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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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| Pre-pregnancy overweight or obesity moderates the association between prenatal maternal depressive symptoms and infant outcomes | |
| Author information | Role |
| Lauren Costello, NYU Grossman School of Medicine, United States | Presenting author |
| Katherine Ziegler, Avera Research Institute, Avera Research Institute, & University of South Dakota, United States | Non-presenting author |
| Lacey McCormack, Avera Research Institute & University of South Dakota, United States | Non-presenting author |
| Anahid Akbaryan, NYU Grossman School of Medicine, United States | Non-presenting author |
| Julianna Collazo Vargas, NYU Grossman School of Medicine, United States | Non-presenting author |
| William S. Harris, University of South Dakota & Fatty Acid Research Institute, United States | Non-presenting author |
| Kristina H. Jackson, Fatty Acid Research Institute & OmegaQuant Analytics, United States | Non-presenting author |
| Maria Barber, Avera Research Institute & University of South Dakota, United States | Non-presenting author |
| Santiago Morales, University of Southern California, United States | Non-presenting author |
| Amy J. Elliott, Avera Research Institute & University of South Dakota, United States | Non-presenting author |
| Christine Hocket, Avera Research Institute & University of South Dakota, United States | Non-presenting author |
| Lauren C. Shuffrey, NYU Grossman School of Medicine, United States | Non-presenting author |
| Abstract | |
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Background: Empirical evidence has demonstrated associations between pre-pregnancy obesity and perinatal maternal depressive symptoms. Omega-3 is an essential fatty acid derived from dietary sources that is critical for fetal brain development. Pre-pregnancy obesity is associated with higher omega-3 intake, but a weaker association between dietary intake and respective maternal and cord blood omega-3 levels. Further, lower intake of omega-3 during pregnancy has been linked to higher depressive symptoms. Yet, prior studies have not examined the interactive effects of pre-pregnancy overweight or obesity (OWOB) and prenatal maternal mental health symptoms on infant cord blood omega-3 levels. Method: Participants included 394 maternal-infant dyads from the NIH Environmental influences on Child Health Outcomes (ECHO) - Safe Passage Study in South Dakota. A pre-pregnancy body mass index > 25 was used to dichotomize participants as OWOB (54%) vs. non-OWOB (46%). Prenatal maternal depressive symptoms were measured using the Edinburgh Postnatal Depression Scale (EPDS) and prenatal maternal anxiety symptoms were measured using the State-Trait Anxiety Inventory (STAI). We implemented linear regression models to examine the interaction term between pre-pregnancy OWOB and prenatal maternal mental health symptoms on cord blood omega-3 levels. Secondary analyses were stratified by pre-pregnancy OWOB status. Results: We observed a significant interaction between pre-pregnancy OWOB and prenatal maternal depressive symptoms with cord blood omega-3 (F (4,379) = 6.21, p < .0001, adj. R2 = 0.05). Stratified models revealed an association between prenatal maternal depressive symptoms with lower cord blood omega-3 levels only among individuals with pre-pregnancy OWOB (β = -0.06, 95% CI = -0.11, -0.02; F (2,208) =4.00, p < .05, adj R2 = 0.03). No associations were observed among non-OWOB participants. Conclusion: Findings suggest maternal-placental transfer of omega-3 may represent one pathway by which maternal metabolic and mental health impacts infant development. |
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| Paper #2 | |
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| Developmental science and nutrition: Pregnancy cortisol associated with infant iron status in diverse US cohort | |
| Author information | Role |
| Dr. Brie M. Reid, Northeastern University, United States | Presenting author |
| Georgia Celestin, Northeastern University, United States | Non-presenting author |
| Caroline Glaser, Northeastern University, United States | Non-presenting author |
| Janet Joseph, Brown University, United States | Non-presenting author |
| Laura Stroud, Brown University, United States | Non-presenting author |
| Abstract | |
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Background: The prenatal period is a crucial window for biopsychosocial vulnerability and developmental opportunity. Changes in biological processes, such as nutrient metabolism and the hypothalamic-pituitary-adrenocortical (HPA) axis during pregnancy, have been linked to children's neurodevelopment (Reid & Georgieff, 2023). However, research on the HPA axis during pregnancy has largely overlooked its impact on offspring development through essential nutrients like iron. Iron, a key micronutrient for early development, is often depleted under stress, leading to both immediate neurodevelopmental issues and an increased risk of lifelong mental health challenges. Iron deficiency (ID) is one of the most common nutrient deficiencies worldwide, affecting 40% of children under five. Infants born to mothers from