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About this paper symposium
| Panel information |
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| Panel 31. Solicited Content: Integrative Developmental Science |
| Paper #1 | |
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| Maternal Childhood Threat Versus Deprivation: Differential Relations to Neonatal Cortisol Reactivity Levels | |
| Author information | Role |
| Dr. Brie M. Reid, Ph.D., Northeastern University, United States | Presenting author |
| Özlü Aran, Northeastern University, US | Non-presenting author |
| Laura R. Stroud, Brown University, US | Non-presenting author |
| Abstract | |
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Maternal childhood maltreatment has been found to affect intergenerational biopsychosocial development, including offspring cortisol levels (Brand et al., 2010; Khoury et al., 2021). Recent work has proposed that different types of early life adversity—namely, "threat" (such as physical violence and intense family conflict) vs. "deprivation" (such as neglect)—may have different neurobiological and psychopathological outcomes (McLaughlin et al., 2012). It is less clear whether there are also distinct pathways connecting different types of maternal childhood maltreatment to distinct child developmental outcomes, including infant cortisol responses. In this study, we investigated associations between maternal childhood maltreatment and newborn cortisol output in response to a neurobehavioral examination, in a cohort of 413 mother-infant dyads followed longitudinally from mid-pregnancy to the first month postpartum. The sample was racially, ethnically, and socioeconomically diverse (34% Hispanic/Latina, 17% Black, 46% White; 39% annual household income <$20k/year). In pregnancy, women self-reported their maltreatment experiences before age 18 with the Adverse Childhood Experiences Scale (Dube et al., 2003). Using threat/deprivation categories used in other samples, 146 women endorsed experiencing “deprivation” operationalized as physical neglect (35.4% of sample) and 40 women endorsed experiencing “threat” operationalized as severe family conflict (9.7% of sample); 24 participants experienced both (5.8% of sample) (methods following Bublitz & Stroud 2013). Infant cortisol output was assessed in one-month-old newborns (Mage=32 days (SD=3 days)) across four samples during the NICU Network Neurobehavioral Scales exam (NNNS; Lester et al., 2004). Infant cortisol output was calculated using area under the curve with respect to ground (AUCg) to capture the total cortisol output over the course of this reliable lab stressor. We fitted a linear model to predict AUCg with maternal childhood neglect and severe family conflict exposure, controlling for infant sex using full information maximum likelihood estimation. Both types of maternal exposure to childhood maltreatment were statistically significant yet operated in different directions. Maternal exposure to childhood neglect was associated with higher infant cortisol output over the NNNS exam (Std. beta = 0.132, p = 0.025), in line with findings in older infants (Khoury et al., this symposium) but in contrast to null findings in older children (Busso et al., 2020). Maternal exposure to severe family conflict in childhood was associated with lower infant cortisol output (Std. beta = -0.154, p = 0.01), consistent with findings on threat and cortisol reactivity in adolescents (Busso et al., 2017). To our knowledge, this is the youngest population of infants studied to show effects of maternal childhood maltreatment on infant salivary cortisol. This study extends the literature in two ways. First, these findings suggest that maternal childhood maltreatment is affecting infant stress responses as early as the neonatal period. Second, the results imply that distinct developmental mechanisms connect distinct types of maternal adversity (e.g. threat versus deprivation) with the neonatal HPA axis and thus may carry differential implications for risk for psychopathology and other developmental outcomes later in childhood. Future work is needed to identify the gestational and/or early postnatal mechanisms that mediate such distinct responses. |
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| Paper #2 | |
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| Maternal Caregiving Moderates Relations Between Maternal Childhood Maltreatment and Infant Cortisol Regulation | |
| Author information | Role |
| Mrs. Miriam Chasson, M.S.W., Harvard Medical School, Israel | Presenting author |
| Jennifer Khoury, Mount Saint Vincent University, Canada | Non-presenting author |
| Michelle Bosquet Enlow, Boston Children’s Hospital, US | Non-presenting author |
| Ayşe Büşra İplikçi, Harvard Medical School, Turkey | Non-presenting author |
| Karlen Lyons-Ruth, Harvard Medical School, US | Non-presenting author |
| Abstract | |
