to assess general stress experienced over the past month (Cohen, Kamarck, & Mermelstein, 1983), whereas the PSI-SF assesses stressors specific to parenting (Abidin, 2012). For physiological measures of stress, we examined hair and salivary cortisol collected at six months postpartum. Our two measures for salivary cortisol were the area under the curve with respect to ground (AUCG) and the area under the curve with respect to increase (AUCI) (Pruessner et al., 2003). We utilized the Postpartum Bonding Questionnaire (PBQ) to measure problems with bonding (Wilhelm et al., 2005) at twelve months postpartum. Multiple regression was used to test associations between psychological and physiological stress and postpartum bonding. Covariates included parental maternal age, level of education, and experiences of early life adversity. We ran separate models for mothers and fathers to explore potential parenting role differences. Results In both mothers and fathers, perceived stress and parenting stress measured at six months postpartum predicted bonding problems at 12 months postpartum (see Table 1). We did not find a significant association between physiological measures of stress and bonding problems among fathers. However, maternal cortisol AUCI (p=0.03) negatively predicted mothers’ reports of bonding issues at 12-months postpartum (Est. = -.41, p = .03). Conclusions Psychological measures of both general and parenting-specific stress reported at six months postpartum predicted bonding problems with the infant at twelve months postpartum among both mothers and fathers. Salivary cortisol AUCi also predicted bonding problems among mothers, but not fathers. Overall, our findings suggest that psychological stress is a better predictor of postpartum bonding problems than cortisol-based measures of biological stress. Future studies should continue to compare measures of stress for biological and psychological outcomes across different populations.

Paper #2
Maternal perinatal cortisol trajectories and infant temperament at 12 months postpartum
Author information	Role
Gabrielle Rose Rinne, University of California - Los Angeles, United States	Presenting author
Kharah Ross, Athabasca University, Canada	Non-presenting author
Christine Dunkel Schetter, University of California - Los Angeles, United States	Non-presenting author
Abstract
Background: Decades of evidence within the Developmental Origins of Health and Disease model demonstrates that the prenatal and early postnatal environment shapes lifespan mental and physical health. The perinatal environment is theorized to influence long-term offspring developmental trajectories partly through variations in maternal neuroendocrine markers, such as cortisol. However, empirical evidence on the associations between maternal perinatal cortisol and offspring outcomes is mixed. Given that maternal diurnal cortisol patterns substantially change across the perinatal period, research on the associations of maternal cortisol trajectories may help to elucidate how maternal neuroendocrine markers shape offspring development. The present study (1) characterizes within-person diurnal cortisol trajectories across the perinatal period and (2) tests associations of perinatal cortisol trajectories with infant temperament. Methods: The present sample includes 196 mother-infant dyads enrolled in a prospective longitudinal study. Study visits occurred during early, mid, and late pregnancy and one, six, and 12 months after birth. Mothers provided saliva samples collected at waking, 30 minutes after waking, at noon, and in the evening over two days that were assayed for cortisol. We calculated the cortisol awakening response (CAR), diurnal slope, and total cortisol output for each study visit using standard approaches. Mothers reported on infant temperament at 12 months of age using the Infant Behavior Questionnaire-Revised, yielding scores for infant effortful control, negative emotionality, and surgency. We used piecewise growth curve models to model maternal perinatal cortisol trajectories and multiple regression to examine associations of cortisol trajectories with infant effortful control, negative emotionality, and surgency, adjusting for household income, infant biological sex, and length of gestation. Results: There were significant changes in total cortisol output and CAR throughout the perinatal period. The cortisol awakening response significantly increased (B=0.09, SE=0.04, p=.049) from early to late pregnancy whereas cortisol output significantly decreased from one to 12 months postpartum (B=-0.29, SE=0.07, p<.001). Regarding associations of within-person cortisol trajectories with infant temperament, infants of mothers with less of a decline in total cortisol output from one to 12 months postpartum were significantly lower in effortful control. However, this association was not significant when adjusting for covariates. In adjusted models, infants of mothers who had greater increases in CAR from early to late pregnancy were significantly lower in negative emotionality (B=-2.14, SE=1.12, p=.048). Additionally, infants of mothers whose cortisol slopes become flatter from early to late pregnancy were lower in surgency (B=-1.09, SE=0.64, p=.088). Conclusions: Changes in maternal neuroendocrine function across the perinatal period are theorized to be essential to maternal and child health, yet few studies have tested how these changes relate to infant outcomes. The present findings corroborate existing evidence demonstrating that CAR increases throughout pregnancy and that cortisol output decreases after birth. Of note, these results extend prior work by showing that within-person changes in cortisol during pregnancy are associated with infant temperament, a critical transdiagnostic indicator of long-term functioning. Overall, these findings highlight the importance of examining the implications of dynamic changes in maternal neuroendocrine markers for maternal-infant health in future research.