socioeconomically and socially marginalized populations in the U.S. and globally are particularly vulnerable. While iron supplementation can support neurodevelopment, growing evidence suggests that treatment during pregnancy may not fully mitigate all neurodevelopmental risks associated with ID. The maternal HPA axis, often dysregulated in stress contexts linked to iron deficiency, may disrupt basic iron metabolism and reduce iron availability for fetal development and brain function. Even with supplementation, iron is prioritized to other tissues before the brain, putting infants at risk for neurodevelopmental impacts, even if they appear clinically iron-replete. Thus, fetal and infant iron status may serve as a key intermediary between prenatal stress and later neurodevelopment. Although animal models link the HPA axis to iron status, no human cohort studies have yet examined how maternal HPA axis function during pregnancy affects offspring iron levels. Method: In a study of 218 women followed longitudinally across pregnancy with offspring cord blood, we characterized diurnal salivary cortisol output across pregnancy in a racially-, ethnically-, and socioeconomically diverse cohort (33.7% Hispanic/Latina, 16% Black, 36.3% White; 36.8% with a household income <$20k/year) to examine associations between diurnal cortisol output (AUC from cortisol measured at wake, 30 minutes after wake, and bedtime over 3 days, across three time points in pregnancy) and offspring iron status at birth, indexed as serum ferritin measured in cord blood (mean ferritin =148±65.4 ug/L, Mean GA at birth = 39.4±1.72 weeks, infants were 47.2% female). Result: Longitudinal latent class mixed modeling (controlling for wake time) showed that diurnal cortisol output (ln transformed) became steeper with increasing gestational age (B=.02, p<.001). Higher levels of diurnal cortisol output across pregnancy were associated with lower ferritin in cord blood (ln transformed, B =- .123, p=.033). Conclusion: These preliminary results are the first to demonstrate an association between elevated diurnal cortisol output during pregnancy and offspring iron status. This research underscores the urgent need for rigorous studies to explore how stress and iron metabolism interact to influence brain development. By advancing our understanding of the HPA axis and nutrient interactions, this work could open new avenues for improving maternal and child health globally. It highlights a critical and timely area of study in developmental science, with direct implications for addressing bio-psychosocial vulnerabilities in pregnancy and early in life. |
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| Paper #3 | |
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| Maternal allostatic load in pregnancy is prospectively associated with child adiposity and metabolic function | |
| Author information | Role |
| Lauren E. Gyllenhammer, University of California, Irvine, United States | Presenting author |
| Jerod M Rasmussen, University of California, Irvine, United States | Non-presenting author |
| Karen L Lindsay, University of California, Irvine, United States | Non-presenting author |
| Wen-Pin Chen, University of California, Irvine, United States | Non-presenting author |
| Daniel L. Gillen, University of California, Irvine, United States | Non-presenting author |
| Kristen Boyle, University of Colorado Anschutz Medical Campus & Lifecourse Epidemiology of Adiposity and Diabetes Center, United States | Non-presenting author |
| Claudia Buss, Charité-Universitätsmedizin Berlin & University of California, Irvine, Germany | Non-presenting author |
| Sonja Entringer, Charité-Universitätsmedizin Berlin & University of California, Irvine, Germany | Non-presenting author |
| Pathik D Wadhwa, University of California, Irvine, United States | Non-presenting author |
| Abstract | |
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Background: Empirical evidence suggests that the origins of obesity and metabolic dysfunction can be traced to stress-related exposures in prenatal life. The aim of the present study was to examine the prospective association of a composite, multi-system measure of maternal biological stress in pregnancy -- allostatic load (AL) -- with offspring adiposity and insulin resistance across infancy and early childhood. Method: In N= 55 mother-child dyads, maternal allostatic load was operationalized as a latent variable representing the following components: pre-pregnancy BMI, cortisol, interleukin-6, C-reactive protein, homeostasis model assessment of insulin resistance (HOMA-IR), free fatty acids, and systolic/diastolic blood pressure. Offspring percent total (%FM) and abdominal (%AbFM) fat were quantified with dual-energy X-ray absorptiometry (DXA) at birth (newborn), 6-mo, and ~5 yrs age, and HOMA-IR was quantified at ~5 yrs age. Generalized estimating equation modeling was used to estimate effects of maternal AL on serial (repeated) measures of child adiposity, and linear regression was used to estimate effects on child HOMA-IR. A priori model covariates included maternal race and ethnicity, socioeconomic status, infant feeding practices, child age, and sex. Results: Maternal AL was positively associated with child %FM and %AbFM before as well as after adjustment for key maternal and offspring covariates (%FM: adjusted β=0.38, p=0.0074; %AbFM: adjusted β=0.37, p=0.0013). Maternal AL also was positively associated with child insulin resistance (adjusted β= 0.011, p=0.0324). Conclusion: Our findings suggest that exposure to a higher biological stress milieu during prenatal development predisposes towards elevated early life adiposity and insulin resistance in early childhood, a proximate cause of type 2 diabetes and cardiometabolic disease. Collectively, these results provide evidence that a multi-systems approach to quantify early life exposures is useful in prospectively predicting variation in childhood adiposity and metabolic function. |