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Introduction. Children of mothers who have experienced childhood maltreatment are at increased risk for adverse physical and psychological outcomes, including difficulties in self-regulation and elevated rates of mental health issues (Delker et al., 2014; Racine et al., 2018). Alterations in offspring biological stress systems, particularly the hypothalamic-pituitary-adrenal (HPA) axis and limbic brain regions, have been proposed as key mechanisms involved in this intergenerational transmission (Buss et al., 2017; Moog et al., 2018). Caregiving quality also has an important influence on regulation of the infant stress response in both animal and human studies (Del Cerro et al., 2010; Gunnar & Hostinar, 2015). However, fewer studies have assessed whether maternal childhood maltreatment interacts with caregiving quality to influence infant HPA axis activity. Aims. The current study assessed how maternal childhood maltreatment and maternal caregiving interrelate in influencing infant cortisol regulation. Analyses assessed whether 1) maternal history of childhood abuse and/or neglect were related to infant cortisol output during a mild laboratory stressor, and 2) whether any effects of maternal childhood maltreatment on infant cortisol output were additive to or moderated by low nurturing (disorientation, withdrawal) or aversive (negative-intrusive) caregiving behaviors. Methods. 181 mother-infant dyads participated (59% White, 41% Hispanic, Black, Asian, or multi-racial/ethnic), with 57.4% of mothers having experienced one or more forms of childhood maltreatment. The dyads were assessed for maternal caregiving quality and infant salivary cortisol output (area under the curve with respect to ground, AUCg) at 4 months during the Still-Face Paradigm (SFP; Tronick et al., 1978). Severity of both maternal childhood abuse and neglect prior to age 18 were assessed using the Maltreatment and Abuse Chronology of Exposure interview (MACE; Teicher & Parigger, 2015). Caregiving quality was reliably coded using the well-validated Atypical Maternal Behavior Instrument for Assessment and Classification (AMBIANCE; Lyons-Ruth et al., 1999). Results. Higher levels of maternal disorientation in interaction with higher levels of maternal childhood neglect were associated with higher infant cortisol output (β = 0.643, CI [0.153, 1.132]; Figure 1). In contrast, higher levels of maternal negative-intrusive interaction potentiated a negative association of maternal childhood abuse with infant AUCg, such that lower infant AUCg was observed in the joint context of higher maternal childhood abuse and higher negative-intrusive interaction (β = -0.745, CI [-1.402, -0.088]; Figure 2). Conclusion. Study findings suggest that maternal childhood abuse and neglect may be associated with different effects on stress response systems among offspring. Furthermore, maternal childhood maltreatment and quality of postnatal care may need to be considered together to fully understand mechanisms of intergenerational transmission. Finally, interventions to prevent the intergenerational transmission of adversity may need to reach maltreated mothers prenatally and continue into the postnatal period to be most beneficial. |
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| Paper #3 | |
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| Intergenerational transmission of maternal early life stress and sleep on infant neural circuits and behavior | |
| Author information | Role |
| Catherine Demers, Ph.D., University of Colorado Anschutz Medical Campus, United States | Presenting author |
| Melissa Nevarez-Brewster, University of Denver, US | Non-presenting author |
| Merecedes Hoeflick Haase, University of North Carolina, US | Non-presenting author |
| Khalid-Al-Ali, University of North Carolina, US | Non-presenting author |
| Maria Bagonis, University of North Carolina, US | Non-presenting author |
| John Gilmore, University of North Carolina, US | Non-presenting author |
| M. Camille Hoffman, University of Colorado Anschutz Medical Campus, US | Non-presenting author |
| Martin A. Styner, University of North Carolina, US | Non-presenting author |
| Benjamin Hankin, University of Illinois at Urbana-Champaign, US | Non-presenting author |
| Elysia Poggi Davis, University of California, Irvine, US | Non-presenting author |
| Abstract | |
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Background: Adverse childhood experiences (ACEs) are robust predictors of mental health for both the exposed individual and the next generation. However, the pathway through which such intergenerational risk is conferred remains unknown. The current study applies an intergenerational framework to evaluate the association between maternal ACEs and infant white matter microstructure. We then consider maternal sleep during pregnancy as a biological pathway by which maternal ACEs might exert intergenerational consequences. Finally, we examine implications for offspring behavior by assessing whether prenatal maternal sleep and infant neurocircuitry changes predict infant negative emotionality. Methods: In 116 participants, maternal ACEs were assessed using the Adverse Childhood Questionnaire dichotomized into low (0 or 1) and high (2+) groups. Prenatal maternal sleep quality was measured at three gestational time points using the Pittsburgh Sleep Quality Index. White matter was assessed using diffusion tensor imaging (DTI) in infants (41.6–46.0 weeks postconceptional age). Alterations in white matter microstructure of circuits implicated in emotion regulation (e.g., uncinate fasciculus) and sensory processing (inferior longitudinal fasciculus) were measured through fractional anisotropy (FA), a summary metric of the overall directional coherence of fiber tracts. Infant negative emotionality was measured using the Infant Behavior Questionnaire at six months postpartum and laboratory observations. Results: High maternal ACEs correlated with poor sleep during pregnancy (b=.50, p=.001). High ACEs additionally predicted lower neonatal FA in the inferior longitudinal fasciculus compared to the low ACE group (left: F(1,94)=7.78, p<.006; right: F(1,95)=4.29, p<.041). Further, increased prenatal sleep problems were associated with higher FA in the uncinate fasciculus (left: b = 0.20, p = .004; right: b = 0.15, p = .0127). The consequences of maternal ACEs and prenatal sleep on infant neurocircuitry likely also have implications for behavior as