Paper #3
Testing Associations Between Placental Corticotropin Releasing Hormone and Children’s Age 8 Internalizing Outcomes
Author information	Role
Dr. Alexandra Sullivan, Ph.D., Department of Psychiatry and Behavioral Sciences, Center for Health and Community, Weill Neurosciences Institute, University of California, San Francisco, United States	Presenting author
Emily S. Barrett, Department of Biostatistics and Epidemiology, Rutgers School of Public Health; Environmental and Occupational Health Sciences Institute, Rutgers University, United States	Non-presenting author
Alexis Sullivan, Department of Psychiatry and Behavioral Sciences, Center for Health and Community, Weill Neurosciences Institute, University of California, San Francisco, United States	Non-presenting author
Michael Coccia, Department of Psychiatry and Behavioral Sciences, Center for Health and Community, Weill Neurosciences Institute, University of California, San Francisco, United States	Non-presenting author
Amanda Noroña-Zhou, Department of Psychiatry and Behavioral Sciences, Center for Health and Community, Weill Neurosciences Institute, University of California, San Francisco, United States	Non-presenting author
Brent Collett, Department of Psychiatry & Behavioral Sciences, University of Washington, Seattle Children’s Research Institute, Seattle, WA, USA, United States	Non-presenting author
Karen Derefinko, Department of Preventive Medicine, University of Tennessee Health Science Center, United States	Non-presenting author
Danielle Roubinov, Department of Psychiatry and Behavioral Sciences, Center for Health and Community, Weill Neurosciences Institute, University of California, San Francisco ; Department of Psychiatry, University of North Carolina at Chapel Hill, United States	Non-presenting author
Kecia Carroll, Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA, United States	Non-presenting author
Ruby Nguyen, Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, MN, USA, United States	Non-presenting author
Roger Smith, Mothers and Babies Research Centre, Hunter Medical Research Institute, Newcastle, NSW, Australia, Australia	Non-presenting author
Qi Zhao, Department of Preventive Medicine, University of Tennessee Health Science Center, United States	Non-presenting author
Kaja Z. LeWinn, Department of Psychiatry and Behavioral Sciences, Center for Health and Community, Weill Neurosciences Institute, University of California, San Francisco, United States	Non-presenting author
Nicole R. Bush, Department of Psychiatry and Behavioral Sciences, Center for Health and Community, Weill Neurosciences Institute, University of California, San Francisco; Department of Pediatrics, Division of Developmental Medicine, UCSF , United States	Non-presenting author
Abstract
Background Placental corticotropin-releasing hormone (pCRH) is a peptide that is essential in fetal neural development and birth timing. Prenatal programming research identifies pCRH as a key maternal neuroendocrine mechanism in the intergenerational transmission of stress, contributing to increased risk of offspring internalizing problems, though empirical evidence is sparse. We investigated associations between pCRH rate of rise during pregnancy and cumulative level of exposure at delivery with multi-informant indicators of offspring internalizing psychopathology during middle childhood. Aligned with literature on sexual dimorphism in pCRH associations with offspring psychiatric outcomes, we also conducted exploratory analyses to assess whether fetal sex moderated the associations tested. Methods We used data from racially and socioeconomically diverse mother-child dyads (n = 838) who were followed prospectively from pregnancy as a part of the Conditions Affecting Neurocognitive Development and Learning in Early Childhood study. We estimated pCRH rate of rise during the 2nd and 3rd trimesters of pregnancy and estimated level of exposure at delivery using circulating maternal pCRH from maternal blood plasma and used the R nlme to fit a linear mixed-effects model of log(pCRH) by gestational age, with random intercept and slope for each participant. Random slopes were used to capture between-person variability in pCRH rate of rise across pregnancy. We then used this model to predict log(pCRH) levels on the date of birth for each participant. Child internalizing psychopathology at age eight was measured using multiple well-validated methods: maternal reports of internalizing problems (CBCL), child self-reported depression (CDI-2) and anxiety (SCARED) symptoms, and three task-based indicators of threat sensitivity using the dotprobe task. We used covariate-adjusted multiple regression models to estimate associations between pCRH and offspring outcomes and whether fetal sex modified associations. Results Neither pCRH rate of rise nor cumulative exposure were associated with any of the six multi-method, multi-informant child outcomes tested (see Tables 1 and 2), including child self-reported depression and anxiety, mother-reported internalizing problems, and three indices of task-based threat sensitivity from the dotprobe task, including measures of disengagement, bias, and facilitation. Fetal sex did not modify any associations between pCRH rate of rise or cumulative exposure and any of the six child internalizing outcomes tested, including child self-reported depression (bslopeXsex=0.53, 95% CI[-0.58, 1.63], bdeliveryXsex=-0.07, 95% CI[-0.85, 0.71]) and anxiety (bslopeXsex=0.57 95% CI[-1.84, 2.98], bdeliveryXsex=-0.35, 95% CI[-2.03, 1.34]), mother-reported internalizing problems (bslopeXsex=0.11, 95% CI[-0.75, 0.98], bdeliveryXsex=-0.06, 95% CI[-0.67, 0.55]), and three indices of task-based threat sensitivity (disengagement: bslopeXsex=1.14, 95% CI[-8.04, 10.31]), bdeliveryXsex=-5.09, 95% CI[-11.63, 1.45]; bias: bslopeXsex=-3.61, 95% CI[-13.38, 6.15], bdeliveryXsex=-1.43, 95% CI[-5.56, 8.42]; facilitation: bslopeXsex=-2.77, 95% CI[-12.30, 6.75], bdeliveryXsex=-2.03, 95% CI[-8.85, 4.79]). Conclusions Despite theoretical attention to pCRH as a plausible maternal neuroendocrine mechanism for the intergenerational transmission of stress effects to offspring, the lack of associations with child internalizing psychopathology indicators in this large, rigorous study are inconsistent with theories of transmission. Future research exploring other maternal neuroendocrine mechanisms (e.g., prenatal immune functioning) is warranted.

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