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| Paper #4 | |
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| Interactive associations between prenatal metals and childhood socioeconomic status on adolescent allostatic load | |
| Author information | Role |
| Dr. Olivia M. Halabicky, Ph.D., University of Michigan, United States | Presenting author |
| Sara Stein, University of Michigan, United States | Non-presenting author |
| Scott Roberts, University of Michigan, United States | Non-presenting author |
| John Meeker, University of Michigan, United States | Non-presenting author |
| José Luis Figueroa-Oropeza, National Institute of Public Health, Mexico | Non-presenting author |
| Martha Téllez-Rojo, National Institute of Public Health, Mexico | Non-presenting author |
| Karen E. Peterson, University of Michigan, United States | Non-presenting author |
| Abstract | |
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Background: Early-life exposures to metals (i.e., trace and heavy) and psychosocial risk factors, such as poverty, can co-occur. Both exposure types may impact developing biological pathways involved in the stress response. Yet, it is not well-understood how these exposures may interact to shape stress physiology across sensitive developmental periods. Allostatic load (AL) is a construct indicating the cumulative body burden of physiological stress. Lower socioeconomic status (SES), a psychosocial risk factor, has been associated with increasing AL in children and some metals have been associated with components of AL (cortisol). Modeling the interactions of early-life exposures on sensitive developmental periods is important for identifying which exposures synergistically accentuate risk or provide protection. We hypothesized that prenatal trace and heavy metal exposure would associate with adolescent AL and that SES would modify this association, such that lower SES will compound risk and higher SES provide protection. Method: The analytic sample comprised 186 adolescents (mAge 13.4 yrs; 51.61% female) in ELEMENT, a longitudinal cohort study of mother-child dyads followed from pregnancy. Maternal spot urinary (Se, As, Cd, Co, Cu, Mn, Mo, Ni, Sb) and blood (Pb) metals were collected in the 3rd trimester. SES data, measured via the Mexico-specific AMAI tool, was collected at 3 years and categorizes households into 6 ordinal levels based on household ownership, housing conditions, access to services, and head of household education. Due to the small number of participants in some categories, SES was recoded into ‘higher’ and ‘lower’ groups. The AL variable consisted of 14 biomarkers from 4 biological systems (cardiovascular, metabolic, immune, and neuroendocrine). To create the AL index, quartiles were created for each biomarker based on the sample distribution to quantify ‘high=1’ and ‘low=0’ risk and then summed. We utilized Poisson regressions to model each individual log-transformed metal and SES predicting AL adjusting for urine specific gravity, child age and sex, maternal schooling and smoking. Results: Prenatal Sb was significantly associated with increasing percent change in AL (IRR= 1.16 95%CI 1.04,1.28) and Ni was marginally associated (IRR= 1.104 95%CI 0.99,1.23). Those in the highest category of SES showed a marginal decrease percent change in AL compared to other categories (IRR= 0.57 95%CI 0.31,1.02). There were significant interactions between several essential trace metals and SES including Se, Cu, Mo, and Ni, where the effect of metals on change in AL was greatest for those in the lower SES categories (Figure 1). Conclusion: Our results suggest there are interactive effects of metals with psychosocial risk on AL in adolescence. Specifically, results suggest that SES may operate as a key factor moderating the effects of essential trace metals on adolescent stress physiology. More research is needed on identifying sources of exposures to essential trace and heavy metals and examining their interaction with SES as well as protective factors to understand stress physiology development and how it may affect later AL, which could inform critical intervention targets and relevant policy initiatives. |
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Environmental exposures, stress and metabolic pathways during pregnancy: An integrative approach to understand offspring health
Submission Type
Paper Symposium
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| Session Title | Environmental exposures, stress and metabolic pathways during pregnancy: An integrative approach to understand offspring health |