both ACEs and prenatal maternal sleep predicted increased infant negative emotionality. Increased uncinate FA predicted greater infant negative emotionality and mediated the link between prenatal sleep quality and negative emotionality (see Figure 1). Conclusion: These findings support the significance of prenatal sleep as an important environmental factor impacting the developing neonatal brain, particularly in circuits integrating visual and socio-emotional processing. Specifically, alterations in white matter development were observed within the uncinate fasciculus, a primary frontolimbic tract implicated in emotion regulation, and the inferior longitudinal fasciculus, a large white matter tract connecting occipital-temporal regions that governs visual-emotional functioning. Such associations may differ by exposure to early life adversity and have enduring consequences for infant negative emotionality. Thus, these data highlight sleep as a biological pathway through which early maternal adversity may shape long-term offspring outcomes. |
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| Paper #4 | |
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| Maternal Childhood Neglect is Linked to Increased Infant Cortisol Output and Stress-Sensitive Brain Volumes | |
| Author information | Role |
| Jennifer Khoury, Ph.D., Mount Saint Vincent University, Canada | Presenting author |
| Miriam Chasson, Harvard Medical School, Israel | Non-presenting author |
| Banu Ahtam, Boston Children’s Hospital, US | Non-presenting author |
| Leland L. Fleming, McLean Hospital, US | Non-presenting author |
| Yangming Ou, Boston Children’s Hospital, US | Non-presenting author |
| Michelle Bosquet Enlow, Boston Children’s Hospital, US | Non-presenting author |
| P. Ellen Grant, Boston Children’s Hospital, US | Non-presenting author |
| Karlen Lyons-Ruth, Harvard Medical School, US | Non-presenting author |
| Abstract | |
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Introduction: Research has linked maternal childhood maltreatment (MCM) to adverse offspring outcomes, including mental health problems (Plant et al., 2018; Racine et al., 2018). While there is extensive literature linking direct experiences of maltreatment to child neurodevelopment (McLaughlin et al., 2019) and dysregulated cortisol (Khoury et al., 2020), limited work has shown associations between MCM and altered infant brain volumes (Khoury et al., 2022; Lyons-Ruth et al., 2023; Moog et al., 2018). In particular, no research has examined infant cortisol as a potential mechanism linking MCM to infant brain outcomes, despite rodent studies finding a causal relation between elevated glucocorticoids and enlarged amygdala volume (Vyas et al., 2004; Vyas et al., 2006). Aims: This study examined whether a) maternal childhood abuse or neglect was associated with infant cortisol output, b) infant cortisol was associated with infant brain volumes in stress-regulatory regions, and c) infant cortisol mediated relations between maternal childhood maltreatment and brain volumes. Study Population: Participants were N=57 mother-infant dyads, stratified for maternal childhood maltreatment. Infants were 51% female and between 4 and 25 months (M = 11.74, SD = 6.12) at the time of the MRI. 57.9% were White/Non-Hispanic, 26.3% were multi-racial/ethnic, 8.8% were Black, 5.3% were Hispanic, and 1.8% were Asian. Methodology: Mothers completed the Maltreatment and Abuse Chronology of Exposure questionnaire (MACE; Teicher & Parigger, 2015), which consists of four abuse subscales and two neglect subscales. At 4 months, dyads participated in the Still-Face Paradigm (SFP) and infant saliva was collected at baseline, +20 and +40 minutes after the SFP. Area under the curve with respect to ground (AUCg) was computed using three cortisol samples to represent infant total cortisol output. Under natural sleep, infants completed a T1-weighted MRI scan between 4 and 25 months. Whole brain, amygdala, hippocampus, thalamus, basal ganglia, and insular cortex volumes were extracted via automated segmentation. Regression and mediation models were conducted, in Mplus Version 8, using FIML and robust standard errors to account for missing data. Results: Maternal childhood neglect, but not maternal abuse, was associated with higher infant AUCg (β = 0.361, CI =0.056, 0.666). Infant AUCg was related to larger volume of the amygdala (β = 0.429, CI = 0.247, 0.610), hippocampus (β = 0.466, CI =0.270, 0.661), thalamus (β = 0.373, CI =0.128, 0.617), and basal ganglia (β = 0.549, CI =0.321, 0.776). Maternal neglect was indirectly associated with larger infant amygdala (β = 0.126, CI = 0.009, 15, .238), hippocampal (β = 0.147, CI = 0.002, 0.269) and thalamic (β = 0.160, CI =0.030, 0.289) volumes, but not basal ganglia volume (β = 0.203, CI = -0.009, 0.416). No indirect effects were observed for maternal childhood abuse. See Figures 1 and 2. Conclusions: Study findings add to the growing literature supporting the intergenerational effects of maternal childhood maltreatment on infant neurodevelopment. Maternal childhood neglect, but not abuse, was associated with higher infant cortisol levels, which, in turn, mediated the indirect association between maternal childhood neglect and larger infant brain volumes in stress-regulatory regions. |
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Maternal Childhood Maltreatment Influences Emerging Infant Neurobiology: Examining Mechanisms of Effect
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Paper Symposium
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| Session Title | Maternal Childhood Maltreatment Influences Emerging Infant Neurobiology: Examining Mechanisms of Effect |